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NEUROLOGY
SANKET
SHAH
(KESAR SAL)
Available on www.mysarthee.co.cc
NORMAL CSF
Differential
Lymphocytes 60–70%
Monocytes 30–50%
Neutrophils None
a
Since cerebrospinal fluid concentrations are equilibrium values,
measurements of the same parameters in blood plasma
obtained at the same time are recommended. However, there is
a time lag in attainment of equilibrium, and cerebrospinal levels
of plasma constituents that can fluctuate rapidly (such as
plasma glucose) may not achieve stable values until after a
significant lag phase.
b
IgG index = CSF IgG(mg/dL) x serum albumin(g/dL)/Serum
IgG(g/dL) x CSF albumin(mg/dL).
CSF IN BACTERIAL
MENINGITIS
The diagnosis of bacterial meningitis is made by
F
l
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d
(
C
S
F
)
A
b
n
o
r
m
a
l
i
t
i
e
s
i
n
B
a
c
t
e
r
i
a
l
M
e
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i
n
g
i
t
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Use of the CSF/serum glucose ratio corrects for
hyperglycaemia that may mask a relative decrease in the
CSF glucose concentration.
The CSF glucose concentration is low when the
CSF/serum glucose ratio is <0.6.
A CSF/serum glucose ratio <0.4 is highly suggestive of
bacterial meningitis but may also be seen in other
conditions, including fungal, tuberculous, and carcinomatous
meningitis.
1. INTRO
Acute infections of the nervous system are among the most
important problems in medicine because early recognition, efficient
decision-making, and rapid institution of therapy can be lifesaving.
2. DEFINITION
• Bacterial meningitis is an Acute purulent infection within the
subarachnoid space.
• It is associated with a CNS inflammatory reaction that may
result in decreased consciousness, seizures, raised intracranial
pressure (ICP), and stroke.
3. EPIDEMIOLOGY
Currently, the organisms most commonly responsible for community-
acquired bacterial meningitis are
• Streptococcus pneumoniae (~50%),
• N. meningitidis (~25%),
• Group B streptococci (~15%),
• Listeria monocytogenes (~10%).
• H. influenzae now accounts for <10% of cases of bacterial
meningitis in most series.
4. ETIOLOGY
• S. pneumoniae
the most common cause of meningitis in adults >20 years of
age
Predisposing factors
1) pneumococcal pneumonia.
2) coexisting acute or chronic pneumococcal sinusitis or
otitis media,
3) alcoholism,
4) diabetes,
5) splenectomy,
6) hypogammaglobulinemia,
7) complement deficiency,
8) head trauma with basilar skull fracture and CSF
rhinorrhea.
• N. Meningitides
children and young adults between the ages of 2 and 20.
The risk of invasive disease following nasopharyngeal colonization
depends on both bacterial virulence factors and host immune
defense mechanisms
Individuals with deficiencies of any of the complement
components, including properdin, are highly susceptible to
meningococcal infections.
• Enteric gram-negative bacilli
common cause of meningitis in individuals with chronic and
debilitating diseases such as diabetes, cirrhosis, or alcoholism and
in those with chronic urinary tract infections
Gram-negative meningitis can also complicate neurosurgical
procedures, particularly craniotomy.
• Group B streptococcus,
previously responsible for meningitis predominantly in neonates,
but it has been reported with increasing frequency in individuals
>50 years of age, particularly those with underlying disease
• L. Monocytogenes
important cause of meningitis in neonates (<1 month of age),
pregnant women, individuals >60 years, and
immunocompromised individuals of all ages.
Foodborne human listerial infection
• H. influenzae type b
meningitis in children has declined dramatically since the
introduction of the Hib conjugate vaccine
More frequently, H. influenzae causes meningitis in unvaccinated
5. PATHOPHYSIOLOGY
6. CLINICAL PRESENTATIONS
• PRESENTATION
an acute fulminant illness that progresses rapidly in a few hours
1)
OR
2) subacute infection that progressively worsens over several
days
• CLASSICAL TRIAD
1) fever,
2) headache,
3) nuchal rigidity
• OTHER IMPORTANT
1) decreased level of consciousness
2) Nausea,
3) projectile vomiting,
4) photophobia
• Seizures
1) Focal
2) Generalised
• RAISED ICP
1) major cause of obtundation and coma
2) 90% of patients will have a CSF opening pressure >180 mmH2O,
7. DIAGNOSIS
• CSF
The diagnosis of bacterial meningitis is made by
F
l
u
i
d
(
C
S
F
)
A
b
n
o
r
m
a
l
i
t
i
e
s
i
n
B
a
c
t
e
r
i
a
l
M
e
n
i
n
g
i
t
i
s
Use of the CSF/serum glucose ratio corrects for
hyperglycaemia that may mask a relative decrease in the
CSF glucose concentration.
The CSF glucose concentration is low when the
CSF/serum glucose ratio is <0.6.
A CSF/serum glucose ratio <0.4 is highly suggestive of
bacterial meningitis but may also be seen in other
conditions, including fungal, tuberculous, and carcinomatous
meningitis.
8. DIFFERENTIAL DIAGNOSIS
1. Viral meningoencephalitis, and particularly herpes simplex
virus (HSV) encephalitis
2. Rickettsial disease can resemble bacterial meningitis
3. Ehrlichioses
4. Focal suppurative CNS infections , including subdural and
epidural empyema and brain abscess
5. Subarachnoid hemorrhage
6. chemical meningitis due to rupture of tumor contents into the
CSF
7. sarcoid, systemic lupus erythematosus (SLE), and Behçet's
syndrome
9. TREATMENT
• GOAL
Bacterial meningitis is a medical emergency.
The goal is to begin antibiotic therapy within 60 min of a patient's
arrival in the emergency room
• Empirical antimicrobial therapy
initiated in patients with suspected bacterial meningitis before the
results of CSF Gram's stain and culture are known
Antibiotics Used in Empirical Therapy of Bacterial Meningitis
and Focal CNS Infectionsa
Indication Antibiotic
1. Preterm infants Ampicillin + Cefotaxime
to infants <1
month
2. Infants 1–3 Ampicillin + Cefotaxime or
mos ceftriaxone
3. Immunocompe vancomycin + Cefotaxime or
tent children >3 ceftriaxone
mos and adults
<55
4. Adults >55 and Ampicillin + cefotaxime or ceftriaxone
adults of any age + vancomycin
with alcoholism or
other debilitating
illnesses
5. Hospital- Ampicillin + ceftazidime +
acquired vancomycin
meningitis,
posttraumatic or
postneurosurgery
meningitis,
neutropenic
patients, or
patients with
impaired cell-
mediated
immunity
Indication Antibiotic
1. Preterm infants Ampicillin + Cefotaxime
to infants <1
month
2. Infants 1–3 Ampicillin + Cefotaxime or
mos ceftriaxone
3. Immunocompe vancomycin + Cefotaxime or
tent children >3 ceftriaxone
mos and adults
<55
4. Adults >55 and Ampicillin + cefotaxime or ceftriaxone
adults of any age + vancomycin
with alcoholism or
other debilitating
illnesses
5. Hospital- Ampicillin + ceftazidime +
acquired vancomycin
meningitis,
posttraumatic or
postneurosurgery
meningitis,
neutropenic
patients, or
patients with
impaired cell-
mediated
immunity
me
Vancomyc 60 (mg/kg)/d, q6h 2 g/d, q12h
in
Meningococcal Meningitis
o Although ceftriaxone and cefotaxime provide adequate
empirical coverage for N. meningitidis, penicillin G remains the
antibiotic of choice for meningococcal meningitis caused by
susceptible strains
Pneumococcal Meningitis
o Antimicrobial therapy of pneumococcal meningitis is initiated
with a cephalosporin (ceftriaxone, cefotaxime, or cefepime)
and vancomycin
o A 2-week course of intravenous antimicrobial therapy is
recommended for pneumococcal meningitis.
