Dr. Rami Abo Ali

1. NEUROLOGY
Dr. Rami Abo Ali
Neurology
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Dr.
Rami
Abo
Ali
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2. VASCULAR DISEASES OF THE
NERVOUS SYSTEM
Neurology
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Dr.
Rami
Abo
Ali
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3. CEREBROVASCULAR DISEASE
 Cerebrovascular disease is a significant cause of
mortality and morbidity in the developed world.
 Strokes of all types rank third as a cause of death
 Stroke is a syndrome of clinical features, but an
accurate diagnosis requires the localization of the
anatomical region involved, the underlying
pathology (infarction or haemorrhage), the
mechanism (e.g. embolism), the underlying
etiology (e.g. atherosclerosis) and contributing
risk factors (e.g. smoking)
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4. DEFINITIONS
 Stroke
 Stroke is a focal, neurological deficit caused by a
compromise of the cerebral circulation.
 The onset is sudden and the symptoms last longer
than 24 hours, if the patient survives.
 Transient ischaemic attack
 A transient ischaemic attack (TIA) is a focal, sudden
onset, neurological deficit lasting less than 24 hours,
with complete clinical recovery, caused by focal hypo
perfusion within the brain.
 The distinction of a TIA from a stroke is largely
arbitrary, as the mechanisms underlying both may be
identical, and the main difference is that of duration.
 Up to 15% of patients with TIA may suffer a
stroke within the first 2 weeks. 4
Neurology
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Dr.
Rami
Abo
Ali

5. TYPES OF STROKE
 The main subdivisions of stroke are :
 cerebral infarction (ischaemic stroke)
 intracranial haemorrhage (haemorrhagic stroke)
 About 80% of strokes are caused by infarction.
 In 12% of cases stroke is caused by primary hemorrhage
(intracerebral hemorrhage or ICH) within the brain
which may affect deep structures or more superficial
lobes of the brain.
 In 8% of stroke cases, bleeding occurs primarily within
the subarachnoid space (subarachnoid haemorrhage or
SAH).
 Sometimes a SAH can be complicated by cerebral
infarction due to vasospasm.
 Cerebral venous thrombosis is a rare cause of stroke but
can present with either cerebral infarction or
hemorrhage or both in venous region of the brain
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7. INCIDENCE OF STROKE
 The incidence of stroke is approximately 150–200
cases per 100 000 persons per annum in the UK,
and approximately 20% of patients will die
within 30 days.
 The incidence of TIA is 30 cases per 100 000
persons per annum, although many probably go
unreported.
 The rates increase markedly with advancing age
and 20–25% of individuals over the age of 45
years will have a stroke
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Dr.
Rami
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Ali

8. ETIOLOGY OF STROKE
 Atherosclerosis:
 This causes thrombotic stroke in large extracranial
arteries, most commonly the bifurcation of the carotid
arteries or intracranial arteries arising from the circle
of Willis, especially the origin of the middle cerebral
artery.
 Cardiac or carotid embolism:
 Embolic stroke usually arises from pieces of ruptured
atherosclerotic plaques or cardiac thrombus.
 The bifurcation of the common carotid and the
akinetic segments of myocardium, e.g. after a heart
attack or in atrial fibrillation, are the most common
sources of emboli.
 Valvular heart disease is another important cause. 8
Neurology
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Dr.
Rami
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9. ETIOLOGY OF STROKE
 Intracerebral haemorrhage :
 This is most often secondary to chronic untreated
hypertension, but can be caused by other factors, e.g.
trauma, anticoagulant therapy, neoplasia, and
coagulation disorders, such as hemophilia or
abnormalities of platelet number or function.
 Lipohyalinosis of small arteries:
 This degenerative process especially affects small
perforating arteries that supply structures deep to the
cortex, e.g. basal ganglia, internal capsule and pons.
 It usually occurs in patients with chronic untreated
hypertension.
 Occlusion of these penetrating arteries causes
subcortical infarcts, less than 1.5 cm in diameter,
which are called ‘lacunes’.
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Neurology
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Dr.
Rami
Abo
Ali

10. ETIOLOGY OF STROKE
 Arterial dissection :
 in the younger population, dissection of either the
carotid or vertebral arteries is a relatively common
cause of stroke.
 This may occur spontaneously or there may be a history
of injury to the neck such as sudden twisting movements
or flexion–extension injuries such as ‘whiplash’.
 Non-atherosclerotic diseases of the vessel wall and
hematological conditions :
 these are rarer than the above causes but should always
be considered, especially in young patients who present
with stroke.
 Causes include rheumatoid vasculitis, systemic lupus
erythematosus, polyarteritis nodosa and temporal
arteritis (in the elderly).
 Infections involving the base of the brain, such as TB
meningitis, can occlude large blood vessels.
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Dr.
Rami
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Ali

