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NEUROSURGERY —
A COMPREHENSIVE
REVIEW
directed by Ian F. Dunn, MD, FAANS
BRIGHAM AND WOMEN’S HOSPITAL
Neurosurgery –
A Comprehensive Review
Provided By:
WARNING:
The copyright proprietor has licensed the picture
contained on this recording for private home use only
and prohibits any other use, copying, reproduction, or
performance in public, in whole or in part (Title 17 USC
Section 501 506).
DESIGNATION
Oakstone Publishing, LLC designates this enduring
material for a maximum of 35.00 AMA PRA Category 1
Credits™. Physicians should claim only the credit
commensurate with the extent of their participation in
the activity.
DISCLOSURE
Oakstone Publishing, LLC has assessed conflict of interest
with its faculty, authors, editors, and any individuals who
were in a position to control the content of this CME activity.
Any identified relevant conflicts of interest were resolved for
fair balance and scientific objectivity of studies utilized in
this activity. Oakstone Publishing’s planners, medical
reviewers, and editorial staff disclose no relevant financial
relationships with commercial interests.
Adam S. Kanter, MD
Chief of Spine Services,
Associate Professor of Neurological
Services,
University of Pittsburgh Medical Center,
Pittsburgh, PA
Reports no commercial interest
Henrikas Vaitkevicius, MD
Instructor in Neurology, Brigham and
Women’s Hospital, Harvard Medical
School, Boston, MA
Reports no commercial interest
LEARNING OBJECTIVES
After viewing this program, participants will be better able to:
• Evaluate the most current neurosurgical techniques available in
order to treat patients with neurosurgical problems.
• Analyze recent literature and data regarding clinical trials relevant to
the practice of neurosurgery.
• Describe best practices in the management of patients requiring
surgery for vascular disorders.
• Explain the latest techniques used in functional neurosurgery.
LEARNING OBJECTIVES
After viewing this program, participants will be better able to:
• Differentiate among the techniques used for spine surgery.
• Discuss the most appropriate procedures for the management of
brain tumors and spinal tumors.
• Identify the most optimal methods for nerve injury and tumors.
• Assess the best neurosurgical treatment plans for pituitary
disorders.
Ischemic and
Hemorrhagic Stroke
Henri Vaitkevicius MD.
Brigham and Women’s Hospital
Harvard Medical School
Date: May 19, 2016
Disclosures
1
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Objectives
Public Health
2
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3
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4
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Ischemic Pneumbra
Revascularization
Outcome
Mortality
Stroke. 2007;38:967-973.
5
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Revascularization
Outcome
Mortality
Stroke. 2007;38:967-973.
TPA
0-3 h
3-4.5 h
6
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TPA
0-3 h
3-4.5 h
Acute Stroke
Time from ED arrival to TPA treatment (min)
180
TPA Response Times
150
120
Door to needle
90
60
30
0
0 30 60 90 120 150 180
Time from stroke onset to ED arrival (min)
Modified from Albers JAMA 2000;283:1147
LSN
7
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Time = brain
Stroke.2006;37:263-266.
4.0
3.5 n = 2775
Adjusted Odds Ratio
3.0
2.5
2.0
1.5
1.0
0.5
Minutes
Lancet 2004;363:768-74
8
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Age > 18
Brain trauma/stroke/surgery > 3 months
Major surgery > 2 weeks
GI hemorrhage > 3 weeks
Plt > 100K; INR < 1.7
SBP <185/110
Bad candidates
9
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NIHSS
1A Wakefulness (3)
1B Month and Age (2)
-1 if intubated
1C commands (2)
10
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NIHSS
2 Gaze (2)
3 Fields (3)
4 Face (3)
5 Motor arms (10s) (4) Drift / hit bed / gravity / none
6 Motor legs (5s) (4) Amputation?
NIHSS
7 Ataxia (2)
8 Sensation (2)
9 Language (3)
10 Dysarthria (2)
Intubated (UN)
11 Extinction (2)
11
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NIHSS
Big picture
POINT,
0-3 Mild
CHANCE
Telestroke
Received TPA in < 90min
Arrives to our hospital < 180min
No change in exam
12
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Telestroke
Received TPA in < 90min
Arrives at BWH < 180min
Stroke. 2004;35:2418-2424
13
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Stroke. 2004;35:2418-2424
Stroke. 2004;35:2418-2424
14
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JAMA 1999;282:2003
15
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Revascularization
Stroke. 2009;40:2761-2768
Revascularization
Stroke. 2009;40:2761-2768
16
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Better device …
MR CLEAN
500 patients
195/233 mechanical interventions
17
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Recanalization
MR RESCUE
SYNTHESIS
IMS III
MR CLEAN
Neurology 2009;73:1066–1072
Recanalization
MR RESCUE
SYNTHESIS
IMS III
MR CLEAN
Neurology 2009;73:1066–1072
18
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Recanalization
MR RESCUE
SYNTHESIS
IMS III
MR CLEAN
Neurology 2009;73:1066–1072
Recanalization
MR RESCUE
SYNTHESIS
IMS III
MR CLEAN
Neurology 2009;73:1066–1072
19
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Recanalization
MR RESCUE
SYNTHESIS
IMS III
MR CLEAN
Neurology 2009;73:1066–1072
Recanalization
MR RESCUE
ESCAPE
Extend-IA
SYNTHESIS Swift Prime
REVASCAT
IMS III
MR CLEAN
Neurology 2009;73:1066–1072
20
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Successful trials
ESCAPE
(n = 316)
EXTEND-IA
(n = 70)
SWIFT-PRIME
(n = 196)
REVASCAT
(n = 193)
Successful trials
ESCAPE
(n = 316)
3 4
2
EXTEND-IA
(n = 70)
1
SWIFT-PRIME
(n = 196) 1
REVASCAT 2
(n = 193)
21
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Primary Outcomes
Complications
EXTEND-IA 6/0% 20 / 9 %
SWIFT PRIME 3/0% 12 /9 %
REVASCAT 1.9 / 1.9% 16 / 18 %
22
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Unique
23
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Outcome at 60 days
Few definitions …
ASPECTS SCORE
-normal = 10
TICI score
-normal = 3 Score
0
Definition
No flow
1 < 20%, flow limiting
2a 20-50%, 2/3 territory
2b 50-99%, delayed
3 Normal
24
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Bottom line:
Speed
- Decision to TPA
- Decision to transfer
- Decision to intervene
- IA team mobilization
Follow up
- Multidisciplinary stroke service
- Feedback to the teams
25
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26
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Significance of TOAST
Vascular imaging
US
-Velocity and direction
MRI/MRA
-Velocity and direction
TCDs
-Velocity and particulates
27
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28
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29
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30
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Treatment
Antiplatelets Cholesterol
-Aspirin/dipyridamole -LDL < 100 (70)
-Clopidogrel Blood pressure
Full anticoagulation -7-14 days
CEA/CAS -ACE/HCTZ
-140/90 (130/80)
Intracranial bypass
Glucose
Intracranial stenting
Smoking, BMI, Physical activity,
Hormones
31
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BMJ 2002;324:71–86
Stroke. 2008;39:1358-1363
• NIHSS < 3
• Clopidogrel 90 d.
+ASA 21 d.
• Aspirin 90 d.
32
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Lipids (SPARCL)
Blood pressure
Autoregulation (24h)
Decrease by 10/5
Goal 120/80
? 140/90
Diuretics
ACEI
Stroke. 2003;34:2741-2748
33
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Glycemic control
-What is HgA1C target ?
Smoking
-Must stop
Alcohol
-1-2 drinks per day
Physical activity
-sweat or rise in HR
-1-3x per week
Carotid disease
Strokes
Trial Pts. Yr. Stenosis
Med CEA CAS
Symptomatic
34
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35
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Timing: 2 weeks
High surgical risk = CAS
-High riding bifurcation (C3)
-History of radiation
-Significant CAD
Intervention threshold
>70% on US = >50% on angio
Case (continued)
36
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Risk scales
Cardioembolic
37
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Incidence of stroke
Rivaroxaban
Dabigatran
Edoxaban
Apixaban
Warfarin
Placebo
ASA
Trial
150 mg
110 mg
AFASAK 4.2 2
BAATAF 3.0 0.4
SPAF 7.0 2.3
CAFA 3.8 2.6
VA 4.3 0.9
EAFT 12.3 3.9
Lancet. 1989 Jan 28;1(8631):175-9
RE-LY 1.7 1.5 1.1 Am Heart J. 1992 Dec;124(6):1567-73
J Am Coll Cardiol. 1991 Aug;18(2):349-55
Rocket AF 2.2 1.7
Am J Cardiol. 1996 Jan 25;77(3):38A-44A
ARISTOTLE 1.6 1.3 Circulation. 1995 Oct 15;92(8):2178-82
J Med. 2010 Nov 4;363(19):1877
AVERROES 3.7 1.6 N Engl J Med. 2011 Sep 8;365(10):883-91
N Engl J Med 2013;369:2093-104
ENGAGE AF 1.5 1.2 Stroke. 2012 Dec;43(12):3291-7
38
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Anticoagulation
Warfarin
Direct thrombin inhibitors
Factor Xa inhibitors
Efficacy (stroke)
Dabigatran Apixaban
Rivaroxaban Edoxaban
39
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Risk (bleeding)
Rivaroxaban
Dabigatran
Edoxaban
Apixaban
Warfarin
ASA
Trial
150 mg
110 mg
Comparisons to Warfarin
Bleeding risks
-13 trials
-102,707 patients
NOACs Warfarin
Fatality 7.6% 11%
Major bleeding 0.16 per 100 pt-years 0.32 per 100 pt-years
Fatal bleeding RR 0.53
Mortality RR 0.91
Blood. 2012;119(13):3016
Ann Intern Med 2015; 163:382
Mayo Clin Proc 2014; 89:896
J Thromb Haemost 2015; 13:2012
JAMDA 16 (2015) 1103.e1e1103.e19.
40
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Case (continued)
Epidemiology
Stroke. 2015;46:2032-2060
41
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How to treat?
Some data
Expert opinions / guidelines
(AHA and ASA)
Stroke. 2015;46:2032-2060
Stroke. 2007;38:1641-1644
42
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Stroke. 2007;38:1641-1644
Stroke. 2008;39:2304-2309
43
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Stroke. 2008;39:2304-2309
1,038 US patients
Mortality rates
44
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Stroke. 2004;35:1130-1134
45
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Stroke. 2004;35:1130-1134
Hematoma Expansion
46
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Hematoma Expansion
Coagulopathy Summary
Anticoagulant Agent Dose
INR >6 → 50 IU/kg
4 factor PCC
INR >4 → 35 IU/kg
(heparin) INR < 4 → 25 IU/kg
47
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Reversing Warfarin
Vitamin K (2 hours)
FFP
Reversing Warfarin
Vitamin K (2 hours)
FFP
NOVO VII
-399 patients
-4 hours
-7% MI or CVA
48
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Reversing Warfarin
Vitamin K (2 hours)
FFP
NOVO VII
-399 patients
-4 hours
-7% MI or CVA
3/4 factor PCC
(II,IX,X) /(II,IX,X,VII)
Platelets
CHANT trial
-NXY-059
Creutzfeldt et al
-368 patients
-Identical ICH volume, MRS, Mortality
Ducruet et al
-66 patients
-No difference in ICH
Neurology® 2009;72:1397–1402
J Stroke Cerebrovasc Dis. 2009;18:221-228
Neurol Res. 2010;32:706-710
Neurocrit Care (2012) 16:82–87
BMC Neurology 2010, 10:19
49
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Platelets
CHANT trial
-NXY-059
Creutzfeldt et al
-368 patients
-Identical ICH volume, MRS, Mortality
Ducruet et al
-66 patients
-No difference in ICH
Naidech et al
-44 patients
- <12h to receive platelets
-activity 472±50 -> 561±92 ARU Neurology® 2009;72:1397–1402
J Stroke Cerebrovasc Dis. 2009;18:221-228
Neurol Res. 2010;32:706-710
Neurocrit Care (2012) 16:82–87
BMC Neurology 2010, 10:19
Platelets
CHANT trial
-NXY-059
Creutzfeldt et al
-368 patients
-Identical ICH volume, MRS, Mortality
Ducruet et al
-66 patients
-No difference in ICH
Naidech et al
-44 patients
- <12h to receive platelets
-activity 472±50 -> 561±92 ARU Neurology® 2009;72:1397–1402
J Stroke Cerebrovasc Dis. 2009;18:221-228
PATCH trial Neurol Res. 2010;32:706-710
-Netherlands Neurocrit Care (2012) 16:82–87
-190 patients BMC Neurology 2010, 10:19
-6 hours
50
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INTERACT 2 (6 hours)
2839 patient
SBP <140 vs. <180
Primary outcome:
MRS > 2: OR 0.87; p = 0.06
Secondary outcome:
Improved MRS: OR 0.87; p = 0.04
Small bleeds (<20cc)
Slow to reach target SBP
INTERACT 2 (6 hours)
2839 patient
SBP <140 vs. <180
Primary outcome:
MRS > 2: OR 0.87; p = 0.06
Secondary outcome:
Improved MRS: OR 0.87; p = 0.04
Small bleeds (<20cc)
Slow to reach target SBP
51
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ATACH (6 hours)
60 patients IPH Expansion
SBP 110-139
SBP 140-169
SBP 170-199
ATACH 2 (3 hours)
1280 Patients (stopped at 1000 this fall)
SBP <140 v.s. <180
MRS > 3
Arch Neurol. 2010;67(5):570-576
Steroids
93 patients
Stopped early
52
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Steroids
93 patients
Stopped early
Seizure Prophylaxis
CHANT Trial
295 Patients
1.7% seizures
53
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Seizure Prophylaxis
CHANT Trial
295 Patients
1.7% seizures
Seizure Prophylaxis
54
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Ventricular TPA
Ventricular TPA
55
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1,033 patients
Early < 24h
Mortality
Functional outcome
1,033 patients
Early < 24h
Mortality
Functional outcome
26% surgery
56
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21% surgery
57
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15 trials
3,366 patients
Hemicraniectomy
9 studies
226 cases
GCS < 8 and ICH > 60cc
May be safe
Improves mortality and functional outcome
58
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59
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60
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Thank You
61
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Treatment of Aneurysms
Endovascular Microsurgery
(coiling, stent- (clipping, clip
assisted coiling, reconstruction,
flow diversion, bypass)
WEB)
72
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Microsurgical Treatment
• (%,,%*#
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Surgical Techniques
81
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Brain Relaxation
• mannitol
• drainage of CSF
• from Sylvian fissure or basal cistern
• ventriculostomy or lumbar drain
• positioning
• avoid impairing venous return
• head elevation
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Hydrocephalus
• Acute hydrocephalus in 20-27%, chronic in 14-23%
• More frequent in poor grade patients
• Ventriculostomy for patients with Hunt and Hess grade 3 or higher
• 50-80% of patients improve neurologically after EVD placement
• Caveat: sudden and large release of CSF may precipitate
rebleeding
• Complications: hemorrhage, infection
1 30 3
2 44 5
3 98 30
4 19 42
5 19 26
Milhorat, Neurosurgery, 1987
98
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• management of hypertension:
• Recommend nicardipine
• Nitroglycerin and other vasodilators are
contraindicated in patients with cerebral edema
(Cottrell et al., JNS, 1980)
• Caveat: only use for extreme hypertension to
avoid reducing cerebral perfusion prior to
placement of EVD
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• .(8(4)..%*
108
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)*3.2'--/()/*.*.+.(
•
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• ((++**#%+,(/08
• +.*+)%9C+*0.+((0.%(/
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•
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109
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#)&*2
110
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Moyamoya Disease
Disclosure Statement
111
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Moyamoya Disease
112
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Proliferative angiopathy
MMD control Takagi, Y., K. Kikuta, et al. (2007).
Neurol Med Chir (Tokyo) 47(1): 1-4.
Moyamoya Disease
• Initially identified in Japan, 1950’s
• Felt to be a disease affecting Asian population
• Prevalence: 6-10/100,000 (Asia)
• Bimodal onset:
1st decade, 3rd-4th decades
113
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Stages of Moyamoya
Moyamoya Stage 6
4 5 “bottleneck sign”
114
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Moyamoya Disease
Treatments
• Medical (not effective)
– Antiplatelet agents, coumadin, steroids, vasodilators, mannitol
– Ca++ antagonists
• Surgical
– Cervical sympathectomy (not effective)
– Extracranial-intracranial grafts
• Revascularization: rationale
– improves cerebral perfusion
→ prevent ischemia
– reduces stress on collateral vessels
→ prevent hemorrhage
115
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Moyamoya Disease
Treatments
Revascularization techniques (↑ CBF)
– Direct
• STA-MCA anastomosis
– Indirect
• Encephalo-duro-arterio-synangiosis (EDAS)
• Encephalo-myo-synangiosis (EMS)
• Encephalo-duro-arterio-myo-synangiosis (EDAMS)
• Omental transposition
• Burr holes
Alaska
1 Moyamoya State Distribution
(47 states, District of Columbia, Puerto Rico, and U.S. Virgin Islands)
4 Minnesota Massachusetts 4
3
New
Oregon
Idaho
4 Wisconsin York
12 South Dakota
Michigan
25 Rhode Island 3
3 1 19 Connecticut 7
Wyoming 25 Pennsylvania
2 Nebraska
Iowa
19 New Jersey 11
Delaware
4 Indiana Ohio
Nevada 3 Illinois
18 1 Maryland 10
Utah
31 10 West
Virginia
13 Colorado Virginia District of Columbia 1
California 6 Kansas Missouri Kentucky 20
23 12 12 8 North
292 10 12 Carolina
Tennessee
Oklahoma 4 South
Arkansas Carolina
Arizona
New Mexico 8
5 4 Alabama
Guam 2 5
Georgia
15 9
Texas 16 Mississippi
1 35 Louisiana
Florida
29
Hawaii
51
2
866 patients
Puerto Rico
U.S. Virgin
Islands 1
1389 revascularization procedures
116
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Saudi 1 Korea 1
Arabia
1
Qatar
1 1
Vietnam
1
Australia
South 2
Argentina
Africa
1
12/04 started collecting blood, CSF, STA and M4 MCA *annualized from 4 mos
117
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Pediatrics, 350,
25%
Adults
Pediatrics
Adults, 1039,
75%
200
Number of patients
201
150
184
100 123
119
115
50
101
23
0
9
9
0-
-1
-2
-3
-4
-5
-6
10
20
30
40
50
60
Age group
118
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Male, 251,
29%
Asian
Black
Caucasian
Hispanic
Other
Female,
615, 71%
Black, 40, 5%
Caucasian,
456, 53%
Male
Female
Moyamoya Angiopathy
1. Moyamoya Disease – isolated disorder ( 755 pts )
- Neurofibromatosis - Leptospirosis
- Sickle cell disease - Connective tissue defect
- Post-irradiation - Marfan’s syndrome
- TB - Tuberous sclerosis
- Pyogenic meningitis - Pseudoxanthoma elesticum
- Fanconi’s anemia - Apert’s syndrome
- Glycogen storage disease - Coarctation of the aorta
- Down syndrome - Hemocystinuria
- Sneddon’s syndrome - Vasculitis
- Alagille syndrome - Primordial dwarfism
- Graves disease
119
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Primordial Dwarfism
(MOPD II) and
Moyamoya Syndrome
Pericentrin gene mutation
120
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19 years later finally had MRA and then angio: MMD; bypassed 2010
2003 2010 2010
121
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Superficial
temporal artery
Temporalis
muscle
Line of incision
Superficial
temporal artery
122
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Reflected
temporalis muscle
Dural incision
Superficial
temporal artery
Superficial
Reflected dura and temporal artery
temporalis muscle
Temporal lobe
M4 branch of middle
cerebral artery
Frontal lobe
123
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M4 branch of middle
cerebral artery
Completed STA-MCA
anastomosis
124
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Moyamoya Disease
Intraoperative Management
• Normocapnia (end tidal CO2 35mm Hg)
• MAP: nl to high range
• Mild hypothermia (33°C)
• Monitor EEG (don’t monitor SEPs, MEPs)
• Thiopental/Propofol for occlusion
• Quantitative CBF (Transonic Flowmeter)
(M4, STA) pre- & post-bypass
125
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126
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127
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1.0
0.5
† P<0.0001
* P=0.0056
0.0
STA MCA STA MCA
128
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129
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7
Frequency(# of surgeries)
0
9 16 23 30 37 44 51 58 65 72 79 86
Minutes
30
15
10
0
9 16 23 30 37 44 51 58 65 72 79 86
Minutes
130
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Moyamoya Disease
Post-operative F/U
• Post-op MR scan
• 6 month, 3 yr, 10 yr, 20 yr F/U
Clinical
Angiography, MR
CBF studies
– MR perfusion, Xenon CT, SPECT (+/- Diamox)
Neuropsychological testing
131
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STA size
Lt ICA Rt ICA
132
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Indirect revascularization
133
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134
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ADC Ax Diff
135
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Pre-Operative Lt ICA
Rt ICA Rt ICA
136
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1993
Xenon CT
Pre-operative Post-operative
(4 mos)
2012
Pre-Diamox
2014
Post-Diamox
137
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* 22.2
25
* p<0.0001
20
Normal MCA flow:
10-20 ml/min
ml/min
15
10
4.4
5
0
Pre-anastomosis Post-anastomosis
Total MCA Flow Before & After Bypass Surgery
75
R2=0.11
P<0.0001
Proximal MCA
flow (ml/min)
50
25
0
0 1 2 3
STA diameter (mm)
138
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Nadia Khan, Robert Dodd, Michael P. Marks, Teresa Bell-Stephens, Joli Vavao,
Gary K. Steinberg
• 5 patients
• Angioplasty: 1
• Angioplasty/stenting: 4
vertebrobasilar
139
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140
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141
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Natural History
Washington Univ (St. Louis)
Medical Treatment
5-year risk of recurrent
ipsilateral stroke of 65%
after the initial symptom
(17% after revascularization)
Stanford series:
5-yr risk of having a stroke (any Hallemeier CL, et al Stroke 2006
distribution) after revascularization
surgery was 5.5%
Clinical outcome
(modified Rankin scale)
P<0.0001 0: no symptoms
2 1: symptoms, no disability
2: slight disability
MRS
1 3: moderate disability
4: mod-severe disability
5: severe disability
0
Pre MRS Post MRS 6: dead
90% of the patients had a mRS 0-2 (mean follow-up: 4.1 years)
142
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15.3%
% of patients with
post-OP TIA within 1st
TIA 1st month month
% of patients TIA free
84.7% within 1st month
8.8%
% of patients with
post-op TIA after 1st
year
TIA after 1st year % of patients TIA free
after 1st year
91.2%
Moyamoya Disease
Long Term Outcome 1991-2007
143
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Mortality:
3 patients (2 bleeds, 1 multiple strokes- MELAS)
0.7% of procedures; 1.1% of patients
Major Morbidity/Mortality:
5.7% per patient; 3.6% per procedure
Pre-op
144
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Rt hemiparesis,
expressive
aphasia
5 mos later,
complete
recovery
● Patency of grafts
● Perioperative complications
stroke, hemorrhage, transient neurologic deficits
145
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• ? Hyperperfusion ? Hypoperfusion
Treat by ↓ or ↑ BP?
146
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35 * 28.8
30
25
20
ml/min
20
15
10
5
0
Control TND
* P=0.036
147
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2 days post-op:
Mild expressive aphasia.
Resolved over next 11 days
Delayed TND
71.1 27.1
Pre-op 83.8 28.7
148
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Local Hypoperfusion
149
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Conclusions
Transient Neurologic Deficits following STA-MCA bypass for
MMD is due to local relative hypoperfusion (flows initially higher)
Treatment: Maintain ↑ BP
AJNR (2015)
• Retrospective, case-control
• Included all adult cases 2005-2011
• Separated into 2 groups
Index cases – large territorial strokes (>15 ml volume)
• 6 patients with 9 operated hemispheres
• Mean Age (Range): 44 (27-67) yrs; 4 female
• Mean DWI Lesion size (SD): 95±55 ml
Controls – no post-op DWI lesions, no post-op symptoms (even
transient)
• 25 patients with 36 operated hemispheres
• Mean Age (Range): 38 (18-59) yrs; 18 female
150
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Pre-operative acute
infarcts (DWI +)
– Patients with poor
outcomes 4/6 (66%)
(another pt subacute infarct:
DWI+/ADC-) (5/6; 83%)
P=0.0004
151
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Pre-diamox (Baseline)
Post-ACZ
New post-op large infarct not always in same hemisphere as pre-op infarct
152
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Right Left
After EDAS
After additional
STA-MCA grafts
153
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46 yo female,
Moyamoya Disease
Bilateral
Hemisphere TIAs
Right Hemisphere
Left EC-MCA TIAs
Vein Graft
154
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1996
1996
155
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10 Days Post-Op
156
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Omental-Cerebral
Transposition
157
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158
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Omental-Cerebral Transposition
21 for Moyamoya disease
1991-2000: 9
2011-2016: 12, laparoscopic harvesting
New Rt hemisphere
motor TIAs & Lt sided
choreiform movements
Rt hemisphere
Rt gastroepiploic artery
injection
159
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Immediate post-op
6 mos Post-Op: Improved CBF and reserve
6 mos post-op
Gastroduodenal artery
Gastroduodenal artery
Gastroduodenal artery
160
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Lt ECA
Rt ECA
161
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3 ½ yrs post op
162
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57 patients
Conclusions
Repeat revascularization is safe and effective in preventing future
ischemic events in patients with failed prior revascularization
procedures
163
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Moyamoya Genetics
Moyamoya Genetics
164
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Moyamoya Genetics
• RNF213 (MIM 613768), gene at 17q25, encodes a ring finger
protein, is a MMD susceptibility gene
(polymorphism c.1457G>A in 95% familial & 75% sporadic MMD,
in 1% Japanese population)
165
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166
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•Appropriate matched control data from 1000 Genomes, but now have
in-house control data
167
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Genetics of Moyamoya
Certain gene mutations may predispose to MMD
According to the testing, my sister and I have the mutated RNF213 gene. My mom
does not. Miya does not have the mutated gene. SUCH wonderful news! We were
told this "drastically reduces her chance of developing Moyamoya", although the
genetics of MM is not completely clear, so it is not with certainty, of course.
168
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Lumen
Lumen
Unresolved Questions
Is Indirect bypass as effective/safe as Direct bypass for adults?
169
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Arias et al 2015 J Stroke USA, 15 pts Direct bypass provides more consistent &
Cerebrovas Dis Missouri complete cerebral revascularization
Kazumata 2014 JNS 121: 432- Japan, 2032 direct, 4171 Direct bypass: higher extent of angiographic
et al 440 Sapporo indirect revascularization. Comparable postop stroke
Systematic review risk in direct and indirect group (5.4% v
5.5%) Recurrent stroke risk is higher in
indirect bypass group
Abla et al 2013 NeuroSx 73: USA, 39 indirect Direct bypass: Significantly greater
430-439 BNI 29 direct improvement in symptoms. Both direct &
indirect equally effective in preventing stroke
Bang et al 2012 NeuroSx 70: Korea, 65 pts, 75 bypasses Direct bypass: greater extent of angiographic
625-633 Seoul revascularization at 6 months
Czabanka 2011 Cerebrovasc Germany 24 patients STA-MCA/EMS: superior to single EMS in
et al Dis 32: 361- Berlin 24 direct, 24 restoring CVRC. Better angiographic
369 indirect collateralization
Kawaguchi 2000 JNS 93: 397- Japan, 22 patients Direct bypass significantly reduce the risk of
et al 401 Nara 11 cons, 6 direct recurrent hemorrhage. Direct bypass
bypass, 5 EDAS significantly reduce the risk of recurrent
ischemic events
Houkin et 2000 Acta Neurochir Japan, 85 pts Direct bypass useful in over 90% of adult
al 142: 269-276 Sapporo 22 sides in adult cases
cases assessed Poorer rate of neo-angiogenesis by indirect
bypass in adults
170
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No antiplatelet agents
171
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Unresolved Questions
172
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Unresolved Questions
Are CBF studies useful in deciding when to revascularize an
asymptomatic hemisphere?
173
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Symptomatic patients
usually with prior MR watershed infarcts
usually with poor angiographic filling
& impaired hemodynamic reserve
Patients with recent stroke (DWI +), esp with cerebrovascular steal
174
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175
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176
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177
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Stanford University
178
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Disclosure Statement
179
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180
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Imagine my
surprise!
181
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182
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Asymptomatic Trials
Symptomatic Trials
183
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• Asymptomatic (ACAS)
– >60 % - surgery
• Symptomatic (NASCET, ECST, VASST)
– >50 % - surgery (NASCET final data)
– <50 % - best medical management
184
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185
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• Carotid dissection
• High cervical carotid aneurysms
• Extreme high exposures
• Medically unstable cases
• Fibromuscular dysplasia
• Second side cases with CN palsy
• Patient choice by CMS criteria
186
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187
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LICA
RICA post-stent
188
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189
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R.J.
61y.o. female
TIA’s
STENT
190
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191
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CREST 2
• Carotid revascularization for primary prevention of stroke
(CREST-2) is two independent multicenter, randomized
controlled trials of carotid revascularization and intensive
medical management versus medical management alone in
patients with asymptomatic high-grade carotid stenosis.
One trial will randomize patients in a 1:1 ratio to
endarterectomy versus no endarterectomy and another will
randomize patients in a 1:1 ratio to carotid stenting with
embolic protection versus no stenting. Medical
management will be uniform for all randomized treatment
groups and will be centrally directed.
192
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193
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Preoperative
• Ultrasound ☹
• MRA
• CTA
• Catheter Angiography
194
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CTA Left
Carotid
(Asymptomatic)
195
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CVA patient
Duplex 70-
79%
NASCET 13%
Wisp of ulcer
196
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197
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Scanlan
“Loftus”
carotid
set
Loftus Shunt
Clamps for
ICA
198
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199
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200
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Pre-Op R CEA
Post-Op
201
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Pre-Op R CEA
Post-Op
202
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203
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1+coumadin =
3
4
204
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No Go
Slow Go
E-Z Go
Low Go
205
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• Spine anatomy
• ECA branches on lateral A/G
• Color change in vessel
• Hard or soft digital feel
• Doppler auscultation of ICA
C2 Body
Top of
Marker ICA
branch on plaque
ECA
206
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Sternomastoid Muscle
207
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208
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Hypoglossal
Sternomastoid Nerve
Artery
209
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210
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211
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212
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213
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214
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215
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Anticoagulants in CEA
• Stop plavix/ticlid/coumadin 1 week
preop
• Continue ASA throughout
surgery/restart plavix later
• Heparin common - no problem
• Check ACT in heparinized patients
– Most often surprisingly low
• Heparin bolus 5000U or weight-based
216
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217
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Arteriotomy
• EEG notified
• Clamps applied (ICA, ECA, CCA)
• Arteriotomy with #11 blade and
Pott’s scissors
• Shunt if required
218
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Is a Shunt Needed?