o Patients with S. pneumoniae meningitis should have a repeat
• ADJUNCT THERAPY
Dexamethasone exerts its beneficial effect by inhibiting the
synthesis of IL-1 and TNF at the level of mRNA, decreasing CSF
outflow resistance, and stabilizing the blood-brain barrier.
The rationale for giving dexamethasone 20 min before antibiotic
therapy is that dexamethasone inhibits the production of TNF by
macrophages and microglia only if it is administered before these
cells are activated by endotoxin.
3) mannitol.
10. PROGNOSIS
• MORTALITY
Mortality is 3–7% for meningitis caused by H. influenzae, N.
meningitidis, or group B streptococci;
15% for that due to L. monocytogenes;
20% for S. pneumoniae.
• SEQUELE
Moderate or severe sequelae occur in ~25% of survivors, although
the exact incidence varies with the infecting organism.
Common sequelae include
i. decreased intellectual function,
ii. memory impairment,
iii. seizures,
iv. hearing loss and dizziness,
v. gait disturbances.
Neurocysticercosis
INTRO
• Neurocysticercosis is the most common parasitic disease of the CNS
worldwide.
• Humans acquire cysticercosis by the ingestion of food contaminated with
the eggs of the parasite T. solium.
Clinical Presentation
1. The most common manifestation of neurocysticercosis is new-onset
partial seizures with or without secondary generalization.
2. When present in the subarachnoid or ventricular spaces, cysticerci can
produce increased ICP
3. Spinal cysticerci can mimic the presentation of intraspinal tumors.
Diagnosis
• The lesions of neurocysticercosis are readily visualized by MRI or CT
scans.
• A very early sign of cyst death is hypointensity of the vesicular fluid on
T2-weighted images when compared with CSF.
• Parenchymal brain calcifications are the most common finding and
evidence that the parasite is no longer viable.
Treatment
• Anticonvulsant therapy is initiated when the patient with
neurocysticercosis presents with a seizure.
• Antiepileptic therapy can be stopped once the follow-up CT scan shows
resolution of the lesion.
• Long-term antiepileptic therapy is recommended when
1)seizures occur after resolution of edema and resorption
2) calcification of the degenerating cyst.
ACUTE STROKE
MANAGEMENT
1. PRIMARY STEPS
• After the clinical diagnosis of stroke is made, an
orderly process of evaluation and treatment should follow
• The first goal is to prevent or reverse brain injury.
• Attend to the patient's (ABC)airway, breathing,
circulation, and treat hypoglycemia or hyperglycemia if
identified.
• Perform an emergency noncontrast head CT scan in
order to differentiate between ischemic stroke and
hemorrhagic stroke; there are no reliable clinical findings
that conclusively separate ischemia from hemorrhage,
although
1. a more depressed level of consciousness,
2. higher initial blood pressure, or
3. worsening of symptoms after onset
2. Medical Support
• When ischemic stroke occurs, the immediate goal is to
optimize cerebral perfusion in the surrounding ischemic
penumbra.
3. Intravenous Thrombolysis
• recombinant tPA (rtPA)
• The time of stroke onset is defined as the
Indication Contraindication
Clinical diagnosis of
1. 1. Sustained BP >185/110
stroke despite treatment
2. Onset of symptoms 2. Platelets <100,000;
to time of drug 3. HCT <25%;
administration <=3 h 4. glucose <50 or >400
3. CT scan showing no mg/dL
hemorrhage or edema 5. Use of heparin within 48
of >⅓ of the MCA h and prolonged PTT, or
territory elevated INR
4. Age >=18 years 6. Recent myocardial
5. Consent by patient infarction
or surrogate 7. Prior stroke or head
injury within 3 months;
8. prior intracranial
hemorrhage
9. Major surgery in
preceding 14 days
10. Gastrointestinal
bleeding in preceding 21
days
11. Minor stroke symptoms
12. Rapidly improving
symptoms
13. Coma or stupor
Administration of rtPA
1. Intravenous access with two peripheral IV lines (avoid
arterial or central line placement)
2. Review eligibility for rtPA
3. Administer 0.9 mg/kg intravenously (maximum 90 mg) as
4. Endovascular Techniques
• Ischemic stroke from large-vessel intracranial occlusion
results in high rates of mortality and morbidity.
• Occlusions in such large vessels [middle cerebral artery
(MCA), internal carotid artery(ICA), and the basilar
artery(BA)] generally involve a large clot volume and
often fail to open with IV rtPA alone.
• Endovascular mechanical thrombectomy has recently
shown promise as an alternative treatment of acute stroke
in
1. patients who are ineligible for, or have
contraindications to, thrombolytics or
2. in those who have failed to have vascular
recanalization with IV thrombolytics.
• endovascular thrombectomy device to restore patency of
occluded intracranial vessels within 8 h of ischemic
stroke symptoms.
5.Antithrombotic Treatment
Platelet Inhibition
• Aspirin is the only antiplatelet agent that has been proven
effective for the acute treatment of ischemic stroke;
6.Neuroprotection
• Neuroprotection is the concept of providing a treatment that
prolongs the brain's tolerance to ischemia.
• Hypothermia is a powerful neuroprotective treatment in
patients with cardiac arrest and is neuroprotective in animal
models of stroke, but it has not been adequately studied in
patients with ischemic stroke.
CEREBRAL VENOUS
THROMBOSIS - MX
Medical Care
• Medical management of the patient with cerebral venous thrombosis
(CVT) is similar to that of patients with arterial stroke as far as stabilizing
the patient is concerned.
• Patients with altered mental status or hemiplegia should be given
nothing by mouth to prevent aspiration.
• Intravenous fluids should not be hypotonic solutions. Normal saline is
recommended at a rate of approximately 1000 mL in 24 hours.
• To decrease intracranial pressure, the head should be elevated 30-40° at
all times.