11. RISK FACTORS
 Non modifiable
 Age ( more than 60)
 Gender (male > female, except in the very young and very old)
 Race (Afro-Caribbean > Asian > European)
 Heredity
 Previous vascular event, e.g. myocardial infarction, stroke or
peripheral embolism
 Modifiable
 High blood pressure
 Heart disease (atrial fibrillation, heart failure, endocarditis)
 Diabetes mellitus
 Hyperlipidemia
 Smoking
 Excess alcohol consumption
 Polycythemia
 Oral contraceptives
 Social deprivation
 History of TIA or stroke
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Dr.
Rami
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12. VASCULAR ANATOMY
 A knowledge of the arterial blood supply to the brain and of
the common sites for atheromatous plaque formation is
important for an appreciation of the various presentations
and significance of cerebrovascular disease.
 The circle of Willis is supplied anteriorly by the two carotid
arteries and posteriorly by the basilar artery, which is
formed by the union of the two vertebral arteries.
 It is therefore common to classify strokes into those affecting
the anterior (carotid) and posterior (vertebrobasilar)
circulations.
 The most common sites for atheromatous plaques are:
 the origin of the internal carotid arteries
 within the carotid syphon
 the origin of the vertebral arteries.
 The anterior, middle and posterior cerebral arteries arise
from the circle of Willis.
 These supply specific portions of the cerebral hemispheres;
thus, reduction in perfusion in each territory will cause
different and specific deficits
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15. CLINICAL SYNDROMES
TRANSIENT ISCHAEMIC ATTACKS
 The symptoms typically represent loss of function
(negative symptoms), are maximal at onset and last 5
to 30 minutes.
 Any cause of an ischemic stroke can cause a TIA
 The most common cause is embolic
 Clinical features :
 Amaurosis fugax: is a sudden transient loss of vision in one
eye for more than a few seconds. It usually occurs from an
embolus that becomes stuck within a retinal arteriole .
Then the embolus breaks up or passes, flow is restored and
vision returns quickly to normal.
 hemiparesis,, aphasia, dysarthria/dysphagia
 vertigo, diplopia.
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Dr.
Rami
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Ali

16. CLINICAL SYNDROMES
MIDDLE CEREBRAL ARTERY OCCLUSION
 The middle cerebral artery is the largest branch of the
internal carotid artery and supplies the largest area of
the cerebral cortex.
 It is the most commonly involved artery in stroke.
 As well as supplying the motor and sensory cortices, the
middle cerebral artery supplies the areas of the cortex
pertaining to the comprehension (Wernicke’s area) and
expression (Broca’s area) of speech
 These areas are found in the dominant hemisphere only,
and thus, in the majority of right-handed individuals,
speech production will be affected only when there is
occlusion of the left middle cerebral artery.
 Nondominant lesions often cause visuospatial problems,
e.g. inattention.
 Lesions of either side can be associated with a
hemianopia (loss of vision in half of the visual field) .
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Dr.
Rami
Abo
Ali

17. CLINICAL SYNDROMES
MIDDLE CEREBRAL ARTERY OCCLUSION
 Signs of middle cerebral artery occlusion
 Contralateral hemiplegia (including the lower
part of the face and relative sparing of the leg)
 Contralateral cortical hemisensory loss
 Dominant hemisphere (usually left): aphasia
 Non-dominant hemisphere: neglect of
contralateral limb and dressing apraxia
 Contralateral homonymous hemianopia
 Conjugate eye deviation (towards the side of the
lesion)
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20. CLINICAL SYNDROMES
ANTERIOR CEREBRAL ARTERY OCCLUSION
 The anterior cerebral artery is a branch of the internal
carotid artery and runs above the optic nerve to follow
the curve of the corpus callosum.
 The two arteries are linked by the anterior
communicating artery and thus the effect of occlusion
depends on the relation with respect to the anterior
communicating artery
 Occlusion proximal to the anterior communicating
artery is normally well tolerated because of adequate
cross-flow and thus few symptoms result.
 Occlusion distal to the anterior communicating artery
causes contralateral weakness and cortical sensory loss
in the leg .
 Incontinence is often present, and occasionally a
contralateral grasp and other primitive reflexes (
glabellar reflex).
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Rami
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Ali

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(glabellar reflex).