• Awake: deficit • TCD: MCAV 0-15%
within 60 seconds pre-clamp
• Stump: CSP • EEG:
<50mmHg – unilateral attenuation 8-
• CPP: stump-IJP 15hz fast
<18mmHg – 2x increase 1hz delta
• rCBF: 18- • SSEP:
20ml/100g/min – 50% amplitude decrease
– 5% latency increase in
CCT (Kearse 20%)
219
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Right
Left
220
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Insertion of Shunt
• Total exposure above plaque
• Shunt in CCA first
• Evacuation of shunt
• Gentle ICA insertion
– Backbleeding
– Shunt open to distend ICA lumen
• Doppler of shunt
• Monitoring must return
221
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222
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• Functional
– recovery of EEG or SSEP
• Vascular
– Return of MCAV by TCD
– Ocular plethysmography
– Return of rCBF
– Doppler of shunt
223
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Plaque removal
• Plane developed at lateral edge
• Feathered edge in ICA
• Sharp dissection in CCA
• Marsupialized in ECA/ opened
PRN
• Tacking sutures in ICA 40% of
cases
• Careful attention to retained
fragments
224
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225
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226
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227
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228
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229
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230
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231
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232
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233
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Backbleeding Check
234
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Stubborn External
235
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Declamping Sequence
(Flushing step)
• External carotid
• Common carotid
• WAIT 10 seconds
• Internal carotid
236
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237
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238
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Rip-Stop x 3
239
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240
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Wound Closure
241
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Complications in CEA
242
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• Medical complications
• Cranial nerve injuries
• Stroke
• Wound problems, residual stenosis,
and vessel integrity
• Medical complications
• Cranial nerve injuries
• Stroke
• Wound problems, residual stenosis,
and vessel integrity
243
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Complications - Medical
Complications - Medical
244
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Dysautoregulated
Hypertensive
Patient on
Heparin Postop
• Medical complications
• Cranial nerve injuries
• Stroke
• Wound problems, residual stenosis,
and vessel integrity
245
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Fixed
Retractors,
the old way
246
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N.B. - Fish-
hooks, the
new way
Lone Star +
247
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• Medical complications
• Cranial nerve injuries
• Stroke
• Wound problems, residual stenosis,
and vessel integrity
248
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Complications - Stroke
Monitoring
changes 43
minutes in
while sewing
up the lateral
wall of the
repair….
249
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1 2
Red =
Baselin
3
e
Complications - Stroke
250
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Assure Patency
• Medical complications
• Cranial nerve injuries
• Stroke
• Wound problems, residual stenosis,
and vessel integrity
251
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JD0229406
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Ian F. Dunn, MD
Associate Professor of Neurosurgery
Department of Neurosurgery
Brigham and Women’s Hospital
Boston, MA
Disclosure Statement
258
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Outline
• Epidemiology
• Definition of TBI
• Assessment
• Concussion
TBI
• Who gets it?
TBI:
– Young men, age 15 – 20s (MVAs) and those older than
65 (falls)
– 1.7million TBIs; >75% mild; about 10% severe
– 52,000 deaths/year
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Epidemiology
• The numbers:
• 2 million people per year (1% of all injuries presenting to ER)
• 250,000 hospitalized per year
• 75,000 die
• 50% of trauma deaths
• Who’s at risk:
• men
• 2 peaks: 15-30yo, >75yo. Mortality also highest in these groups.
• Mechanism of injury:
• MVA: most common cause of TBI (about 50%)
• Firearms: account for largest proportion of deaths from TBI nationwide
• Age:
• Young and elderly: falls are most common cause of TBI
Contact:
Epidural hematoma*
Subdural hematoma*
Skull fracture
Coup contusion
Inertial injuries:
Translational acceleration:
Contracoup contusion
Intracerebral hematoma
Subdural hematoma
Rotational acceleration (+ angular)
Concussion
Diffuse Axonal Injury (DAI)*
Subarachnoid hemorrhage (SAH)*
Intraventricular hemorrhage (IVH)
Gliding contusion
Tissue tear hemorrhage
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Epidural/subdural
Epidural
hematomas
Subdural
Orrison, W. Neuroimaging
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• Injury:
• Differences in density between gray/white matter
• Not just axonal!
• MICROscopic findings are pathognomonic
• CT may dramatically underestimate injury—look for small hemorrhagic foci. MRI may
show more due to edema collection.
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Contralateral EDH
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Management Goals
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• Primary injury
– The direct injury
Observe/Admit Discharge
•Abnormal CT •If doesn’t meet any of admission criteria
•Penetrating injury •“Return to ED STAT if....” be thorough
•LOC/declining MS •F/U in clinic
•EtOH/drugs
•Skull fx
•Amnesia
•Distracting injuries
•Social factors
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Intubation
Fluid Resuscitation: LR/NS
Ventilation (PaCO2 = 35-40mmHg)
O2
Sedation +/- pharmacologic paralysis
Head CT
ICU
SAH Surgical lesion OR Monitor ICP
Treat IC HTN
Nimodipine: 60mg
q4hrs x 21 days
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IC HTN? RepeatHead CT
YES
Last resort
Hyperventilate to
PCO2 =30-35mmHg
High dose barbiturates (pentobarbital):
Loading: 10mg/kg over 30 min
IC HTN? 5mg/kg every hour x 3 doses
YES Maintenance: 1mg/kg/hr
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Intracranial Compartment
1,500 ml
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ICP-Volume Relationship
ICP
Imminent
Compensated state herniation
Volume
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1. Cingulate herniation
2. Uncal herniation
4. Tonsilar herniation
5. Extracranial
Narayan, R. Neurotrauma.
Contralateral hemiplegia
CP CP
Obtundation coma
PCA PCA
RULE OF THUMB:
mass lesion is ipsilateral to dilated
pupil
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• Formal guidelines:
– Monitor ICP if GCS 3-8 with abnormal CT OR
– Normal CT and age > 40, posturing, SBP < 90
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Ventriculostomy Anatomy
nasion
10cm
tragus
1-2cm
3cm
Coronal suture
Midline
Mid-pupillary line
Inter-tragal line
ICP control
Elevate head of bed to 30 degrees; head in neutral position;
avoid cervical venous compression
If refractory, consider:
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ICP, continued
• ICP control improves outcome
• Highly useful predictor of worsening
underlying surgical pathology
• Can’t measure CPP without measuring ICP
• Management principles:
– Avoid O2 sat < 90, PaO2<60
– Avoid SBP < 90mmHg
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Hyperosmolar therapy
• Mannitol: 0.25g/kg – 1g/kg bolus
– “buying time” maneuver vs repeated
administration in the ICU for ICP control
– Rebound effect
Hypothermia?
• There are currently no data to convincingly
suggest that hypothermia improves outcome
in TBI
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Sedatives
• Propofol: sedative/hypnotic, rapid
onset/offset of action
– Propofol infusion syndrome: >5mg/kg/h
– Lipemia, metabolic acidosis, etc
Pressure autoregulation
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PARAMETER RATE
Global CBF ~50 ml/100g/min
CBF (Gray)) ~80 ml/100g/min
CBF (White) ~20 ml/100g/min
CMR oxygen ~3.5 ml/100g/min
CMR glucose ~4.5 ml/100g/min
CBF/CMR oxygen ~15 ml/100g/min
ICP 5-12 mm Hg
Venous PO2 >35 mm Hg
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Hyperventilation:
Intense cerebral vasoconstriction: ischemia
Profound chronic hyperventilation (PCO2 <30
mmHg) contraindicated.
Maintain PCO2 > 35 mmHg
• Control Agitation
• Control Ventilation
• Decrease Cerebral Metabolic Rate (CMRO2) and
reduces ischemic threshold
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Maintain euvolemia
Normal saline
Monitor balance, weight
Avoid:
Dehydration
Free water
Glucose
Hyponatremia
Use of Mannitol
Mannitol is effective for control of increased ICP in
severe CHI.
Limited data suggests intermittent doses may be
more effective than a continuous infusion
Maintain serum osmol < 320.
AVOID DEHYDRATION
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Use of Mannitol
One of the few interventions (1 of 6) that achieved the level of use as a
guideline.
There are two Class I studies and one class II studies that support the use of
Mannitol in ICP control.
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Mechanism
2) Osmotic effect, delayed for 15-30 minutes
until gradients are established between
plasma and cells.
Reflection coefficient 0.9
(Defined as the ability of BBB to exclude a
compound)
Mechanism
3) Free radical scavenging,
4) Removal of fluid even from brain tissue in which
the blood-brain barrier is damaged,
5) Reduced volume and rigidity of red blood cells,
6) Compensatory cerebral vasoconstriction in
response to increased cerebral blood flow
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Mechanism: Precautions
Large continuous levels can cause “opening”
of BBB, where Mannitol and other small
molecules can pass into the interstitium.
Mannitol should be administered as repeated
boluses
Serum osmolality > 320 and hypovolemia
should be avoided, monitor renal function.
• Hypertonic saline
– Recent interest shows that hypertonic saline is
equivalent to mannitol
– Reflection index of 1.0 in intact BBB.
– Goal to maintain Na+ 145-155 meq
– Non osmotic effects.
– No randomized trials
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– Hemodynamic effects
– 1) Improve and maintain MAP
– Plasma volume expansion
– Centrally mediated increases in CO
– 2) Improving CO, brings improvement in CPP and
cerebral oxygen delivery
– ICP effects
– 1) Ability to dehydrate edematous tissue via
transendothelial gradient
– 2) No osmotic diuretic properties that decrease
circulating volume
– 3) Improvement in restoration of transcellular
cerebral osmolytes by improving cellular
cotransporter systems
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• Osmolar effects
– Dehydration of brain tissue by creating
transendothelial osmotic gradient
Immunomodulating effects
1)Decrease leukocyte adherence and migration and
reduce certain prostaglandins and other inflammatory
mediators
2)Increase levels of cortisol and ACTH
3)Reduce neutrophil marginalization and trafficking,
possibly protecting against bacterial infection
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– Neurochemical effects
– In face of lower Na levels, cell wall polarity is lost
with accumulation of extra cellular excitatory
amino acid, i.e., glutamate.
– HTS reverses these changes and restores cell wall
membrane transport systems.
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• Barbituate coma
– Coupled reduction of CBF/CMRO2 with decrease
ICP
– Significant hemodynamic compromise
– Randomized Controlled Trials show no
improvement in outcome
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Principles:
• Reverse question mark incision for hemispheric access--muscle
taken anteriorly
Incision
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Sinus proximity
Craniotomy/craniectomy
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Post-craniectomy
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Post-craniectomy
Durotomy
Hematoma evacuation
Duraplasty/Gelatin membrane
Bifrontal
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11-15 93% 7%
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Concussion
Defintion
https://myaans.aans.org/en/sitecore/content/MyAANS/Resources/Concussion%20and%20Sports.aspx
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• Recreation sports
– Alpine Skiing
– Cycling
– Equestrian
• Organized Sports
– Football
– Boxing
– Ice hockey
– Rugby
– Soccer
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Identify
immediate Prevent
neurologic catastrophic
emergency Prevent
outcome from
permanent
second impact
brain injury
syndrome
from repeat
concussions
Spectrum of Concussion
• 80-90% of concussions resolve spontaneously
over 3-7 days.
• 10% of concussions have prolonged
symptoms.
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Disclaimer:
“managing the athlete with mild
traumatic brain injury may be more
of an art than a science”
Role of Imaging
• By definition standard imaging should be
normal (ie. concussion is a physiologic
process).
• Functional imaging studies may play a role in
the future, but not of current practical value.
• If symptoms persist or show focality, CT or
MRI should be obtained to be sure that no
brain injury exists.
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Brain Rest
• Key component of management
– Cognitive rest during symptomatic period
• Medications should be avoided, except to
treat headache
• Consider referral to specialist for prolonged
symptoms.
– Brown NJ, Mannix RC, O'Brien MJ, Gostine D, Collins MW, Meehan WP 3rd. Effect of cognitive
activity level on duration of post-concussion symptoms. Pediatrics. 2014 Feb;133(2)
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Sports concussion
Graded Exertion Protocol
Exercise Goal
1. No activity –complete rest 1. recovery
2. Light aerobic exercise 2. Increase HR
3. Sport-specific training 3. Add movement
4. Non-contact training drills (may 4. Exercise +
start resistance training) coordination +
5. Full contact practice after thinking
medical clearance
6. Return to play
Are there
any indications YES
Initial medical assessment
for neurosurgical
intervention?
NO
Sports Stepwise
concussion return to
specialist sport
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Prevention
• CDC estimates:
– 475,000 pediatric TBI occur annually
– 2% of Americans have sequelae of TBI.
• Poorly funded
• Underappreciated
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Hit Counts
• Does limiting hits to the head prevent long
term problems?
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Pitch Counts
105
VS
106
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Practice
• Soccer
– Limit headers, especially for younger players
108
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Rules Changes
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Resources
• State laws and education programs
• CDC
– Head’s Up Program
• Online training module
• ACE “acute concussion evaluation” worksheets
• Consensus Conferences
– Publications and forms are widely available.
– “Consensus statement on concussion in sport: the 4th
International Conference on Concussion in Sport held
in Zurich, November 2012”
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Pediatric Concussions
• No athlete should be allowed to return
to play while still experiencing signs or
symptoms of a concussion.
• Clinical judgment and graded return to
play criteria are important, but
increasingly science is adding objective
criteria for return to play.
• Concussion prevention must come on
several levels, including science,
education, legislation, and advocacy and
commitment by the medical profession.
315
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Rocco A. Armonda, MD
MedStar-Washington Hospital Center &
Georgetown University Hospital
Washington, DC
Disclosure Statement
• Reports no commercial interest
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Mechanism of Trauma
• Blunt
– MVA
• Penetrating
• Blast
– Blunt/Blast Wave/Fragments
• Iatrogenic
– Transphenoidal
– Skull Base Tumor Surgery
Management Algorithm
• Decompress The Brain!
• Stop The Bleeding!
• Restore Anatomic Continuity
• Water-tight Dural Closure
• Frontal Sinus Management and Skull Base
Foundation Re-establish/Orbital Bando to
allow further reconstruction
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T-Bar Incision
Subtemporal
Decompression
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Management Algorithms
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Case Presentation
• 25 yo Soldier Struck by roadside explosive
on the passenger side.
• Initially following commands, left side
paretic, intubated for transport
• Right Pupil Traumatic Dilation, with
Suspected Globe Injury
• Open Depressed Contaminated Scalp
Wound
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Roadside Explosive:
Passenger Side Beneath Kevlar
334
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335
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3D Reconstructions
Entry Wound
336
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337
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Maxillofacial Fixation
338
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Orbit-Reconstruction
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• Identified/Quantifie
s Best Tailored
Surgical Approach
• Based on the
Nasofrontal
Outflow Tract
Plastics and Reconstructive Surgery,
Vol122:1850,2008
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Clinical History
• L hemispheric decompressive craniectomy
• Frontal craniotomy- anterior skull base
mesh/pericranial flap
• Failed cranioplasty X2
– Bone
– PMMA
• CSF leak/ fungal meningitis
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Operative Plan
• Frontal craniotomy/ central bandeau
• Mesh removal
• Obliterate sinuses
• Bone graft reconstruction-anterior cranial
fossa
• Interpose vascularized tissue
– Free flap
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Mesh
Pericranial flap
350
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Nasofrontal ducts
Pedicle
351
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Anterior
ALT flap
Posterior
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Extent of Bifrontal
Decompression
354
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BLAST OVERPRESSURE:
EXPANSILE SKULL BASE
FRACTURE
356
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GSW: Management
• Cerebral Angiogram Assess
Neurovascular Structures
– ICAs, ACA, Venous Sinus
• Combined Neurosurgery/OMFS
Reconstruction
• Frontal Sinus Exeneration
• Skull Base/Orbital Bando Reconstruction
• Dural Repair/Re-inforcement
• OMFS Mandible/Palate Repair
Delayed Complications
• Pneumocephalus
– CSF Leak
• Endoscopic Repair
– Delayed CSF Infection
– Low-Pressure Hydrocephalus
• Skull Base Sealed Second Intracranial
Procedure
• Delayed Bifrontal Cranioplasty 6 months
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ENTRY ENTRY
Pre-Cavernous Aneurysm
Projecting into Sphenoid
Sinus: Massive Epistaxis
360
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Neck Remnant:
Reangio/Retreat 4-6 weeks
361
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Initial CT:GCS4
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5 minutes Later
Post-ICA Occlusion:
Hemicraniectomy
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Conclusions
• Assess Risk for Neurovascular Injury
– DSA may be more Diagnostic than CTA/MRA
• Decompress the CNS
– Brainstem
– Optic Nerve (Anterior Skull Base; Early)
– Facial Nerve (Lateral Skull Base)
• Restore Anatomic Continuity/Separation
with Dural Repair
– Avoids Delayed CSF Leak, Infection,
Encephalocele
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Case Presentation
• 58 yo male assaulted at a nightclub several
hours earlier found confused agitated.
• No Medical History, Unknown Meds
• Intubated, Not Following Commands
• Left Hemiparasis, Pupils Asymmetric R>L,
Localizes with Right UE withdraws R LE
• HTN 170/90
• Stat CT Obtained
368
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Unknown?
• 1. Coagulation Status and Meds?
• 2. How long since injury?
• 3. Associated Injuries (ie Cspine,
Abdomen,Occult Vascular Injury)?
• 4. What is his best expected outcome?
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Post-Op Coronal CT
Acute SDH
• 1. In General ASDH worse prognosis than EDH
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Spectrum of Injury
• Chronic SDH(After 20 days)
– Older, Brain Atrophy, Anticoagulation, Minor
Trauma, Slow Onset of Symptoms…
• Subacute SDH (4-20 days)
– Usually within a 2-3 week history of minor
trauma, anticoagulation (ASA vs Anticoagulation).
• ASDH (3 days of Trauma)
– Severe Trauma, Significant Underlying Brain Injury
Possible, Diffuse Brain Swelling may be delayed.
8-58/100K >65
3.4/100K<65
7.24/100K US Pop
79.6/100K in VA pop
10.35/100k Japan
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Chronic SDH
• Risk Factors
– Age >65
– Hx of Fall
– Anticoagulation
• Warfarin 42.5 X Higher
• Those Anticoagulated
– 750K Acute Coronary Syndromes
– 2.4 Million with Atrial Fibrillation (Increased SDH
Risk)
cSDH: Etiology
• Trauma?
• Neovascular Membranes + More Friable
Subdural Bridging Veins
• Increased Brain Atrophy + Anticoagulation Use
• Alcohol Contributes: Brain Atrophy and
Coagulopathy, Estrogen More Ectatic Blood
Vessels
375
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Recurrence Rate/Treatments
• Up to 33.3%
• Neovascular Membrance
– High Vascular Endothelia Growth Factor (VEGF)
• Use of ACE-Inhibitors to decrease Recurrence
– Lower VEGF (Vascular Endothelia Growth Factor)
– 5% Recurrence vs 18%
– NNT 8 to see a difference
(Weigel et al NS 61:788-793, 2007)
Non-Operative Treatments
• Tranexamic Acid (TRACS Canadian Trial)
– Background Japanese Study: 21pts 100%
resolution at 28-137 days CT every 3 wks.
Kageyama et al JNS 2013: 119; 332-7
– 750 of TXA q day.
– 130 pts
– Radiologic Resolution by 20 weeks
– Excluded pts with Thromboembolic Risks
– If surgery outer-membrane is sampled
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Non-operative Treatment:
Chronic Subdural Hematomas
• Atorvastatin (ATOCH Trial)
• 25% Recurrence with 11-13.5% Mortality
• Background Study: 23 pts Chronic SDH with
Atorvastatin (J of Neurol Sci. 2014; 336 (1-2):
237-42.
• Mechanism Statin Inhibits: VEGF,
Pseudoenvelope Abnomal Blood Vessels,
Inflammatory Reaction Modulator
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Outcomes Treatment:
World NS Review (86:399-418,Feb 2016)
Drain Lower Recurrence (8 vs 22%; 8 NNT)
evidence quality Moderate
Drain Place Frontal (5% vs 20%) Parietal
Recurrence (evidence quality Low)
Small Difference Twist vs Burr Hole
Evidence quality low
HOB Small Difference (30.6% vs 25% overall
complications flat vs upright)
Outcomes Treatment:
World NS Review (86:399-418,Feb 2016)
• Irrigate with Thrombin Solution vs Saline
– 5.6 % vs 25.6% Recurrence (NNT=5)
– Moderate Grade GRADE Evidence
• ACE-Inhibition vs Placebo Post-Drainage (No
Recurrence either group)
• Twist Drill No Irrigation 48 vs 96 hrs Closed
Drain
– 2.9% vs 23.3% General Complications (NNT=5)
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When to Restart
Anticoagulation/Antiplatelets?
• Small Study 12 pts
• After 2 wks for Mechanical Heart Valves
– Neurocritical Care 2013; Aug:19(1):90-94.
– Average 14 days Anticoagulation Held; 9 days
postoperative
– Length of Stay 19 days
– No Deaths nor Thromboembolic Events
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When to Restart
Anticoagulation/Antiplatelets? JNS
124; 750-759, 2016
• 479 Pts Chronic SDH 2007-2012 231 prior AT of which 120
Restart AT with Postop Hemorrhage:
– 14.8 % Major Hemorrhage
– 23% Minor Hemorrhage
– 1.67% Thromboembolism
Conclusions
• Those Restart AT lower ICH risk than those not
restart AT (26.9% vs 2.2.%)
• Prior AT more likely to have Postop Recurrence (19 vs
10%)
• Recommendation Restart AT no earlier than 3 days
due to increased risk of Thromboembolic
Complications
• > 75% Restart by 2 weeks, median 52 days.
JNS 124:750-759, 2016
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Results: 2009-2013
106 managed under the protocol/inclusion
•Favorable Outcome 66.1% unfavorable 33.9%
– (p=0.0001)
– Mortality 25.4%, 70.1 deaths with Penetrating TBI
•Factor Poor outcome:
– ISS>35.62, SDH at first CT, Absent Cisterns, Non-
reactive pupils at ER arrival.
•ICU Good vs Bad: 13+/-2.7 vs 27 +/-5 (.0002)
•Hospital Stay: 26.6 +/- 6, 48 +/- 13(p=.0001)
385
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Initial CT
386
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Post-OP CT
T-Bar Incision
387
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Bifrontal Craniectomy:
Without Falx Release
388
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389
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390
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Day#4
391
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392
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Post-Decompression
393
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Post-Decompression
Immediate Imaging
394
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395
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396
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397
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Immediate Post-OP
398
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Delayed Post-OP
PRE/POST
399
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400
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Post-Op Drain
401
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402
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403
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404
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405
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406
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0700 am
407
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Post OP Day#1
408
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409
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Immediate Post-Op:
Pneumocephalus
Pneumocephalus
410
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Post-OP Day 5
411
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Conclusions
• Acute SDH
– Underlying Brain Injury Dictates Outcome
– Early Decompression when Significant Edema
– Correct Coagulopathy
• Chronic SDH
– Rising Number expected
– Use of Drains, Frontal Placed
– Consider Tranexamic Acid (TXA), ACE-Inhibition,
Statin Adjucts drecrease Recurrence
– Consider Thrombin Irrigation decrease Recurrence
412
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Decompressive Craniectomy
for TBI
Jamie S. Ullman, MD, FACS
Associate Professor
Department of Neurosurgery
Hofstra Northwell School of Medicine
New York
Disclosure Statement
Reports no commercial interest
413
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Severe TBI
414
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Severe TBI
Primary Injury
Moment of Impact
Irreversible
Secondary Injury
Anytime thereafter
Especially first 24 hours
Potentially preventable
Severe TBI
Secondary Injury:
ISCHEMIA
State of oxygen deprivation
Anaerobic metabolism
Lactate production
increased in acidity (decreased pH)
Ischemic cascade
415
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Biochemical Changes in
Ischemia
Ischemic Cascade
1. Influx calcium ions
Decreases transmembrane potentials
increases voltage-dependent Ca++ channels
Decreases transmembrane Na+ gradient
Slows outward transport of Ca++
2. Ca++ release from ER due to decrease in ATP
3. Increase EAA release (glutamate)
increased activation of NMDA receptor-gated
Ca++ channels
EAA- excitatory amino acids NMDA- N-methyl-D-Aspartate
Biochemical Changes in
Ischemia
Increased intracellular calcium
Decreases mitochondrial phosphorylation,
decreases ATP production
Increases membrane permeability/breakdown
Phospholipases
Free fatty acids
Arachadonic acid (cyclooxygenase)
Prostaglandins– edema
Lipooxygenase– edema
Thromboxanes– vasoconstriction, platelet aggregation
Cell Death
Apoptosis
416
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ICP Monitoring
Allows for early warning for significant
intracranial developments
Flourishing contusions
Increased brain swelling
Complications after surgery
Enables Cerebral Perfusion Pressure
(CPP) measurement
ICP >40 mm Hg associated with poor
outcome
417
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Severe TBI
Decompressive Craniectomy:
The Past
418
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DC in Head Injury
Controversial
Biphasic use
1960’s-1970’s
1990’s-2000’s+
Era of Doubt:
April 2011+
419
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DC Indications
Trauma
Ischemic stroke
High-grade subarachnoid hemorrhage
Venous sinus thrombosis
Malignant brain tumors
Other neurological conditions
eg. encephalitis
Purpose of DC
Cranial Vault
Closed Cavity
Three components
Brain
Blood
CSF
420
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Monro-Kellie Doctrine
From
Rosner
Purpose of DC
Cranial Vault
Three Components
Brain
Evacuate mass lesion, lobar resection, infarct resection
Blood
Vasoconstriction
CSF
Ventricular drainage
Closed Cavity
Take off bone and dura– protect brainstem
421
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Monro-Kellie Doctrine
Decompressive Craniectomy
Benefits
Has reduced infarct volume in experimental
models
Increase brain perfusion
Preserve/improve penumbral areas
Reduce need for intensive therapy
Pressors in trauma
Hyperosmolar therapy
422
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Decompressive Craniectomy
Types:
Suboccipital
Unilateral frontotemporoparietal
“Hemicraniectomy” 12-15+ cm in AP direction
+/- Anterior temporal lobar resection
Bifrontal
Subtemporal/ temporal
Cushing (1905): 6x8 cm opening
Stellate dural opening
DC in TBI
Kjellberg and Prieto (JNS 34:488-493, 1971)
73 cases (trauma, tumor, hemorrhage,
encephalopathy, pseudotumor) Mass
General
Last resort therapy
Bifrontal craniectomy
Ligated sinus/cut falx
18% (13) survival
12 TBI, 7 bilat fixed pupil
5 excellent, 4 some deficit, self care
423
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DC in TBI
Ransohoff J, et al. Hemicraniectomy in
the management of acute subdural
hematoma JNS 34:70-76, 1971
35 pts with acute SDH, posturing, uni-or bilateral
pupillary dilation
Post op management with normothermia, no
steroids
Mortality: 60% (vs.>90), 50% independent outcome
among survivors (7 of 14)
9 underwent cranioplasty
DC in TBI
424
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DC “Career-ending” trials:
Cooper PR, et al., “Hemicraniectomy in the
treatment of acute subdural hematoma: a
reappraisal.” Surg Neurol 5:25-8, 1976.
Additional 50 patients treated since 1971 report
10% total survival rate
4% functional survival rate
“Operation…should be restricted to those
patients…obtunded but without demonstrable
brain stem dysfunction, only to deteriorate
subsequently because of increased hemispheric
edema and/or subdural clot.”
DC “Career-ending” trials
Cooper PR, et al., “Enhancement of
experimental cerebral edema after
decompressive craniectomy: implications in
the management of severe head injuries.”
Neurosurgery 4:296-300, 1979.
Cryogenic lesions in 10 dogs (5 immediate DC, 5
control), injected with Evans blue dye, sacrificed
after 8 hours. All but one hyperventilated <30
DC: better ICP, higher volume of Evans Blue Staining
around lesion (1.96 vs. 0.27 ml)
IVF: Ringers Lactate
425
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DC “Career-ending” trials
Cooper, et al, 1979.
Conclusion: “Massive bony decompression
effectively controls intracranial pressure, but at the
cost of enhanced edema production. The long-
term complications of this are still unknown.”
? Cryogenic lesion, hypotonic fluids
DC “Career-ending” trials
Cooper, et al, 1979: Comment
426
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“Traditional” Management of
Severe Head Injury
Hyperventilation to PCO2 = 25 mm Hg
Mannitol
Especially in suspected ICH or herniation
Prophylacitc or routine
Maintain osm 300-320
Fluid restriction
Decadron
Strict BP control
HOB 30 degrees
DC in Head Injury
Literature
Paucity of randomized, control trials
Anecdotal evidence in recent literature
indicates that DC has a role in treating
patients with elevated ICP.
427
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DC in Stroke
Malignant Cerebral Edema
15% of MCA infarctions
80% mortality
DC in Stroke
Three European Randomized Trials
DECIMAL
DESTINY
HAMLET
428
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DC in Stroke
DECIMAL (Stroke 38:2506-17, 2007)
Early DEcompressive Craniectomy in
Malignant Middle Cerebral Artery Infarction
France
Age 18-55
38 pts, stopped by Data Monitoring Committee
58% absolute reduction in mortality with DC
Favorable outcome (6 mo and 1 yr f/u)
Surgery: 25% and 50%
Medical: 5.6% and 22.2%
DC in Stroke
DESTINY
DEcompressive Surgery for the Treatment
of Malignant INfarction of the Middle
Cerebral ArterY (Stroke 38:2518-25, 2008)
Germany
32 pts
Mortality: Surgery (12%) Medical (53%)
Functional Outcome (6 mo and 1 yr f/u)
Surgery: 47%
Medical: 27%
429
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DC in Stroke
HAMLET
Hemicraniectomy After Middle Cerebral
Artery Infarction with Life-threatening
Edema Trial (Lancet 8: 326-33, 2009)
Netherlands 64 pts
Med vs Surg: Mortality 59 vs 22%
32 surgery stratified <48 hrs, 48-96 hrs (11 pts)
Mortality: 19% vs 27
Age <51(N=38) vs 51-60(N=26)
Mortality: 38% vs 6%
DC and Stroke
Pooled Data Analysis of three RCT (Lancet
Neurol 6:215-22, 2007)
Favorable outcome (mRS </=4)
75% (surg) vs. 24%; ARR 51%
mRS </=3
43% vs. 21%; ARR 23%
Survival
78% vs. 29%; ARR 50%
Conclusions: DC within 48 hours reduces
mortality and increases functional outcome
(incl those w/aphasia; younger did better)
430
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DC
Stroke vs. TBI
Continuum
Ischemic Stroke
Univariate: infarct/penumbra
TBI
multivariate- heterogeneous
Hemorrhage, structural damage,
ischemia, penumbra
Can results be more definitive?
DC Present times
Changes in ICU
management Jennett, et al, JNNSPSY, 40:
CT 291-8, 1977
ICP/CPP
Maintain physiological
parameters
431
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DC in TBI
Questions/Criticisms
Are we accomplishing anything with DC?
Are we reducing mortality at the expense of
increasing incidence of severe disability
and vegetative state?
Severe TBI
There is no magic
bullet to completely
reverse the effects of
the primary and
secondary effects of
severe TBI in humans.