• supplemental oxygen only when level of consciousness is decreased.
Heparin
Adult
Initial infusion: 18 U/kg/h IV; aPTT checked in 6 h and q6h after any dosage
change, as well as every am;
adjust dose according to following parameters
aPTT = <1.2 times control: 80 U/kg bolus with increase of 4 U/kg/h
aPTT = 1.2-1.5 times control: 40 U/kg bolus with increase of 2 U/kg/h
aPTT = 1.5-2.3 times control: No change in infusion rate needed
aPTT = 2.3-3 times control: Decrease infusion rate by 2 U/kg/h
aPTT > 3 times control: Hold infusion for 1 h and decrease rate by 3
U/kg/h
Warfarin
• warfarin treatment should be maintained for 3-6 mo
Adult
Initial: 5 mg PO qd; adjust dose by monitoring INR (target, 2.5)
Thrombolytics
• These agents cause lysis of the clot.
• This treatment at present is limited to specialized centers but should be
considered for patients with significant deficit.
Urokinase
• Given in CVT by catheterization of venous sinus or by direct instillation at
surgery during thrombectomy.
Adult
2,50,000 U/h instilled directly or via venous sinus catheter; additional doses
of 50,000 U; total dose 1,000,000 U over 2 h
Streptokinase
Adult
Instilled directly or via venous sinus catheter
Surgical Care
• In cases of severe neurologic deterioration, open thrombectomy and
local thrombolytic therapy have been described as beneficial.
• Recently, decompressive craniectomy has been reported as a treatment
strategy, with varied results.
CAUSES
occlusion of any of five vessels may be responsible—
1) vertebral,
2) posterior inferior cerebellar,
3) superior lateral medullary arteries,
4) middle lateral medullary arteries,
5) inferior lateral medullary arteries
CLINICAL FEATURES
• This syndrome is characterized by
1. sensory deficits affecting the trunk and extremities on the
opposite side of the infarction
2. sensory deficits affecting the face and cranial nerves on
the same side with the infarct.
• On side of lesion
1) Impaired pain and thermal sense over half the body, sometimes
face: Spinothalamic tract
TREATMENT
Treatment for lateral medullary syndrome involves focusing
on
1. relief of symptoms and
2. active rehabilitation
IMMEDIATE
1. A feeding tube inserted through the mouth or gastrostomy
may be necessary if swallowing is impaired.
2. Speech therapy may be beneficial
3. In some cases, medication may be used to reduce or
eliminate pain.
4. One of the most unique and difficult to treat symptoms that
occur due to Wallenberg syndrome are interminable,
violent hiccups. The hiccups can be so severe that patients
often struggle to eat, sleep and carry on conversations.
5. Depending on the severity of the blockage caused by the
stroke, the hiccups can last for weeks. Unfortunately there
are very few successful medications available to mediate the
inconvenience of constant hiccups.
LONG TERM
1. Long term treatment generally involves the use of blood
thinners like warfarin.
2. Patients will often remain on these medications or an aspirin
regimen for the rest of their lives in order to minimize the
risk of another stroke.
3. Other medications may be necessary in order to suppress
high blood pressure and risk factors associated with strokes.
Transient Ischemic
Attacks
DEFINITION
• TIAs are episodes of stroke symptoms that last only briefly; the
standard definition of duration is <24 h, but most TIAs last <1 h.
• Amaurosis fugax, or transient monocular blindness, occurs from
emboli to the central retinal artery of one eye. This may indicate
carotid stenosis as the cause or local ophthalmic artery disease.
RISK
• The risk of stroke after a TIA is ~10–15% in the first 3 months,
with most events occurring in the first 2 days.
Risk Factors for Ischemic Stroke and TIA
• Identification and control of modifiable risk factors is the best
strategy to reduce the burden of stroke, and the total number of
strokes could be reduced substantially by these means
1. Hypertension
2. Atrial fibrillation
3. Diabetes
4. Smoking
5. Hyperlipidemia
6. Asymptomatic carotid
stenosis
7. Symptomatic carotid stenosis
(70–99%)
8. Symptomatic carotid stenosis
(50–69%)
CAUSES
Common Causes
Uncommon Causes
Thrombosis Hypercoagulable disorders
Lacunar stroke (small
vessel) Venous sinus thrombosis
Large vessel thrombosis
Dehydration Fibromuscular dysplasia
Embolic occlusion
Artery-to-artery Vasculitis
Carotid bifurcation
Aortic arch Cardiogenic
Uncommon Causes
Arterial dissection Mitral valve calcification
Cardioembolic Atrial myxoma
Atrial fibrillation Intracardiac tumor
Mural thrombus
Myocardial infarction Subarachnoid hemorrhage
Dilated cardiomyopathy vasospasm
Valvular lesions
Mitral stenosis Drugs: cocaine, amphetamine
Mechanical valve
Bacterial endocarditis Eclampsia
Paradoxical embolus
Atrial septal defect
Patent foramen ovale
MANAGEMENT PLAN
• FIG 364-1 HARRISON
mg/d.
• Tobacco smoking should be discouraged in all patients
Antiplatelet Agents
• Platelet antiaggregation agents can prevent atherothrombotic
events, including TIA and stroke
• Aspirin, clopidogrel, and the combination of aspirin plus extended-
release dipyridamole are the antiplatelet agents most commonly
used for this purpose.
• Ticlopidine has been largely abandoned because of its adverse
effects.
• The choice of antiplatelet agent and dose must balance the risk of
stroke, the expected benefit, and the risk and cost of treatment.
Anticoagulation Therapy and Embolic Stroke
• Several trials have shown that anticoagulation (INR range, 2–3) in
patients with chronic nonvalvular (nonrheumatic) atrial fibrillation
prevents cerebral embolism and is safe.
• For primary prevention and for patients who have experienced
stroke or TIA, anticoagulation with warfarin reduces the risk by
about 67%, which clearly outweighs the 1% risk per year of a
major bleeding complication.
• If the embolic source cannot be eliminated, anticoagulation should
in most cases be continued indefinitely.
• Many neurologists recommend combining antiplatelet agents with
anticoagulants for patients who "fail" anticoagulation (i.e., have
another stroke or TIA).
Weber's syndrome
INTRO
• Weber's syndrome is a form of stroke characterized by the presence of
an oculomotor nerve palsy and contralateral hemiparesis or hemiplegia.