22. CLINICAL SYNDROMES
POSTERIOR CEREBRAL ARTERY OCCLUSION
 The posterior cerebral arteries are the terminal branches
of the basilar artery.
 In addition to cortical branches to the medial inferior
temporal lobes and occipital and visual cortices, there are
perforating branches that supply the midbrain and
thalamus.
 Occlusion is typically embolic and most patients are in
atrial fibrillation.
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Dr.
Rami
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Ali

23.  The effect of occlusion depends on the site:
 Proximal occlusion: which includes midbrain syndrome
(Weber’s syndrome : ipsilateral oculomotor 3rd nerve palsy
and contralateral hemiplegia ).
 Thalamic or temporal lobe involvement may cause confusion,
memory impairment and hemisensory disturbance.
 Cortical vessel occlusion: homonymous hemianopia with
macular sparing (the macular area is additionally supplied
by the middle cerebral artery).
 Bilateral occlusion: Anton’s syndrome (cortical blindness) is
rare. The patient is blind but lacks insight into the degree of
visual loss and often denies it.
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Dr.
Rami
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CLINICAL SYNDROMES
POSTERIOR CEREBRAL ARTERY OCCLUSION

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25. CLINICAL SYNDROMES
CAROTID ARTERY OCCLUSION
 Often an internal carotid artery occlusion does
not present as a stroke due to the presence of a
collateral blood supply from the circle of Willis.
 A stroke will only occur if the collateral supply is
inadequate or thrombosis spreads or embolizes to
involve the middle cerebral artery or its
branches.
 Thus, clinically, carotid artery occlusion may
present similarly to a middle cerebral artery
stroke
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Dr.
Rami
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Ali

26. CLINICAL SYNDROMES
LACUNAR STROKE
 Lacunar infarction is caused by occlusion of small
penetrating vessels to the subcortical deep white
matter, internal capsule, basal ganglia or pons.
 Although these vessels supply a very small area, a
number of extremely important structures pass
through this space.
 A very small lesion can cause a marked neurological
deficit.
 Lacunar infarcts are most commonly caused by
lipohyalinosis and microatheroma affecting the small
perforating vessels, as opposed to embolic disease.
 Most patients have hypertension, diabetes or
hypercholesterolemia. 26
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Rami
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27.  Clinically, patients present with unilateral weakness or sensory loss
affecting at least two of the face, arm or leg.
 Other symptoms :
 Pure motor stroke – affects two limbs
 Pure sensory stroke
 Sensory-motor stroke
 No higher cerebral dysfunction (e.g. confusion, dysphasia, neglect, apraxia)
and no cognitive difficulties or hemianopia.
 A CT brain may not detect lacunar infarcts, and MRI is more sensitive.
 Multiple lacunar infarcts in multiple domains can cause vascular
dementia
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Dr.
Rami
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CLINICAL SYNDROMES
LACUNAR STROKE

28.  The most common signs and symptoms of a stroke are a
sudden onset of facial drooping, extremity weakness,
speech difficulty, and visual loss.
 If you recognize a stroke, you need to BE FAST:
 Balance issues
 Eye problems (loss of vision)
 Facial dropping
 Arm or leg weakness
 Speech difficulties
 Time (sudden onset)
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Rami
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Ali