432
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Severe TBI
Current Armamentarium
ICP monitoring
Oxygen monitoring
Induced normothermia
Hyperosmolar therapy
Barbiturates
Hypothermia
Decompressive Craniectomy
DC in TBI
Guerra, et al (JNS 90:187-96, 1999)
Resurrected DC
57 pts. prospective series, 1977+
Unilateral DC with focality, bifrontal for diffuse
Not section falx and left bone over sinus
Result: 19% mortality; 58% achieved “social
rehabilitation”
Advocated advancing DC early to 2nd tier therapy
Not indicated with irreversible herniation
433
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DC in TBI
Polin et al (NS 41:84-94, 1997)
35 pts with historical control (92) (TCDB)
Bifrontal, diffuse injury without mass lesion
Poor outcome if ICP>40 and no operation
within 48 hours
6.7% favorable vs 60% without above
Medical management (control)
3.8x risk of unfavorable outcome vs DC
Pediatric: 44% favorable vs 29% adult
DC for TBI
Aarabi et al (JNS 104:469-479, 2006)
50 pts retrospective
DC for malignant swelling
49 pts unilateral
Mortality 28%
51% favorable GOS among survivors
434
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DC for TBI
Taylor, et al. A randomized trial of very early
decompressive craniectomy in children with traumatic
brain injury and sustained intracranial hypertension.
Child’s Nerv Syst 17:154-162, 2001
27 children, medical vs. early DC, diffuse
Surgery: bitemporal craniectomy, no durotomy
Good outcome 54% vs. 14% (med)
ICP reduction greater in DC
9 mm vs. 3.7 mm HG (P = 0.57)
DC in Head Injury
DC and Therapeutic Intensity
Weiner et al. (Neurosurg 66:111-19, 2010)
10 severe TBI pts with BTPO2 monitoring
DC performed mean 2.8 days post admission
ICP immediately reduced (by ave. 7.8mm Hg)
Therapeutic intensity Level reduction correlated
with ICP reduction
Cumulative ischemic burden as measured by
BTPO2 was reduced.
30-day mortality: 10% (40% were GCS 3 on
admit)
435
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DC in Head Injury
DC and Functional Outcome
Williams, et al. (J. Trauma 66:1570-76, 2009)
171 pt underwent DC for severe head injury
Single institution: Memphis
1-6 yr follow-up
32% mortality, 117 survived with 95% f/u
Good Outcome (GOSE): 82% survivors (56% of
all)
Younger age (26 vs. 43 yrs)
Greater change in ICP (pre DC ICP not diff in survivors
vs. non-survivors)
DC in Head Injury
Whitmore, et al (JNS 116:1106-13, 2012)
Is aggressive treatment of TBI [including DC]
cost-effective
436
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DC in Head Injury
Cochrane Review, 2006
Literature analysis
Due to lack of randomized, controlled trials, DC
cannot be recommended for routine use in
adults.
Taylor trial lends to conclusion that DC would be
beneficial in pediatric patients with refractory
ICP
DC in Head Injury
Important questions:
At what stage do we perform DC?
At initial operation for mass lesion when swelling
is encountered or anticipated?
As third tier therapy when all other medical
management has failed?
As second-tier therapy when initial measures
(sedation, ventricular drainage, mannitol) not
effective?
Would you rather use hypothermia/barbiturates
first?
437
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DC in TBI
DECRA (NEJM 364:1493-502,2011)
Early Decompressive Craniectomy in
Patients With Severe Traumatic Brain
Injury
155 pts; DC 73 pts, Standard care 82 pts
Pts with diffuse injury
DECRA
Craniectomy (Bifrontal, Standard Care
falx /SSS intact)
ICP >20 x 15 min in 1 hr First Tier: Sedation
Sedation EVD
EVD Normocapnea
Normocapnia Mannitol
mannitol Second Tier:
Hypothermia
Barbiturates
DC permitted >72 hours
(15 pts total, 4 <72 hrs)
438
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DC in TBI
DECRA
DC group higher incidence of fixed pupils
(27% vs 12%)
DC (35 hrs mean to rand.) Standard Care
DC in TBI
DECRA
Conclusions:
DC decreased ICP and ICU LOS in patients with
ICP refractory to first tier therapy.
439
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DC in TBI
DECRA
Critique:
1. ICP threshold for DC (a big procedure)
may be too low- often easy to meet
CPP requirements at this level)
2. More bilaterally fixed pupils in DC
group
DECRA (cont)
3. Corrected analysis of pupils showed no
difference in outcome not carried over to
final conclusions
4. Falx not cut, but ICP still significantly
lower
5. When non-DECRA pts in Australia
analyzed:
Mortality: 18.4%
Favorable outcome: 54% (Honeybul JNT 27:1225-
32, 2010)
440
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DC in TBI
DECRA
Take home message:
Bifrontal craniectomy in pts with diffuse injury
likely has no advantage over continued
medical management early in the post-
injury course.
Ho et al,
Continued improvements in pts upon 18 month
f/u (Crit Care Med 39:2495-2500, 2011)
CONCLUSIONS:
Our study underscores the importance of continued
international prospective data collection for assessing types
of surgical interventions in addition to DC and their timing in
patients who suffer from severe TBI. Additionally, in
geographical areas with limited access to advanced
medical treatment for severe TBI, DC is of benefit when
performed < 5hr after injury in younger patients with
GCS>5.
441
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DC in TBI
RESCUEicp
Randomised Evaluation of Surgery with
Craniectomy for Uncontrollable Elevation
of Intracranial Pressure
May 2014
43+ Centers
400/400 patients
Analysis is Pending
DC in TBI
RESCUEicp
Inclusion Criteria:
Age 10-65
Abnormal CT
ICP monitoring
ICP > 25 for <1-12 hours
Immediate OR allowed for mass lesion but no
DC
442
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DC in TBI
RESCUE-ASDH
New study: beginning recruitment of patients
and sites.
“Randomization” of pts to craniotomy vs
craniectomy at initial procedure for acute
SDH
All cranis need to be at least 11 cm
N=990
http://rescueasdh.org/
443
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Third Tier
8. Burst Suppression (Barbs, Propofol)
Other therapies:
Moderate Hypothermia
444
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Decompressive Craniectomy
Technical points:
Hemispheric:
Large: Good temporal,
12-15+, 1 cm from
midline
Bifrontal:
Midline bone island vs.
none
Cut falx vs. not
Decompressive Craniectomy
Technical points:
Open dura
Yoon, et al. “Ventricular pressure monitoring
during bilateral decompression with dural
expansion.” (JNS 91:953-9, 1999)
20 pts with brain swelling
50% decrease in ICP after craniectomy
Additional 34.5% decrease in ICP after durotomy
Hinge craniotomy as alternative
445
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Decompressive Craniectomy
Complications
*Subdural hygromas
High shearing forces, diffuse injury more prone
*Hydrocephalus
Mental status deterioration
Focal deficits
“Syndrome of the Trephined”
Headaches, seizures, irritability, psychiatric
symptoms
DC Trauma
446
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DC Trauma
DC Trauma
447
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DC Trauma
DC Trauma
448
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DC Trauma
Hinge Craniotomy
Schmidt, et al
Use of hinge craniotomy for cerebral decompression.
Technical note.
J Neurosurg. 2007 Sep;107(3):678-82.
Kenning et al.
A comparison of hinge craniotomy and decompressive
craniectomy for the treatment of malignant
intracranial hypertension : early clinical and
radiographic analysis
Neurosurg Focus 26 (6): E6 2009
449
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Hinge Craniotomy(plasty)
DC Trauma
450
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The Repair
The Repair
451
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The Repair
The Repair
452
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The Repair
The Repair
453
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The Repair
454
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DC
Evidence vs Experience
Marrying RCT results and clinical experience
Negative/Equivocal RCT
1. Denial
2. Anger
3. Bargaining
4. Depression
5. Acceptance/Resignation
DC “Career-ending” trials
Cooper, et al, 1979 (2011): Comment
455
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Disclosure
Reports no commercial interest
456
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-Management Options
Evaluation and
Assessment
History
Clinical Exam
Radiographic Tests
457
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Evaluation and
Assessment
Clinical factors
– Age
Younger- occult ligamentous injury?
Older- pre-existing stenosis?
– Co-morbidities
Rheumatoid arthritis
Ankylosing spondylitis increases risk of Chance fracture
– Mechanism of Injury
High speed vs. low speed
Flexion, rotation, axial loading?
Seatbelt?
C-Spine Clearance
Clinical Exam
– Awake, co-operative patient
No Pain, Normal Neurologic
– Cleared, no need for further work up
Pain to palpation or abnormal neurologic
– Imaging required
– Options include Xray and CT
458
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C-Spine Clearance
Clinical Exam
– Awake, non co-operative patient
Cannot rely on exam
Wait for reliable exam
Imaging
C-Spine Clearance
Clinical Exam
– Obtunded/comatose patient
Cannot rely on exam
Imaging required
459
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Evaluation and
Assessment
Radiographic Tests
– Xray
With flexion/extension (dynamic)
Good for awake patients with low index of suspicion for
injury
– CT
Test of Choice for bony evaluation
Completely negative CT can be used to clear C spine
– MRI
Test of Choice for spinal cord compression evaluation
Recommended if CT positive or if CT negative but
neurologic deficit present.
Evaluation and
Assessment
Radiographic Tests
– Xray
Must visualize from Foramen Magnum to C7-
T1 disc space
Flexion/Extension views to assess ligamentous
stability
1-2 mm of physiologic subluxation
460
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Evaluation and
Assessment
Posterior Spinal Line
Facet line
Evaluation and
Assessment
Radiographic Tests
– CT
Will identify majority of injuries
Highly sensitive for fractures
Debate regarding using CT to “clear” spine in
all trauma patients
461
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Evaluation and
Assessment
Radiographic Tests
– MRI
Increasing use to screen and clear spines,
especially in obtunded patients
High sensitivity to soft tissue/ligamentous
injury
Evaluation and
Assessment
Spinal Injury
Awake,
Awake, co-operative Obtunded/comatose
non co-operative
Abnormal exam
Imaging with CT MRI if abnormal CT
High suspicion
Imaging with CT
Negative CT, with abnormal exam: obtain MRI and flexion/extension Xrays
462
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Types of Injuries
Types of Injuries
Occipital Condyle fracture
– Type I
– Type II
Same as type I with extension to
foramen magnum
Stable- external orthosis
– Type III
466
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Types of Injuries
Occipital Condyle fracture
– Type I
– Type II
– Type III
Wedge shaped alar avulsion fracture of condyle
Fragment can be displaced
May be unstable requiring surgery if severe
Types of Injuries
Occipital Cervical Dislocation
– Type I: anterior subluxation of condyle
– Type IIa: vertical distraction Occ-C1 > 2 mm
– Type IIb: vertical distraction C1-C2 > 2 mm
– Type III: posterior dislocation of condyle
467
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Types of Injuries
Occipital Cervical Dislocation
– All unstable requiring surgery
– I/III may be reduced with LIGHT traction
– Severe injury: may be fatal
Types of Injuries
468
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C1 Jefferson’s fracture
Rule of Spence
>7mm total lateral displacement of C1 lateral
mass on C2 – unstable due to ligament disruption
469
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C2 Odontoid/Dens Fractures
Type I
Type II
Type III
Odontoid Fractures
• Type I
• Type II
• Type III
• Type II unstable
470
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– Odontoid Fracture
MRI imaging is recommended to rule out
disruption of the transverse ligament.
Injury to the transverse ligament is an
unstable injury
Disruption of the transverse ligament is a
contraindication for an anterior odontoid
screw
HALO/collar
Anterior Odontoid screw
– Contraindications
– Use bi-planar C-arm
C1-2 posterior fusion
Transarticular screw
471
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C1-C2 subluxation
Atlanto axial subluxation (C1-C2)
– Ligamentous injury of transverse ligament
– May avulse medial lateral mass of C1
– Lateral Xray or CT
– MRI evaluation by gradient echo for ligament
integrity
472
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C2/Axis fracture
– Fracture through pars/pedicle of C2
– Rarely causes neurologic deficit
– CT test of choice, no need for flex/ex
– Vertebral artery injury?
CTA
473
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– Type I
<3mm translation, no angulation
Hyperextension with compression
External orthosis 2-3 months (HALO)
– Type II
>3mm translation, >11 degrees angulation
Hyperextension with axial load and flexion
Goal is to reduce gaps to allow union
HALO or surgery
474
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– Type III
Consists of Type I fracture with facet
dislocation
Initial flexion-distraction, followed by extension
High rate of neurologic deficits
Surgery for fixation
– C1-C3 posterior fusion or O-C fusion
475
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Facet Injury
476
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Highly unstable
Chance –type fracture (DISH/AS)
477
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C2 pedicle/pars screws
Visualize superior and medial borders
– Aim slightly medial and superior
478
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479
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Thank you!
481
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Disclosures
• Consultant for DepuySynthes, Medtronic, Stryker,
and Globus
482
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484
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485
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Mechanism of Injury
• Most T-L junction injuries are caused by indirect
trauma
• Combinations of flexion, axial load, lateral
compression, rotation, distraction, shear and
extension result in injury
• Loading rate is a critical determinant of type and
severity of injury
• The appearance on radiographic studies is not the
same as the moment of injury
L-1
486
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Classification of Fractures
• There is no universally agreed upon classification
• We will examine the evolution of a few different
classification schemes.
Classification of Fractures
• An ideal classification would be:
– Simple
– Include vast majority of injuries
– Reflect mechanism of injury
– Correspond to anatomic pathology
– Determine treatment options
– Determine prognosis
487
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Fracture - dislocation
488
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Compression Fracture
Ligamenti
ntact
Canal intact
Loss of height
Canal occlusion
Angulation
Comminution
No Posterior
Column Injury
Neuro intact
489
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Unstable Burst
Fracture
Loss of
Body Height
Posterior
Column
Injury
SCI
Flexion - Distraction
Injury and Chance
Fracture
Posterior
ligament
disruption
+ / - body
fracture
490
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Fracture Dislocation
Shear &
Translation
Dislocation
Injury to all 3
Columns
High incidence
Globally neuro deficit
unstable
AO Classification
• Introduced by Magerl et al. in 1994
• Based on a ten-year review of 1,445 consecutive
cases at five different institutions.
• Intended to serve as a comprehensive
classification system that could guide treatment
491
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AO Classification
• Initial report by Magerl included 53 separate injury
patterns
• Comprehensive, but complex
492
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Thoracolumbar Injury
Classification and Injury Severity
Scale
Three Part Description
Injury Morphology
Integrity of PLC
Neurologic Status
493
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Point System
Injury Morphology
Select one
Translation /
Compression fx Rotation
Axial, Flexion 1 3
Burst - add 1
Distraction injury
4
•Only one morphologic subgroup is scored when multiple are present (highest one)
Intact 0
PLC
Suspected/
(displaced in tension)
Indeterminant 2
Injured 3
Evaluated by MRI, CT,
Plain X-rays, Exam
494
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Neurology-Point System
Intact
0
Cauda equina Nerve root
3 2
Cord
And conus medullaris
Incomplete Complete
3
2
495
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Treatment
TLICS Algorithm
Identify fracture morphology Assess integrity of PLC
Assign points Assign points
496
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497
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Validation
• Reliability
– Harrop, J Neurosurgery Spine, 2006
– Forty-eight spine surgeons reviewed 58 clinical
thoracolumbar injury case histories at 3 month intervals
– More than 90% of the surgeons agreed with the
treatment recommendations of TLICS
N0 = intact
N1 = resolved symptoms
N2 = radiculopathy
N3 = incomplete
N4 = complete
NX = cannot obtain exam Vacarro, 2015
498
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5 Treatment Goals
499
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500
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Non-operative Treatment
– Non-operative does not always =
conservative treatment
– Only a certain amount of immobilization
can be tolerated.
501
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502
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• More instability or
deformity or poor bone
quality = more failure with
short segment posterior
instrumentation
– More points of fixation
– May require anterior column
support
503
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Case 1, History
• 30 yr old male MVC
• Back pain
• Decreased motor and
sensory function at T12
– Iliopsoas 2/5
• Head, chest, abdomen,
and pelvis negative
Physical Examination
• Thoracolumbar pain
• May have palpable defect
posteriorly
• Motor strength 2/5 below
Illiopsoas
• Diminished sensation
below T12 level
• Intact perianal pin prick
sensation
504
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Radiographs
Plain Radiographs
• T12 fracture
• 40° kyphosis
• 50% loss of height
• Posterior element
splaying
Radiographs
CT
• T12 burst fracture
• 40% canal compromise
• Facet joint widening T12-
L1
505
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Radiographs
MRI
• T12 burst fracture
• T2: PLC signal changes
• No spinal cord edema
• 40% canal compromise
506
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Surgical Approaches
A. Bed rest/ TLSO
B. Anterior corpectomy/fusion/
instrumentation
C. Posterior
fusion/instrumentation
D. Posterior
Decompression/fusion/
instrumentation
E. Anterior
?
Decompression/Fusion/
Posterior Instrumentation
Postoperative Radiographs
507
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Case
• Patient is a 69 year old woman with a history of
osteoporosis presents to ER after ground level
fall. Chief complaint of mid thoracic back pain.
• Past Med Hx also includes COPD, and previous
T3-T7 fusion performed
• Patient is a smoker, and has a 60 pack year history
• Physical Exam: Neurological intact
508
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Surgical Options
• No surgery
• Extend fusion caudally with multiple Smith
Peterson osteotmies
• Anterior/Posterior Surgery
• Extend fusion caudally with single pedicle
subtraction osteotomy.
Before After
509
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Post-Op Course
• Patient developed post-op deep wound infection
requiring 2 washouts.
510
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511
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INFECTION
512
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513
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Pedicle Anatomy
• Familiar visual and tactile landmarks are not
available with percutaneous screws
• Therefore, knowledge of pedicular anatomy is
critical to successful screw placement
514
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nerve
Medial
515
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Set up ⇒ AP-image
Pedicles in
upper half of
vertebral
body. Endplates
parallel
Spinous
Process
Equidistant
Set up ⇒ Lateral
Endplates
Parallel
Pedicles
Superimposed
516
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517
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20 mm
Mark Jamshidi !
20-25mm from the skin
Skin 25mm
Pedicle
518
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25mm
Lateral View
519
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520
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Hybrid Approach
521
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522
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523
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524
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Aknowledgement
525
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Disclosures
526
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Disk Herniation
• Caused by a defect in the annulus
– excessive stress applied to the disk.
• Mostly occurs on the posterior or
posterolateral aspect of the disk.
– Due to morphology of the annular fiber bundles
– Directs the herniation toward the exiting and
traversing nerve roots
Disk Herniations
• About 20-30% of all herniations of the cervical
region occur at the C5-6 level; 60-75% occur at
the C6-7 level.
• About 90% of all lumbar disk herniations occur at
the L4-5 and L5-S1 levels, about equally.
– 93% occur inside the spinal canal
– 3% in intervertebral foramen
– 4% are extraforaminal or occur far laterally
• Thoracic herniations account for less than 1% of
all diskectomies
Carette S, Fehlings MG. N Engl J Med. Jul 28 2005;353(4):392-9.
Battie MC, Videman T. J Bone Joint Surg Am. Apr 2006;88 Suppl 2:3-9.
527
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528
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529
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530
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Study Overview
• 541 Patients
– 276 PRESTIGE
– 265 Control
• Largest medical device study in the cervical spine
– Level I, Prospective, Randomized Controlled Clinical
Trial
• 32 Centers
• No Training Cases
• Gold Standard Control Group
– Single Level ACDF with Allograft and Plate
Results
• Neck Disability Index: Disc replacement
showed statistically significant difference at
6 weeks and 3 months
531
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Statistically lower rate of revisions and supplemental fixations at the treated level
532
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• 48 month f/u
• Patient outcome scores for satisfaction, NDI, SF-12
all significantly higher for arthroplasty group
• Re-operation rate was 4% versus 15% for
arthroplasty versus ACDF
• 5 year follow-up
• Significantly higher
satisfaction, NDI, and SF-
12 scores in arthroplasty
group
• Reoperation rate
significantly lower in
arthroplasty group (4%
versus 16%)
533
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Other Options:
Anterior Microforaminotomy
Anterior Microforaminotomy:
Not the way to go if not experienced
with this approach
Hacker et al. JNS 98, 2003 23 patients 1998-2000
30 % re-operation
534
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Other Options:
Posterior Cervical Microforaminotomy/diskectomy
535
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Thoracic Disks
536
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Posterolateral Approaches
In 1958 Hulme used costotransversectomy to treat
thoracic disc herniation.
rib resection and removal of the transverse
process - more ventral window
537
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Posterolateral Approaches
In 1978, Patterson and Arbit
described transpedicular
approach involving removal of
the entire pedicle and facet
direct line of exposure to the
ventrally located disc space.
Potential advantage to the
transpedicular approach over
costotransversectomy and
transthoracic is less damage to
radicular vessels.
(Adamkiewicz (arteria magna
radicularis) usually arises on
the left side at T8-L2.)
Ventral Approach
1958, Crafoord et al. reported thoracotomy and ventral
approach for a thoracic disc.
1969, Perot and Munro reported this technique for
thoracic disc herniation in two patients. Since then,
multiple series support this approach.
Excellent ventral exposure of the spinal cord
Permits multiple levels to be addressed via the same
approach if required.
The obvious disadvantage to the transpleural approach
is the risk of pulmonary morbidity.
Considerable amount of pain secondary to the
thoracotomy and chest tube.
Limited to treatment of the T-5 disc space or below.
538
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Sciubba et al: J Spinal Disord Tech Volume 23, Number 2, April 2010
539
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Sciubba et al: J Spinal Disord Tech Volume 23, Number 2, April 2010
Thoracoscopic Approach
Videoscopic-assisted thoracoscopic surgery (VATS)
Endoscope is established tool in thoracic surgery – good use for
spine surgery
Rosenthal and Dickman compared the rate of complications between
VATS, thoracotomy, and costotranversectomy.
no instances of postoperative neurological deterioration in
thoracoscopic or ventral group but in costotransversectomy
group, 7% experienced neurological deficits.
Intercostal neuralgia (16% rate in the VATS group versus
50% in thoracotomy group)
Rate of retained disc fragments
0% in thoracotomy group
4% in VATS
13% in costotransverstectomy group.
540
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Thoracoscopic Approach
Burke and Caputy, Neurosurg Focus. 2000 Oct 15;9(4):e9.
541
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542
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543
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544
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545
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546
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547
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548
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Conclusions
Disc Herniation: a leading cause of of morbidity
in the US, with huge socio-economic
implications
As neurosurgeons, it our is our job to
understand what techniques are appropriate
under what circumstances to get patients to
return to maximal function
Despite the fact that technology is constantly
evolving, our gold standard treatments are well
established and very successful. Extensive
studies will be required to make changes in
standard of care
549
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550
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• Muscle splitting
• Ligament sparing
• Large implants (e.g., 26 x 55 x 12mm)
• Maximizes stability; anterior support
• Indirect decompression
• Minimizes OR time, blood loss, …
Anatomy
A. Psoas Muscle
Muscle on lateral aspect of
lumbar vertebral bodies
Contributes to hip flexion
B. Lumbar Plexus
Lies in the posterior 1/3 of the
psoas muscle
C. Dorsal Lumbar Musculature
Erector Spinae/Quadratus
Lumborum
Enter retroperitoneal space
lateral to Erector Spinae
D. Retroperitoneal fat
Safe triangle of fat used for
access to psoas muscle
E. Peritoneum
Falls anterior when space is
created with finger in
retroperitoneal space
551
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Psoas tapering
552
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( apophyseal ring )
• INDICATIONS
• DDD W/RADIC, STENOSIS (MODERATE), LG SPONDY
• DIRECT INTERVERTEBRAL DISTRACTION
• DISC HEIGHT RESTORATION (APOPHYSEAL RING)
• INDIRECT DECOMPRESSION
• LIGAMENTOTAXY (ALL & PLL)
• MECHANICAL IMMOBILIZATION
• ANTERIOR FUSION, SUPPLEMENTAL FIXATION
553
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• Patient selection
• stenosis, hypertrophic ligamentum fl,
spondy
• Lack of intervertebral distraction
• Endplate compromise / subsidence
(improper graft sizing, overdistraction)
• Lack of immobilization
• Inadequate discectomy
• Instability inadequately addressed (PSF)
Intervertebral height
restoration
554
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Indirect decompression /
ligamentotaxy
555
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Pre-op Post-op
Preop Post Op
556
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Clinical Indications:
LIMITATIONS
Anatomic
• scoliotic rotational deformities
• Iliac crest limits L5-S1 (~L4/5) access
• Nerves: lumbar plexus
Retroperitoneal scarring
• e.g. kidney surgery
557
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Surgical Technique
Patient Positioning
A-
B-
C-
D-
Before
breaking
table!
558
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THEN BREAK
PRE-INCISION LOCALIZATION
Optimize AP & Lateral images
Adjust table (not C-arm)
Linear endplates
Linear posterior cortex
Superimposed pedicles
559
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TARGETING ENTRY
TARGETING ENTRY
560
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LATERAL INCISION
EMG NEUROMONITORING
561
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562
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563
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564
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565
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566
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567
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568
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569
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570
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571
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572
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573
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574
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575
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• Compare:
• 18 mm standard cage alone
• Cage with lateral plate
• Cage with spinous process fixation
• Cage with lateral plate + sp process fixation
• Cage with Ipsilateral pedicle screws
• Cage with Bilateral pedicle screws
576
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Supplemental fixation
Lateral plate
Supplemental fixation
Pedicle screws (unilateral or bilateral)
577
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Supplemental fixation
Spinous process fixation device
Supplemental fixation
Combinations…
578
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•
•
•
•
•
•
•
•
•
•
Flexion - Extension
40
A A
35
30
25 B
20 BC BC
C
15
10
0
Standalone lat Ipsilat Sp process Lat plate + Bilatped
plate Ped screws fixation Sp process screws
579
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Lateral bending
40 A
A
35
30
25 B
B
B
20
B
15
10
0
Standalone Sp process Ipsilateral Lateral Lat plate + Bilateral
fixation screws plate Sp process screws
Axial rotation
80 A A
70
B B
60
BC
50 C
40
30
20
10
0
Standalone Sp Lat plate Ipsilat Lat plate + Bilat PS
process screws Sp process
580
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Supplemental Fixation
• Standalone cages provide very good rigidity in flexion-
extension (31.6% of intact ROM)
581
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Youssef et al., Minimally Invasive Surgery: Lateral Approach Interbody Fusion. Spine 35: S302-311, 2010.
0%
30 %
Youssef et al., Minimally Invasive Surgery: Lateral Approach Interbody Fusion. Spine 35: S302-311, 2010.
582
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• N: 100
• Surgical time: 74 mins
• LOS: 1.5 days
2007 • VAS reduction: 68.7%
• F/U: 6 months
• Complications: 2%
• No infections
• No transfusions
• N: 58
• F/U: 15 months
• Overall complication rate: 22.4%
• (13.8% approach related)
583
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584
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Scoliosis
• N: 25
• EBL: 53cc/level
• Mean f/u: 11 mon
• Mean VAS improvement: 70.4%
• Mean ODI improvement: 44.2%
• Fusion (CT): 100%
No CSF leaks
No wound infections
No visceral injuries
No vascular injuries
No postoperative
weakness
No deep venous
thromboses, urinary
tract infections, or
ileus identified.
585
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Spinal Deformity
• N: 23
• Circumferential fusion:
transpsoas + perc screws
+/- TLIF @ L5/S1
• Levels: 3.7
• Mean f/u: 13.4 months
• EBL: 477cc
• Mean VAS (bk) delta: 3.96
• Fusion rate: 97.6%
• Cobb
Pre-op 31.4 deg
Post-op 11.5 deg
• Complications
• “Thigh Sx”: 30.4% (1 persistent)
2 returns to OR
(CSF lk, hardware failure)
• N: 107 (prospective)
• Mean: 4.4 levels/pt
• Supp PS fixation: 75.7%
• Lateral fixation: 5.6%
• Stand-alone: 18.7%
• Mean Op time: 178 mins
• Mean LOS: 3.8 days
• Transfusions: 4.7%
• ICU: 2.8%
• Inpatient Rehab: 0.9%
• Complications: 11.2%
MIS only: 7.7%
Open: 20.7%
(*wound infections = open only)
586
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587
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Post-op infections :
3.6% TLIF
3.1% MIS TLIF
11% PLIF
3.2% Endoscopic ALIF
2.3% MIS decompression
0.0% LLIF
588
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Durotomy :
5 - 20% posterior fusions
0.2% ALIF
5 - 19.6% TLIF
7.7% MIS decompression
0.0% LLIF
LOS (days) :
4 ALIFs
3-6 PLIFs and instrumented
3-6 TLIFs
1.2 LLIF
Prospective study
N: 53
No vascular injuries
1 psoas hematoma
589
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HF weakness:
L 1/2 0%
L 2/3 25%
L 3/4 33%
L 4/5 57%
Psoas tapering
590
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4 institutions, N: 568
8 / 10 recovered without
intervention within 6 months
rectus abdominis
internal oblique
external oblique
transverse abdominis
innervated by
subcostal nerve
iliohypogastric nerve
ilioinguinal nerve
591
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FINAL
TIPS
&
PEARLS
Positioning
592
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PRE-INCISION LOCALIZATION
Optimize AP & Lateral images
Adjust table (not C-arm)
Linear endplates
Linear posterior cortex
Superimposed pedicles
593
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NEUROMONITORING
594
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ALL retractor
595
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596
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597
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Be cognizant of
graft over-sizing
598
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Be cognizant of
graft over-sizing =
over-distraction
Post-op
Subsidence …
BEGINS in the OR
599
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1 month
6 months
600
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MINIMIZE SUBSIDENCE
•
•
• NOT
•
Conclusion
The lateral transpsoas approach is a safe and
effective less invasive option for the treatment
of a variety of lumbar pathology and should
exist in the tool belt of contemporary spine
surgeons.
601
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602
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Disclosure
• Research Grants: AO spine
• Employment:UCSF
• Honoraria:AO spine
• Ownership Interests:Spinicity/ISD
603
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In 2025…
• According to World Health Organization:
– The world population will be 8 billion people
– People age 65+ will number 800 million
(currently 600 million)
604
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605
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– Open Approach
– Mini-open approach
via expandable tube
– MIS/Tubular approach
via nonexpandable
tube
606
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MIS Procedures
• Spinal Decompression/Discectomy
• Spinal Lami for Tumors
– Intradural
– Extradural
• Lumbar Fusion for Degenerative
Disease
• TL Deformity Correction
607
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Indications
• Cervical foraminal
stenosis
• Posterolateral or
foraminal disc
herniation
• Symptoms refractory
to conservative
treatment
Advantages
• Excellent access to
eccentrically located disc
fragments
• Avoids retraction on the
esophagus and laryngeal
nerve
608
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“Success” rates of
MIS Foraminotomy Range
from 54-97%
• Adamson - “Excellent or good” in 97%
– 100 pts
• Ruetten – 87.4% no longer had arm pain
– 175 pts
– 9.2% with residual pain
• Hilton – 85% with complete pain relief
– 222 pts
• Fessler – 92%
– 25 pts
– 54% with complete resolution of radiculopathy
Contraindications
• Significant kyphosis
or mechanical
instability
• Signs or symptoms of
cervical myelopathy
• Spinal cord
compression on
imaging studies
609
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610
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Nuances
• Limited view
• Need to drill some of
the pedicle
• Blind sweeps under
the nerve root can
cause root
inflammation
• Can not reach
centrally located disc
pathology
MIS foramenotomy
• Less expensive than ACDF
• Not as reliable as ACDF???
