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• Rapidly developing clinical signs of focal

(at times global) neurologic dysfunction
lasting more than 24hrs or brain infarction
is demonstrated on imaging.
• TIA:
• “A transient episode of neurologic
dysfunction caused by focal brain, spinal
cord or retinal ischemia without acute
infarction.” 1

Types of Stroke
85% 15 %
Ischemic hemorrhagic 2
• Ischemic 80-85%
Atherosclerotic CVD in 20%
Lacunar in 25%
Cardiogenic embolism in 20%
Cryptogenic 30%
Unusual causes 5%
• Hemorrhagic
10 ICH 10-15%
SAH 5% 3
• The 3rd leading cause of death

• Incidence increases with age

• 100-300/100,000 pop/yr

• Slightly more common in male

• poor prognosis in women 4
 AF  increased age
 Smoking  male gender
 HTN  Family historyy of
 Hyperlipidemia stroke
 DM
 Asxm Carotid Stenosis
 Heavy Alcohol use
 Oral CP 5
Risk factors
Single most important risk factor
It increases risk for stroke of all types
Also plays a role in SAH
Continuous association b/n both systolic and
diastolic BP and the risk of stroke
• Cardiac disease
Cardio embolism is responsible for ~20% of all
ischemic stroke
Most significant causes are AF, MI, RHD and
Non rheumatic AF is the most common cause of
cerebral embolism : average annual risk ~ 5% 6
• Risk factor for stroke with AF
older age, HTN , poor LV function, prior cardio
embolism, DM, thyrotoxicosis, LA enlargement,
• RHD usually causes ischemic stroke when there is
prominent MS or AF
• MI uniformly ischemic and generally embolic
90% in 1st 2 weeks
increased in older age , prior stroke, AF, ant.
Apical MI, thrombosis in LV 7
• Carotid artery stenosis • Cigarette smoking
common cause of  Major independent risk
factor for ischemic
stroke stroke
Depends on degree  The risk associated with
of stenosis smoking is present at
all ages in both sex and
Natural hx of among different racial
Asymptomatic and ethnic groups
stenosis is ~ • DM
2%/yr/stroke rate • Hyperlipidemia
Symptomatic pt • Alcohol
~13% /yr risk of
stroke • Hypercoagulable states 8
Risk factors for stroke
Risk factor Cerebral infarction Intracerebral Subarachnoid
haemorrhage haemorrhage
Greater age ++ ++ +
Hypertension ++ ++ +
Ischaemic heart disease ++ 0 0
Atrial fibrillation ++ 0 0
Diabetes mellitus ++ 0 0
Peripheral vascular disease ++ 0 0
Raised haematocrit + 0 0
High cholesterol + 0 0
Low cholesterol 0 + 0
High plasma fibrinogen + 0 0
Smoking ++ + ++
Alcohol _ ++ +
Obesity + + ?
Transient ischaemic attack ++ 0 0

++, strong association; + moderate association; 0, no association; -, protective in moderation 9
Stroke Mimics

• Hypoglycemia
• Hyperglycemia
• Seizure
• Subdural
Hematoma 10
Stroke Mimics

• Hypoglycemia Altered consciousness

• Hyperglycemia Glucose <50 or
Glucose >300
• Seizure
• Subdural 11
Stroke Mimics

• Hypoglycemia
• Hyperglycemia
• Seizure Altered consciousness
• Subdural (Todd’s paralysis)
History of seizures
Seizure medications 12
Stroke Mimics

• Hypoglycemia
• Hyperglycemia
• Seizure
• Subdural Altered consciousness
Signs of trauma 13

• HIV positive
 consider CNS infection, e.g. toxoplasma, CMV. Also
• Syphilis
• Cerebral abscess
• Neurocysticercosis
• Tuberculoma
• Echinococcus cysts 14
Transient ischemic attacks (TIA)
• Symptoms and signs resolve within 24
hours (most within 30 minutes).
• As many as 20% may sustain a small
infarct visible on CT.
• 5-10 times risk of subsequent stroke.
• Only 15% of strokes are preceded by a
TIA. 15
TIA - differential
• Focal epilepsy and migraine may cause
transient focal neurological symptoms.
• Transient global amnesia causes loss of
recent memory without other cognitive
• Hypoglycaemia may cause transient
• Vertigo and dizziness rarely due to TIA. 16
Pathophysiology of Ischemic stroke
• Occlusion of intracranial vessel

