Cerebrovascular Disease

Cerebrovascular Disease (CVD)

• Sudden focal (or global) neurologic deficit
caused by a vascular pathology
• Transient Ischemic Attack- transient episode
of neurological dysfunction caused by focal
brain, spinal or retinal ischemia without
evidence of infarction in which clinical
symptoms typically lasts less than an hour
– Unstable condition (warning of an impending
stroke)
– Risk of stroke - 10% in 7 days and 15% at 30 days
 Blood Vessel Signs and Symptoms
Involvement
• Contralateral weakness of UE/LE leg>arm, face
Anterior Cerebral • Contralateral numbness s of UE/LE leg>arm, face
Artery • Incontinence

• Contralateral weakness of UE/LE face,arm>leg

Middle cerebral Artery
• Contralateral numbness s of UE/LE face, arm>leg
(proximal • Preferential gaze looking towards the lesion
segment/maintrunk)
• Contralateral hemineglect
• Contralateral homonymous hemianopia
• Receptive and expressive aphasia if dominant hemisphere
involved (Global aphasia)
MCA superior division • Expressive/Motor aphasia (Broca’s aphasia)
only
MCA inferior division
only • Comprehensive/Sensory aphasia (Wernicke’s aphasia)
 Blood Vessel Signs and Symptoms
Involvement
• Homonymous hemianopia
Posterior Cerebral or
Artery • Bilateral visual loss

• Contralateral weakness of extremities

Posterior Cerebral
artery • Ipsilateral cranial nerve III palsy (ptosis, dilated pupil)
(Weber Syndrome)

• No affectation of consciousness
Basilar artery/pontine
perforators • Quadriplegia
(Locked In Syndrome) • Unable to verbally communicate
• ONLY vertical eye movements are intact
• Pons
Millard Gubler Syndrome
• Ventro-lateral pons
• Basilar artery perforator
• Ipsilateral 6th and 7th nerve palsy and contralateral
hemiplegia

Locked in syndrome
• Bilateral basis pontis
• Basilar artery perforators
• Quadriplegia, bilateral facial palsy, no eye movement
except for vertical gaze
• Consciousness intact
• Lateral Medulla
– Wallenberg syndrome
– Posterior inferior cerebellar artery
– Ipsilateral facial numbness and contralateral extremity
numbness
– Ipsilateral ataxia
– Dysphagia, vertigo, nystagmus

• Medial Medulla
– Branch of the vertebral artery
– Ipsilateral tongue deviation and contralateral extremity
weakness
2 Major types of CVD
1. Ischemic stroke – results from
blockade of an artery and
infarction of CNS tissue

2. Hemorrhagic – results from a

rupture of a blood vessel or an
abnormal vascular structure
directly into and around the brain
 Ischemic Stroke Subtypes
1. Atherosclerotic infarction (20%)- thrombotic
infarct/Large vessel disease

2. Lacunar infarct (25%)- penetrating arteries

affecting the deeper parts of the brain (basal
ganglia, thalamus, white matter) and in the brain
stem
- Small vessel disease – lipohyalinosis
- *Penetrating arteries- lateral lenticulostriate a.
(MCA), medial lenticulostriate a. (ACA), pontine
perforators (basilar a.)
Ischemic Stroke Subtypes
3. Cardioembolic (20%)
- Common site of occlusion: branching points of
vessels

4. Cryptogenic/Unknown (30%)

5. Infarction of other determined cause (5%)

Normal Physiology
• 15% of cardiac output supplies the brain
• Normal cerebral blood flow (CBF): 50-
55ml/100 g brain tissue per minute
• Reduction of CBF below 10 to 12 mL/100
g/min causes infarction, almost regardless of
its duration.
 CELL
Apoptosis DEATH

Glutamate release
Concept of ischemic penumbra

Cells are active, trying to survive

Cells are dead

Hemorrhagic stroke/CVD bleed/ICH

• Chronic HTN weakens the

blood vessel wall
• Formation of Charcot
bouchard aneurysm usually
at the bifurction of small
vessels
 Etiologies of ICH
• Chronic uncontrolled hypertension- most common
• Vascular malformation
• Aneurysm
• Venous Angioma
• Capillary telangiectasia
• Blood dyscrasia
• Trauma
• Amyloid angiopathy
• Excessive anticoagulation
• Illicit drug use - meth, shabu, cocaine
• Tumor bleed
 Common Sites of ICH
• Putamen and adjacent internal capsule (40-
50%)
• Thalamus (10-15%)
• Cerebellar- 10%
• Pons (5%)
Hematoma can expand within first 24 hours in
hypertensive ICH
38% will have hematoma expansion within 24
hours, most within 1st 6 hrs
 Diagnostic Exams
• Complete blood count with platelet count
• CBG
• Electrolytes
• Urinalysis
• Chest X ray
• BUN, crea, LFTs
• PT INR and PTT
• 12 L ECG
• Fasting blood sugar
• Lipid profile
• Non contrast cranial CT scan
 Management Principles
• Early recognition of signs of stroke
• Exclude common stroke mimickers such as
hypoglycemia, Todd’s paralysis
• Provide basic emergent supportive care
(ABCs of resuscitation)
• Monitor neuro vital signs, BP, MAP, RR,
temp, pupils. Treat if MAP >130
• Ascertain type of stroke: If ischemic, check if
eligible for rTPA (within 4.5 hours post ictus)
 Management Principles
• Ensure appropriate hydration. IVF: 0.9% NaCl
• DO NOT use D5 containing fluids
• For moderate to severe stroke, provide medical
decompression
– Mannitol 20% 0.5-1 g/kg BW q 4-6 hrs for 3-7
days or longer
– Hypertonic saline
• Rehabilitation within 72 hours or once patient is
stable
BP Management in Acute Stroke