611
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Posterior Incisions/Approaches
• What kind of incision?
– Linear
– C shape?
– J shape?
– Can we do this
minimally invasively?
612
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613
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614
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Nuances
• Patient selection is key
– Can consider for
paramedian soft
herniated thoracic discs
– Avoid calcified
“rocks”
• Unlikely to remove
with an MIS approach
as you can NOT retract
the cord
• Ventral approaches are
preferable for large
calcified herniated discs
615
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616
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Durotomy…
• Watch K-wires and
smallest dilator tube
with flouro
– Both can enter
interlaminar space
617
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Avoiding Durotomy
• Use a woodson to free
adhesions betw dura
and lig flav
• Use “sucker-retractor”
to push nerve roots
and dura away from
discectomy
instruments
Thoracolumbar Tumors
• Intradural
– Extramedullary
– Intramedullary
• Extradural
618
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– Open Approach
• Midline spinal incision
• Muscle Retraction
• Wide exposure of tumor
Location of the
Minimally Invasive Incision
1 2 3
1- Disc
1- Midline intradural tumors
2 – Paramedian intradural or
2 – PLIF
extradural tumors 3 - TLIF
3 – Foraminal tumors
619
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36
620
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Traditional Approach:
Intradural Spinal Tumor
+ Proven safety and
Efficacy
(McCormick Clin Neurosurg, 1994;
Tobias: Childs Nerv Syst 2008)
37
38
621
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Midline incision
● Utilizing expandable
retractors
● Preserve lateral lamina,
facets and muscle
attachments
39
A B C D
E F G H
40
622
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A B C D
Cadaveric Study:
Comparison of MIS vs Open Exposure of the T6-7 levels:
MIS affords 50-75% smaller incision
Lu, Dhall, Mummaneni: World Neurosurgery 2010
E F G H
41
42
623
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43
• Paramedian Incision
• Dilate paraspinal
muscles
• Place retractor to
expose hemilamina
624
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• Hemilaminectomy
• Leave Spinous Process and Interspinous
Ligaments Intact
45
625
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• 20 yo woman with
back pain, bilateral leg
radicular pain
• Unable to sit for 1
minute
• Urinary urgency
626
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3. Mini-Open
Foraminal Tumor
Resection
Nerve Sheath Tumors account for one-
third of all primary spinal neoplasms
(Nittner, Acta Neurol Psych, 1968).
627
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Mini-Open Resection of
Nerve Sheath Tumor
(Lu, Dhall, Mummaneni, JNS Spine 2009)
Mini-Open Removal
of Foraminal Tumors
628
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Results
Case Illustration
• 48 y/o obese male
– h/o L3-S1
circumferential fixation
with one year of knee
pain and right knee
flexion weakness
54
629
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Case Illustration
• Mini-open paramedian
approach
– Pseudarthrosis found at L3-4
level.
– Tumor resection performed.
– L3-4 instrumentation and
fusion performed.
• Follow-up at 1 year
demonstrated complete
recovery of motor strength.
Improving knee pain.
55
SECTION HEADING
Preop
Postop
56
630
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Thoracolumbar
Decompression and Fusion
Magerl-1982
631
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Foley 2001
Wiltse 1968
• Described a
sacrospinalis splitting
technique for doing
posterior spinal fusion
in patients with
spondylolithesis
• Allows access to
Kambin’s Triangle
632
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Indications for
Minimally Invasive Lumbar Fusion
– Spondylolisthesis
• Neural compression
• Failed conserv tx
• Mobile
– Spondylosis or DDD
• 1 level
• Nonsmoker
• No secondary gain
• Back pain
• Often radiculopathy
– Deformity?
• Lumbar Guidelines:
JNS Spine 2005
Spondylolisthesis
• Often associated with
stenosis
• Is it mobile on flexion
and extension x-rays?
• If Immobile – consider
MIS decompression
• If Mobile and painful,
may need fusion
633
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TLIF Options
– Open Approach
– Minimally Invasive
(Tubular) TLIF via
nonexpandable tube
– Mummaneni, Haid,
Rodts: JNS Spine, July
2004
634
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Comparison of Mini-open
to Open TLIF
Comparison of
Open and Mini-open TLIF
635
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Learning Curve?
Pseudarthrosis example
636
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637
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Degen Vs Deformity
• In Degenerative 1-2 level spinal disease, MIS
approaches decrease hospital stay and EBL
– The operations are interchangeable for Most cases
MIS Deformity
• Can decompression be achieved? Yes
• Can hardware be placed safely? Yes (even iliac
screws)
• Can sag balance be restored? Maybe
• Will you match LL-PI within 10 degrees? Maybe
• Will it take a long time to do? Initially - yes
• Can a succesful fusion be established?
– This is the Challenge…
638
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• Complication rates
high
• Pseudarthrosis rates
problematic
639
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Schwab et al:
Eur Spine J 2012
Risk Factors for
Major Peri-operative
Complications in
Adult Spinal
Deformity Surgery
A Multi-center Review
of 953 Consecutive
Patients
640
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Conclusion
• Patient related risk factors
– Age, sex, BMI, number of co-morbidities, ASA, percentage of revision cases, number of redo
surgeries were not significantly different in patients with and without major complications
– May make a difference in minor complications?
641
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642
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Tormenti, et al.
NS Focus 2010
Complications
• Pitfall:
– The authors
concentrated on
coronal curve and not
on sagittal balance
643
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• 23 patients,
retrospective review
• High pseudo rate if no
interbody fusion is
done, can not rely on
MIS posterolateral
fusion
644
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645
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Class I Treatment
• MIS Decompression without fusion or with limited
one level fusion
52 year old woman with radicular right leg pain. Minimal back pain. MRI with
Right L3-4 lateral recess stenosis from disc bulge (axial shown below).
CA 15
PT 3
PI-LL -7
SVA<5
A B D
646
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Level I Treatment
• Decompression alone
– Neurogenic claudication secondary to central stenosis
• Requires limited decompression
• Minimal or no back pain
– Radiographic findings
• Decompression w/ limited instrumented PL Fusion
– Stenosis with minimal back pain
– Anterior supporting osteophytes
– No global imbalance, cobb <20,
– No LL-PI Mismatch
647
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Case Example
• 67 year old woman with low back pain and
bilateral sciatica and anterior thigh pain
Dynamic X-rays
648
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MRI
L3/4 L4/5
649
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650
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651
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A B
652
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HPI
• 59 yo female with mechanical low back
pain and left leg radiculopathy
– The pain radiates in the left L5 distribution
• She has failed conservative therapy
including multiple ESI and facet injections
• PMHx: negative
653
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654
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CT L-s Spine
655
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What to do??
• T3 – pelvis
• T9 – pelvis
• L5-S1 psf
• L5-S1 alif
• L5-S1 alif and psf
• MIS or open?
656
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Positioning
657
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Mini-open ALIF
• Midline incision,
infraumbilical, 1-4 cm
above pubic
symphysis
Mini-Open ALIF:
Retroperitoneal of Transperitoneal
658
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Serial dilations
659
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660
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661
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662
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663
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Bilateral mini-open
foraminotomy
664
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665
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666
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Conclusion:
MIS is NOT Ideal for Class 3
• Avoid 0
– Curves with Cobb >30
– Apical rotation > Grade II
– Lateral olisthesis >6mm
– Sag imbalance requiring PSO
– Thoracic kyphosis
• These characteristics predict
failure with limited MIS
decompression/fusion surgery
• Need to do OPEN surgery
• BUT IN FUTURE CAN WE
DO IT?
667
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Incremental
costs for MIS
Incremental
savings for
MIS
132 *Other perioperative events Included emergency room visits, hospital readmissions (excluding reoperations), postoperative rehabilitation,
and additional diagnostics.
668
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Biomaterials
• Match Modulus of Elasticity of Bone
– PEEK?
– Stronger than PEEK?
– MRI compatible?
• Bio-absorbable instrumentation
669
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Cost-effectiveness analysis in
minimally invasive spine
surgery. Al-Khouja et al:
Neurosurg Focus 2014
670
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Cost-effectiveness analysis in
minimally invasive spine
surgery. Al-Khouja et al:
Neurosurg Focus 2014
671
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Conclusions
• Prepare for the influx of “elderly” osteoporotic but active
patients who live for a century and have worsening
degenerative deformity…
• Must innovate to find cost effective solutions
– Cost per Qaly calculations…
• Appropriate Indications for surgery must be
followed
672
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Disclosures
• Consultant for DepuySynthes, Globus,
Medtronic, and Stryker
673
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Syringomyelia Epidemiology
674
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Chiari Malformations
• In 1891, German pathologist Hans von Chiari
described the post mortem findings of hindbrain
malformations:
– Type I: cerebellar tonsils herniated into the cervical
spinal canal
– Type II: herniation of the medulla, vermis, and tonsils;
medullary kinking; 4rth ventricle is usually below the
foramen magnum; usually associated with
meningomyelocele
– Type III: rare (herniation of cerebellum and brain stem
into a high cervical meningocele
Chiari Malformation
675
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Old
Theories I
II
Gardner's
Hydrodynamic
Williams' Craniospinal Dissociation
676
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• Pathophysiological mechanism
behind the progression of
syringomyelia associated with
the Chiari I malformation has
been poorly defined.
• Purpose of this prospective
study was to define the
pathophysiology of syrinx
development and its resolution
with surgery.
677
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PreOp Evaluation
• Radiological Imaging of Anatomy
• Radiological Imaging of Physiology – cine
MRI
• Spinal Subarachnoid Pressure Recording
and Physiological Testing
• Cervical, lumbar SA pressure during rest, Valsalva
and jugular compression (Queckenstedt’s Test)
• Rate of rise and fall of pressure
• Compliance (ml of CSF/mmHg)
678
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PostOp Evaluation
• 6 days
• cine MR (while syrinx is still present)
• 6 months postop
• anatomical MR scan
• cine MR
• Pressure testing
• 12 months postop assessment of:
• Sx of headache, dysesthetic pain, extremity
weakness, sensory loss, and impaired ambulation
• Neurological signs: weakness, atrophy, and ataxia
Results
679
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Results (cont’d)
680
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Results of cine MR
Craniospinal Compliance
C= ∆Vol./∆Pressure
681
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Intraoperative Ultrasound
Results (Cont’d)
682
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Clinical Results
Conclusions
• Results support the proposed theory:
The Chiari I malformation produces a
block to the flow of CSF (shown by
MR, CINE MR, Jug Comp tests)
• Brain expansion during systole forces
the cerebellar tonsils into the partially
enclosed spinal subarachnoid space
(which has low compliance)
• Tonsillar decent has results in large
cervical subarachnoid pulse pressure
waves, which are transmitted through
the wall of the spinal cord.
• Pulsatile caudal flow of the syrinx
fluid during systole leads to syrinx
progression.
683
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Significance of Study
• Evidence that mechanism of syrinx origin and
resolution arises from outside the spinal cord (not
inside)
• Supports the craniocervical decompression +
duraplasty technique
• This technique will become adopted in a greater
number of academic and clinical centers, as it
arrests syrinx progression without invading the
CNS parenchyma or CSF pathway. Very limited
in its complication rate when compared to other
treatment modalities such as shunting.
684
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685
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Pathophysiology of Failed
Craniocervical Decompression
Pathophysiology of Primary
Spinal Syringomyelia
686
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687
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Rate of
CSF Entry
into the
Syrinx
30 30
20 20
10 10
0 0
0 10 20 30 40 50 60 0 10 20 30 40 50 60
688
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
• Series of 8 patients
• Removal of arachnoid cyst and restoration
of CSF flow results in syrinx resolution.
689
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690
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Idiopathic Syringomyelia
• Must take very careful history
• Infection, Trauma, etc
• Must check for subarachnoid space
adhesions
• Must check for small posterior fossa
691
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Acknowledgements
• Drs. John Heiss and Edward Oldfield at
NIH and UVA, respectively
692
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Disclosure Statement
Reports no commercial interest
693
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694
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695
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696
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697
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698
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699
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700
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701
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702
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703
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704
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705
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706
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707
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708
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709
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710
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711
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712
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713
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714
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715
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716
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717
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718
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719
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720
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721
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722
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723
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724
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725
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726
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727
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728
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729
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730
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731
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732
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733
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734
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735
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736
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737
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738
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739
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740
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741
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742
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743
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* No disclosures
744
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Patterns
745
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
746
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Imager/Interpreter
747
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Tumors Lesions
• To identify tumors and • To distinguish tumors
distinguish between from other lesions
benign and malignant
forms • To define treatable from
untreatable disease
• To assess resectability • To localize site for
of large tumors
highest yield, safest
• To accurately biopsy
characterize them to • Can obviate need
help guide surgery for biopsy in some
cases
Tumors
Benign Malignant
Intraneural Extraneural
748
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
749
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Schwannoma
750
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Schwannoma
NS Clinics 2008
751
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+/- deficit
On same nerve (different fascicles) =
? SYNDROME
752
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Schwannomatosis
NS Clinics 2008
753
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754
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
755
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
756
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
JPRAS 2015
JNS 2010
757
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Plexiform schwannoma
JNS 2010
758
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Spectrum of Schwannomas
759
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Neurofibroma
• Often several
entering/exiting
fascicles
• 70-80% nerve
function preserving
Neurofibroma
760
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Neurofibromatosis I
• Benign
• Malignant
• Difficult to tell
what’s what
761
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Resectable
JNS 2006
Resectable
JNS 2006
762
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JNS 2006
Plexiform neurofibroma
763
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Unresectable
JNS 2006
Plexiform neurofibroma:
Subtotal (palliative) resection
764
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
• Ganglia
• Perineuriomas
• Lipofibromatous hamartomas
• Neuromuscular choristomas
765
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Intraneural Ganglia
An anatomical explanation:
New MRI technologies help visualize
connections
766
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
JNS 2003
Intraneural ganglia:
A clinical problem
• Suboptimal neurologic
outcomes
• High recurrence
rates (20%*)
• * underestimated
767
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Intraneural ganglia
JNS 2003
768
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Intraneural Ganglia:
Occam’s Razor
• What works for the
peroneal nerve at
fibular neck should
work elsewhere
769
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Hypertrophic neuropathy
(perineurioma)
• Characteristic clinical
and MRI features
• Slowly progressive
predominant motor
deficit affecting young
(Brain 2009)
770
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Perineurioma
NS Clinics 2008
peroneal
tibial
771
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Congenital Lesions
Hamartoma Choristoma
Fibrolipomatous hamartoma +
nerve territory bony and soft tissue
overgrowth
NS Clinics 2008
772
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
• When it involves
median nerve at
wrist in adults,
perform carpal
tunnel release
• No need to biopsy;
characteristic MRI
NS Clinics 2008
NS Clinics 2008
773
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Nerve-Territory Overgrowth =
Tumors
JPRAS 2014
Neuromuscular choristoma +
nerve-territory undergrowth
774
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MRI
Biopsy
775
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NF S100 EMA
776
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F/U
• FIBROMATOSIS (DESMOID)
777
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778
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779
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780
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Benign Extraneural
• Lipoma
• Ganglia
• Others (any lesion in the
neighborhood)
Extraneural Lipoma
NS Clinics 2008
781
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Extraneural Lipoma
JNS 2012
NS Clinics 2008
Lipoma
NS Clinics 2008
782
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Extraneural Ganglion
783
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Desmoid
• Infiltrative but benign
• Usually occur in difficult locations to
get wide resection
784
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Desmoid
• Best treatment when gross total
resection (GTR) is not achievable? -
Nothing works very reliably
NS Clinics 2008
785
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NS Clinics 2008
NS Clinics 2008
786
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Approach to MPNST
• Suspect
• Stage
• Biopsy (percutaneous or limited
open)
• Multidisciplinary approach for
surgery (wide resection or
amputation) in combination with
chemo, radiation preop and/or postop
787
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The Principle
Leksell Gamma
Knife
788
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789
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Concept:
Robbing the bank without getting caught
SAFETY/EFFICACY
Methods
790
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Technique
An MRI Target
791
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An MRI Target
NS Focus 2015
792
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Perineurioma
793
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Results
Results
Most common:
• Inflammatory demyelination
• Inflammatory/vasculitis
• Perineurioma
• B-cell lymphoma
• “Metastatic” breast CA
794
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795
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Target-specific Therapy
• Stem Cell
Transplantation: a
potentially effective
therapy for neuro-
lymphomatosis
Ghobriel et al.
Cancer 2004
796
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797
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Results
Rare:
• Undiagnosed carcinomas
• Neuroleukemiosis
• Amyloidosis
• Etc.
798
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Rare Ones –
e.g., prostate CA to LS plexus/sciatic
799
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Perineural spread:
more common than thought
NS Focus 2015
NS Clinics 2008
800
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Patterns
Treatment
801
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What’s new?
Pathogenesis Treatment
Improved understanding
Improved outcomes
802
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Disclosure Statement
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Metastatic Brain
Tumors
Charles S. Cobbs, M.D.
Director, Ben and Catherine Ivy Center
for Advanced Brain Tumor Treatment
Swedish Neuroscience Institute
Seattle, WA
1093
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Conflicts of Interest
Acknowledgements
No conflicts of interest
Overview
Overview Brain Mets Questions:
Overview biology Who gets surgery?
Who gets treated Who gets SRS?
Should WBRT be given
Survival too?
Symptom SRS with or without
management WBRT?
Types of therapy What to do for
Surgery recurrence?
SRS Guidelines
Chemo Case Examples
1094
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Introduction
10 times more common than primary CNS
tumors; about >200,000 / yr in USA
About 20-25% of metastatic CA goes to CNS
Mostly lung, breast, melanoma, renal cell
and colon
Presenting symptoms include HA, seizure,
encephalopathy, ataxia, and sensory and
motor deficits
Lung ~50%
Breast 15-20%
Melanoma 10-15%
Unknown (1/3 lung) 10-15%
Colorectal 2-12%
Kidney 1-8%
Thyroid 1-10%
Lymphoma ?
1095
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1096
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Intravasation / Invasion
Intravasation:
(invasion into vasculature) poorly understood
Invasion:
Matrix Metalloproteinases: degradation of
basement membrane
Heparanase: breaks down heparan sulfate
proteoglycans (HSPG)
1097
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1098
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Symptom Management
Prevention and Treatment:
DVT, Infection, Pain, Neurologic, cognitive, emotional
dysfunction
Cerebral Edema
Dexamethasone (potent, CNS penetration, limited
mineralocorticoid effect)
Radiation Necrosis
Surgical Resection, steroids, hyperbaric oxygen,
anticoagulants
Seizures
AEDs, but no good evidence for prophylactic AEDs
1100
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Steroids
Level III recommendation
4-8 mg/day provide temporary relief of
symptoms related to increased ICP,
peritumoral edema.
For severe symptoms of increased ICP,
higher doses such as 16 mg/day can be
considered
Dexamethasone is recommended
1101
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1102
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WBRT
Goal: Treatment of existing and future mets
Typically uses parallel-opposed external beams
to deliver 30 Gy (3 Gy/d x 10 days over 2 weeks)
Acute complications: encephalopathy, brain
edema, nausea, vomiting, alopecia, mucositis
Delayed complications: RN, dementia, optic and
otic toxicities, neurocognitive, endocrine deficits
Used as sole therapy for RPA class III patients,
and can improve survival from 1-2 to 4 months.
May be used in conjunction with local therapy
(surgery or SRS) in RPA class I/II patients
WBRT
Best for patients with:
Massive brain edema
>10 mets
Impending herniation
SCLC
Patients who cannot have local /
focal therapy
1103
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WBRT: Why 30 Gy in 10
fractions?
9 RCTs evaluated, class I evidence
obtained from a meta-analysis
Altered dose fractionation schedules do not
significantly result in change in median
survival, local control or neurocognitive
outcomes
< 30 Gy in 10 fractions suggests a trend
toward poorer survival
> 30 Gy in 10 fractions shows no benefit
1104
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WBRT Toxicity
Vascular injury
Endothelial cell death
Vascular sclerosis
Leukoencephalopathy
Accelerated brain atrophy
Neural stem cell death
Depressed hippocampal dependent
learning, memory, spatial processing
1105
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Surgery
Goals:
Establish diagnosis (in 80%)
Local control in non-eloquent locations
Rapid relief of symptoms of mass effect, hemorrhage,
hydrocephalus
Complications:
Infection, neuro deficits, hemorrhage, infarction, death
Most often used in RPA class I/II patients with
single met and minimal or controlled systemic
disease
Minimal impact on control of distant brain mets
or overall survival (without additional RT)
Surgery
1106
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Stereotactic Radiosurgery
(SRS)
Goal: Treatment of single or more mets in
outpatient setting, local control for eloquent
brain, relative cost-effectiveness compared with
surgery
Limitations: Indistinct lesions, Mets > 3cm
Complications: radiation necrosis, theoretical
risk of secondary malignancy
Control Rates (for most histologies): 60-75% at 2
yrs, distant brain met control rats of 46% at 2
yrs.
Overall Survival: 10 months
Similar to surgery with respect to min. impact on
distant brain mets and overall survival
Curr Oncol Rep (2010) 12:34–40
1107
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Gamma Knife
Cyber Knife
1108
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SRS
Gamma Knife: Multiple intersecting Co-60 gamma
ray beams
Linear Accelerator (E.g., Cyberknife): High energy
X-ray beams
For both, dose is inversely proportional to diameter
of tumor
Typical dose 15-24 Gy to 50% isodose line
Biologically = 5-6 weeks of daily conventional
radiotherapy
No evidence that one system better than other
Typical treatment ½-3 hrs
Suh J, NEJM, 2010
Stereotactic Radiosurgery
1109
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1110
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Lin, 2007
1111
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Chemotherapy
Should patients with brain metastases
receive chemotherapy?
1112
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1113
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SRS Alone
Guidelines? Evolution of
Thinking?
Category 2B evidence
For RPA class I patients
High KPS
Low systemic disease
1-3 mets
Nicholas F. Marko and Robert J. Weil (2010) Neurocognitive considerations in the treatment of brain
metastases
Nat. Rev. Clin. Oncol. doi:10.1038/nrclinonc.2010.30
1118
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1119
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Chang et al.
1120
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43 yo High Functioning
Executive with Stable Systemic
Breast CA
1121
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Recurrence
No prior WBRT > consider WBRT or best
supportive care
Prior WBRT > best supportive care or re-
irradiation (?SRS) if prior positive response
to RT
Case 1
45 year old female with metastatic
breast adenocarcinoma (HER2+,
treated with Herceptin) presents
with 1 week history of headaches.
Systemic work up shows stable
small chest lesions. Brain MRI as
shown. KPS 80 on steroids. Your
treatment recommendations likely
include:
Surgical resection plus WBRT
Surgical resection plus SRS boost to
resection cavity
Surgery followed by observation
WBRT followed by SRS
SRS alone
Other (feel free to specify in chat box)
1125
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Case 1 Management
Would recommend surgery followed by
SRS boost to tumor bed.
Resection confirms diagnosis
Would wait a couple of weeks prior to SRS for
tumor bed to shrink and edema to go away
Most patients with high KPS may wish to
follow with SRS alone, and hold off of
WBRT
Case 2
A 47 year old male (smoker) with
history of NSCLC (he had a 3 cm
LUL lesion treated 6 months prior
with surgery; there were clear
margins and clear nodes),
presents to your clinic with
headaches. His body imaging
shows no obvious systemic
disease. Brain MRI shows 4
enhancing lesions as shown. KPS
90. No neurological deficits. Your
treatment recommendations would
likely include which of the
following:
WBRT
WBRT followed by SRS boost
SRS Alone
Other (feel free to specify in
chat box)
1126
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Case 2 Management
Would recommend SRS to 4 lesions +/- WBRT
Improved survival (Andrews study) only found in
patients with 1 brain met, but suggestive in cases of 3
mets
Other considerations:
This patient has developed several brain mets within
months of primary tumor diagnosis
Suggests aggressive disease
Suggests other micrometastases are probably
already present
Case 3
46 yo man with cutaneous
melanoma resected 2 yrs
prior (Clark level IV)
presents with left focal
seizure. PET/CT is
negative. Stable on
steroids. 3 lesions are seen:
Recommend:
SRS
SRS + WBRT
WBRT
Resection plus SRS
1127
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Case 3 Management
Young person, relatively radioresistant primary
Melanoma has greatest risk of multiplicity, thus more
lesions may be present when re-scanning
SRS alone makes sense
SRS plus WBRT makes sense
WBRT alone doesn’t make sense due to radioresistance
Surgery (with mapping?) of one lesion plus radiotherapy
doesn’t make sense
Consider addition of Temozolomide?
Crosses BBB
anti-melanoma properties
synergizes with radiotherapy
? Give concomitantly or after radiotherapy
1128
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Malignant Glioma
Management and
Novel Therapies
No conflict of interest
1129
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Overview
Definitions Chemotherapy
Biology Focal therapies
New concepts MGMT
Radiographic features 1P/19Q
Advanced imaging Stupp Protocol
Surgical Extent of Recurrence
Resection Options
Pathology Novel / New
Molecular Profiling Approaches
Radiation Therapy Clinical Trials
Focal Therapies Immunotherapy
Virotherapy
1130
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p53 mutation,
FGF2, PDGF, EGFR
PDGFR-α amplification
overexpression (7p)
Low Grade
INK4A/ARF
Astrocytoma loss
CDK4 amplification (p16/p19
RB loss pathway)
Anaplastic
Astrocytoma PTEN loss
(10q)
PTEN loss
(10q)
GBM GBM
(secondary) (primary)
Modified after E.C. Holland, 2001
1131
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1132
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Proneural = Good
Mesynchmal/Proliferative
=Bad
1133
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1134
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1135
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1136
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1137
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1138
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1139
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TYPE 2 – IDH MUTANT ASTROCYTOMA. Lower grade glioma type 2 is characterized by IDH1
mutation, TP53 mutation, and ATRX mutation, and corresponds to IDH1-mutant astrocytoma.
TYPE 3 – IDH NON-MUTANT LOWER GRADE GLIOMAS. This type carries genetic alterations
that are characteristic of glioblastoma, and are not IDH mutated.
1140
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1141
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1142
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1143
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Neuroradiology: Guidelines
Level I recommendation
Gadolinium enhanced MRI
Level II recommendation
CT with contrast
Level III recommendation
MR Spectroscopy
Functional MRI may help define speech and motor areas
Diffusion-weighted MRI, perfusion imaging to measure
relative cerebral blood volume, are helpful especially in
the era of bevacizumab (Avastin)
CT Scan
1144
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1145
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Pseudoresponse
1146
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Pseudoprogression
1147
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1148
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Frameless Stereotaxis
1149
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1150
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1151
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1152
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1153
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1154
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Extent of Resection
Level II evidence:
Stummer et al, Lancet Oncology 2006:
RCT, 270 patients, extent of resection of MG with
use of fluorescence (5-aminolevulanic acid)
65% GTR (5-ala group) vs. 35% GTR (non 5-ala
group) based on post op MRI enhancement
6 month PFS 41% vs. 21% (p<.0001)
Non blinded
Pre-Temozolomide era
1155
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1156
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1157
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Neuropathology
Tissue diagnosis is critical
Biopsy size important to avoid sampling artifact
Biopsy of tumor edge may provide inaccurate tumor
grade diagnosis
Grade of tumor will determine treatment
Misdiagnosis of e.g., grade III astrocytoma vs.
malignant oligodendroglioma may impact
therapy
1p/19q codeletion
IDH1
ATRX, p53
1158
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1159
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1160
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Standard Therapy
1161
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Chemotherapy
Nitrosourea (BCNU) were previously used
in combination with radiation therapy with
minimal effect
RCT of Temozolomide has clearly
established this agent as important
additive agent
Carmustine wafers have shown modest
effects in RCT
1162
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1163
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RT + TMZ
Trial Age (yrs) N Median
RT60
RT45
RT34
TMZ
survival
(mo)
Wick W, et al. J Clin Oncol. 2010;28(15s). LBA2001; Malmstrom A, et al. J Clin Oncol. 2010;28(15s). Abstract
LBA2002; Dirier A, et al. J Clin Oncol. 2010;28(15s). Abstract 2048; Perry JR, et al. Neuro-oncology. 2010;12(suppl 3).
Abstract P.072.
Local Therapies
Brachytherapy (Implanted radioactive seeds)
Gliasite
1164
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Gliadel
Phase III RCT BCNU wafer vs placebo
in newly diagnosed malignant glioma
International, multicenter, double-blind, placebo-controlled trial
of 240 patients with primary high grade gliomas
Randomized to resection and RT +/- Gliadel wafer vs. placebo
BCNU Placebo
Median survival (+2.3 mos) 13.9 months 11.6 months
(p=0.03)
1165
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1166
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Recurrence
What is recurrence?
1990’s Macdonald criteria based on
enhanced tumor size
But what about Avastin, and radiation
necrosis (pseudo-progression)
In 2009 T2 and FLAIR sequences were
recommended to evaluate both enhancing
and non enhancing tumor progression
1167
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Recurrence
Nearly all glioblastomas will recur …
Three FDA-approved therapies
1. Gliadel…Carmustine wafer indication
For “recurrent glioblastoma multiforme patients as an
adjunct to surgery”
2. Bevacizumab indication
For “progressive disease in adult patients following prior
therapy as a single agent”
Based on “improvement in objective response rate”
3. Novo TTF-100A device
Wen PY and Kesari S. N Engl J Med. 2008;359(5):492-507; Stupp R, et al. J Clin Oncol. 2007;25:4127-4136;
Gliadel prescribing information. Available at: http://www.gliadel.com/Docs/Pdf/201241R1_Gliadel_PI.pdf and Avastin prescribing
information. Available at: http://www.gliadel.com/Docs/Pdf/201241R1_Gliadel_PI.pdf. Accessed April 11, 2011.
1168
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Targeted Agents
1169
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Targeted Agents
T1 Gad
FLAIR
Bevacizumab and
EGFR and mTOR
irinotecan
inhibitor
Bevacizumab (Avastin) +
Irinotecan
First trial in GBM, BEV+Irinotecan
Stark-Vance et al. 2005, 21 pts.
response rate of 43% and 52% stable dz in
21 pts with recurrent GBM
Vrendenberg et al., JCO, 2007, 35 pts.
6 month PFS 46%
1170
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1171
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Bevacizumab/Avastin:
Take Home Message
Does not prolong survival in newly
diagnosed GBM
Helpful/indicated for:
Symptomatic/bulky tumors
Patients maxed on steroids
Herniation with edema
Progressive GBM
1172
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T1 Gad
FLAIR
CMV antigens
1173
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1174
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Checkpoint Inhibitors
A phase III trial testing Opdivo® (nivolumab) and Yervoy® (ipilimumab)—anti-PD-1 and anti-
CTLA-4 antibodies, respectively—in patients with recurrent glioblastoma (NCT02017717).