29. INVESTIGATION OF STROKE
AND TRANSIENT ISCHAEMIC ATTACK
 The following routine investigations should be performed:
 CBC
 Renal function and electrolytes
 Clotting screen: all patients with hemorrhagic stroke and those
on anticoagulants
 Erythrocyte sedimentation rate (ESR); C-reactive protein
(CRP): inflammatory disease
 Thyroid function tests: all patients with atrial fibrillation
 Blood sugar: hypoglycemia and diabetes mellitus
 Fasting lipids
 Blood culture: if endocarditis or a superadded infection is
suspected
 Autoantibodies and coagulation studies in young patients:
connective tissue or vasculitic disease or prothrombotic disorder
 Electrocardiography (ECG): arrhythmia, myocardial
ischaemia/infarction and left ventricular hypertrophy
secondary to hypertension
 Chest X-ray: neoplasia and enlarged heart.
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Dr.
Rami
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30. SPECIAL INVESTIGATIONS
IMAGING
 All patients should have a computed tomography (CT)
or a magnetic resonance imaging (MRI) of the brain.
 CT is more commonly available acutely and can
differentiate between an ischaemic and a haemorrhagic
stroke.
 It can also reveal stroke mimics such as subdural
haematomas or tumours.
 CT may appear normal, depending on the time from
onset of the stroke to imaging and the size and severity
of the infarct.
 Only 75% of infarcts are ever visible on CT.
 CT is a critical tool in determining a patient’s
suitability for thrombolysis.
 .
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31.  MRI should be considered if the clinical signs
localize to the posterior fossa (i.e. brainstem and
cerebellum) because these regions are poorly
visualized by CT due to artifacts caused by the
surrounding bone.
 MRI should also be considered in patients who may
have had a small stroke, which may not be visible
on CT, or where the diagnosis is uncertain.
 Vascular reconstructive imaging using CT
angiography (CTA) and MR angiography (MRA) is
helpful in visualizing the intra- and extracranial
carotids and the posterior circulation to look for
atheromatous disease, dissections and aneurysms
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33. SPECIAL INVESTIGATIONS
CAROTID DOPPLER
 The carotid Doppler is an extremely effective,
noninvasive means of demonstrating internal
carotid artery stenosis when carotid
thromboembolism is suspected.
 A carotid endarterectomy is considered if there is
greater than 50–70% stenosis in the vessel, and a
history of a non-disabling ischaemic stroke or TIA
within the last 6 months.
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34. SPECIAL INVESTIGATIONS
CEREBRAL ANGIOGRAPHY
 The advent of carotid Doppler and MRA has meant
that conventional cerebral angiography is used
infrequently in stroke patients, primarily to locate
intracerebral aneurysms, and for the diagnosis of
cerebral vasculitides, which are both still poorly
detected with MRA.
 In patients with a recent completed stroke,
angiography should not be considered until 1–2
weeks have elapsed
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35. SPECIAL INVESTIGATIONS
ECHOCARDIOGRAPHY AND HOLTER MONITORING
 Echocardiography is useful in patients with
suspected cardiogenic embolism and may define
wall-motion abnormalities or the presence of
atrial or ventricular thrombus.
 Holter monitoring or more prolonged monitoring
using a REVEAL device may confirm paroxysmal
atrial fibrillation in patients with suspected
cardiogenic embolic stroke, but normal ECG.
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Rami
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36. MANAGEMENT OF STROKE
 The aim of management:
 minimizing the volume of brain that is irreversibly
damaged (saving penumbra)
 preventing complications
 reducing the patient's disability and handicap
through rehabilitation
 reducing the risk of recurrent episodes
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37. ACUTE STROKE MANAGEMENT
 • non-specific
 ABC: maintain adequate airway to prevent aspiration, O2
saturation should be ≥ 95%, IV fluid for adequate
hydration (isotonic saline or glucose saline).
 Nutrition: Consider nutritional supplements; start feeding
via a nasogastric tube in persistent dysphagia.
 Blood pressure: Unless there is heart failure or renal
failure, evidence of hypertensive encephalopathy or aortic
dissection, do not lower the blood pressure in the first
week since it will often return towards the patient's
normal level within the first few days.
 Blood glucose: Hyperglycemia (≥200mg/dl) may increase
infarct volume, therefore use insulin but monitor closely to
avoid hypoglycemia.
 Temperature : fever may increase infarct volume, so treat
any cause and give antipyretics early
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38. ACUTE STROKE MANAGEMENT
 • Specific treatment
 Thrombolysis treatment :Intravenous thrombolysis with
recombinant tissue plasminogen activator (rt-PA) –
alteplase increases the risk of haemorrhagic transformation
of the cerebral infarct with potentially fatal results.
However, if given within 3-4.5 hours of symptom onset to
highly selected patients, may improve overall outcome
 After an acute persistent stroke, aspirin 300mg started
within 48 hours of onset improves long-term outcome. . For
people who have a contraindication or intolerance to both
clopidogrel and aspirin, dipyridamole alone is recommended
as a treatment option.
 Heparin increases in the risk of both intracranial and
extracranial hemorrhage and does not result in better long-
term outcomes . Therefore it should not be used in the