Cause
o It is caused by midbrain infarction as a result of occlusion of the
paramedian branches of the posterior cerebral artery(PCA) or of
basilar bifurcation perforating arteries.
o Weber's Syndrome has presented as a manifestation of
decompression illness in a recreational scuba diver.[2]
Presentation
This lesion is usually unilateral and affects several structures in the midbrain
including:
Structure
Effect
damaged
1. substantia
contralateral parkinsonism
nigra
2. corticospinal contralateral hemiparesis and typical upper motor
fibers neuron findings
3. corticobulbar difficulty with contralateral lower facial muscles and
tract hypoglossal nerve functions
4. oculomotor ipsilateral oculomotor nerve palsy with a drooping
eyelid and fixed wide pupil pointed down and out. This
nerve fibers
leads to diplopia
Benedikt syndrome
INTRO
• Benedikt syndrome,or paramedian midbrain syndrome, is a rare
type of posterior circulation stroke of the brain, with a range of
neurological symptoms affecting the midbrain, cerebellum and other
related structures
Causes
• Benedikt syndrome is caused by a lesion ( infarction, hemorrhage,
tumor, or tuberculosis) in the tegmentum of the midbrain and
cerebellum.
• Specifically, the median zone is impaired.
• It can result from occlusion of the posterior cerebral artery.
Characterization
Neuroanatomical structures affected
include CNIII nucleus,
Red nucleus,
corticospinal tracts,
brachium conjunctivum, and
cerebellum.
• It is characterized by the presence of
1)an CN III oculomotor nerve palsy and
2)contralateral hemiparesis (weakness) and
3)cerebellar ataxia including tremor.
Treatment
• Deep brain stimulation may provide relief from some symptoms of
Benedikt syndrome, particularly the tremors associated with the disorder
Foville's syndrome
INTRO
• Foville's syndrome is caused by the blockage of the perforating
branches of the basilar artery in the pons.
Structures affected
1. the PPRF, (paramedian pontine reticular formation)
2. nuclei of cranial nerves VI and VII,
3. corticospinal tract,
4. medial lemniscus,
5. the medial longitudinal fasciculus.
Presentation
1. ipsilateral horizontal gaze palsy
2. facial nerve palsy
3. contralateral hemiparesis,
4. hemisensory loss,
5. internuclear ophthalmoplegia.
MULTIPLE
SCLEROSIS
DEFINITION
• Demyelinating disorders characterized by inflammation and
selective destruction of central nervous system (CNS) myelin. The
peripheral nervous system (PNS) is spared, and most patients
have no evidence of an associated systemic illness.
CHARACTERISTIC FEATURES
• Multiple sclerosis (MS) is characterized by a triad of inflammation,
demyelination, and gliosis (scarring);
• the course can be relapsing-remitting or progressive.
• Lesions of MS typically occur at different times and in different
CNS locations (i.e., disseminated in time and space).
EPIDEMIOLOGY
• MS is approximately threefold more common in women than men.
• The age of onset is typically between 20 and 40 years, but the
disease can present across the lifespan.
• Geographical gradients have been repeatedly observed in MS,
with prevalence rates increasing at higher latitudes. high rates are
found throughout northern Europe, the northern United States,
and Canada. By contrast, the prevalence is low in Japan , in other
parts of Asia, in equatorial Africa, and in the Middle East.
• viral infections (e.g., poliomyelitis and measles viruses), human
Clinical Manifestations
• The onset of MS may be abrupt or insidious.
• Clinical course of multiple sclerosis (MS).
A. Relapsing/remitting MS. (RR)
B. Secondary progressive MS. (SP)
C. Primary progressive MS. (PP)
D. Progressive/relapsing MS.(PR)
Symptom
1. Sensory loss
2. Optic neuritis
3. Weakness
4. Paresthesias
5. Diplopia
6. Ataxia
7. Vertigo
8. Paroxysmal attacks
9. Lhermitte
10. Pain
11. Dementia
12. Visual loss
Symptom
13. Facial palsy
14. Impotence
15. Myokymia
16. Epilepsy
17. Falling
Diagnostic Criteria
Diagnostic Criteria for MS
(a). MRI may be used to document a second lesion when only one
site of abnormality has been demonstrable on examination.
• A confirmatory MRI must have either four lesions involving the
white matter or three lesions if one is periventricular in
location.
• Acceptable lesions must be >3 mm in diameter.
(b). Evoked response testing may be used to document a second
lesion not evident on clinical examination.
DIFFERENTIAL DIAGNOSIS
Disorders that Can Mimic MS
Migraine Headache
INTRO & TRIGGERS
• Migraine, the second most common cause of primary
headache,
• affects approximately 15% of women and 6% of men.
Symptom
1) Nausea
2) Vomiting
3) Diarrhea
4) Light headedness
5) Scalp tenderness
6) Visual disturbances
7) Photophobia
8) Photopsia
9) Vertigo
10) Seizure
11) Syncope
12) Alteration of consciousness
13) Confusional state
14) Paresthesias
MANAGEMENT-
• refer KDT
CLUSTER HEADACHE
Cluster Headache
1. Gender M>F
2. Pain
Toxic
headache
• Toxic headache Is usually caused by fever from acute bacterial illnesses
or from exposure to various chemicals including from fumes, pollution
and allergens.
• Causes
1) Nitrite.
2) carbon tetrachloride
3) organophosphate pesticides,
7) amphetamines
• Treatment
Caffeine can be used to alleviate a vascular headache by constricting
dilated arteries.
CT vs MRI
CT Scans
INDICATIONS
• If initial evaluations indicate a skull fracture or intracranial
bleeding, a CT (or CAT) scan is usually ordered.
• The CT scans can reveal
1) hematomas,
2) hemorrhages, and
3) skull fractures
•giving the neurologist exactly the information necessary for
deciding if emergency treatment is needed and precisely
where.
TECHNIQUE
• a way to obtain detailed X-ray pictures of cross-sections
through the body.
ADVANTAGE
• Testing is fast and results are quick; making it exceptionally
valuable when prompt diagnosis and treatment are critical.
• Unlike some other scanning methods, the CT scan can be
taken while the patient is hooked up to IV’s or other medical
equipment.
DRAAWBACKS
• Irradiation
MRI
INDICATIONS
• Magnetic Resonance Imaging (”MRI”) is not often used in
acute head injury cases.
• After the acute phase has passed, the doctor may want an
MRI to evaluate the location and extent of brain injury to
determine further treatment and rehabilitation options.
TECHNIQUE
• MRI uses powerful magnetic fields and the magnetic
reaction of the body’s cells to construct cross-sectional
images Similar to CT scans.
ADVANTAGE
1) Because it doesn’t use X-rays, it can be safer than CT if
multiple imaging sessions are expected.
2) Variations of MRI technology can also examine brain
functioning and identify injuries not visible in CT scans. But
even the detail available using MRI cannot detect mild
concussions.
3) It gives finer details than CT.
DRAWBACKS INCLUDE:
1) Longer to perform
2) Not as readily available as a CT scanner in most hospitals
3) Is not practical for patients hooked up to medical
equipment
4) Cannot be used if patient has metal embedded anywhere
in the body
5) Is not tolerated well by some patients because of the
confined space inside the MRI machine
6) Expensive
Alzheimer's
Disease
INTRO
• AD can occur in any decade of adulthood, but it is the most common
cause of dementia in the elderly.