A phase II trial testing MEDI4736 (durvalumab), an anti-PD-L1 antibody, in patients with
glioblastoma (NCT02336165).
A phase II trial testing Keytruda® (pembrolizumab), an anti-PD-1 antibody, with or without
Avastin® (bevacizumab), in patients with recurrent glioblastoma multiforme
(NCT02337491).
1175
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Adjuvant Immunotherapies
A phase I/II trial testing indoximod, an IDO inhibitor, in patients with recurrent glioma
(NCT02052648).
Monoclonal Antibodies
A phase I/II trial testing TRC105, an anti-endoglin antibody, in patients with recurrent
glioblastoma multiforme (NCT01648348).
Malignant Glioma
Conclusion
1176
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Meningiomas
Disclosure Statement
• Reports no commercial interest
1177 1
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meningioma
“MENINGIOMA”
1178 2
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Arachnoid cap
cell
1179 3
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1180 4
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1181 5
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7/98
2/00
8/99
1182 6
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6/93 11/04
1183 7
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•They need no
“control”
when they Are
self controlled
1184 8
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Fibroblastic
Meningeothelial
1185 9
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Transitional
Psammomas Body
Psammomatous
1186 10
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•Meningothelial
•Fibrous (fibroblastic)
•Transitional (mixed)
•Psammomatous
•Angiomatous
•Microcystic
9o%
•Secretory
•Lymphoplasmacyte- rich
•Metaplastic
Atypical
1187 11
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Atypical meningioma
Increased mitotic activity (> 4mitoses /10 HPF)
or three or more of following features:
•increased cellularity
•small cells with high nucleus
•cytoplasm ratio
•prominent nucleoli
•sheet-like growth
•foci of necrosis
•Atypical
•Clear cell
•Chordoid
1188 12
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1189 13
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•Rhabdoid
•Papillary
•Anaplastic (malignant)
1190 14
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1191 15
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1192 16
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1193 17
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1194 18
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7ys f-up
8/95 3/02
Preop. Postop.
3ys 1y
1195 19
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Presence of progesterone
receptors in meningioma is a RU 486
favorable prognostic factor
1196 20
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1197 21
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68%
ER+
6q25.1
PR+
11q22
7%
25% -non
Aggressive pathology
35%
**
*
30%
25%
20%
*, **
15%
10%
5%
0%
PR NON ER
Aggressive pathology
1198 22
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14
*
12
**
10
*,**
8
6
*
4
2
*
0
PR NON ER
Chromosome abnormalities in de
novo meningiomas
70%
60%
**
50%
*
40%
**
30%
20% *,**
*,** * *
10%
*
0%
PR NON ER
1199 23
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80
70
60
50
40
30
20 *
10
*, ** **
0
PR NON ER
*
20%
15%
10%
5%
*
0%
PR NON ER
3% 8% 22%
1200 24
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ETIOLOGY
Trauma
Viruses Papovavirus antigen
BK viral DNA
SV40 viral DNA
Radiation Low dose
High dose
1201 25
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12/96 Postop.
1/00 recurrence
11/99 recurrence
12/23/99 -Postop. F-up GK 5/02
1202 26
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1203 27
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High Dose
Low Dose
1204 28
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TRAUMA
Berlinghieri (1772-1825)
Meningioma might develop
1. as many as 10 to 12 y after
head injury
2. H. Cushing
1897 –U.S. Army General Leonard Wood - head
injury from a low-hanging chandelier
1905 – meningioma, first surgery
1910- two stage surgery for parasagittal
meningioma. Pt was discharged in good health
and in 1920 he was the republican favorite to
succeed Woodrow Wilson as president.
1205 29
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1206 30
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1207 31
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1208 32
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31 5 0
Normal karyotype 29% 16 % 0%
75 31 6
73% 41% 8%
1209 33
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1210 34
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Normal
Tumor
Meyerson, 2010
1211 35
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1212 36
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1213 37
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1214 38
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1215 39
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1216 40
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1217 41
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1218 42
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1219 43
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1220 44
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Bernasconi-Cassinari
artery (1956)
1221 45
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1222 46
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CURE
1223 47
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Recurrence Risk
Simpson’ s Recurrence
Grade Rate (%)
I 9
II 19
III 29
IV 39
V 89
1224 48
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1225 49
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3/88
GRADE 1
6/02- recurrence
8/02- postop.
1226 50
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9/18/03preop. 4
Pathology- Grade II
1227 51
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6/04
9/04
9/04 preop.
1228 52
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Grade III
POSTOP.
1229 53
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He died 3 ms late
from progression
1230 54
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1231 55
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1232 56
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1233 57
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ANTERIOR THIRD
MIDDLE THIRD
POSTERIOR THIRD
OPEN
PARTIALLY CLOSED
OCCLUDED
ONE WALL
TWO WALLS
THREE WALLS
1234 58
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1235 59
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1236 60
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1237 61
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1238 62
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1239 63
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1240 64
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Origin
1241 65
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Alike
But,
quite different
1242 66
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1243 67
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Adcok,
Burden
1244 68
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1245 69
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M.Yasargil, 1984
1246 70
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1247 71
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“Tumor Control”
>90%
1248 72
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F-up > 5 ys
1249 73
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1250 74
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Basal meningioma
γ- Knife
99 pt (89 - skull base meningioma)
Clinical control 93%
(No resection required)
Increase in size 5%
To surgery 7%
Complications 14%
F-up 5-10 ys
1251 75
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179 patients
140 tumor-for f-up 37.3 mos
Complications-25%
1252 76
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4/91 12/94
Add GK post GK
9/99
1253 77
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MENINGIOMAS
Delayed aggressive growth after
initial control by radiosurgery
12 cases
Average of latency- 37.85 mo (6-108)
Rapid growth 10
Change of pathology (B-A) 4 (from 9)
Cytogenetic abnormality 3 (from 5)
1254 78
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53% 67%
1255 79
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VA
20/400
VA
20/20
1256 80
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Visual improvement
Curative removal
1257 81
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1258 82
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The D,D,D,D of
Meningioma Surgery
• D: Disrobe
• D: Devascularize
• D: Debulk
• D: Dissect
1259 83
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1260 84
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Ultra short
1261 85
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Post op
Post op
1262 86
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1263 87
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SURGICAL STRATEGY
Exposure with minimal
brain retraction.
Vascular preservation.
Cranial nerve preservation
1264 88
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1265 89
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1266 90
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1267 91
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1268 92
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1269 93
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ER PR Ki67
1270 94
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1271 95
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VEINS RULE
1272 96
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Defeated
by
BIOLOGY
Preop. Postop.
(R5)
1273 97
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Malignant
High -
proliferative ER+
index
1274 98
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1275 99
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1276 100
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1277 101
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1278 102
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1279 103
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1280 104
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Estrogen is bad
Progesterone is
good
4/04
10/03
1989
3/04
9/03
4/04
12/03
3/01
1281 105
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1282 106
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1283 107
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Planes
1284 108
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1285 109
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1286 110
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1287 111
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Devascularization
Al-Turky
1288 112
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1289 113
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Personal experience
1000 and 1
meningiomas
MEET
ANDI –
The ancestor of the
future perfect human
1290 114
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1291 115
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First pathology
1292 116
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Recurrence
Second recurrence
1293 117
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1294 118
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Second surgery
1295 119
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1296 120
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1297 121
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Adhesion
Wittaker
1298 122
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1299 123
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SRS FSRT
35 pt 18 pt
Dose 1400 cGy 5400 cGy
Volume 6.8 ml 8.8 ml
3y TC 92.7% 93.3 %
WHO Gr I 92.9% 92.3 %
Compl. 2 pt 1pt
F-up 4-97 mo 6-63 mo
1300 124
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ICE
1301 125
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1302 126
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1303 127
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Meningiomas’ Future =
Neurosurgery’s Future
Personal experience
1000 and 1
meningiomas
1304 128
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Francesco Durante
(1844-1934)
1305 129
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1306 130
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1307 131
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1308 132
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1309 133
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1310 134
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1311 135
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1312 136
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810
Witaker
1313 137
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1314 138
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Monfort
1315 139
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1316 140
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1317 141
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1318 142
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Preop
F-up 3 mo
Postop.
1319 143
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1320 144
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GK and I
Actuarial
Prediction
Guess
Wrong Guess?
1321 145
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γ- Knife
159 patients
Average follow-up 35 mo
◊Clinical control 93%
◊Radiological control 94%
1322 146
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8080
ANY Growth
Survival probability (%)
6060
group
mix
4040
2020
00 50
50
100
100
150
150
200
200
Time (Months)
Time
1323 147
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11/99
5/00
11/04
1324 148
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Operated - 28
Mortality / Morbidity - 0
CURE
♦Surgical removal
Forever
1325 149
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1326 150
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1327 151
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1328 152
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1329 153
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1330 154
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1331 155
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Petroclival meningioma
194 cases (1983-2003)
OUTCOME
•Surgical mortality 0%
•Partial resection 10%
•Non cranial nerve morbidity 4 (3%)
Temporal lobe venous infarct 1 pt
Mid brain infarct 2 pt
Repeated intraventricular hemorrhage 1 pt
1332 156
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Parasellar Meningioma
317 cases
1333 157
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Principles in
the Operative
Management
of Low-Grade
Gliomas
Nader Sanai, MD, FAANS, FACS
Associate Professor of Neurological Surgery
Director, Division of Neurosurgical Oncology
Director, Barrow Brain Tumor Research Center
Barrow Neurological Institute
Disclosures
1334
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Median
2-Year 5-Year 10-Year
Age at
Survival Survival Survival
Diagnosis
Grade IV 55 12% 5% 3%
1335
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“Malignant”
9% Grade III: More aggressive
Astrocytoma Oligodendroglioma
WHO Grade III WHO Grade II
1336
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36 % Concordance in tumor
histology, grade,
and MIB-1 labeling
72 % Concordance in tumor
grade
1337
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20
15
10
1338
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* Adjusted for the effects of patient age, KPS, tumor location and tumor subtype.
† Per unit of measure (e.g. log cm3, cm 3, %)
100% 98%
Claus (2005) 156 <0.05
<100% 92%
>90% 97%
Smith (2008) 216 <0.001
<90% 76%
100% 100%
Capelle (2013) 1091 0.0199
<100% 77%
1339
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‘Malignant’ Transformation
Risk of Transformation
Literature is varied: incidence ranges from 11-100%
median time to transformation ranges from 2.1-6.4 years
50-75% of Grade II gliomas become Grade III or IV within 7-8 years*
*Jaeckle et al., J Neurooncol 2011; Aug; 104(1): 253-9
Persistent Growth
Even without transformation, Grade II gliomas continuously grow 4.1mm / year*
‘Malignant’ Transformation
Risk of Transformation
Tumor
Literaturegrowth
is varied:
rate can be incidence
instructive
ranges from 11-100%
median time to transformation ranges from 2.1-6.4 years
Changes
12.0 in growth rate identify LGGs that
50-75% of Grade
have become II gliomas
or will becomebecome Grade
anaplastic in III or IV within 7-8 years*
Jaeckle
*the al., J Neurooncol 2011; Aug; 104(1): 253-9
nearetfuture*
11.8
Tumor Volume (ml)
11.6
Persistent Growth
11.4
11.2
11.0
10.8
10.6
Transformers
10.4
0 6 12 18 24
Non-Transformers
Time (months)
1340
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5-year Malignant
Progression-Free
Survival:
88% with EOR ≥ 90%
71% with EOR < 90%
Sanai et al, J. Neurosurg. 2010; 112(1):1-9
1341
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1342
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80 EOR > 90
Laura Snyder, MD
Assistant Professor of Neurosurgery
60 EOR < 90
Barrow Neurological Institute
40
p=NS
20
0
0 20 40 60 80 100 120
Time (months)
*Smith et al. J Clin Oncol. 2008; 26(8):1338-45
*Sanai et al., J. Neurosurg. 2010; 112(1): 1-9
1343
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High-Grade Glioma
Reported Rates of Gross-Total Resection
30% - 84%
Disaggregated Dataset
1714 of 2616 Tumors = 65.5% GTR
Intraoperative Technology
Fluorescence-guided surgery for low- and high-grade gliomas
Intraoperative MRI for identification of residual tumor
Intraoperative ultrasound to visualize local microvasculature
Intraoperative CT to compensate for brain shift
1344
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1345
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Months Months
Sanai et al., J. Neurosurg., 2011 McGirt et al., Neurosurgery, 2009
1346
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Alexia
LanguageTraditional Targets for Intraoperative Awake Mapping Motor
Broca’s mouth
Motor
Naming
Reading
Sensory
Writing
Visual
Anomia
Speech
Subcortical arrest
Broca’s Area Wernicke’s Area
1347
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En Bloc Approach
Windowing Approach
1348
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1349
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1350
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1351
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1352
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1353
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Email: Nader.Sanai@bnaneuro.net
1354
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Surgical Management of
Pineal Region Tumors
Jeffrey N. Bruce, MD
Columbia University
Disclosure Statement
• Reports no commercial interest
1355
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Histological Considerations
Historical Perspective
1356
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Potential RT complications
• Hypothalamic/endocrine
dysfunction
• cerebral necrosis
• RT-induced tumors
• cognitive impairment
ependymoma
pineocytoma
germinoma
1357
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Pineal cysts
Diagnostic considerations
• tissue diagnosis mandatory
1358
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Stereotactic
Biopsy
vs
Open Resection
Advantages of Open
Resection for Pineal Tumors
• definitive diagnosis
• resection curative for benign tumors
• resection curative for some non-benign tumors
• malignant tumors can benefit from debulking
• operative risks are acceptable
• control of hydrocephalus
1359
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• sampling errors
– 25% of GCT are mixed
• small sample difficult to interpret
• hemorrhage
• ignores benefits of removal or debulking
• bleeding risks
– deep venous
system
– vascular tumors
– vascular
anomalies
1360
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Indications for
stereotactic biopsy
• tumor
dissemination
• medical
contraindications
to craniotomy
• invasive tumors
Endoscopic considerations
1361
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1362
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1363
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ADVANTAGES
• direct midline approach
• avoid deep veins
• gravity assists exposure
DISADVANTAGES
• sitting position
- air embolus
1364
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1365
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1366
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1367
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1368
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1369
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1370
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DISADVANTAGES
• venous system over tumor
• occipital retraction
• +/- sacrifice bridging veins
• visual field deficits
• difficult to resect tumors
projecting anteriorly
1371
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1372
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1373
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Midbrain Gliomas
1374
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Intramedullary ependymoma
1375
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1376
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1377
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preop postop
1378
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ADVANTAGES
• broad exposure
DISADVANTAGES
• venous system over tumor
• parietal retraction
• sacrifice bridging veins
1379
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Operative approaches
n = 181
Infratentorial-supracerebellar - 83%
Occipital-transtentorial - 6%
Interhemispheric-transcallosal - 5%
Stereotactic biopsy - 5%
1380
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Miscellaneous (22%)
TOTAL = 181
Surgical Results
(n=181)
Radical
histology Bx STR STR/GTR
BENIGN 2 5 70
MALIGNANT 12 29 63
Total 14 34 133
1381
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Total - 181
Common Postoperative
Complications
• EOM dysfunction
• Ataxia
• shunt malfunction
1382
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Venous complications
1383
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1384
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Benign tumors
teratoma, dermoid, epidermoid,
pilocytic astro, meningiomas
1385
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OUTCOME
MALIGNANT TUMORS
1386
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Postoperative Staging of
Malignant Pineal Tumors
Radiation Therapy
1387
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Spinal RT
1388
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Germinomas
Malignant NGCT
Before chemotherapy After chemotherapy
• poor prognosis
• recent results promising
• cisplatinum/VP-16 and RT
1389
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Radiosurgery
preop postop recurrence
1390
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Tord D. Alden, MD
Assistant Professor,
Division of Neurosurgery
Ann & Robert H. Lurie Children’s Hospital of Chicago
Feinberg School of Medicine, Northwestern University
talden@luriechildrens.org
Disclosures
• There are no off-label usage described
below
• There is no industry support or affiliation
1391
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History
• 1926 Harvey Cushing presented at
pediatric meeting children with brain
and spinal cord tumors
• 1929 Franc Ingraham started
neurosurgical service at Boston
Children’s Hospital
• 1931 Harvey Cushing lectures on series
of cerebellar astrocytomas
History
• 1939 Drs. Bailey, Buchanan, and Bucy
publish “Intracranial Tumors of Infancy
and Childhood”
– Considered first textbook on Pediatric
Neurosurgery
– Pediatric brain tumors are different than
adult disease
– Sparse and inconsistent data published on
this subject
1392
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1393
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1394
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1395
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1396
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1397
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Neuroimaging Features
• Pilocytic Astrocytoma: cystic tumor,
solid nodule; hypodense on CT
• Medulloblastoma: hyperdense on CT,
midline arising from vermis, enhances
• Ependymoma: expands 4th ventricle,
creeps out lateral recesses, enhances,
calcium
Treatment Modalities
• Surgery
• Chemotherapy
• Radiation therapy
• Autologous Bone marrow transplant
after chemotherapy
• Many factors determine treatment
– Histology type and sub-type
– Age
– Disease burden (extent, location)
1398
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1399
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Surgical Management –
Hydrocephalus
• Endoscopic third ventriculostomy
• External ventricular drain
• Ventriculoperitoneal shunt
Surgical Management –
Hydrocephalus
• Pre-resection CSF shunt
– improves pre-op patient physiology
– provides slack surgical field
– risk of upward herniation of posterior fossa
structures
– potential for shunt-related tumor
dissemination
• Only 10 -30% of patients will need
shunts post operatively
1400
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Fourth Ventricle
• The floor must be
identified along with the
peduncles
• Tumor may be transected
to the plane of the floor
• Tumor resection from the
brainstem is not advised
1401
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Fourth Ventricle
• Complications:
– facial palsy
– abducens palsy
– vocal cord paralysis
– cerebellar ataxia
– injury to peri-aqueductal
structures
• INO
• horizontal gaze palsy
1402
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Sub-Occipital Craniotomy
Approach
• Transvermian
– midline tumors
• Transcortical
– hemispheric tumors
• Cerebello-medullary fissure
– less retraction
• Cerebello-pontine angle
1403
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Complications
• Surgical mortality is near zero
• Postoperative worsening needs evaluation
– hematoma
– pneumocephalus
– cerebellar edema
• Neurological morbidity is high
– Cerebellar ataxia
– Nystagmus
– Hydrocephalus
– Cerebellar mutism
1404
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Complications
• Aseptic meningitis
– Headaches
– Photophobia
– Fever
– Meningismus
• Low dose corticosteroids may be helpful
1405
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Complication – Hydrocephalus
• N=343 1989 to 2003
• age <2 yrs 3
• presence of papilledema 1
• moderate/severe hydrocephalus 2
• cerebral metastases 3
• preop estimated tumor diagnosis
– Medulloblastoma 1
– Ependymoma 1
– Dorsal exophytic brainstem glioma 1
• total possible 10
1406
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Probability of Hydrocephalus at
6 months after Resection
• 0 0.071
• 1 0.118
• 2 0.191
• 3 0.293
• 4 0.422
• 5 0.562
• 6 0.693
• 7 0.799
• 8 0.875
• 9 0.925
• 10 0.950
1407
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Specific Tumors
1408
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Cerebellar Pilocytic
Astrocytoma
JPA – Epidemiology
• 10% of all pediatric brain tumors
• 25% of posterior fossa tumors
• 90% pilocytic: do not reoccur when
totally resected
• Mean age at presentation 6 to 8 years
• M:F ratio equal
• 96% 10-year survival
1409
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Cerebellar Pilocytic
Astrocytoma
• A circumscribed, morphologically and
biologically distinct astrocytoma subtype
• A unique intraaxial tumor
– surgically curable
• Represent 35 - 40% of all posterior fossa
tumors
• Sometimes termed juvenile or cystic
cerebellar astrocytomas
• Usually present between 5 - 10 years of age
– infrequent in neonates and infants
• A second peak occurs in young adults
1410
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JPA – Classification
1411
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Cerebellar Pilocytic
Astrocytoma
• Two histologic patterns:
– densely compact regions with hair like
processes
– loose spongiform foci
• Rosenthal fibers
• Low mitotic activity
• Cysts
• Usually no necrosis
JPA – Surgery
• If the cyst wall enhances or is thickened,
attempt to remove it
• If the cyst wall does not enhance, no need to
remove it
1412
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JPA – Outcome
• 95% 25 year survival after GTR
• If residual
– Re-explore
– Evidence for tumor involution
• 5 to 10% recurrence after GTR
Outcome
• Routine surveillance scanning should be performed on
a regular basis
• Regression or involution of residual disease has been
documented
• Reoperation is the treatment of choice for recurrent
disease
– Adjuvant therapy rarely required
1413
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Outcome
• The most important predictive parameter in
determining outcome is the extent of tumor
removal
– Midline = hemispheric
– Cystic = solid
• Brainstem infiltration is a poor prognostic sign
• Most recurrences occur within three years of
diagnosis
– Late recurrences have been reported
– Residual tumor may not always recur
• Recurrence occurs locally
• CSF dissemination is exceptionally rare
1414
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Medulloblastoma
1415
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Medulloblastoma
• One of the most common tumors of the
posterior fossa
• Comprise between 15-25% of all childhood
brain tumors
• Occur at any age but predominate in
childhood
• Mean age at presentation is 5-6 years
• Most frequently present in the fourth ventricle
• Tend to invade cerebellar tissue and the
cerebellar peduncles
• The brainstem is usually compressed and
often invaded
Medulloblastoma
• Typically protrude through foramen of
Magendie
• Early CSF dissemination is common
• The aqueduct of Sylvius is frequently
enlarged
• Less frequently located laterally within
the cerebellar hemispheres
1416
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Medulloblastoma
• Hyperintense on NECT
• Enhance strongly
• Hemorrhage rare
• Calcification rare
• Displace IV anteriorly
• Hydro is common
Medulloblastoma
• Fills fourth ventricle
• Heterogeneously
hypointense to gray
matter on T1WI
• Enhancement varies
• Variable on T2WI
• Cysts are common
• CSF dissemination ?
1417
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Medulloblastoma
• Disseminated disease occurs in 50% of
cases
• 66% Leptomeningeal
• 15 to 33% extracranial
– bone
• 10-50% of initial images
Medulloblastoma
• Highly cellular
• Round to oval cells
• Hyprchromatic nuclei
• Scant cytoplasm
• Ill defined borders
• Homer Wright rosettes
1418
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Medulloblastoma – surgical
findings
• Blood supply arises at interface with
vermis
• Identify the floor of the 4th ventricle
early
• Residual tumor
– Superior most vermis
– Lateral recess
– Foramen of Luscka
Staging
• Based on surgical impression and post
op imaging
• Whole brain and spinal MRI is required
• Patients with disseminated disease at
diagnosis are at highest risk
• Unfavorable factors:
– Younger age
– Brain stem involvement
– Subtotal resection (1.5 cm3 residual)
– Non-posterior fossa tumor
1419
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Staging
• Average risk
– Age > 3 years with posterior fossa tumor
– Total or “near total” resection (<1.5cc residual)
– No dissemination
• High risk
– Age < 3 years
– Metastatic disease
– Subtotal resection (>1.5cc residual disease0
– Non posterior fossa tumor
– Anaplasia on pathology
Molecular Markers
Medulloblastoma Comprises Four Distinct Molecular Variants. Paul A. Northcott, Andrey Korshunov, Hendrik Witt, Thomas Hielscher,
Charles G. Eberhart, Stephen Mack,Eric Bouffet, Steven C. Clifford, Cynthia E. Hawkins, Pim French, James T. Rutka, Stefan Pfister, and
Michael D. Taylor. J Clin Oncol 29:1408-1414. 2010
1420
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Molecular Markers
Molecular markers
• Shh (Sonic Hedgehog) pathway
alterations (favorable)
• Wnt pathway alterations (favorable)
• c-myc amplification (unfavorable)
1421
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Outcome
• Overall survival after surgery and radiation
therapy:
– 50-60% @ 5 years
– 33-53% @ 10 years
• Recurrence:
– Most occur within two years of diagnosis
– Common sites: posterior fossa, CSF pathways,
cribiform plate, temporal tips
– Systemic metastases: bone, lymph nodes
– Almost all occur within the period of risk defined
by Collins’ rule
– Treatment options very limited
Challenge: Infant
and Adolescent
Medulloblastoma
1422
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Histopathological Features
Medulloblastoma
Classic Anaplastic
Medulloblastoma Medulloblastoma
1423
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Molecular Characterization
1424
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1425
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Ependymoma
Ependymoma
• Ependymal cells are related
to other glial cells
• Ependymomas are slow
growing neoplasms that are
often partially cystic
• Arise most commonly in the
fourth ventricle (60%)
• Have a tendency to “ooze”
through foramina (“plastic
ependymoma”)
1426
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Ependymoma
• Peak age range is 1 to 5 years
• 4 to 6 times more common in children
• 15% of all childhood brain tumors
• Usually have a long clinical history
• Cranial nerve dysfunction is more common
compared to other posterior fossa tumors
– compression or invasion of the floor (VI, VII)
– CPA spread (V, VII, VIII)
– lateral foramen magnum (IX, X, XI)
Ependymoma
• Findings are variable
• Non enhanced CT
– Mixed density mass
– 50% calcified
– inhomogeneous enhancement
– hemorrhage uncommon
– hydrocephalus
1427
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Ependymoma
• Lobulated mass casted or molded into
fourth ventricle
• Extrudes out foramina
• T1WI - iso or hypo
• T2WI - hyper
• Inhomogeneous enhancement
Ependymoma
• Appearance and
architecture is variable
• “Leopard skin”
• Dense palisades of nuclei
around vessels
• “Pseudorosettes” and
“ependymal rosettes”
• Low mitotic index
• Moderately cellular
1428
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Ependymoma
• Grow through foramina of IV vent.
• Frequently in CPA where they displace
the brainstem and cerebellum
• Well demarcated
• Limited infiltration
Surgery
• Resection is frequently limited by
adjacent neural structures
– invades floor
– surrounds cranial nerves
• Most morbidity consists of various
cranial nerve palsies
1429
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Ependymoma
• Careful and full inspection of Foramen
of Luschka
• Blood supply from brainstem
• Can wrap around vessels and CN out
laterally
Results
• Improved progression-free survival with multi-agent
regimens in concert with radiation therapy
• Spinal seeding is uncommon, but can see
intraventricular spread
• Chemotherapy can be used to delay radiation in
patients under 3-yrs of age
• Survival at 5-years:
– Complete Resection with XRT 60-80%
– Incomplete Resection 0-30%
– Complete resection with posterior fossa 3D radiation with high
survival
• Consider “second look” surgery after chemotherapy for
those with incomplete resection
1430
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1431
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1432
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1433
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Brainstem Gliomas
Midbrain
Focal
Tectal
Pontine
Diffuse Intrinsic
Dorsally Exophytic
Focal
Cervicomedullary
1434
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1435
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Brainstem Gliomas
• Excluding the DIPG, other brainstem
tumors can have better prognosis
• Tumors that are exophytic and
surgically accessible are often lower
grade
• Surgical resection may be sufficient
1436
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Brainstem Glioma
• Recent and renewed interest in
obtaining a tissue diagnosis
• Complication rates of biopsy as high at
10 to 25%
• New techniques to stratify
– Proteomic analysis of CSF
– Gene and protein specific markers for
customization of therapy
Other Tumors
1437
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Neonatal tumors
• Blood volume 70cc per kg
• The younger the child, the smaller the
reserve
• Plan operatively
• Pathology is often more aggressive due
to primitive nature
Skull tumors
• Can be found throughout the skull
• Pathology
– Langerhans cell histiocytosis
– Dermoid
– Epidermoid
• Treatment
– Excisional biopsy
1438
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1439
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ATRT
• Most often found at CP angle in
posterior fossa
• Often involving multiple cranial nerves
• Consider monitoring with EMG
stimulation of appropriate CN
• Prognosis is poor with median survival
<12 months
Atypical Teratoid/Rhabdoid
Tumor
• First recognized by Lucy Rorke in 1987
– Senior pathologist at U of Penn
• 1993 the WHO classified ATRT as Grade IV
Embryonal neoplasm
• Incidence
– Unknown given its late recognition
– Children’s Cancer Group (9921) 10-15% of
infants
– Ped Onc Group & Ped BT Consortium – 15% of
malignant tumors < 36m old
• Usually in younger Children (<2y)
1440
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ATRT Pathophysiology
• Prior to its recognition was often
diagnosed as a medulloblastoma or
PNET
– Components of ATRT resememble other
primitive tumor types
• Pathologically resembles malignant
rhabdoid tumors of the kidney
• Immunohistochemically can vary widely
so molecular analysis can but used to
help diagnose
Imaging
1441
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1442
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Surgical Resection
• Goal = gross total resection
1443
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Pathology
• Malignant rhabdoid cells on a
background of primitive neuroectoderm
cells, mesenchymal cells, or epithelial
cells.
– Rhabdoid cell: medium
sized, eccentric nucleus,
pink cytoplasmic
inclusion body
Pathology
H&E
Vimentin
EMA
MIB
1444
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Pathology
• Histological identification can be difficult
• Staining:
– + vimentin, GFAP, EMA, cytokeratin,
synaptophysin, chromagranin, Smooth muscle
actin
– MIB > 50%
Molecular Analysis
• Histological Phenotype can differ
• Molecular Analysis
– Majority of ATRT have mutations of
hSNF5/INI1 gene on chromosome 22
• Encodes for chromatin remodeling complex
1445
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1446
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1447
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Conclusion
• Pediatric brain tumors have been a
challenge since the beginnings of
pediatric neurosurgery
• Surgery still plays a major role in
defining the disease
• Multi-modality treatment paradigms
targeting genes and their protein
products are on the horizon
1448
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Thank You
1449
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Disclosures
Reports no commercial interest.
1450
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1451
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1452
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1453
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1454
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1455
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1456
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1457
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Options
• Conservative follow-up
• Surgical removal
• Radiation treatment
– Stereotactic radiosurgery
– Stereotactic radiotherapy
• Combined surgery and radiation
1458
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50% surgery
25% radiation
25% observation
1459
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1460
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Conservative Management
• What percent of tumors show growth?
• What is at risk over the period of
observation?
1461
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1462
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1463
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VDT:
volume
doubling
time
Surgery
1464
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1465
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Hearing Preservation
with Surgery
• Is it worthwhile?
• Is preserved nonuseful hearing more aggravating?
• Is a total resection possible with hearing
preservation?
• Will hearing preservation be long-lasting?
• Is tinnitus altered by tumor removal?
• Are post-op headaches so severe to preclude
surgery?
• Are CSF leaks still a problem?
• Is quality of life acceptable after surgery?
1466
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Approaches
• Suboccipital transmeatal
• Translabyrinthine
• Middle fossa
Supine Position
1467
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Technical Pearls-1
• Supine position
• Facial nerve monitoring
1468
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Facial Nerve
Monitoring
Technical Pearls-1
• Supine position
• Facial nerve monitoring
• BAER monitoring (or direct VIII)
1469
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Hearing Monitoring
• BAER: scalp electrodes
• measures N1 and N5
• direct recording of VIII - cochlear n.