routine management of acute stroke.
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39. PROGNOSIS
 The risk of recurrence after stroke is 5–15% in
the first year, and by 5 years 30% have had a
recurrence.
 For this reason a key component of the
management of patients who have had strokes or
TIAs is the management of modifiable risk
factors, and secondary prevention with
antiplatelet drugs, anticoagulants and carotid
endarterectomy where appropriate.
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40. INTRACRANIAL HAEMORRHAGE
 Intracranial hemorrhage can be subdivided by
site:
 Primary intracerebral hemorrhage
 Subarachnoid hemorrhage
 Subdural and extradural hemorrhage
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41. SUBARACHNOID HAEMORRHAGE
 Subarachnoid haemorrhage is caused by spontaneous (rather
than traumatic) arterial bleeding into the subarachnoid space.
 The incidence of subarachnoid haemorrhage is 10–15 cases
per 100 000 persons per year and the average age of onset is
about 50 years
 Causes
 Intracranial aneurysms: 85%
 Non-aneurysmal perimesencephalic haemorrhage
(haemorrhage into basal cisterns): 10%
 Arteriovenous malformation: 5%.
 Risk factors
 Family history/genetic factors
 Smoking
 Hypertension.
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42. SUBARACHNOID HAEMORRHAGE
CLINICAL FEATURES
 Patients complain of a severe headache of instantaneous
onset (like a sudden ‘blow to the head’).
 Transient or prolonged loss of consciousness or seizure may
follow immediately.
 Nausea and vomiting often occur due to raised intracranial
pressure.
 Drowsiness or coma may continue for hours to days.
 Signs of meningism occur after 3–12 hours: neck stiffness on
passive flexion; positive Kernig’s sign (lifting the leg and
extending the knee with the patient lying supine, stretches
the nerve roots and causes meningeal pain).
 Focal signs due to intraparenchymal extension of blood or
vasospasm causing ischaemia and infarction may be
present, e.g. limb weakness, dysphasia.
 Papilloedema may be present
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43. SUBARACHNOID HAEMORRHAGE
INVESTIGATION
 CT scanning is the investigation of choice and shows
subarachnoid or intraventricular blood in up to 95% of patients
who present within 24 hours.
 Beyond that, the sensitivity of CT decreases to 80% at 3 days,
50% at 1 week and 30% at 2 weeks.
 A lumbar puncture should be carried out if the clinical
suspicion of a subarachnoid haemorrhage is high, but CT is
normal and only if the patient is alert and orientated without
focal signs
 Xanthochromia, yellow-tinged CSF(indicating the presence of
bilirubin in the cerebrospinal fluid occurs several hours after
bleeding .
 Angiograms are required to localize aneurysms and
arteriovenous malformations prior to intervention and to
confirm the cause of the diagnosis.
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45. SUBARACHNOID HEMORRHAGE
MANAGEMENT
 Immediate management
 General supportive care: regular neurological
observations, bed rest and fluid replacement, analgesia
for headache, and avoidance of hypotension and
hypertension
 Nimodipine (a calcium-channel blocker): reduces risk of
delayed ischemia secondary to vasospasm
 Subsequent management
 Berry aneurysms are the most common finding at
angiography.
 These can be dealt with neurosurgically by clipping of
the aneurysm neck or by endovascular coiling.
 Arteriovenous malformations can be treated
conservatively, or with direct surgery, radiosurgery,
endovascular embolization or a combination of these. 45
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46. SUBARACHNOID HEMORRHAGE
 Prognosis
 Subarachnoid hemorrhage has a poor prognosis, with an
overall mortality rate of almost 50%, and 30% of
survivors have major neurological deficits.
 The risk of rebleeding from aneurysms is high in the
first 2 weeks, and then declines.
 In arteriovenous malformations the risk is lower but
persists
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47. SUBDURAL AND EXTRADURAL HEMORRHAGE
 Subdural hematoma
 Subdural hematoma occurs as a result of rupture of
cortical veins bridging the dura and brain.
 It is almost invariably caused by trauma to the head in
a patient with a shrunken brain (e.g. elderly and
alcoholics).
 In an acute subdural hemorrhage, there can be rapid
accumulation of blood with a space-occupying effect,
leading to rapid transtentorial ‘coning’.
 With a chronic subdural hematoma, the initial injury
may be minor and there may be a latent interval, from
days to months, between injury and symptoms.
 Chronic subdural hematoma is common in the elderly
and in alcoholics.
 Symptoms can be indolent and fluctuate and include
headache, drowsiness (a key feature) and confusion.
 However, focal deficits (usually hemiparesis), seizures,
and coma can occur
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48. SUBDURAL AND EXTRADURAL HEMORRHAGE
 Extradural hemorrhage
 Extradural hemorrhage is caused by a traumatic
tear in the middle meningeal artery, usually
associated with a temporal or parietal skull
fracture.
 Blood accumulates rapidly in the extradural
spaces, over minutes to hours.
 After a lucid period, the patient may then
develop focal signs, coma and transtentorial
coning, leading to death
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50. SUBDURAL AND EXTRADURAL HEMORRHAGE
 Management
 Diagnosis is by CT scan
 Urgent surgical drainage is undertaken for acute
subdural or extradural hematoma.
 Chronic subdural hematoma is often evacuated
through burr holes as an elective procedure
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