Clinical Manifestations
• The cognitive changes with AD tend to follow a characteristic pattern,
beginning with memory impairment and spreading to language and
visuospatial deficits.
• In the early stages of the disease,
1) the memory loss may go unrecognized or be ascribed to
benign forgetfulness.
2) Once the memory loss begins to affect day-to-day activities the
disease is defined as MCI. Approximately 50% of MCI individuals
will progress to AD within 5 years.
3) Slowly the cognitive problems begin to interfere with daily
activities, such as keeping track of finances, following instructions
on the job, driving, shopping, and housekeeping.
• In the middle stages of AD,
1) the patient is unable to work, is easily lost and confused, and
requires daily supervision.
2) Social graces, routine behavior, and superficial conversation may
be surprisingly intact.
3) Language becomes impaired—first naming, then comprehension, and
finally fluency. In some patients, aphasia is an early and prominent
feature.
4) Apraxia emerges, and patients have trouble performing sequential
motor tasks.
5) Visuospatial deficits begin to interfere with dressing, eating,
solving simple puzzles, and copying geometric figures. Patients may
be unable to do simple calculations or tell time.
• In the late stages of the disease,
1) some persons remain ambulatory but wander aimlessly.
2) Loss of judgment, reason, and cognitive abilities is inevitable.
3) Delusions are common and usually simple in quality, such as
delusions of theft, infidelity, or misidentification.
4) Approximately 10% of AD patients develop Capgras' syndrome,
believing that a caregiver has been replaced by an impostor.
5) Some patients develop a shuffling gait with generalized muscle
rigidity associated with slowness and awkwardness of movement.
• In end-stage AD,
1) patients become rigid, mute, incontinent, and bedridden.
2) Help may be needed with the simplest tasks, such as eating,
dressing, and toilet function.
3) They may show hyperactive tendon reflexes.
4) Myoclonic jerks may occur spontaneously or in response to physical
or auditory stimulation.
5) Generalized seizures may also occur.
DIAGNOSIS
• Early in the disease course, other etiologies of dementia should be
excluded.
• Neuroimaging studies (CT and MRI) do not show a single specific pattern
with AD and may be normal early in the course of the disease.
• As AD progresses, diffuse cortical atrophy becomes apparent, and MRI
scans show atrophy of the hippocampus .
• Imaging helps to exclude other disorders, such as primary and secondary
neoplasms, multi infarct dementia, diffuse white matter disease, and
NPH;
• it also helps to distinguish AD from other degenerative disorders with
distinctive imaging patterns such as FTD or CJD.
• Functional imaging studies in AD reveal hypoperfusion or
hypometabolism in the posterior temporal-parietal cortex
• The EEG in AD is normal or shows nonspecific slowing.
• Routine spinal fluid examination is also normal.
Treatment
• The management of AD is challenging and gratifying,
• The primary focus is on long-term amelioration of associated behavioral
and neurologic problems.
• Building rapport with the patient, family members, and other caregivers
is essential to successful management.
• In the early stages of AD, memory aids such as notebooks and posted
daily reminders can be helpful.
EXTRA PYRAMIDAL
SYSTEM
INTRO
BASIC PARTS
o At the same time signals are being transmitted over the pyramidal
system to produce a specific movement, additional signals relative to the
movement are also relayed to the basal nuclei, red nucleus, and
brainstem reticular formation.
o The basal nuclei evaluate the command signal sent down the
pyramidal pathways and may contribute to the establishment of needed
background muscle tone for the movement. The nuclei are able to do
this in part by projecting to the red nuclei, which influence spinal cord
alpha and gamma motor neurons via rubrospinal tracts.
o Similar indirect routing to the spinal cord is achieved through
corticoreticulospinal and corticorubrospinal pathways .
o The function of these indirect pathways to the spinal cord motor
neurons may include more than providing background muscle tone for
movements directed by the motor cortex.
o Even so, because the red nucleus receives input from the basal and
cerebellar nuclei as well as direct input from the cerebral cortex, its
function may include modifying or "fine tuning" the motor neurons which
innervate the muscles involved in a given movement.
Feedback Loops
Mononeuropathy Multiplex
DEFINITION
• Mononeuropathy multiplex refers to the multifocal involvement of
individual peripheral nerves.
• Mononeuritis multiplex more often an inflammatory cause is
responsible, and in such cases the disorder is referred to as
mononeuritis multiplex.
CAUSES
• systemic (67%) and nonsystemic (33%) vasculitis & less commonly,
vasculitic neuropathy may present as mononeuritis multiplex;
Treatment
Therapy of the systemic vasculitis
• can stabilize and in some cases improve the neuropathy.
• Glucocorticoids [prednisone (1.5 mg/kg per day)] plus a cytotoxic agent
(usually oral cyclophosphamide at 2 mg/kg per day) is the treatment of
choice .
• Prednisone can be changed to an alternate-day regimen after 1 month to
minimize side effects.
• Once a clinical response is documented, prednisone may be tapered by
5 mg every 2–4 weeks.
• The cytotoxic agent is usually continued for 1 year.
Guillain-Barré Syndrome
DEFINITION
Required
1. Progressive weakness of 2 or more limbs due to
neuropathy
2. Areflexia
3. Disease course <4 weeks
1. Exclusion of other causes
• vasculitis (PAN,SLE, Churg-Strauss syndrome),
• toxins (organophosphates, lead),
• botulism,
• diphtheria,
• porphyria,
• localized spinal cord or cauda equina syndrome
Supportive
1. Relatively symmetric weakness
2. Mild sensory involvement
3. Facial nerve or other cranial nerve involvement
4. Absence of fever
5. Typical CSF profile (acellular, increase in protein level)
6. Electrophysiologic evidence of demyelination
Treatment
• In the vast majority of patients with GBS, treatment should be initiated
as soon after diagnosis as possible.
• ~2 weeks after the first motor symptoms, immunotherapy is no longer
effective.
• In patients who are treated early in the course of GBS and improve,
relapse may occur in the second or third week. Brief retreatment with
the original therapy is usually effective.
• Occasional patients with very mild forms of GBS, especially those who
appear to have already reached a plateau when initially seen, may be
managed conservatively without IVIg or PE.
8. chest physiotherapy.
• As noted, ~30% of patients with GBS require ventilatory assistance,
sometimes for prolonged periods of time (several weeks or longer).
• Frequent turning and assiduous skin care are important, as are daily
CLINICAL FEATURES
• MG is not rare, having a prevalence of 1–7 in 10,000.
• It affects individuals in all age groups, but peaks of incidence
occur in women in their twenties & thirties and in men in their
fifties & sixties. (20-30/50-60)
• Overall, women are affected more frequently than men, in a
ratio of ~3:2.