BAERs
• Intra-operative use of BAERs to guide vestibular
schwannoma resection
– Wave I-II and I-III interpeak intervals
– Wave I-V interpeak interval latency
• Hearing may be diminished or lost completely
even with anatomic preservation of CN VIII
III IV V
I II
1470
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Results
• A total of 133/205 patients met inclusion
criteria
– 79 female/54 male
– Mean age = 46.9 (SD 10.69)
• 68/133 (51.1%) BAER latencies < 2ms
– 37/68 (54.4%) non-functional hearing
– 31/68 (45.6%) functional hearing
• 65/133 (48.9%) BAER latencies ≥ 2ms
– 60/65 (92.3%) non-functional hearing
– 5/65 (7.7%) functional hearing
Results
• Patients with
100
pre-operative 90
BAER latencies 80
≥ 2ms had 70
Percent (post-op)
Functional
60
Hearing
significantly 50
decreased 40 Non-
30 Functional
functional 20 Hearing
hearing post- 10
0
operatively
< 2ms ≥ 2ms
– p < 0.001 Latency
1471
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Results
• Multivariate analysis:
– Hearing preservation was less likely in patients
harboring larger tumors (p = 0.038)
– Hearing preservation was less likely in patients with
pre-operative BAER latencies ≥ 2ms independent of
tumor size (p < 0.001)
BAER Summary
• A ≥ 2ms latency is statistically significant in
predicting post-operative functional hearing
loss
• We suggest that the utilization of pre-operative
BAERs as a prognosticator of post-operative
hearing is a reliable tool that can guide
decision making in hearing preservation
patients
1472
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Technical Pearls-1
• Supine position
• Facial nerve monitoring
• BAER monitoring (or direct VIII)
• Adequate bone opening (4cm)
• Open dura inferiorly and release CSF
• Keep dura moist
• Expose angle – usually one retractor
1473
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1474
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Technical Pearls - 2
• Drill canal before opening arachnoid
• Wash out all bone dust
• Open arachnoid
• Stimulate entire surface for VII
• ? Place electrode on VIII
• CUSA the core of the tumor
1475
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Post-operative Problems
• Headaches
• Tinnitus
• CSF Leak
Post-op Headaches
1476
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AICA
1477
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AICA Dissection
AICA Dissection
1478
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AICA Free
1479
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1480
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1481
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1482
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Technical Pearls -3
• Identify VIII, isolate vestibular and cut
• Identify VII
• Decompress tumor in canal
• Identify intracanalicular VII and VIII
• Gentle teasing with countertraction or sharp
dissection
• Papaverine irrigation
• Nothing on VIII
1483
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1484
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1485
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Papaverine irrigation
1486
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15mm Schwannoma
Canal drilled
1487
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1488
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Follow planes
Final view
1489
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1490
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Technical Pearls - 4
• Inspect lateral end of canal
• Bone wax/cement and muscle/fat
• Dural closure
• Cranioplasty
• Steroids for 1-2 weeks
• Serial LPs
1491
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1492
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1493
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4 1 (1%) - 1 (1%)
5 2 (1%) 3 (2%) -
1494
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99.9% is:
+ tinnitus - tinnitus
Pre-op 10 16
1495
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+ tinnitus - tinnitus
Pre-op 23 28
1496
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1995
Tumor 1.5-2.0cm
pre-op good 27 11 (41%) 6 (22%) 10 (37%)
Tumor >2cm
pre-op good 73 7 (10%) 5 (7%) 61(84%)
2003
1497
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Audiogram Results
• Pre-Operative
– PTA average 23.02dB
– Range 5-57 dB
• Immediate Post-Operative
– PTA average 34.95dB
– Range 8-69 dB
Audiogram Results
• Pre-Operative
– Discrimination average 89.91%
– Range 60-100%
• Immediate Post-Operative
– Discrimination average 82.35%
– Range 8-100%
1498
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•Immediate Post-Operative
–PTA average 35.09dB
–Range 8-69 dB
–Discrimination average 82.48%
–Range 8-100%
1499
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1500
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1501
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1502
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• CSF Leak
• Headache
• Facial Weakness
• Wound Infection
• Meningitis
• Ataxia
• Diplopia
• Keratitis
1503
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1504
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1505
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1506
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1507
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1508
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1509
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1510
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1511
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1512
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1513
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1514
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1515
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• Single surgeon
• 135 consecutive patients, 101 responded
• minimum of 6 months post op
1516
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Debate
Radiosurgery Microsurgery
Size
Age
1517
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• 95 patients 2000-2002
• 48 patients followed > one year
• 67% preserved serviceable hearing (50/50 level)
• 82% preserved hearing if Class I to begin
• No new trigeminal dysfunction
• One patient with previous VII weakness worsened
at one year fu
1518
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1519
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1520
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1521
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1522
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1523
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1524
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1525
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Summary
1526
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1527
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1528
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1529
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1530
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1531
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1532
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Issue #5 Mortality
• Radiosurgery: 0
• Microsurgery: 1-2%
• Radiosurgery: 0
• Microsurgery: 5-10%
1533
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Issue #7 Cost
• Advantage Radiosurgery
Issue #8 - Oncogenesis
• The concerns that stereotactic radiosurgery
may lead to the development of delayed
radiation-induced neoplasms remain
unsubstantiated; an increased incidence of
new neoplasm development has not been
reported despite more than 26 years of
experience and the treatment of more than
20,000 patients worldwide.
• Kondziolka D. NEJM, 82:1426-1432, 1998.
1534
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• Reports conflicting
• Samii – Nerves are paler and more tenuous.
• Malis – No change
1535
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1536
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1537
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1538
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Debate
Radiosurgery Microsurgery
Size
Age
1539
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1540
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1541
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1542
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Z.B. Wu, et al
J. Neurosurgery (2005)
1543
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Type I
1544
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Z.B. Wu, et al
J. Neurosurgery (2005)
Z.B. Wu, et al
J. Neurosurgery (2005)
1545
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Type II
Type II
1546
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Type II
Z.B. Wu, et al
J. Neurosurgery (2005)
1547
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Type III
1548
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Type III
Type III
1549
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Z.B. Wu, et al
J. Neurosurgery (2005)
1550
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Z.B. Wu, et al
J. Neurosurgery (2005)
1551
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1552
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Leonetti et al
Otolaryngology-Head and Neck Surgery (2006)
Leonetti et al
Otolaryngology-Head and Neck Surgery (2006)
1553
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Leonetti et al
Otolaryngology-Head and Neck Surgery (2006)
1554
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1555
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1556
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1557
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1558
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Petroclival meningiomas
• A different entity
• Aggressive, but incomplete surgery
• Combination therapy
1559
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1560
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CPA Meningiomas
Is total resection reasonable if nerves need to be
sacrificed?
The selection of operative approach and the goal of
surgery should be part of the whole treatment strategy
The attempt to achieve complete resection can be
justified only if the associated long-term morbidity is
minimal.
The retro sigmoid suboccipital approach is the most
effective and safe approach – i.e. The gold standard
for lesions in the CPA.
1561
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1562
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1563
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1564
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1565
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1566
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1567
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1568
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1569
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1570
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1571
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Proposed Algorithm
Age Tumor Presentation First therapeutic Following
Size option evaluation
Young small no signs conservative growing tumor: GKS
signs GKS
Large or microsurgery residual tumor
brainstem (optimal radical small: GKS
compression resection or planned large: another surgery or
two-step strategy) radiotherapy (also if
malignant)
Elderly small conservative growing tumor: GKS
large no signs conservative growing tumor: total sub-
optimal removal
signs microsurgery (total Residual tumor:
suboptimal removal) small: GKS
stereotactic radiotherapy if
too large
1572
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Disclosure Statement
1573
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Critical Advances in
Neurosurgical Treatment
Technique Decade Need
What is “stereotactic
radiosurgery”?
• The delivery of a very high dose of
irradiation to a small and critically
located intracranial volume
through the intact skull
• Alternative and adjunct to surgery
and radiation therapy
• Tumor, vascular malformations,
functional disorders
• Use of:
– Stereotactic principles/guidance
– 1-5 fractions
– High conformality
– Steep fall off
1574
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GK Icon
Modern Stereotactic
Systems
• Incorporate all
advanced
neuroimaging (e.g.
SPECT, PET,
functional MRI)
• MR compatible
• Accurate and precise
• User friendly
• Concept of “minimally
invasive surgery”
1575
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Stereotactic radiosurgery
Symptom Diagnosis
Radio
surgery
1576
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Basic Units
Measurement Common Units Official (SI) Unit
Joules (J), Mega Joules (J)
Energy
electron-volts (MeV)
Activity –
disintegrations per Curie (Ci) Becquerel (Bq)
unit time
Exposure – Coulombs/kg
Roentgen (R)
ionization (C/kg)
Absorbed Dose – Gray (Gy)
energy deposited in Rad
tissue 1 Gy = 1 J/kg
Dose equivalent –
Rem Sievert (Sv)
biological effect
http://deepseanews.com/2013/11/true-facts-about-ocean-radiation-and-the-fukushima-disaster/
1577
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Dosimetric calibration
Patient positioning
Target definition
3D Imaging
Biological model
Target localization
Computer
displays
this…..
You
deliver
this!
Image courtesy of Stan Benedict, UC Davis
1578
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Step 2: Neuro-Imaging
1579
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Step 3: GK Planning
Dose Planning
• Isocenter based dose planning.
• 4^8 (i.e. 65,536) unique
combinations per isocenter
• Multiple isocenters per target.
• All make for highly conformal
plans and shielding around
eloquent structures.
1580
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Step 4: Treatment
Step 5: Follow-up
1581
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Multidisciplinary Approach to
Stereotactic Radiosurgery
1582
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Types of Stereotactic
Radiosurgery
• Gamma Knife
• Modified LINAC’s
• Proton Beam
• Cyberknife
• X-Knife
• Versa HD
• Tomotherapy
• Novalis
• Edge
1583
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Arteriovenous Malformations
1584
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• Intent
– 400 patients
– Followed for 5 to 10 years
– Randomized to medical tx vs. intervention
1585
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Aruba Results
• Risk lower in
Death or Stroke
medical tx group
• However mean f/u
33.3 months (SD
19.7 months)
• What about long-
term risk?
Risk of Hemorrhage
1586
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AVM Illustration
1587
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Predictors of an
unfavorable outcome
N=2236 patients
Prior Hemorrhage
Prior Embolization
Larger Volume
Eloquent location
Lower dose
More isocenters (likely related to volume but possibly
dose heterogeneity)
Dose-Volume-Location
Interrelationship 100
% obliteration
80
• Dose impacts 60
40
– Obliteration
20
– Complications through V12
0
• Limitations of dose 0 4 10 16 20
dose (Gy)
24
related primarily to
– Volume
– Location
• Deep vs. superficial
• Eloquent vs. noneloquent
– Prior radiation
– Neurological function
1588
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Unfavorable
Favorable
N=2236 patients
1589
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Unruptured AVM’s—Does it
Matter in terms of obliteraton?
• Should we treat
AVM’s with GKRS
That have not
ruptured?
• Analyzed 2236
patients from 7 busy
SRS centers
• Isolated 509 ARUBA
eligible pts
GKRS Obliteration of
Unruptured, ARUBA eligible
AVM’s
1590
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1591
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1592
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Trigeminal Neuralgia
The Problem
• Trigeminal neuralgia
(TGN) is a
– Paroxysmal lancinating pain
– Confined to a distribution
encompassing one or more
of the branches of the
trigeminal nerve
– Usually on one side of the
face
• Other kinds of facial pain
associated with post-
herpetic neuralgia,
multiple sclerosis,
diabetes, or trauma.
• Incidence 4/100,000/year
• Rare familial incidence
1593
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Patient Demographics
1594
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Radiosurgical History
of Facial Pain
• In his book Brain Fragments, Dr.
Leskell wrote,
“One can accept death, but one cannot
accept the deep, devastating pain.
Sharp, intractable pain is like hell
‘without escape, without hope and
without Heliotrope when Venom burns.’
Standing at the bedside without ever
having experienced pain, it is
impossible to imagine the patient’s
agony, and it is impossible to
understand that a short time without
pain can be extreme happiness.”
1595
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• Stereotactic frame or
mask for maximum
accuracy and precision
• High resolution MRI (1.5
or 3T, 1mm slices) or CT
cisternography
• T1 and T2 sequences for
MR
• Dose planning
• Dose delivery via small
beamlets (3 to 5mm)
Ridder NS 2002
1596
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Dose Planning
• Affected by length of
cisternal segment of
trigeminal nerve
• Must consider
– Integral nerve
A B dose
– Brain stem dose
– Prior nerve
dysfunction
– Prior treatments
C D
1597
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SRS Mechanism
• Disruption of
myelin
• Possibly some
intimal
hyperproliferation
of adjacent vessels
1598
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Results
• Median follow-up of 31 months
• BNI pain score of 1 was achieved in
59.4% of patients
• Vessel impingement was seen in 63
patients (59%)
• No difference was seen in the pain
relief between those with and without
vascular impingement following GKRS
1599
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Vascular Impingement
1600
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Results
– 1 year= 90% ,6
– 2 years=77% ,4
– 3 years=70% ,2
0,0 censored
0 30 60 90 120 150 180 210
1601
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Proximal
Proximal
Distal
Distal
Complications:
“No Free Lunch” (Burchiel)
• Pain relief maintained longer in
those with some numbness
• 9% of patients had new onset of
facial numbness
– Pollock et al. (2002) showed New numbness
this correlated with a dose of
90+Gy
• 19% had new or worsened facial
numbness
• No cases of new onset corneal
reflex loss or anesthesia dolorosa No numbness
• New onset of facial numbness
following SRS correlates with
– more than one SRS
– pain relief
1602
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• Evaluate patients
with TGN
undergoing SRS
– VAS
– BNI pain scale
– SF-36
1603
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1604
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Brain Metastasis
1605
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Lung: 48%
Brain Metastases
1606
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Approaching
Brain Metastasis
Patients
• Symptom management
• Staging of extracranial
disease
• Chemotherapy
• Intracranial disease staging
– 1 Lesion
• With evidence of systemic
disease (single)
• Without evidence of
systemic disease (solitary)
– Multiple Lesions
• 2-3
• All others
• KPS, RPA, GPA, and
Disease specific GPA status
Historical Treatments
• Surgical resection of solitary, symptomatic
metastases in patients fit for a craniotomy
• Corticosteroids
• Whole brain radiation therapy (WBRT)
• Chemotherapy
1607
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RTOG-9508:
Randomized SRS Trial
• Enrollment
Arm 1: WBRT (37.5 Gy) +
SRS: n=164
Arm 2: WBRT (37.5 Gy)
alone: n=167
• Stratification
1. Number of brain
metastases (1 vs 2 - 3)
2. Extracranial mets
(none vs present)
Andrews DW, et al. Lancet 2004;363:1665-1672.
RTOG-9508 Results
Survival Analyses WBRT + SRS WBRT P-value
(months) (months)
Overall 6.5 5.7 0.13
1608
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
SRS+WBRT
Based on level I evidence presented,
SRS alone coupled with close clinical
3
other histologies.
0.0 0.2 0.4 0.6 0.8 1.0
Event Probability
1609
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Myth #1:
Number of Metastases
• There is no holy 1…3…
grail for cut-off 4… 5?
number of brain
mets
• SRS devices allow
almost limitless
number of lesions
to be treated
1610
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Myth #2:
Micrometastases are everywhere
• Modern volume acquisition,
3T post contrast MRI can
detect even small mets
• Surveillance scanning
detects
– Early local or distant progression
– Leptomeningeal spread
• Intervene when it is
prudent
1611
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Myth #3:
All Mets Need Treatment
• Some mets are asymptomatic
• A number of studies have shown that a
disconnect between intracranial disease
control and overall survival
• We are not curing these patients. Our
intervention is palliative.
Myth #4:
All patients with WBRT suffer
neurocognitive decline
1612
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Myth #5:
All Brain Mets are Created Equal
• Outcomes vary
tremendously by
– Type of cancer
– Histological subtype
– Genetic subtype
Myth #6:
Brain Mets are Genetically Identical to Regional
and Extracranial Mets
1613
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1614
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Radioresistant
Metastasis
Pt with metastatic melanoma;
KPS=100;
At SRS (above left) and 7 months
post Gamma surgery (below right)
>35 month median local control 14.4 month median local control
For radioresistant mets For radioresistant mets
1615
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Radiosurgery to a Tumor
Resection Cavity
• Following a gross total
resection of a brain
metastasis, recurrence
occurs 47% of time.
• WBRT reduces the
chance of recurrence.
• Radiosurgery with a 2
mm margin around
– Also reduces recurrence
– May avoid sequelae of
WBRT
– Hold WBRT until really
needed
1616
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
JLGK0901 Study
Up to 10 BM is reasonable for SRS
• Comparable
survival for
those with
5-10 versus
2-4 BM’s
1617
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1618
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Conclusions
• Radiosurgery is a safe
and effective strategy
for many intracranial
pathologies.
– Low morbidity
• Minimally invasive
• Low risk of delayed
neurological deficits
• Rare incidence of
radiation injury
1619
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Conclusions
• Stereotactic radiosurgery
frequently affords:
– Tumor volume stabilization
– Preservation or improvement of
neurological function
– Enhanced quality of life
– Extended life expectancy in
patients with malignant tumors
– Pain relief
• Dose escalation or repeat
radiosurgery may be
needed to treat certain
malignant lesions.
1620
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Neurosurgery – A Comprehensive
Review
Michael W. Groff, MD
Director of Spinal Neurosurgery
Disclosures
Independent Contractor:
BestDoctors, Inc
1621
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Goals: NOMS
Neurologic
• Decompression
Oncologic
• Resection
Mechanical Stability
• Instrumented Fusion
Systemic Disease
• Death or Prolonged Hospital Stay
Mark Bilsky
Metastatic Primary
• Palliation • Cure
• Intra-lesion • En bloc
• Adjuvant therapy • Limited adjuvant
1622
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Primary Tumor
Breast 22%
Lung 15%
Prostate 10%
Myeloma 9%
Lymphoma 7%
Renal 6%
Thyroid 3%
1623
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Spinal Level
Thoracic 70%
Lumbar 20%
Cervical 10%
Probability of met =
f (number of bodies,
size of bodies)
1624
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Back Pain
Cord Compression
Pathologic fracture - 8% incidence
1625
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Pathologic Fracture
1626
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Pathologic Fracture
1627
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1628
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Work-up
History
• Ambulation, B/B, Pain worse at night or positional
Physical exam
• LE weakness, long tract signs, sensory level, point
tenderness
MRI of the spine - compression
CT of the spine - stability
Restage primary
• CT chest, abdomen, and pelvis
• FDG PET
• 10 - 30% with synchronous lesions
Labs with LFT’s
1629
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Stability Assessment
Anatomic
• 2 column
• 3 column
Physiologic
• History positional pain
Trauma is not Oncology
Harms
Case EW
1630
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What to do?
Do No Harm!
1631
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Case CM
CM intraop
1632
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Post op - 1 year
MRI
Study of choice
Unsuspected lesions
in 30%
Whole body fast-imaging
techniques:
• STIR 30-45 min
• Echo-planar 6 min
False positives
1633
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Radionuclide Imaging
2% cold
1634
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
SPECT or PET/CT
1635
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Myelography
Importance of Biopsy
Benign tumors
Myeloma/plasmacytoma
Primary bone sarcomas
Paget’s disease
DDX - CT guided biopsy
• Core bx preferable to FNA
1636
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Breast CA
50 year old woman
Back and leg pain
Worse s/p XRT
Known Breast CA
Only known met
Intraop - LECA
1637
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
IntraOp
1638
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Postop
1639
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Study Design
All patients
• Underwent MRI
• Treated with Decadron
• Diagnosis confirmed with biopsy
Stratification based on
• Tumor type
• Ambulatory status
• Spine stability
Randomized to
• surgery with XRT or XRT alone (30Gy)
Treatment
Radiation started within 24 hours
Surgery within 24 hours
Goals
• Remove as much tumor as possible
• Immediate decompression
• Stabilization when needed
XRT started less than 14 days post-op
1640
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Entry Criteria
Known cancer
Symptomatic lesion
Resectable based on MRI
Not paraplegic > 48 hours
No prior XRT
Exclusion: lymphoma, leukemia, multiple
myeloma, germ cell tumor, primary spinal tumor
Endpoints
Primary
• Ambulation
Secondary
• Continent
• ASIA and Frankel grade
• Narcotic and steroid use
• Survival
1641
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Results
Ambulation
• Surgery + XRT 126 days
• XRT alone 35 days
• For non-ambulatory patients 56% vs 19%
Continent
• Surgery + XRT 142 days
• XRT alone 12 days
Survival
• Surgery + XRT 129 days
• XRT alone 100 days
Results
1642
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
25
Number of Patients
20
15
10
0
Sun Mon Tues Wed Thu Fri Sat
Day of Week
Conclusion
1643
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Laminectomy + XRT
Is a thorocotomy necessary?
Pros
• Direct visualization of decompression
• Reconstruction of anterior column
Cons
• Transpedicular/costotransversectomy is
better tolerated
Katonis Spine ‘99, Vornanen Spine ‘95
1644
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Thoracic Approaches
Laminectomy
Transpedicular
Transfacet-pedical sparing
Costotransversectomy
Lateral Extracavitary
Retroplural
Transthoracic
Trans-sternal
Thoroscopic/Endoscopic
1645
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
History of LECA
Exposure 1
1646
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Exposure 2
Exposure 3
1647
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Exposure 4
Exposure 5
1648
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Exposure 6
Definition of LECA?
1649
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1650
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Incision Design
1651
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Cage insertion
1652
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1653
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Summary
Decompression
Optimize ventral exposure
Bilateral exposure
Anterior column reconstruction
Remove proximal rib head
Anterior/Posterior versus LECA
Not Anterior versus LECA
1654
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
VP/KP
1655
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Complications
T4
1656
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Intraop
1657
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Spinal Radiosurgery
Radiosensitive Metastasis
1658
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
CyberKnife Overview
Frameless image-guided stereotactic
radiosurgery
A lightweight linear accelerator mounted on a
robotic arm that has 6 axes of rotation
Two ceiling mounted cameras perform near
real-time image tracking
Mathematical transformation from image space
to target space
Target is radiated by robot controlled linear
accelerator
CyberKnife
0.3 mm accuracy
< 1 mm clinical accuracy
Arbitrary beams
Over 100 nodes
Over 1200 beams
Approximately $3 x 106
1659
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Management Goals
NOMS
SRS
VP
Separation Surgery
Summary
1660
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1661
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1662
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1663
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Diagnosis/Management
Sensitivity of, access to diagnostic
imaging
Earlier diagnosis
Incidental/asymptomatic
Sensitivity>Specificity
Differentiation from non-neoplastic,
non-surgical conditions
1664
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Diagnosis,
localization,
characterization
Earlier diagnosis
Smaller size
Less edema
Higher level of
function
Incidental tumors
Biologically
indolent
Can’t make
normal patient
better
Post-op posterior
column deficits
are expected
1665
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Medical myelopathy
Multiple Sclerosis
Transverse Myelitis
Sarcoidosis
1666
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Medical myelopathy
Multiple Sclerosis
Transverse Myelitis
Sarcoidosis
Extrinsic
myelopathy
Medical myelopathy
Multiple Sclerosis
Transverse Myelitis
Sarcoidosis
Extrinsic
myelopathy
1667
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1668
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Current Techniques
Positioning, exposure
Spinal cord/tumor access
Myelotomy, retraction
3 hands better than 2
Tumor/cord interface
Internal decompression
Monitoring
1669
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1670
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Unencapsulated
Histologically benign
Slow growth
1671
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1672
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1673
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1674
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1675
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1676
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1677
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Neurologic Morbidity
20 40 60 80 100
Extent of Resection
Disease Free Survival (Yrs)
20 40 60 80 100
Extent of Resection (%)
1678
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1679
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1680
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1681
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1682
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1683
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1684
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1685
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1686
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1687
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1688
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1689
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1690
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1691
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Paul C. McCormick
Columbia University
College of Physicians and Surgeons
1692
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Solitary schwannomas
Origin
Preganglion (intradural)
Postganglion
(extradural)
Dumbbell extension
Nerve of origin
Access/exposure
Stability
1693
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Lack of well
defined connective
tissue supportive
matrix (epineurium,
perineurium,
endoneurium)
Nerve root of origin
Non-functional
Not salvageable
Well defined
connective tissue
supportive matrix
(epineurium,
perineurium,
endoneurium)
Spinal nerve of
origin
Sacrifice single
fascicle
Functional fascicles-
salvageable
1694
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Type
Nerve of origin II
Pre vs. post ganglionic
Pre-ganglionic I, II
Post-ganglionic III, IV
Dumbbell (spinal Type IV
canal)
II (intradural),
IV(extradural)
Functional nerve of
origin- III, IV
Origin: Intradural
No extension through root
sleeve
Sacrifice non-functional root of
origin
Spare functional corresponding
sensory or motor
Access: laminectomy
Stabilization: No
1695
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Corresponding
functional root may be
attached to tumor
within common
arachnoid sheath
Applied to tumor
surface but separable/
salvageable up to DRG
1696
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1697
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Origin: Intradural
Extradural extension through
root sleeve
Sacrifice entire nonfunctional
motor/sensory nerve root
Access:
laminectomy/facetectomy
Stabilization
1698
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Origin: Postganglionic
Peripheral nerve tumors
Functional nerve
displaced onto tumor
capsule
Sacrifice only fascicle of
origin
1699
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Origin:
Postganglionic
Variable paraspinal
extension
Spare functional
nerve root
Access:
Posterolateral/
anterolateral
No stabilization
1700
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Origin: Postganglionic
Significant intraspinal
extension (extradural)
Spare functional nerve
root of origin
Access: Posterolateral
May need stabilization
1701
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Type IV
1702
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1703
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1704
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Ventral to dentate
Tumor type
Tumor
consistency/
vascularity
Level
Cord rotation
Extension beyond
midline
1705
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Pure Ventral
No cord rotation
Meningioma
Nerve sheath tumor
Pial based
hemangioblastoma
AV fistula
1706
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Standard anterior
cervical exposure
Corpectomy
Midline durotomy
Tumor resection
Corpectomy
reconstruction and
stabilization
1707
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Primary dural
closure
Duragen
Wide strut allograft
Gelfoam lateral
gutters
Bedrest 3 days
Spinal drain 3-5
days
Fibular allograft
Translational plate
Hard Collar 8
weeks
1708
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1709
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1710
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1711
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1712
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1713
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1714
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Ian F. Dunn, MD
Associate Professor of Neurosurgery
Skull base and pituitary surgery
Brigham and Women’s Hospital
Disclosure Statement
1715
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Overview
• Meningiomas
• Schwannomas
• Chordomas/chondrosarcomas
• Paragangliomas
1716
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Cranio-orbitozygomatic
Extended middle fossa approach
Transcondylar
Petrosal approaches
1717
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1718
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Surgical anatomy
1719
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1720
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1721
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1722
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1723
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Parasellar meningiomas
• Cavernous sinus 160
• Tuberculum sella 65
• Clinoidal 44
• Sphenoid wing 62
• Sphenopetroclival 48
Outcomes
• Mortality within 30 days 0.6%
• Stroke 2.2%
• Complete resection 90%
• Recurrence 7%
1724
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1725
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1726
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
• Falciform ligament/dura
• Drill bony canal--
constant irrigation
1727
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
• Falciform ligament/dura
• Drill bony canal--
constant irrigation
• Open optic sheath
• Careful tumor resection
1728
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1729
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Cranio-orbitozygomatic
1730
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1731
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Superior access
1732
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
163 cases:
1733
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Petroclival meningiomas
Symptom
Diplopia
Facial numbness/pain
Hearing loss
Headache
1734
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
AP
PP
1735
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1736
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Outcomes
GTR: 35/55 patients with “true” petroclival meningioma
Other complications:
CSF leak
PE
respiratory failure
DVT
brainstem stroke
venous infarction
seizure
IVH
Anterior petrosal
Combined petrosal
Hearing + Hearing -
1737
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1738
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Trigeminal schwannomas
28 cases (3yr mean follow-up):
• Relief of pain 73%
• Improv. of V sensory 40 %
• Improv. of V motor function 80%
• Improv. of VI function 63%
• Perm. worsening of V sensory n 8%
1739
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1740
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Meckel’s cave
• Sleeve of arachnoid covering trigeminal
nerve
1741
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1742
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1743
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1744
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Chordoma
Sacrococcygeal region -49-50%
Spheno-occipital region
(at the clivus) -30-35%
Vertebral chordomas
(lumbar, cervical, thoracic) -15% of
total chordomas
1745
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Cytokeratin + Cytokeratin -
EMA + EMA -
1746
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1747
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Metastases
12%
10%
8%
6%
4%
2%
0%
Chordoma Chondrosarcoma
1748
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
% of children under 17 yo
40%
35%
30%
25%
C
20%
CS
15%
10%
5%
0%
C CS
Recurrence
100
90
Chondrosarcoma
Survival probability (%)
80
70
60
50
40
30 Chordoma
20
10
0
0 20 40 60 80 100 120 140 160 180 200
Time
1749
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Treatment of Chordoma
Surgery (as many surgical approaches) Proton Beam radiotherapy
Chondroid
60 60
Chordoma
40 40
20 20
Chordoma
0 0
0 50 100 150 200 0 50 100 150 200
Time (months) Time (months)
1750
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
• Chordoma 35%
• Chondroid chordoma 29%
• Low-grade chondrosarcoma 0%
1751
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Clival involvement
Upper clivus 32 cases (86%)
1752
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Complications
• Meningitis 5%
• Cranial nerve palsy 25%
• Hemiparesis 4%
• Hydrocephalus 3%
• CSF leak 7%
• Radiation necrosis 6%
1753
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1754
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1755
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
death 16
progression 11
stable disease 1
Chordoma
Chondroid chordoma
Rec. chordoma
1756
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1757
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1758
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1759
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1760
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
80 80
60 60
Group Group
40 A 40 DA
N DN
20 RA
20
RN
0 0
0 20 40 60 80 100 120 0 20 40 60 80 100 120
Time Time
Recurrence Recurrence
100 100
Survival probability (%)
80 80
60 group 60 Group
3 13
40 N 40 N
20 20
0 0
0 20 40 60 80 100 0 20 40 60 80 100
Time Time
1761
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
80 80 No residual
60 60
D
40 40
Residual
20 20
R
0 0
0 30 60 90 120 150 180 0 30 60 90 120 150 180
Time (months) Time (months)
Paragangliomas
1762
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Paraganglioma signs/symptoms
• Hoarseness
• Hearing deficit
• Dizziness
• Swallowing difficulty
• Tinnitus
• Hypertension
• Headache
• Neck pain
• Ear pain/mass
Secreting tumors
• Can secrete catecholamine, Dopamine,
Serotonin, etc.