CPP = MAP-ICP
MAP = SBP + 2 DBP
3
Target MAP 110 – 130
Infarct: 120-130
Bleed: 110-120
 BP Management in Acute Stroke

• Avoid precipitous drop in BP (not > 15% of

baseline MAP). Do not use rapid-acting
sublingual agents; when needed use easily
titratable IV (ie nicardipine) or short-acting
oral antihypertensive medication
 Management of CVD Infarct

• Reperfusion
– Thrombolysis--IV rTPA in carefully selected pts
within 3-4.5 hours after the stroke
– Prevents ischemia from progressing into infarction
• Neuroprotection
• Aspirin within 48 hours- prevents new clot
formation

GOAL: Salvage the ischemic penumbra

 Recombinant Tissue Plasminogen
Activator (rTPA)
• Initiates local fibrinolysis by binding to fibrin
in a thrombus (clot) and converts entrapped
plasminogen to plasmin
• Synthetic, developed by DNA technology
• Risks with treatment- bleeding (Intracranial
hemorrhage); not an easy drug to give
• With strict inclusion and exclusion criteria
 NINDS rTPA Trial
• Dose: 0.9 mg/kg IV (Maximum of 90 mg)
– 10% to be given as bolus and 90% as drip for 1 hour
• e.g. 56 kg F; Total dose = 50 mg => 5mg IV bolus,
45 mg as drip for 1 hour

• IV rTPA patients within 3 hours are 30% more

likely to have minimal to no disability at 3 months
 ECASS trial
• European Cooperative Acute Stroke Study
(ECASS) III study explored the safety and
efficacy of rtPA in the 3- to 4.5-hour time
window
 Management of CVD Infarct

• Antiplatelets
– Aspirin 160-325 mg/day as early as possible
– Other antiplatelets: clopidrogrel, cilostazol, triflusal,
dipyridamole
• If cardioembolic, start anticoagulation with warfarin
or novel oral anticoagulants (NOACs)
– Goal PT INR 2-3 (if on warfarin)
– May defer initially if with large infarcts
• Allow permissive hypertension during the first week
post ictus (MAP 120-130)
 Management
Management of ICH
of CVD bleed

• Maintain MAP of 110-120

• Newer studies suggest that BP lowering to SBP
<140 is safe among patients with CVD bleed
• Prophylactic antiepileptic drugs and steroids
are NOT recommended
• Correct coagulation/bleeding abnormalities if
present
 Etiologies of ICH
• Chronic uncontrolled hypertension- most common
• Vascular malformation
• Aneurysm
• AV Malformation
• Venous Angioma
• Capillary telangiectasia
• Blood dyscrasia
• Trauma
• Amyloid angiopathy
• Excessive anticoagulation
• Illicit drug use - meth, shabu, cocaine
• Tumor bleed
Aneurysmal Subarachnoid Hemorrhage
• thin-walled focal dilatations that protrude from
the arteries of the Circle of Willis

Common Locations
• ACOM 4O %
• PCOM 3O %
• MCA 2O %
• Basilar tip 5 %
• Others 1-3%
 SAH
– “worst headache of my life” in 80% of patients
– May be associated with vomiting, stiff neck, loss
of consciousness or focal neurologic deficits,
seizures in 20%
– PE: signs of meningeal irritation, decreased
consciousness, CN III or IV palsy, may or may not
have focal deficits
 Hunt and Hess Grading of SAH
Grade Clinical Manifestation
1 Asymptomatic or mild headache, slight nuchal
rigidity
2 Moderate to severe headache, nuchal rigidity,
CN palsy
3 Drowsiness, confusion, mild focal signs
4 Stupor, moderate to severe hemiparesis
5 Coma, decebrate rigidity, moribound
appearance
 SAH: Diagnostics and Management
• 4 vessel cerebral angiogram (gold standard)

complete bed rest - Ca channel blockers [Nimodipine] to

Analgesics prevent vasospasm
anti-emetics - anticonvulsant prophylaxis
manage inc ICP - BP target, SBP < 15O
H2 blockers of PPI as GI prophylaxis - correct hyponatremia
Stool softeners - Maintain normothermia,
normoglycemia
• Secure aneurysm either by clipping or coiling
in good grade patients ASAP
 Complications of SAH
1. Re-bleed rate- 4% for 24 hours; 20% for 2 weeks
- most feared complication because it carries
the highest mortality
2. Vasospasm leading to cerebral ischemia /
infarction
- within 3 to 21 days
3. IV extension and hydrocephalus
4. Hyponatremia
5. Seizures