INVESTIGATIONS
2 Electrodiagnostic Testing
3 Anticholinesterase Test
4 Single-fiber electromyography:
TREATMENT
1. Anticholinesterase Medications
2. Thymectomy
3. Immunosuppression
Glucocorticoid Therapy
Mycophenolate mofetil
• A dose of 1–1.5 g bid is recommended.
• This drug has become the choice for long-term treatment
of myasthenic patients.
• Unfortunately, the cost of mycophenolate is still very high
AZATHIOPRENE
• An initial dose of 50 mg/d should be used to test for adverse
side effects.
• If this dose is tolerated, it is increased gradually until the white
blood count falls to ~3000–4000/uL.
• The typical dosage range is 2–3 mg/kg total body weight.
Cyclophosphamide
• a course of high-dose cyclophosphamide may induce long-
lasting (possibly permanent) benefit by "rebooting" the immune
system.
4. Plasmapheresis
• The indications for the use of IVIg are the same as those
for plasma exchange
• This treatment has the advantages of not requiring special
equipment or large-bore venous access.
• The usual dose is 2 g/kg, which is typically administered over 5
days (400 mg/kg per day).
Management of Myasthenic Crisis
• Myasthenic crisis is defined as an exacerbation of weakness
sufficient to endanger life; it usually consists of respiratory
failure caused by diaphragmatic and intercostal muscle weakness.
Antibiotics
• Aminoglycosides: e.g., streptomycin, tobramycin, kanamycin
• Quinolones: e.g., ciprofloxacin, levofloxacin, ofloxacin, gatifloxacin
• Macrolides: e.g., erythromycin, azithromycin,
Beta-blocking agents
• Propranalol, atenolol, metoprolol
Botulinum toxin
• Botox exacerbates weakness
Magnesium
Penicillamine
Quinine derivatives
• Quinine, quinidine, chloroquine, mefloquine
• Cyclosporine
• Azathioprine Avoid allopurinol—combination may
result in myelosuppression.
CLINICAL FEATURE
• The seizure usually begins abruptly without warning, although some
patients describe vague premonitory symptoms in the hours leading up
to the seizure.
INVESTIGATIONS
• Laboratory Studies
1. Routine blood studies are indicated to identify the more common
metabolic causes of seizures, such as abnormalities in electrolytes,
glucose, calcium, or magnesium, and hepatic or renal disease.
2. A screen for toxins in blood and urine should also be obtained from all
patients in appropriate risk groups, especially when no clear
precipitating factor has been identified.
3. A lumbar puncture is indicated if there is any suspicion of meningitis or
encephalitis, and it is mandatory in all patients infected with HIV, even in
the absence of symptoms or signs suggesting infection.
• Electrophysiologic Studies
1. All patients who have a possible seizure disorder should be evaluated
with an EEG as soon as possible.
2. The EEG during the tonic phase of the seizure shows a progressive
increase in generalized low-voltage fast activity, followed by generalized
high-amplitude, polyspike discharges.
3. In the clonic phase, the high-amplitude activity is typically interrupted by
slow waves to create a spike-and-wave pattern.
4. The postictal EEG shows diffuse slowing that gradually recovers as the
patient awakens.
• Brain Imaging
1. Almost all patients with new-onset seizures should have a brain
imaging study to determine whether there is an underlying structural
abnormality that is responsible.
2. MRI has been shown to be superior to CT for the detection of cerebral
lesions associated with epilepsy.
3. Functional imaging procedures such as positron emission tomography
(PET) and single photon emission computed tomography (SPECT) are
also used to evaluate certain patients with medically refractory seizures
MANAGEMENT
STATUS
EPILEPTICUS
DEFINITION
• Status epilepticus refers to continuous seizures or
repetitive, discrete seizures with impaired
consciousness in the interictal period.
• The duration of seizure activity sufficient to meet the
definition of status epilepticus has traditionally been
specified as 15–30 min.
• However, a more practical definition is to consider
status epilepticus as a situation in which the duration of
seizures prompts the acute use of anticonvulsant
therapy. For GCSE, this is typically when seizures last
beyond 5 min.
SUB-TYPES
• Status epilepticus has numerous subtypes, including
• generalized convulsive status epilepticus (GCSE)
1. persistent generalized electrographic seizures,
2. persistent coma,
GCSE
CLINICAL
• GCSE is obvious when the patient is having overt
convulsions.
• However, after 30–45 min of uninterrupted seizures, the
signs may become increasingly subtle. Patients may
have mild clonic movements of only the fingers or fine,
rapid movements of the eyes.
• There may be paroxysmal episodes of tachycardia,
hypertension, and pupillary dilation. In such cases, the
EEG may be the only method of establishing the
diagnosis.
• Thus, if the patient stops having overt seizures, yet
remains comatose, an EEG should be performed to rule
out ongoing status epilepticus.
MANAGEMENT
• GCSE is an emergency and must be treated
immediately
• The first step in the management of a patient in GCSE is
1. to attend to any acute cardiorespiratory problems
or hyperthermia,
2. perform a brief medical and neurologic
examination,
3. establish venous access,
4. send samples for laboratory studies to identify
metabolic abnormalities.
• Anticonvulsant therapy should then begin without
delay; a treatment approach is shown in harrison fig
363-3.
Brown-Séquard syndrome
INTRO
Subacute Sclerosing
Panencephalitis (SSPE)
DEFINITION
• SSPE is a rare chronic, progressive demyelinating disease of the CNS
associated with a chronic nonpermissive infection of brain tissue with
measles virus.
INCIDENCE
• The incidence has declined dramatically since the introduction of a
measles vaccine.
CLINICAL FEATURES
• Most patients give a history of primary measles infection at an early age
(2 years), which is followed after a latent interval of 6–8 years by the
development of progressive neurologic disorder.
• patients are between 5 and 15 years old at diagnosis.
• Initial manifestations include
1) poor school performance
2) mood and personality changes.
• Typical signs of a CNS viral infection, including fever and headache, do
not occur.
• As the disease progresses, patients develop
1) progressive intellectual deterioration,
2) focal and/or generalized seizures,
3) myoclonus,
4) ataxia,
5) visual disturbances.
• In the late stage of the illness, patients are
1) unresponsive,
2) spastic quadriparetic,
3) hyperactive tendon reflexes
4) extensor plantar responses.
Diagnostic Studies
• MRI is often normal early, although areas of increased T2 signal
develop in the white matter of the brain and brainstem as
disease progresses.
• The EEG may initially show only nonspecific slowing, but with disease
progression, patients develop a characteristic periodic pattern with
bursts of high-voltage, sharp, slow waves every 3–8 s, followed
by periods of attenuated ("flat") background.
• The CSF is
1) acellular
2) normal or mildly elevated protein concentration
3) a markedly elevated gamma globulin level (>20% of total CSF
protein).
4)CSF anti-measles antibody levels are invariably elevated,
5)oligoclonal anti-measles antibodies are often present.
• Measles virus can be cultured from brain tissue using special
cocultivation techniques.