• Incidence of catecholamine secretion is 4%
• Potentially serious complications
of intraoperative or perioperative
hypertension crisis
• All patients need to be evaluated
for catecholamine secretion
• Anesthetic management considerations
1763
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Multiple tumors
Occur in more than 10% of cases
1764
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
1765
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Outcomes
• Of 43 cases:
1766
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Approaches
Cranio-orbito-zygomatic (“COZ”) Supra-orbital
Transsphenoidal
Middle fossa
zygomatic
Transpetrosal
Transcondylar
Transtemporal
1767
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Disclosure Statement
Reports no commercial interest
1768
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Endocrine Evaluation
of Pituitary
Anterior the Neurosurgical
Hormone Regulation
Patient
Adriana Ioachimescu, MD, PhD
Neurosurgery Grand Rounds
October 30, 2008
1769
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
Pituitary Adenomas: “1 in 5”
Epidemiology
20% general population at autopsy
10-20% incidentally by brain imaging
Prevalence ↑ w/ age
Except prolactin- and ACTH-secreting tumors (peak 20-40 y.o.)
Gender: PRL- and ACTH-secreting adenomas more frequent in
women
Familial predisposition is rare
Syndromal associations: MEN-1 (11q13), Carney complex
(PRKAR1), McCune Albright (X-linked)
In patients with sporadic pituitary adenomas younger than 30,
AIP (germline aryl hydrocarbon receptor interacting protein)
mutations were detected in 8.6% cases and MEN-1 mutations
in 3.4%
1770
Copyright © Oakstone Publishing, LLC, 2016. All Rights Reserved.
MicroRNAs downregulation
Asa SL, Ezzat S. Annu Rev Pathol. 2009;4:97-126.
Evans CO, et al. Cancer Res. 2003 Jul 15;63(14):4218-24.
D'Angelo D, et al. J Clin Endocrinol Metab. 2012 Jul;97(7):E1128-38.
Clinical Manifestations
Pituitary hormone oversecretion
PRL
GH: acromegaly
ACTH: Cushing’s disease
TSH: central hyperthyroidism
FSH or LH: hypergonadism
Mass effect
Headaches
Vision loss: bitemporal hemianopia
Diplopia: cranial nv. III, IV, VI (apoplexy)
Compression of the stalk or normal pituitary gland
(hypopituitarism, galactorrhea)
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Cushing’s disease
Cushing’s Disease
1. Feelders RA et al. Presented at ENEA, Napoli, Italy, 4–6 December 2009;Poster 18. 2. Data from CDC statistics and NHANES III (2005–
2006) 2011. Available at: http://www.cdc.gov/nchs/nhanes.htm
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AND
Differentiate between CS and reactive hypercortisolemia
Severe obesity
Psychiatric disorders: depression, anxiety disorder,
anorexia nervosa, OCD
Chronic alcoholism
Poorly controlled DM
Obstructive sleep apnea
1773
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Surgical Strategy
Wide opening of the sella
Selective adenomectomy
Hypophysectomy or hemi-hypophysectomy
1774
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1775
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1776
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Adjuvant to surgery/radiotherapy
Side effects common and limiting
Unsatisfactory in most cases
Response rates poor ∴
⇒ Poor surgical candidates
⇒ Preoperative preparation
⇒ Awaiting results from XRT
1777
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Pasireotide
1778
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Major drawbacks:
Biochemical parameters are not useful to establish cortisol status at
end organ level
Both ACTH and cortisol ↑during tx, although patient may have
clinical signs of adrenal insufficiency
Hypokalemia
http://www.corcept.com/news_events/pr_1307237503
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Acromegaly
Acromegaly/ Gigantism
10-15% of pituitary adenomas; mostly macroadenomas
Changes in appearance, headaches, sweating, joint pain
hypogonadism
HTN, DM, OSA, cardiomyopathy, colon polyps, thyroid
nodules
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Medical
SST analogues (short, pump, long)
Dopamine receptor agonists (Parlodel, Dostinex)
GH Receptor antagonist (Pegvisomant)
Radiotherapy
SRS
Fractionated SRT
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1783
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Cabergoline
~0.5-1.0mg twice weekly
Normalizes IGF-1 in 35% of patients, ↑prolactin favorable
Tumor shrinkage ~50% of patients
Nausea, GI, postural ↓BP
1784
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10-20 mg sc qd
Normalizes IGF-1 in 80-90% patients after ≥ 12 mths
Improves symptoms
Long-term impact on tumor growth?
Indication: failed surgery and other medical therapy
GH levels increase up to 6 mths after Rx
MRI monitoring of tumor size, monitor LFTs
Well-tolerated
1786
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Prolactinoma
1787
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Prolactinomas
Non-tumoral causes of
hyperprolactinemia
1788
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Prolactinoma
Women
Microadenomas (≤1 cm)
Amenorrhea/galactorrhea
Infertility, osteoporosis
Men
Macroadenomas
Headaches /visual loss
Sexual dysfunction
Gynecomastia, infertility
Osteoporosis
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Goals of therapy:
1. Suppress clinical
consequences of increased
PRL level
2. Control tumor mass
- Significant decrease in size is
not a goal for
microprolactinomas if
symptoms are controlled
Medical Rx in prolactinomas
Long-term tx:
Until menopause in women, lifelong in most
macroadenomas
1790
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1791
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1792
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Failure of medical Rx
Cystic macroprolactinoma
Rate of remission
67% in intolerant vs. 36% in dopamine agonists-
resistant patients
75% for microprolactinomas vs. 30% for
macroprolactinomas
Rate of recurrence
18% for microprolactinomas vs. 23% for
macroprolactinomas
Recurrence defined by reappearance of
hyperprolactinemia *Hamilton DK, Pituitary, 2005
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1794
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Nonfunctioning
Pituitary Tumors
and Pituitary
Incidentalomas
Clinically
Nonfunctioning
Pituitary Adenomas
Asymptomatic* Symptomatic
*Incidentalomas
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Pituitary Incidentalomas
Questions to be asked
Is it Functioning or Nonfunctioning
Is it causing mass effects?
Headache
Visual field defects
Hypopituitarism
Who needs surgery?
If surgery is done, what postoperative
surveillance is needed?
What therapy is indicated if there is
postoperative residual tumor?
1796
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Size
Macroadenomas – 29 (63%)
Microadenomas – 13 (37%)
Hypopituitarism – 19 (41%)
Prolactinomas – 7 (15%)
Hyperprolactinemia – 10 (22%)
Visual Field Defects – 10 (33 % of macros)
Surgery in 17 (37%) – 1 cranio, 16 adenomas
Gonadotropinomas – 23%
Plurihormonal – 31%
Somatotropinomas – 15%
No staining – 31%
Fainstein Day et al., Pituitary 2004;7:145
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Reinecke et al., JAMA 1990;263:2772 Donovan & Corenblum, Arch Int Med 1995;155:181
Nishizawa et al., Neurosurgery 1998;43:1344 Feldkamp et al., Clin Endocrinol 1999;51:109
Igarashi et al., Neuro Med Chir 1999;39:592 Sanno et al., Eur J Endocrinol 2003;149:123
Fainstein Day et al, Pituitary 2004;7:149 Arita et al., J Neurosurg 2006;104:884
Karavitaki et al., Clin Endocrinol 2007;67:938 Dekkers et al., Eur J Endocrinol 2007;156:217
Pituitary Incidentalomas
Indications for Surgery
Secreting tumors other than prolactinomas
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Normalized 45%
Improved 28%
No Change 27%
Worsened 0%
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Nonfunctional Adenomas
Giant Adenomas
TS (± staged)
Craniotomy
Extended TS
Extracapsular
Surgical enhancements:
LD/Image Guidance/
Intraoperative MRI/
Endoscope
Limitations:
Fibrous (5-8%)
Dumbbell tumors
Eccentric parasellar extension
1801
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SURGICAL OPTIONS
69
1802
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3D Endoscopy
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Observation
Second Surgery
Medical Therapy
Dopamine agonists
Bromocriptine
Cabergoline
Octreotide
Radiotherapy
Conventional
Gamma Knife
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1805
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Pituitary Tumors
Conclusions
1806
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Edward R. Laws
Brigham & Women’s Hospital
Harvard Medical School
Pituitary Adenomas
Third Most Common Primary Brain Tumor
20% of Routine Autopsies
19% of Primary Brain Tumors are
Operated Upon Transsphenoidally at US
Training Centers
1807
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The Pituitary
The “Master Gland”
Controls
Growth Metabolism
Sexual maturation Stress response
Reproduction Fluid balance
Pituitary Tumors
Common Complaints
Depression Weight gain
Apathy Fluid retention
Sleep disorders Sexual dysfunction
Memory Loss Infertility
Anger, Agitation Fatigue, weakness
Irritability Visual loss
Moodiness Emotional lability
Anxiety Headache
1808
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1809
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1810
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The Microadenoma
Selective Microsurgical
Removal
1811
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CSF Rhinorrhea 93
Hypophysitis 29
Hypophysectomy 23
Miscellaneous Sellar 160
Lesions
Total 5099 04/09
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1814
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Visual Improvement – 87 %
Relief of Headache - 95 %
Preservation of Normal Function – 95 %
Restoration of Normal Function – 30 %
Recurrence – 16 % (6 % symptomatic)
Living & Well at 10 Years- 83 %
1816
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Active Acromegaly
Mass Effect – Visual
Loss
Hypopituitarism
Apoplexy
1817
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1818
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1819
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GH Adenomas
Outcomes
Relief of Mass Effect – 95%
Improvement in Acromegalic Symptoms
and Signs – 95 %
Normalization of GH Secretion – 50-72 %
Preservation of Normal Pituitary Function
– 95 %
Recurrence – 1.3 – 8 %
Living & Well at 10 Years – 70 %
Prolactin Microadenoma
1820
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Prolactin Adenomas
Outcomes
1821
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1822
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1823
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Cushing’s Disease
Association with Cerebral Atrophy
1824
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1825
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Normalization of Cortisol/ACTH
Improvement in Symptoms, Signs and Co-
Morbidities
Cushing’s Disease
Outcomes
Relief of Mass Effect – 97 %
Normalization of ACTH – 55- 91 %
Preservation of Normal Function – 95 %
Recurrence – 12 % (10 yrs)
Living and Well 10 Years after Surgery
– 75 %
1826
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Extended Transsphenoidal
Approaches
1827
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Craniopharyngioma
1828
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It is Here to Stay
Endoscopic Anatomy
1829
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1830
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1831
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1832
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Arachnoid cyst
1833
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chordoma
1834
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1835
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1836
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Craniopharyngioma
A Treatment Algorithm
R. Michael Scott, M.D.
Department of Neurosurgery
The Boston Children’s Hospital and Harvard Medical
School, Boston, Massachusetts
May 2016
NO DISCLOSURES
May 2016
1837
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May 2016
May 2016
1838
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May 2016
May 2016
1839
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May 2016
May 2016
1840
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May 2016
May 2016
1841
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May 2016
Treatment of Craniopharyngioma
1842
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May 2016
May 2016
1843
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May 2016
May 2016
1844
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May 2016
May 2016
1845
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May 2016
May 2016
1846
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May 2016
May 2016
1847
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May 2016
May 2016
1848
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May 2016
May 2016
1849
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In 1995, patient age 22, moyamoya was diagnosed following left MCA stroke;
In 1997, a malignant meningioma was diagnosed and removed
In 2000, she died at age 27 from tumor invasion of brain stem,
17 years after initial diagnosis and radiotherapy
May 2016
May 2016
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May 2016
1851
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May 2016
1852
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May 2016
May 2016
1853
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May 2016
1854
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May 2016
May 2016
1855
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May 2016
May 2016
1856
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Deaths
• No operative deaths
• 2 deaths in the first year after surgery in children
who had made excellent recoveries from surgery
• Their deaths were due to overwhelming sepsis
unrelated to and remote from craniotomy:
– J.Ch--from strep. Pneumoniae, 6 months post-op
– K. M-J-- from upper respiratory infection, 3 months
post-op
• These cases emphasize importance of post-op
endocrine supervision and stress steroids (no
similar deaths in past 20 years)
May 2016
Other complications:
• Endocrine--most total resections have DI
• New or worsened visual deficits (4)
• Behavior and/or appetite changes (3)
• Intraoperative bleeding from vessels on basilar-
posterior cerebral artery (1)
• Subdural hygroma (1)
• Stroke -- Huebner artery territory (asymptomatic) (1);
MCA stroke 2 months post-op of unknown cause (1)
• 1 year postop chickenpox encephalitis -->devastating
encephalopathy
• Arteriopathies – ectasia, aneurysms (2)
May 2016
1857
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May 2016
May 2016
1858
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May 2016
May 2016
1859
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May 2016
1860
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May 2016
Age 27.
One year after
gastric bypass,
16 years post-op.
Weight loss of
130 lbs, holding
steady
(picture used by
permission)
May 2016
1861
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Surgical Lessons
• Plan operative exposure based on tumor location
and size, but leave intraoperative options open --
wide exposure or provide opportunity to extend
initial opening
• Clearly identify all normal anatomy before
working on tumor; split sylvian fissure
• Clear tumor from vessels and nerves before
decompressing it when possible
• Identify and protect vascular supply to optic
apparatus
• Reoperation is feasible in the event of recurrence
and can be curable in certain patients
• Surgically implanted metastases can occur
• Vascular injury is not uncommon, leading to
stroke or ectasia
May 2016
CONCLUSIONS
May 2016
1862
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May 2016
1863
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Hydrocephalus and
Arachnoid Cysts
Tord D. Alden, MD
Assistant Professor, Neurological Surgery
Northwestern University, Feinberg School of Medicine
Ann and Robert H. Lurie Children’s Hospital of Chicago
talden@luriechildrens.org
Disclosures
1864
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Cerebrospinal Fluid
• Mechanical buffer
– Systole
• Blood moves caudally from the brain
• CSF moves to the lumbar cistern
– Diastole
• Blood moves from the brain to the heart
• CSF moves cranially from the lumbar cistern
• Removes waste
• Provides a stable environment for the CNS
Cerebrospinal Fluid
• Produced • Absorbed
– Choroid Plexus – Arachnoid granulations
– Ependymal surface – Ependymal surface
– Subarachnoid space – Meninges
– Pia – Pia
– Brain Parenchyma – Perineural space
– 300 to 500 ml/day
• Pathologic states
– Over production
– Under absorption
1865
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CSF flow
Childs Nerv Syst. 2006, 22(7):662-9. Proposal of "evolution theory in cerebrospinal fluid
dynamics" and minor pathway hydrocephalus in developing immature brain. Oi S, Di Rocco C.
1866
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CSF dynamics
• Oi (Childs Nervous System, 2006)
• Describes major and minor pathways of CSF
circulation
• Minor pathways during gestation and first
year of life
• Major pathways start during end of gestation
but do not dominate absorption until 1 year of
age
What is Hydrocephalus?
• Production of CSF in excess of ability to
reabsorb
– Too much production
– Too little absorption
• Classified
– Communicating vs Non-communicating (Dandy
1914)
– Obstructive vs Non-obstructive (Russel 1949)
– Congenital vs Acquired
1867
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Classification
• Terminology can be confusing
• Important for surgical treatment
– Ventriculoperitoneal shunt
– Endoscopic third ventriculostomy
– Surgical removal of cause
• Choroid plexus tumor
• Tumor in CSF pathway
1868
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Causes of Hydrocephalus
• increased production • decreased absorption
– Choroid plexus tumor – Abnormal brain
• decreased absorption development
– Mechanical blockage • Myelomeningocele
• Foraminal atresia • Encephalocele
• Colloid cyst • Holoprosencephaly
• Aqueductal stenosis • X-linked hydrocephalus
• Arachnoid cyst • Dandy-Walker
• Tumor malformation
– Poor absorption
• IVH
• Infectious (meningitis /
ventriculitis)
11
Causes
• Congenital
– Genetic
– Infection
– Malformations
• Tumors
– Increased CSF production
– Obstruction of pathway
• Increased venous sinus pressure
• Iatrogenesis
• Idiopathic
• Acquired
– Infection
– Intraventricular hemorrhage
1869
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Hydrocephalus
• Pediatric
– Congenital
– Prematurity / Intraventricular hemorrhage (IVH)
– Open neural tube defect
– Meningitis
• Adult
– Idiopathic
– Subarachnoid hemorrhage
– Meningitis
– Normal pressure hydrocephalus
1870
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Epidemiology
• Congenital 3/1000 live births
• Acquired hydrocephalus depends on cause
– 10% of patients with SAH
• Bimodal age distribution
– Children 0 to 10
– Adults 40 to 70
1871
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Work-up
• History
• Clinical exam
• Imaging
– Ultrasound (open fontanel)
– CT
– MRI
• Thin section through the aqueduct
• Examine space in front of brain stem
1872
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Consequences of Hydrocephalus
• Altered neuronal cell proliferation and migration
• Axonal degeneration
– focal neuronal loss
– decrease in synapses
– Gliosis
• Thinning of the cerebral cortex
• White matter suffers from chronic hypoperfusion
• Delay/Prevention of normal myelination
19
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Surgical treatment
• Treat Cause
– Choroid plexus tumor
• Over production and Under absorption
– Lesions in pathway
• Foramen of Monro
• Third ventricle
• 4th ventricle
• Arachnoid cysts
• CSF diversion
– Endoscopic third ventriculostomy (ETV)
– Ventriculoperitoneal (ventriculo-extracranial site) shunt
– Ventriculo-ventricular shunt
Shunts
• Many devices in use
• Pressure versus Flow control valves
• Siphon versus Anti-siphon devices
• Adjustable versus Fixed valves
• Many possible locations
1874
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Terminus of shunt
• Peritoneum (abdominal pseudocyst)
• Right atrium of heart (cor pulmonale)
• Pleural space (symptomatic effusion)
• Gall bladder
• Urinary bladder (infection)
• Ureter (loss of kidney)
Shunt Infection
• 5-15% incidence
• Most in first 6 months
• Skin flora
– Staphylococcus aureus
– Staphylococcus epidermidis
– Proprionobacter acnes
– Enterococcus faecalis
• Symptoms:
– Fever
– Redness along shunt tract
– Abdominal pain/Shunt peritonitis
– CSF collection
• Abdominal pseudocyst
• Pleural effusion
1875
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Shunt Infection
Shunt Infection
• The use of protocol to
standardize insertion
• Overall infection rate of
6.0 percent
1876
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Shunt Malfunction
• 40% in first 2 years
• 80% in the first 10 years
• Proximal shunt failure
most common (95% of
time)
• Failure anywhere along
the system
Shunt Malfunction
• Drainage
– Over-drainage
• Low pressure headaches
• Subdural hygroma/hematoma
– Under-drainage
• Increased ICP
• Increased ventricular size
• Improper placement
– Intracranial
– Intra-abdominal
• Obstruction of component
– Ventricular catheter
– Valve
– Distal catheter
• Disconnection
• Failure of absorption of CSF
1877
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1878
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Shunt Malfunction
1879
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34
1880
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35
Anatomy
• Foramen of Monro
36
1881
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Lateral Ventricle
• Foramen of Monro
• Anterior Septal Vein
• Thalamostriate Vein
• Anterior Caudate Vein
37
Anatomy
• Third Ventricle
– Mamillary bodies
– Infundibular recess
– Tuber cinereum
– Basilar artery
38
1882
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Anatomy
• Third Ventricle
39
Ventricular anatomy
1883
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Anatomy
41
Third Ventriculostomy
• Approach
42
1884
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Third Ventriculostomy
• Obstructive hydrocephalus
– Third ventricle
• Pineal region lesions
– Aqueduct
• Aqueductal stenosis
• Tectal plate tumors
– Fourth ventricle
• Posterior fossa tumors
• Chiari malformation
• Posterior fossa arachnoid cyst
1885
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ETV
1886
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ETV: Outcome
Potential Complications
• Infections
• Intraventricular hemorrhage
• Fornices: memory
• Hypothalamus: diabetes insipidus
• Optic tracts
• Basilar artery
1887
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ETV
ETV – Outcome
• Most series report success rate of 50 to 95%
• Poor predictors
– Age less than 12 months
– Etiology
• Myelomeningocele
• Meningitis
• IVH
• Highest success
– Tectal plate glioma
– Aqueductal stenosis
1888
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Arachnoid Cyst
• Account for 1% of intracranial mass type lesions
• Estimates are highly variable
– Prevalence of 0.2 to 2.6% reported
• Incidental finding
• Male to Female ratio of 2:1
• Left side more common than right
• Most common locations
– Posterior fossa
– Temporal
– Suprasellar
– Frontal
1889
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Etiologies
• Temporal hypoplasia
– Unlikely to see re-expansion after treatment
• Secretory elements
– Na/K pump activity
– Enlargement over period of time.
• CSF trapping
– Ball-Valve mechanism demonstrated on cine MRI and
endoscopy
• Cysts may develop as diverticulum
• CSF absorption abnormality.
1890
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Prevalence and natural history of arachnoid cysts in children. Wajd N. Al-Holou, M.D., Andrew Y. Yew, M.D.,
Zackary E. Boomsaad, M.D., Hugh J. L. Garton, M.D., M.H.Sc., Karin M. Muraszko, M.D., and Cormac O. Maher,
M.D. JNS Pediatrics 2010
1891
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1892
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1893
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1894
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Suprasellar Cyst
• MRI
64
1895
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65
1896
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Conclusions
• Understanding the CSF dynamics will guide
treatment
• Hydrocephalus is the common pathway of
multiple disease processes
• Arachnoid cysts warrant treatment if
symptomatic – defining what is symptomatic
is debated by many
1897
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Disclosure Statement
• Reports no commercial interest
1898
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1899
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1900
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• Epilepsy
– Resection, ablation, intracranial electrodes, VNS, DBS
• Movement Disorders
– Pallidotomy, Thalamotomy, DBS, fUS
• Pain
– Rhizotomy, MVD, Spinal cord stimulation, cingulotomy, cordotomy,
intrathecal morphine
• Spasticity
– Myelotomy, selective rhizotomy, intrathecal baclofen
• Psychiatric Illness
– Cingulotomy, anterior capsulotomy, limbic leucotomy, DBS
1901
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Localizing Value
**** Neuroimaging
*** EEG
** Clinical semiology
* Neuropsychology
1902
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Functional MRI
24 y.o. M with new onset seizures and secondary generalization
1903
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1904
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Anteromedial TL Selective AH
EcoG
1905
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• 42 yo RH female
engineer
• Focal sensory
seizures involving R
side of tongue with
speech arrest
• Frequency: 2 - 4 / day
1906
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1907
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Epilepsy Surgery -
Resection
1908
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1909
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1910
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1911
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1912
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Indications:
Tremor
Parkinson’s Disease
Dystonia
Other……..
1913
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1914
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1915
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Outcome Measurements -
• Responder
– > 50% improvement in BDI or Ham-D
– > 35% improvement in YBOCS
• Partial Responder
– > 25 - 50% improvement in BDI or Ham-D
– > 25 - 34% improvement in YBOCS
• Non-Responder
1916
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Surgical Technique
• local anaesthesia with sedation
– valium 10 mg po; droperidol 5 mg im
• stereotactic MR
• target anterior cingulate
• lesion parameters - 85oC for 90 secs, 10 mm exposed tip
1917
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Sagittal
Sagittal
1918
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24
32
25
• N = 64 pts, 42 M; 22 F
• Mean age 34.7 ( range 16 - 69 yrs)
• Mean duration of illness @ 10 years
• Mean pre-op YBOCS 31.1
• Failed:
– 3 SSRI trials with augmentation ( 12 week
minimum)
– behavioural therapy ( 20 week minimum)
1919
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24
32 Mean YBOCS Improvement
25 26%
24
1920
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– N = 5, ages 29 - 46 yrs
– Disease duration 14 - 30 yrs, mean 22
– F/U: 16 - 47 mos, mean 31.5
– 4/5 improved
– Mean GAF increase of @32.5
– 1/5 remain institutionalized
1921
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1922
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1923
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Disclosures
• None
1924
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Learning objectives
At the conclusion of this program, participants will be
able to:
• List the clinical manifestations of the
neurofibromatoses and von Hippel Lindau
disease
• Describe the genetics and molecular biology
underlying these disorders
• Understand treatment options and surveillance
paradigms available to patients with central and
peripheral nervous system lesions associated
with NF1, NF2, Schwannomatosis & VHL
Neurocutaneous disorders
• NF1, NF2, Schwannomatosis
• VHL
• Sturge-Weber
• Ataxia-Telangectasia
• Tuberous sclerosis
1925
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Neurocutaneous disorders
• Common theme - rare diseases
- US definition - less than 200K affected
in US (1 in 1500)
- Autosomal dominant transmission vs.
sporadic mutation
Neurocutaneous disorders
• Tumor suppressor gene syndromes
• Multiple neoplasia syndrome
1926
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Neurocutaneous disorders
• Common findings (descending order of
neurosurgical impact)
- Benign tumors of the central and peripheral
nervous system
- Seizures
- MSK - Skeletal dysplasia, weakness, ataxia,
deformity, spasticity
- Pain
- Ophthalmologic manifestations
- Learning disability, developmental delay
- Visceral manifestations
- Cancer (Renal cell CA, MPNST)
1956
Crowe et al. series
1992 & 1994
reports 5% of patients
Evans et al.
1822 with multiple
Parry et al.
Wishart - first probable neurofibromas have
Clinical characteristics
case report of NF2 acoustic neuromas
of NF2
2007
1916 1971 Germline mutation of
Harvey Cushing brackets central NF & von INI1/SMARCB1 in familial
the disorders as von Recklinghausen’s Schwannomatosis
Recklinghausen’s disease are distinct identified
disease clinical entities
1 1 1 1 2
8 9 9 9 0
0 0 5 9 0
0 0 0 0 0
1930
Gardner & Frazier
suggest BAN represent a
central form of von
Recklinghausen’s
disease
2003
1882 1993 Schwannomatosis and
von Recklnghausen’s NF2 gene cloned & NF2 are clinically and
report product identified as molecularly distinct
Merlin / Schwannomin
1987
NIH Consensus Statement
on Neurofibromatosis
1927
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Neurofibromatoses
• NF1
• von Recklinghausen’s disease
• peripheral nf
• “cafe-au-lait” spots, (plexiform) neurofibromas,
intertriginous freckling, Lisch nodules, skeletal
abnormalities, optic nerve gliomas
• NF2
• central nf
• bilateral acoustic nf (BANF)
• Schwannomatosis
• Multiple schwannomas w/o Vestibular
schwannomas
NF2
• multiple neoplasia syndrome
1928
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Genotype-phenotype correlations
Increasing disease severity
Somatic mosaicism
1929
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Somatic mosaicism
• 1 in 8 transmission
• 1 in 12 transmission
1930
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Schwannomas
Schwannomas
1931
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Meningiomas
Meningiomas
1932
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Ependymomas
Ophthalmologic manifestations
1933
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Cutaneous manifestations
NF2 diagnosis
1934
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Clinical presentation
Age at diagnosis
1-19
20-39
40+
1935
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Vestibular schwannomas
• hearing loss & tinnitus, usually unilateral
• 60% adults, 30% children
1936
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VS treatment
Buchman CA, Chen DA, Flannagan P, Wilberger JE, Maroon JC. The learning curve for acoustic tumor surgery. Laryngoscope. 1996;106(11):1406-11.
Charabi S, Tos M, Thomsen J, Borgesen SE. Suboccipital acoustic neuroma surgery: Results of decentralized neurosurgical tumor removal in Denmark. Acta Oto-Laryngologica.
1992;112(5):810-5.
Fayad, J.N., Bassim, M.K., Brackmann, D.E. Hearing preservation and rehabilitation in vestibular schwannoma surgery (2010) Neurosurgery Quarterly, 20 (2), pp. 53-59.
Brackmann, D.E., Fayad, J.N., Slattery III, W.H., Friedman, R.A., Day, J.D., Hitselberger, W.E., Owens, R.M. Early proactive management of vestibular schwannomas in neurofibromatosis
Type 2 (2001) Neurosurgery, 49 (2), pp. 274-283
Kida Y, Kobayashi T, Tanaka T, Mori Y. Radiosurgery for bilateral neurinomas associated with neurofibromatosis type 2. Surgical Neurology. 2000;53(4):383-90.
Mathieu D, Kondziolka D, Flickinger JC, Niranjan A, Williamson R, Martin JJ, et al. Stereotactic radiosurgery for vestibular schwannomas in patients with neurofibromatosis Type 2: An analysis
of tumor control, complications, and hearing preservation rates. Neurosurgery. 2007;60(3):460-8.
Roche PH, Regis J, Pellet W, Thomassin JM, Gregoire R, Dufour H, et al. Neurofibromatosis type 2. Preliminary results of gamma knife radiosurgery of vestibular schwannomas.
Neurofibromatose de type 2 Resultats preliminaires de la radiochirurgie gamma knife des schwannomes vestibulaires. 2000;46(4):339-54.