• Viral antigen can be identified immunocytochemically,
• viral genome can be detected by in situ hybridization or PCR
amplification.
Treatment
• No definitive therapy for SSPE is available.
• Treatment with isoprinosine (100 mg/kg per day), alone or in
combination with intrathecal or intraventricular alpha interferon, has
been reported to prolong survival and produce clinical improvement in
some patients
Wernicke encephalopathy
INTRO
• Wernicke encephalopathy is a syndrome characterised by
1) ophthalmoplegia,
2) ataxia,
3) confusion,
4) impairment of short-term memory
•
Cause
1. thiamine (vitamin B1) deficiency
2. prolonged alcohol, amphetamine consumption resulting in thiamine
deficiency.
3. gastric disorders as carcinoma, chronic gastritis,
4. Crohn's disease,
5. repetitive vomiting, particularly after bariatric surgery.
Presentation
• Wernicke's encephalopathy begins abruptly, usually with
1) eye movement disorders (nystagmus, gaze palsies, and
ophthalmoplegia, especially of the lateral rectus muscles),
2) gait ataxia,
3) confusion,
4) confabulation,
5) short-term memory loss.
• The classic triad of the syndrome is
1) encephalopathy (brain damage),
2) ophthalmoplegia (eye paralysis),
3) ataxia (loss of coordination).
• Untreated, it may progress to Korsakoff's psychosis, coma and death.
Treatment
• Treatment begins with intravenous or intramuscular injection of
thiamine, followed by assessment of central nervous system and
metabolic conditions.
• In the presence of sub-clinical thiamine deficiency, a large dose of sugar
(especially glucose) can precipitate the onset of overt encephalopathy;
therefore, correcting hypoglycemia should not be attempted before
thiamine replenishment.
• Rehydration to restore blood volume should follow, as needed.
• When treated early, recovery may be rapid and complete; though there
are almost always some minor neurological signs that persist
CLINICAL FEATURES
• Because alcohol has a short half-life, these withdrawal symptoms
generally begin within 5–10 h of decreasing ethanol intake, peak in
intensity on day 2 or 3, and improve by day 4 or 5.
• Features include
1) tremor of the hands (shakes or jitters);
2) agitation and anxiety;
3) autonomic nervous system overactivity including an increase in
pulse, respiratory rate, and body temperature;
4) insomnia, sometimes accompanied by frightening dreams.
5) 2 TO 5% of alcoholics experience withdrawal seizures, often within
48 h of stopping drinking
• Anxiety, insomnia, and mild levels of autonomic dysfunction may
persist to some degree for 4–6 months as a protracted abstinence
syndrome, which may contribute to the tendency to return to drinking.
TREATMENT
• The first step is to perform a thorough physical examination in all
alcoholics who are considering stopping drinking, including a search for
1. evidence of liver failure,
2. gastrointestinal bleeding,
3. cardiac arrhythmia,
4. infection,
5. glucose or electrolyte imbalance.
• The second step is to offer reassurance that the acute withdrawal is
short lived and to offer adequate nutrition and rest.
1. All patients should be given oral multiple B vitamins, including
50–100 mg of thiamine daily for a week or more.
2. Because most alcoholics who enter withdrawal are either
normally hydrated or mildly overhydrated, IV fluids should be
avoided unless there is evidence of significant recent bleeding,
vomiting, or diarrhea.
3. Medications can usually be administered orally.
• The third step in treatment is to recognize that most withdrawal
symptoms are caused by the rapid removal of a CNS depressant, in this
case, alcohol.
1. While most CNS depressants are effective, benzodiazepines have
the highest margin of safety and lowest cost and are, therefore, the
preferred class of drugs.
2. Benzodiazepines with short half-lives are especially useful for
patients with serious liver impairment or evidence of preexisting
encephalopathy or brain damage.
• Treatment of the patient with DTs can be challenging, and the
condition is likely to run a course of 3–5 days regardless of the therapy
employed.
1. The focus of care is to identify and correct medical problems and
to control behavior and prevent injuries.
2. Many clinicians recommend the use of high doses of a
benzodiazepine (as much as 800 mg/d of chlordiazepoxide),
3. Other clinicians recommend the use of antipsychotic medications,
such as haloperidol, Or olanzapine
• Generalized withdrawal seizures rarely require aggressive
pharmacologic intervention beyond that given to the usual patient
undergoing withdrawal, i.e., adequate doses of benzodiazepines.
• The rare patient with status epilepticus must be treated
aggressively .
HAZARD OF ALCHOHOL
(ALCHOHOLISM)
INTRO
Alcohol dependence is defined as repeated alcohol-related difficulties in
at least three of seven areas of functioning that cluster together over a
12-month period.
Alcohol abuse is defined as repetitive problems with alcohol in any one
of four life areas—social, interpersonal, legal, and occupational
Not everyone develops each of the problems described below.
NERVOUS SYSTEM
CNS & PNS
1. a blackout, an episode of temporary anterograde amnesia, in which the
person forgets all or part of what occurred during a drinking evening.
2. disturbed sleep. sometimes disturbing dreams.
3. snoring and exacerbate sleep apnea
4. impaired judgment and coordination, increasing the risk of accidents and
injury
5. Heavy drinking can also be associated with headache, thirst, nausea,
vomiting, and fatigue the following day, a hangover syndrome that is
responsible for significant financial losses in most work environments.
6. peripheral neuropathy
7. cerebellar degeneration or atrophy.
8. Wernicke's (ophthalmoparesis, ataxia, and encephalopathy)
9. Korsakoff's (retrograde and anterograde amnesia) syndromes.
PSYCHIATRY
1. alcohol and/or drug dependence.
2. schizophrenia
3. manic depressive disease
TEMPORARY PSCHIATRIC
1. anxiety disorders such as panic disorder.
2. intense sadness lasting for days to weeks
3. temporary severe anxiety
4. auditory hallucinations
Cancer
1. breast cancer
2. oral and esophageal cancers
3. rectal cancers
Hematopoietic System
1. If heavy drinking is accompanied by folic acid deficiency, there can
also be hypersegmented neutrophils, reticulocytopenia, and a
hyperplastic bone marrow;
2. if malnutrition is present, sideroblastic changes can be observed.
3. a possible false-negative tuberculin skin test
4. mild thrombocytopenia
Cardiovascular System
1. a dose-dependent increase in blood pressure
2. increased risk for coronary artery disease
3. an increased risk for cardiomyopathy.
4. Mural thrombi can form in the left atrium or ventricle
5. mitral regurgitation.
6. Atrial or ventricular arrhythmias, especially paroxysmal tachycardia,
can also occur after a drinking binge in individuals showing no other
evidence of heart disease—a syndrome known as the "holiday heart."
This condition is observed transiently in the majority of alcoholics
entering treatment.
MALE
1. decrease erectile capacity in men.