Rowe JG, Radatz MWR, Walton L, Soanes T, Rodgers J, Kemeny AA. Clinical experience with gamma knife stereotactic radiosurgery in the management of vestibular schwannomas
VS treatment
1937
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VS treatment
• Clinical trials
• Bevacizumab (VEGF inhibitor -
angiogenesis)
• Rapamycin (mTOR inhibitor)
• Lapatinib (tyrosine kinase inhibitor)
Meningiomas
1938
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Meningiomas
17
44
Convexity
23
Parasagittal
9
10
20
Falcine
16
11
Tentorial
Sphenoid Wing
8
Intraventricular
5
Olfactory groove
2
4
Cavernous Sinus
1
2
Optic Sheath
1
1
1939
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Meningiomas
Exponential (7.8%)
Quiescent periods / tumor 10 tumors
• Mean - 1.36 ± 0.7
• Range - 1 to 4
• Frequency - every 4.5 years
Duration
• Mean – 2.4 ± 2.3 years Stuttering (60.9%)
• Range – 0.4 to 11.7 years 78 tumors
Linear (31.2%)
40 tumors
Meningioma management
• Symptom driven
• Skull base tumors
• Surgical debulking + radiotherapy
1940
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Nonvestibular schwannomas
• Nonvestibular nerve cranial nerve
schwannomas
• up to 50% of patients
• III, V, VII most frequent
• Lower cranial nerves most frequently
symptomatic
NF2
• Nonvestibular nerve cranial nerve
schwannomas
• up to 50% of patients
• III, V, VII most frequent
• Lower cranial nerves most frequently
symptomatic
1941
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Ependymomas
• 18-53% of patients
• Typically confined to spinal cord
• less than ⅓ need operation
NF2 surveillance
• Annually:
• Brain/spine MRI annually (when feasible)
• Audiology (starting at 10)
• Ophthalomology - at diagnosis
1942
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NF1 genetics
• Multiple neoplasia syndrome
• Autosomal dominant inheritance
• NF1 tumor suppressor gene located on
17q
• Penetrance of 100% by age 20
• Significant variability in expressivity
• Half of cases due to new mutations
NF1 epidemiology
• Most common form of Neurofibromatoses
• 1 in 3,000 live births
• No gender, race or ethnic specificity
1943
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1944
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NF1 diagnosis
Must have 2 or more of the following:
• 6 or more cafe´ au lait macules (.5 cm in children or
.1.5 cm in adults)
• 2 or more cutaneous/subcutaneous neurofibromas or
one plexiform neurofibroma
• Axillary or groin freckling
• Optic pathway glioma
• 2 or more Lisch nodules (iris hamartomas seen on slit
lamp examination)
• Bony dysplasia (sphenoid wing dysplasia, bowing of
long bone pseudarthrosis)
• First degree relative with NF1
Neurocutaneous manifestations
1945
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Clinical course
• Features usually present by age 8
• Generally progressive
• Disfigurement (dermal / plexiform
neurofibromas)
• 2.7x relative risk - development of cancer
• Reduced life expectancy of 54/59 years (vs
70/74)
• Cumulative risk for development of CNS
tumor is 7.9% (vs .46%)
1946
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Brainstem gliomas
• Prevalence in NF1 (4-18%)
• Distinguish from UBO (unidentified bright
objects) - do not progress
• Incidental discovery (most common)
• WHO Grade I through IV
• Favorable imaging findings
• Medullary / midbrain
• Focal tumor
• Up to 89% may remain stable
1947
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Brainstem gliomas
• Treatment is generally reserved for cases
with radiographic and clinical progression
• Focal tumors - surgical resection attempt
• Diffuse tumors - radiotherapy
• CED
• chemotherapeutics
Plexiform neurofibromas
• 10% lifetime risk of developing an MPNST
• Complete resection will likely cause
neurological deficit
1948
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MPNST
• 5-10% of all soft tissue sarcomas
• Risk Factors
• NF1 (10% lifetime risk)
• (internal) plexiform neurofibroma (not dermal)
• radiation
MPNST
• Diagnosis = low index of
suspicion
✓rapid increase in size
✓new/progressive
neurologic deficit
✓subacute/acute onset of
pain
✓hard and immobile on
palpation
1949
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MPNST
• Diagnosis
✓ MRI/CT (hemorrhage,
necrosis, cystic areas,
heterogenous
enhancement are not
dependable markers)
✓ 18FDG PET
✓ Percutaneous biopsy
MPNST
• Treatment
• Wide local
excision (including
amputation if
needed)
• Radiation therapy
(60-70 Gy with 5
cm margin)
• Sarcoma based
therapeutics forequarter amputation, 2009
(ineffective)
1950
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MPNST
Age at diagnosis
40-62 26-36
(yrs)
Development De novo in PN
Chemotherapy
55 18
response (%)
NF1 surveillance
• Under 16
• Annually:
• Pediatric evaluation (scoliosis, painful
cutaneous lesions/rapid growth,
neurologic examination)
• Ophthalmology
• Endocrine, cardiology, neurosurgical
evaluation as needed
1951
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NF1 surveillance
• Over 16
• Annually:
• Scoliosis less important
• Ophthalmology less important
• Primary care evaluation
• MPNST evaluation
1956
Crowe et al. series
1992 & 1994
reports 5% of patients
Evans et al.
1822 with multiple
Parry et al.
Wishart - first probable neurofibromas have
Clinical characteristics
case report of NF2 acoustic neuromas
of NF2
2007
1916 1971 Germline mutation of
Harvey Cushing brackets central NF & von INI1/SMARCB1 in familial
the disorders as von Recklinghausen’s Schwannomatosis
Recklinghausen’s disease are distinct identified
disease clinical entities
1 1 1 1 2
8 9 9 9 0
0 0 5 9 0
0 0 0 0 0
1930
Gardner & Frazier
suggest BAN represent a
central form of von
Recklinghausen’s
disease
2003
1882 1993 Schwannomatosis and
von Recklnghausen’s NF2 gene cloned & NF2 are clinically and
report product identified as molecularly distinct
Merlin / Schwannomin
1987
NIH Consensus Statement
on Neurofibromatosis
1952
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Schwannomatosis
genetics
•Multiple neoplasia syndrome
•Tumor suppressor gene
•Similar annual incidence to NF2
➡1 in 30,000 live births
•No gender, race or ethnic specificity
•Majority of cases are sporadic
➡INI1/SMARCB1 (50% familial cases, 10% sporadic cases) -
22q11.23
➡ LZTR1 (80% of SMARCB1 negative familial cases)
๏ MUST EXCLUDE NF2 (vestibular nerve, ophthalmic findings)
Schwannomatosis
• Most common presentation - intractable pain
from peripheral nerve tumor
• Non-vestibular nerve cranial nerve
schwannomas (including facial nerve tumors)
• Management analagous to sporadic tumors
1953
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VHL
• Autosomal dominant
• VHL gene - ch. 3
• 1 in 39,000 live births
*25-33% of patients
presenting with a
hemangioblastoma will
have VHL
1954
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Hemangioblastoma
Brainstem (10%)
Cerebellum (37%)
1955
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Hemangioblastoma
Hemangioblastoma
• Signs and symptoms
• Related to mass effect
•Tumor growth
•Peritumoral cysts
• Presence of a peritumoral cyst and symptoms
• 72% of symptomatic cerebellar tumors
• 75% of symptomatic brainstem tumors
• 95% of symptomatic spinal cord tumors
• Cyst enlarged faster than tumor
• 7 times faster in cerebellum
• 15 times faster in brainstem
• Cyst was larger than tumor
• 34 times larger in cerebellum
• 19 times larger in brainstem
1956
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Hemangioblastoma
Hemangioblastoma
1957
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Hemangioblastoma
• Growth
• 1278 (51% of tumors evaluated) stable and 1227
(49%) grew
•
saltatory (886 tumors [72%])
• linear (76 [6%])
•
exponential (264 [22%])
Hemangioblastoma
• Symptom formation
• 58 (41%) tumors became symptomatic requiring
intervention
•26/58 (45%) of the tumors that eventually produced
symptoms were not apparent on initial imaging
• 49/58 (85%) of symptom producing tumors had an
associated cyst/syrinx
• If surgery for growth only (not symptom formation)
each patient would have had 4 additional
surgeries over 10 years
1958
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1959
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• 20 VHL patients
• 44 CNS hemangioblastomas
• Average age - 37
• Average follow up – 8.5 years
• Treated volume - .5 cm3
• Mean prescribed dose – 18.9 Gy
1960
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Results
1961
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Audiovestibular
symptoms
• Endolymphatic sac
tumors
ELSTs
• Clinical findings (T.J. Manski et al., JAMA, 1997; D.I. Choo et al., J Neurosurg, 2004)
1962
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ELSTs
1963
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ELSTs
Pancreatic
RCC Pheochromocytomas neuroendocrine tumors
(10-20%) (8-17%)
(24-45%)
1964
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VHL surveillance
• AGE > 16
• Annually:
• Eye/retinal examination
• General/neurological examination
• Quality abdominal ultrasound
• Fractionated metanephrines
(normetanephrine blood test or 24-
hour urine test) - MRI or MIBG scan if
abnormal
VHL surveillance
• >16
• during pregancy
• Regular retinal & OB checkup to
anticipate potentially more rapid
progression of lesions.
• Endocrine evaluation each trimester
• 4th month - MRI without contrast
1965
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Key points
• Neurofibromatosis type 1 is associated with the development of brain tumors,
including optic pathway gliomas and brainstem gliomas. These tumors, when
compared to their sporadic counterparts, have a more favorable natural
history and do not require treatment unless clinical and/or radiographic
progression is clearly identified. The lifetime risk of development of a
malignant peripheral nerve sheath tumor in NF1 is 10%.
• VHL is a multiple neoplasia syndrome that results in the formation of CNS and
retinal hemangioblastomas, endolymphatic sac tumors and visceral
manifestations including renal cell cancer and pheochromocytomas.
• Tailored surveillance paradigms need to be made for patients with these rare
disorders.
1966
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Oakstone 2016
Disclosure
1967
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Traditional Approaches
(Anatomical)
• Direct damage to RAS in upper midbrain-lower
midline thalamic nuclei
– Top of basilar stroke, tumor, hemorrhage, inflammation
• Diffuse or large bilateral hemispheral lesions
– Trauma (DAI, subdural hematoma, contusion), global
anoxia-ischemia, hydrocephalus, tumor
• The “herniation” syndromes and secondary
compression of upper brainstem
Herniation Syndromes
• Central • “Uncal”
– Early drowsiness – Early ipsilateral pupillary
– Small reactive pupils enlargement (10%
– Cyclic breathing contralateral)
– Preserved eye movements – Later reduction in alertness
early – Followed by loss of eye
– Later pupils mid-sized and movements and corneals
fixed – Pupils mid-sized and fixed
– Ostensibly from downward – Followed by agonal
displacement and buckling of respiratory patterns
upper brainstem – Ostensibly from lateral
compression of midbrain
1968
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Traditional Approaches
(Physiological)
• Toxins, anesthetics, and drugs
– (probably affect both RAS and cortical neurons)
• Seizures
– (similarly uncertain anatomical locus of action)
• Hypoxia and trauma (sometimes seizures) as
special cases that have initial physiologic and
later destructive effects
1969
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Catatonia
1970
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Unusual Intoxications
• Not cocaine unless NCSE
• Can occur with sympatholytics (e.g., clonidine)
• Anticholinergics (coma especially in children; tricyclics,;
phenothiazines, anti-parkinson, OTC)
• Cholinergics (organophosphates also with atropinic effects)
• Serotonin syndrome (especially with concurrent MAOIs)
• Anion gap acidosis poisonings (ethylene glycol. salicylates,
methanol, toluene, paraldehyde-and uremia, DKA)
– And lactate—i.e., cyanide CO, INH
1971
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1972
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Hashimoto Encephalopathy
• Confusion, stupor, multifocal myoclonus progressing
to coma over days
• Normal MRI and CSF
– Some with rapidly evolving, even unilateral, white matter
lesions that simulate ADEM
• Normal thyroid function in most but characteristic
anti-thyroid peroxidase and anti-thyroglobulin
antibodies
• Differential diagnosis—CJD, lithium intoxications
(commonality of myoclonus)
• Cases appearing in children and young adults
1973
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Prognostication in Coma
1974
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1975
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Mental-Imagery Tasks
1976
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DBS in MCS
• Medial thalamic DBS improved one MCS patient’s
performance on some scales 6 years after head
injury (Schiff et al, Nature 2007)
– Large areas of preserved cortex and connections
– Longer periods of eye opening, functional use of objects
and intelligible speaking with optimized DBS
– No improvement on motor and communication scales
(?ceiling effect or measurement scales)
– Implication that MCS is an arousal defect
Brain Death
• Sociologic, legal and medical dividing line from
severe and irrevocable brain damage
• Clinical diagnosis:
– Irreversibility (cause must be defined)
– Lack of function of
• Cerebrum-deep, unresponsive coma
• Midbrain-fixed, mid-sized pupils
• Pons-absent caloric-induced eye movements
• Apnea by formal testing
1977
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1978
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1979
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Disclosure Statement
1980
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1981
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Part 1: General Principles 14. Heparin-Induced Thrombocytopenia (HIT) by Jeanine M. Walenga and M.
Margaret Prechel
1. Physiology of Hemostasis by Jawed Fareed and Omer Iqbal
15. Anticoagulation in Cardiovascular Diseases by Shermeen B. Memon, Lara
2. Laboratory Assessment of Physiologic and Pathologic Hemostasis by Jeanine Bakhos, and Mushabbar A. Syed 28. Is it Safe to Shunt Anti-coagulated NPH Patients? By Eric W. Sankey, Rory
Goodwin, Ignacio Jusue-Torres, and Daniele Rigamonti
M. Walenga
16. Workup and Treatment of Pulmonary Embolus by Agnieszka A. Ardelt
3. Current anticoagulation drugs and mechanisms of action by Tarik F. Ibrahim, 29. Surgical Hemostasis in the Era of Anticoagulation: Guidelines and
Recommendations Summary by Drew A. Spencer, Paul D. Ackerman, Omer
Sean Maxwell and Omer Iqbal Part 3: Coagulation Issues Specific to Neurosurgery
Iqbal, and Christopher M. Loftus
4. Reversal of Target-Specific Oral Anticoagulants by Walter Jeske 17. Classes of Drugs and Blood Products for Acute Reversal of Anticoagulant
Effect by Christopher D. Witiw, Laureen D. Hachem, and Michael G. Fehlings
5. Overview, Treatment, Measurement, and Modification of Platelet Function by 18. Rescue Strategies to Facilitate Emergency Neurosurgery in Patients on
Daphne Li, Wael Hassaneen-Mostafa, and Asterios Tsimpas Antiplatelet or Anticoagulant Agents by Erinç Aktüre, Andrew Goodwin, and
Bruce Tranmer
6. Role of Antiplatelet Therapy in Neurosurgery: Efficacy and Safety Profiles by
19. Considerations for Coagulation in the Multi-Trauma Patient by Craig Rabb
Nicholas Bowen and Shaker A. Mousa
and Allison Strickland
Part 2: Coagulation Issues Across all Patient Spectrums 20. Cerebral Venous Sinus Thrombosis by William W. Ashley Jr.
7. Congenital Coagulation Disorders by Danielle Sterrenberg and Sucha Nand 21. Coagulation studies in preoperative neurosurgery patients byHugh J.L.
Garton
8. Acquired Coagulation Disorders by Kimberly Kruczek, Kathrine Cooper, Hanh
Mai, and Sucha Nand 22. Safe strategies for gradual suspension and re-institution of anticoagulation to
permit elective surgery by Chirstopher Roark
9. Regulation and Dysregulation of Fibrinolysis by Omer Iqbal, Paul O’Malley, 23. Spontaneous Intracerebral Hemorrhage due to Coagulation Disorders by W.
and Nil Guler Caleb Rutledge, S. Andrew Josephson, and Michael T. Lawton
10. Risks Associated with Administration of Allogeneic Blood Components by
Phillip J. DeChristopher 24. Prophylactic Screening for Venous Thromboembolism in Neurosurgical
Patients by Michael Schneck
11. Common Coagulation Disorders that may arise Intraoperatively by Srikanth 25. Venous Thromboembolism Prophylaxis in Neurosurgery by Vikram C.
Nagalla and Geno Merli Prabhu
12. Evaluation and Management of Untoward Intraoperative Bleeding by Michael 26. Can Patients with known intracranial and intraspinal vascular lesions be
P. Wemhoff and W. Scott Jellish anticoagulated? By Christopher P. Robinson, Michael Star, and José Biller
27. Intrathecal Access and Devices in Patients on Antiplatelet or Anticoagulant
13. Treatment of Disseminated Intravascular Coagulation (DIC) by Marcel Levi Therapy by Kevin N. Swong, Drew A. Spencer, and Christopher M. Loftus
1982
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1983
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CML 12/11
CML 12/11
1984
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CML 12/11
CML 12/11
1985
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CML 12/11
SH 1247052
77 yo RH F PMH of DVTs and possible PEs on Xarelto (rivaroxaban) admitted to trauma after fall down
stairs with CT head demonstrating a left cerebral intraparenchymal hemorrhage with left posterior subdural and
6mm MLS. GCS 13 on arrival. Kcentra administered on admission.
• PMH/PSH: Baseline Dementia, DM, Bone Cancer, Thrombocytopenia, PE, Hypothyroidism
• Home Meds: alendronate, ASA81, donepezil, fexofenadine, insulin, hydroxyurea, lantus, synthroid,
xarelto, simvastatin, vesicare
• Allergies: Amoxicillin
• SH: Denies tobacco use, Denies alcohol use, Denies illicits. Lives at home with daughter who is at bedside.
Retired legal secretary.
• FH: noncontributory
• ROS: Negative except for as specified above.
Recs:
- ICU with Q1 hour neuro checks. Contact Neurosurgery for changes in neurologic exam.
- Please avoid hypo-osmolar and dextrose containing fluids as these can exacerbate cerebral edema and
ischemia.
- Repeat CT head 6 hours after initial scan. Repeat CT head sooner if there is deterioration in neurologic exam
- Avoid hypotension
- Keppra for seizure ppx x 7 days
- Discussed prognosis and potential intervention with daughter at bedside. Daughter states that the patient would
not want a undergo surgical intervention given the poor prognosis.
- Maintain normal body temperature
- Total fluids 83ml / hr
1986
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Cranial Imaging
Initial 6 hours
1987
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Cranial Imaging
18 hours 42 hours
1988
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1989
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MR 2865992
22 M with no PMH hit by car (30MPH) while
crossing the street. Patient was intubated on
arrival to the ED. Injuries include pulmonary
contusions, facial fractures, bilateral
frontotemporal contusions and midline frontal
bone fracture extending to a diastatic fracture
of the sagittal suture.
Initial Exam: intubated, eyes open to voice, full
strength x4
1990
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Initial CTH
1991
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CTV at admission
1992
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1993
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1994
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Neuro Exam:
GCS: 3T
Intubated
Right Pupil 5mm irregular nonreactive
Left Pupil 6mm nonreactive
Negative corneal reflex bilaterally
Negative Gag
Cold calorics performed with no eye movement
1995
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PM 2862516
1996
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This Presentation
1997
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1998
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1999
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2000
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Patients We Encounter
• Atrial fibrillation
• Prosthetic heart valves
• DVT/PE
• Endovascular devices (coronary/cerebral)
• Hypercoagulable states
• Unknown therapy
2001
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Antiplatelet Agents
• 1Aspirin
– COX-1 Arachidonic 2
• 2Clopidogrel, prasugrel, ticlopidine, Acid
3 Aggregation
ticagrelor 1
– ADP binding
• 3Abciximab, eptifibatide, tirofiban Prostaglandin
G2/H2
– GpIIbIIIa inhibition
Thrombo Activation,
xanes
Aggregation,
Degranulation
Anticoagulants
Parenteral Oral
2002
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Anticoagulant Agents
Vitamin K
Inhibit synthesis of
# antagonists Warfarin
II, VII, IX, X
(VKA)
Fondaparinux
Indirectly inhibit Xa
Pentasaccharide
activity via ATIII
Idraparinux
Argatroban
Bivalirudin
Direct thrombin
II
inhibitor (DTI)
Dabigatran
Lepirudin
Apixaban
Rivaroxaban
2003
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Clinical scenarios
• Elective surgery patients on AP/AC
– A) bridge
– B) stop
• Emergencies (non bleed) presenting on AP/AC (tumor, acute disc,
hydrocephalus…)
• Bleeds occurring on AP/AC (cerebral or spinal)
• Surgery patients who develop AP/AC needs postop
– DVT
– PE
– CVST
• Patients who need ICU/office procedures on AP/AC
– LP or LD (CVST, diagnostic)
– EVD (pre/post GDC)
2004
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Neuro exam:
AOX3
R B4/D4/T4/DF 0 otherwise intact
Preoperative
2005
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Postoperative
Argatroban infusion started for one wk till CTV showed patent SSS
2006
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How do we reverse?
• Antiplatelet drugs
• Heparin
• Lovenox
• Warfarin
• TSOAC’s
– DTI type
– Factor Xa type
2007
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75 y/o RH F w/ h/o MI on ASA + Plavix s/p stent + Defibrillator also w/ chronic hyponatremia
related to polydipsia associated w/ B parotid gland resection in the 1980’s complicated
infrequently by seizures though not on daily AED due to polydipsia who presented to the
LUMC ED as a Trauma II after husband found her at the base of their staircase
minimally responsive. CT head demonstrated scattered, largely cortical tSAH. CT
cervical was negative.
On arrival, patient awake, but would not regard. Roving eye mvts w/ nystagmus. Symmetric,
purposeful movements x 4, but would not follow commands. Incomprehensible sounds.
GCS 11 (E: 4|V: 2|M: 5)
Na 112.
Trauma concerned patient not protect airway if still actively seizing Intubation (11:53 am)
NS examined patient prior to intubation and recommended the following:
1. Platelet transfusion for ASA + Plavix
2. Neurology consultation for AED + Na management
3. EEG
4. Repeat CT head in 6’ or w/ exam change
2008
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2009
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• Exam:
– AO X3
– EOMI w horizontal nystagmus
– R PF 4/ EHL 3
– L IP 4/ PF 4/ EHL 3
• INR 4.3, APTT 58.1, Platelet 275
2010
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5.4 cm x 3.8 cm
2011
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• Sequence of events:
– Patient given prothrombin complex concentrate,
Vit K (FFP volume is an issue of course)
– OR for R frontal EVD and SOC and evacuation of
L cerebellar IPH.
2012
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• Post op Exam:
– AOX3
– EOMI, horizontal nystagmus
– L dysmetria
– Motor: 5/5 X4
2013
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1 wk postop
2014
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2015
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2016
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• Plan:
– Prothrombin Complex Concentrate
– L4-S1 laminectomy and evacuation of epidural chronic
abscess/phlegmon 3/12/15
• Cultures: negative
• ID: Abx for 6 wks
2017
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0.5 1 1.5
Hazard Ratio
This chart may not be reproduced for other internal training or for external use.
2018
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0.5 1 1.5
Hazard Ratio
This chart may not be reproduced for other internal training or for external use.
2019
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• To prevent this……
2020
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• Non-bleeding problems
– Trauma EVD on NOAC’s
– Procedures that can’t wait on NOAC’s
• (SAH)
• Critical intracranial lesions (see example next)
• Spinal diseases
• Shunts
2021
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On admission
2022
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Postop
T1WI T1WI + C
2023
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2024
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Idarucizumab (Praxbind®)
2025
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PRT064445 vs Per977
Andexanet (Portola Agonist) Aripazine (Perosphere Agonist)
• Recombinant protein • Synthetic lysine-mimetic
• Large molecule (35,000 D) • Small molecule (1,000 D)
• Specific for FXa • Non-specific effect
• Some enzymatic activity (does it • No enzymatic activity
have procoagulant and other • Able to access clot bound FXa
biological effects?)* • Should not generate antibody
• Able to access clot bound FXa? • Cost of goods may be lower
• May generate antibody
• Cost of goods may be high
2026
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Elective Surgery
• Antiplatelet
– Wait 5-7 days[4]
• Vit K antagonists
– Hold for 5 days
– ~90% of patients will have INR < 1.4 at 5 days (goal
INR 2.0-3.0)[4,5]
• NOACs
– Dabigatran, rivaroxaban (renal clearance)
• 1-2 days if CrCl >50
• 3-5 days if CrCl < 50
• But we can’t measure them….
2027
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Apixaban Eliquis 12 hrs 12-24 hrs 48 hrs Avoid while Avoid redose > 5 hrs
catheter in wait > 24h
place after last dose
Dabigatran Pradaxa 12-17 hrs 4 days CrCl > 50 ml/min 3- Avoid while Avoid while 2 hrs
4 days catheter in catheter in
CrCl < 50 ml/min 5-6 lace place
days
Rivaroxaban Xarelto 7-11 hrs 48 hrs 48 hrs Avoid while Avoid while 6-8 hrs
catheter in catheter in 24 hrs if
place place if trauma
redosed 18 or bloody
hrs minimum tap
2028
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Neuro Exam:
Intubated, sedation held
Eyes open to voice
Sticks tongue out to command
Face symmetric
Left pupil 3-2. Right pupil irregular and non-reactive
Follows commands symmetrically x4
2029
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2 days later: the patient was loaded on ASA 325 and Plavix 300 in a plan for
Stent-assisted coiling
2030
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2031
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DVT Screening
• Symptoms
– Non-specific
– DVT
• swelling/pain most common
– PE
• Dyspnea, tachycardia, tachypnea, pleuritic pain
• Wells score
• D-dimer (reference <250µg/L)
– High NPV (~90%)
• Combined score and D-dimer effective to rule out[7]
• Confirmation
– Compression US
– CT PE or V/Q scan
• Still requires much clinical judgement
2032
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DVT PE
• Active cancer (1) • Signs/symptoms of DVT (3.0)
• Lower extremity immobilization • Alternate diagnosis less likely
(paralysis, paresis, injury) (1) than PE (3.0)
• Bedridden ≥ 3 days in last 12 weeks • HR > 100 (1.5)
(1)
• Immobilization, surgery in last 4
• Local tenderness (1) weeks (1.5)
• Calf swelling (1) • Prior DVT/PE (1.5)
– 3 cm > contralateral
• Hemoptysis (1.0)
• Unilateral pitting edema (1)
• Collateral superficial veins (1) • Cancer (1.0)
• Prior DVT (1) • Probability
– Low < 2.0
• Alternate diagnosis at least as likely
(-2) – Intermediate 2.0 - 6.0
– High > 6.0
• DVT likely if > 2
Prophylaxis recommendations
2033
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IVC Filters
Indications – ACCP Guidelines
• DVT • PE
– Acute proximal lower extremity – Acute PE with AC contra-
– Contra-indication to AC indication
• Bleeding diathesis
• Periop
– Prophylactic
• Severe trauma
• Recurrent VTE
– Including TBI, SCI, long
• VTE through AC therapy bone/pelvic fractures
• Bleeding complications • High risk
• AC therapy complication • Prolonged immobilization
• Fall risk
• Poor compliance
~20-40% still placed without clear indication based on request/preference[8]
2034
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ALN OptEase
2035
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2/17/2015
2036
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3/25/2015
5/12/2015
2037
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5/13/2015
2038
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2039
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11/2013
2040
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C/O HA
Exam: unremarkable
On Therapeutic Lovenox
2041
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Negative
2042
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15 days later: Patient was treated by SRS for the R frontal lesions
2 days later: patient presented to ER with RLE pain and dyspnea
Patient admitted to Oncology and Heparin drip was started for a day
& transitioned to Lovenox
2043
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A day later
• Exam:
– AOX3
– R Hemiparesis
– L full strength
• Troponin I: 7.8
2044
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On Admission
2045
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2046
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2047
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2048
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2049
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9 months postop
Paraplegic in wheelchair
2050
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2051
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SH 1247052
77 yo RH F PMH of DVTs and possible PEs on Xarelto admitted to trauma after fall down stairs with CT head
demonstrating a left cerebral intraparenchymal hemorrhage with left posterior subdural and 6mm MLS. GCS 13 on
arrival. 2188 units of Kcentra administered on admission.
• PMH/PSH: Baseline Dementia, DM, Bone Cancer, Thrombocytopenia, PE, Hypothyroidism
• Home Meds: alendronate, ASA81, donepezil, fexofenadine, insulin, hydroxyurea, lantus, synthroid, xarelto,
simvastatin, vesicare
• Allergies: Amoxicillin
• SH: Denies tobacco use, Denies alcohol use, Denies illicits. Lives at home with daughter who is at bedside. Retired
legal secretary.
• FH: noncontributory
• ROS: Negative except for as specified above.
Recs:
- ICU with Q1 hour neuro checks. Contact Neurosurgery for changes in neurologic exam.
- Please avoid hypo-osmolar and dextrose containing fluids as these can exacerbate cerebral edema and ischemia.
- Repeat CT head 6 hours after initial scan. Repeat CT head sooner if there is deterioration in neurologic exam
- Avoid hypotension
- Keppra for seizure ppx x 7 days
- Discussed prognosis and potential intervention with daughter at bedside. Daughter states that the patient would not want
a undergo surgical intervention given the poor prognosis.
- Maintain normal body temperature
- Total fluids 83ml / hr
Cranial Imaging
Initial 6 hours
2052
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Cranial Imaging
18 hours 42 hours
2053
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2054
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Thank you.
• Any questions?
References
1. Gordon JL, Fabian TC, Lee MD, et al. Anticoagulant and antiplatelet medications encountered in
emergency surgery patients: a review of reversal strategies. J Trauma Acute Care Surg.
2013;75(3):475-86.
2. Grandhi R, Harrison G, Voronovich Z, et al. Preinjury warfarin, but not antiplatelet medications,
increases mortality in elderly traumatic brain injury patients. J Trauma Acute Care Surg.
2015;78(3):614-21.
3. Campbell PG, Sen A, Yadla S, et al. Emergency reversal of antiplatelet agents in patients presenting
with an intracranial hemorrhage: a clinical review. World Neurosurg. 2010;74(2-3):279-85.
4. Yorkgitis BK, Ruggia-Check C, Dujon JE. Antiplatelet and anticoagulation medications and the surgical
patient. Am J Surg. 2014;207(1):95-101.
5. Levi M, Eerenberg E, Kamphuisen PW. Bleeding risk and reversal strategies for old and new
anticoagulants and antiplatelet agents. J Thromb Haemost. 2011;9(9):1705-12.
6. Schulman S, Hwang HG, Eikelboom JW, et al. Loading dose vs. maintenance dose of warfarin for
reinitiation after invasive procedures: a randomized trial. J Thromb Haemost. 2014;12(8):1254-9.
7. Owaidah T, AlGhasham N, AlGhamdi S, et al. Evaluation of the usefulness of a D dimer test in
combination with clinical pretest probability score in the prediction and exclusion of Venous
Thromboembolism by medical residents. Thromb J. 2014;12(1):28.
8. Patel G, Panikkath R, Fenire M, et al. Indications and appropriateness of inferior vena cava filter
placement. Am J Med Sci. 2015;349(3):212-6.
9. Berczi V, Bottomley JR, Thomas SM, et al. Long-term retrievability of IVC filters: should we abandon
permanent devices? Cardiovasc Intervent Radiol. 2007;30(5):820-7.
10. Kaufman JA, Kinney TB, Streiff MB, et al. Guidelines for the use of retrievable and convertible vena
cava filters: report from the Society of Interventional Radiology multidisciplinary consensus
conference. Surg Obes Relat Dis. 2006;2(2):200-12.
2055
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References cont.
11. Buesing KL, Mullapudi B, Flowers KA. Deep Venous Thrombosis and Venous Thromboembolism
Prophylaxis. Surg Clin North Am. 2015;95(2):285-300.
12. Majeed A, Meijer K, Larrazabal R, et al. Mortality in vitamin K antagonist-related intracerebral
bleeding treated with plasma or 4-factor prothrombin complex concentrate. Thromb Haemost.
2014;111(2):233-9.
13. Mavrakanas TA, Samer C, Fontana P, et al. Direct oral anticoagulants: efficacy and safety in patient
subgroups. Swiss Med Wkly. 2015;145:w14081.
14. McCoy CC, Lawson JH, Shapiro ML. Management of anticoagulation agents in trauma patients. Clin
Lab Med. 2014;34(3):563-74.
15. Moussouttas M. Challenges and controversies in the medical management of primary and
antithrombotic-related intracerebral hemorrhage. Ther Adv Neurol Disord. 2012;5(1):43-56.
16. Ortel TL. Perioperative management of patients on chronic antithrombotic therapy. Hematology
Am Soc Hematol Educ Program. 2012;2012:529-35.
17. Spyropoulos AC. Bridging therapy and oral anticoagulation: current and future prospects. Curr Opin
Hematol. 2010;17(5):444-9.
18. Suryanarayan D, Schulman S. Potential antidotes for reversal of old and new oral anticoagulants.
Thromb Res. 2014;133 Suppl 2:S158-66.
19. Thiele T, Sümnig A, Hron G, et al. Platelet transfusion for reversal of dual antiplatelet therapy in
patients requiring urgent surgery: a pilot study. J Thromb Haemost. 2012;10(5):968-71.
20. Yasaka M, Okada Y. [Management of intracranial hemorrhage during anticoagulant therapy with
warfarin or novel anticoagulants]. Rinsho Shinkeigaku. 2012;52(11):1113-6.
2056