2. irreversible testicular atrophy with shrinkage of the seminiferous tubules,
3. decreases in ejaculate volume,
4. a lower sperm count .
FEMALE
1. amenorrhea,
2. infertility,
3. an increased risk of spontaneous abortion.
PREGNANCY
1. serious consequences for fetal development.
2. The fetal alcohol syndrome can include any of the following:
Musculoskeletal
1.skeletal muscle weakness caused by acute alcoholic myopathy
2. increased risk for fractures and osteonecrosis of the femoral head.
VERTIGO
DEFINITION
• an illusory or hallucinatory sense of movement of the body or
environment, most often a feeling of spinning
PHYSIOLOGY
• Three sensory systems subserving spatial orientation and posture;
1. The vestibular system is
2. the visual system (retina to occipital cortex)
3. the somatosensory system that conveys peripheral information
from skin, joint, and muscle receptors.
Physiologic Vertigo
• This occurs in normal individuals when
(1) the brain is confronted with an intersensory mismatch among the
three stabilizing sensory systems;
(2) the vestibular system is subjected to unfamiliar head movements to
which it is unadapted, such as in seasickness;
(3) unusual head/neck positions, such as the extreme extension when
painting a ceiling; or following a spin.
Pathologic Vertigo
• This results from lesions of the visual, somatosensory, or vestibular
systems.
• Visual vertigo
1. caused by new or incorrect eyeglasses or by the sudden onset of an
extraocular muscle paresis with diplopia;
• Somatosensory vertigo,
1. rare in isolation,
2. usually due to a peripheral neuropathy or myelopathy
• vestibular vertigo
1. The most common cause of pathologic vertigo
2. involving either its end organ (labyrinth), nerve, or central
connections.
3. The vertigo is associated with jerk nystagmus and is frequently
accompanied by nausea, postural unsteadiness, and gait ataxia.
4. Since vertigo increases with rapid head movements, patients
tend to hold their heads still.
Labyrinthine Dysfunction
• This causes severe rotational or linear vertigo.
• The fast phases of nystagmus beat away from the lesion side,
• the tendency to fall is toward the side of the lesion, particularly in
darkness or with the eyes closed.
3. ischemia.
o presumably due to occlusion of the labyrinthine branch of the
internal auditory artery, may be the sole manifestation of
vertebrobasilar insufficiency ;
• Acute bilateral labyrinthine dysfunction
o usually the result of toxins such as drugs or alcohol.
o The most common offending drugs are the aminoglycoside
antibiotics
• Recurrent unilateral labyrinthine dysfunction,
o in association with signs and symptoms of cochlear disease
(progressive hearing loss and tinnitus), is usually due to Ménière's
disease
• Positional vertigo
o precipitated by a recumbent head position, either to the right or to
the left.
o Benign paroxysmal positional (or positioning) vertigo (BPPV) of the
posterior semicircular canal is particularly common.
o Although the condition may be due to head trauma, usually no
precipitating factors are identified.
Benign Paroxysmal Positional Vertigo and Central Positional Vertigo
3. Habituation Yes No
• Psychogenic Vertigo
o It should be suspected in patients so "incapacitated" by their symptoms
that they adopt a prolonged housebound status.
o a psychogenic etiology is almost certain when nystagmus is absent
during a vertiginous episode.
DIAGNOSTIC EVALUATION
• The simplest provocative test for vestibular dysfunction is rapid rotation
and abrupt cessation of movement in a swivel chair.
• Patients with symptoms of positional vertigo should be appropriately
tested .
• A final provocative and diagnostic vestibular test, requiring the use of
Frenzel eyeglasses, is vigorous head shaking in the horizontal plane for
about 10 s. If nystagmus develops after the shaking stops, even in the
absence of vertigo, vestibular dysfunction is demonstrated. The
maneuver can then be repeated in the vertical plane.
• If the provocative tests establish the dizziness as a vestibular symptom,
an evaluation of vestibular vertigo is undertaken
MANAGEMENT
Treatment of acute vertigo consists of bed rest (1–2 days maximum) and
vestibular suppressant drugs
Treatment of Vertigo
Agenta
1. Antihistamines
Meclizine
Promethazinec For acute vertigo only
c
2. Benzodiazepines
Diazepam
Clonazepam
3. Phenothiazines
Prochlorperazinec For acute vertigo only
c
Agenta
4. Anticholinergicd d
For motion sickness only.
Scopolamine transdermal
5. Sympathomimeticsd d
For motion sickness only.
Ephedrine
6. Combination d
For motion sickness only.
preparationsd
Ephedrine and
promethazine
7. Exercise therapy
Repositioning For benign paroxysmal positional vertigo.
maneuverse
Vestibular rehabilitationf
8. Other
Diuretics or low-salt (1 g/d) For Ménière's disease.
dietg
Antimigrainous drugsh h
For migraine-associated vertigo
Ménière's disease.
SYNCOPE
DEFINITION & INTRO
• Syncope, a transient loss of consciousness and postural tone due
to reduced cerebral blood flow, is associated with spontaneous
recovery.
CAUSES
DIFFERENTIAL DIAGNOSIS
1 Anxiety Attacks and Hyperventilation Syndrome
• the symptoms are not accompanied by facial pallor and are not
relieved by recumbency.
2 Seizures
Features that Distinguish Generalized Tonic-Clonic Seizure from Syncope
3 Hypoglycemia
4 Hysterical Fainting
TREATMENT
SITE OF CARE
• Patients with syncope should be hospitalized when there is a
possibility that the episode may have resulted from a life-threatening
abnormality or if recurrence with significant injury seems likely.
• These individuals should be admitted to a bed with continuous
electrocardiographic monitoring.
• Patients who are known to have a normal heart and for whom
the history strongly suggests vasovagal or situational syncope
may be treated as outpatients if the episodes are neither frequent nor
severe.
GENERAL
SPECIFIC
• The treatment of syncope is directed at the underlying cause.
Glossopharyngeal neuralgia
Noncompressive
Myelopathies
CAUSES
The most frequent causes of noncompressive acute transverse
myelopathy (ATM) are
1. spinal cord infarction;
2. systemic inflammatory disorders, including SLE and
sarcoidosis;
3. demyelinating diseases, including multiple sclerosis (MS);
4. postinfectious or idiopathic transverse myelitis,
5. infectious (primarily viral) .
INVESTIGATIONS
After spinal cord compression is excluded, the evaluation
generally requires a lumbar puncture and a search for underlying
systemic disease
Evaluation
8) Lyme disease
9) Syphilis
10) Schistosomiasis
11) Toxoplasmosis
o Herpes zoster, HSV, and EBV myelitis are treated with
intravenous acyclovir (10 mg/kg q8h) or oral valacyclovir (2
gm tid) for 10–14 days;
o CMV with ganciclovir (5 mg/kg IV bid) plus foscarnet (60
mg/kg IV tid), or cidofovir (5 mg/kg per week for 2 weeks).