• Reduction in blood flow to the brain region it

• A fall in cerebral blood flow to zero cause death
of brain tissue within 4-10minutes
• If blood flow is restored prior to a significant
amount of cell death
• only transient sxs TIA 17
• Ischemic Penumbra ► tissue
surrounding the core region of infarction is
ischemic but reversibly dysfunctional
• Ischemic penumbra eventually will infarct
if no change in flow occurs
Saving the ischemic penumbra is the
goal of thrombolytic Rx and newer Rx
under Ix 18
Clinical Features of stroke

• Sudden numbness or weakness of the face,

arm or leg, especially on one side of the
• Sudden confusion, trouble speaking or
• Sudden trouble seeing in one or both eyes
• Sudden trouble walking, dizziness, loss of
balance or coordination
• Sudden, severe headache with no known
cause 19
Clinical Features related to location
• The most common C/F Of CVA depends on site of
Lenticulostriate branches 20
• Stem:
contralateral hemiplegia
homonymous hemianopia
with dominant hemisphere : global aphasia
• Upper division
Hemiparesis usually affects face and arm more
than the leg
Broca aphasia more common 21
• Lower division
Wernicke type aphasia with dominant hemisphere
Behavioral change with non-dominant infarction
• Lenticulostriate branches
Lacunar infarction with involvement of theInternal
capsule producing a syndrome of pure motor
hemiparesis 22
 ACA  Posterior circulation
 uncommon <3  P1 3rd CN palsy with
 Contralateral weakness ataxia(Claud’s syndrome)
involving primarily the or with contralateral
lower extremity and to hemiplegia of face, arm
lesser extent the arm and leg(Weber’s
 Impaired memory and syndrome)
abulia  P2 Contralat.
 Ant. Coroidal artery Homonymous
syndrome hemianopia with macular
 Hemi paresis
 Hemi sensory loss
 Hemianopia 23
 Vertebral artery
 Lat. Medullary syndrome/Wallenberg synd.:
• Vertigo, numbness of ipsilateral face and
contralat. Limbs, diplopia, hoarsness,
dysarthria, dysphagia and ipsilateral Horner’s
 Basilar artery
 Locked in syndrome:
 quadriplegia and aphonia
 Complete Basilar occlusion is easy to recognize: bilateral long tract
signs motor and sensory with signs of CN palsy and cerebellar
 Superior Cerebellar artery occlusion
 Severe ipsilateral cerebellar ataxia, nausea and vomiting, dysarthria,
contralateral loss of pain and To sensation over the extremities, body
and face 24
 Lacunar syndrome
 Syndrome of small vessel disease
 Results in infarcts < 2cm in size
 This same vessels are responsible for typical
location of HTNive ICH
>20 described lacunar syndromes
 Pure motor hemiparesis
 Pure sensory stroke
 Ataxic hemiparesis
 Dysarthria – Clumsy hand syndrome 25
• Hx: a number of features in the Hx may be
useful in determining the type of stroke
 Clinical course, etiology, previous TIA,
activity at onset or just before the stroke,
associated sxs 26
Embolic Thrombosis ICH
Clinical course Most often occur Fluctuates Progresses
suddenly, maximal Progressive in gradually during
at onset step wise minutes or few hrs

Etiology Cardiac origin HTN HTN

Common in young More common in
black and Asian
Previous TIA Attacks in >1 Favors No
vascular territory thrombosis
Embolism from
heart or aorta
Activity at onset or Sometimes Can be precipitated
just before the sudden, coughing by sex or other
stroke or sneezing activity
Associated Sxs Fever- Infections Headache, vomiting
Endocarditis Sz is rare and reduced alertness 27
• P/E
• Important clues
• Absent pulses atherosclerosis with thrombosis
• Sudden onset of cold blue limb favors embolism
• Neck bruit Occlusive extra cranial disease
• Cardiac findings
• Fundoscopy
• Neurologic examination Location of the process 28
 CBC, PT, PTT, U/A, ESR,  Documents the extent and
VDRL, ANA, FBS, Lipids, RFT, location of infarction in all
CXR, ECG, ECHO areas of the brain
Imaging:  Is less sensitive than CT in
 CT performed to deff ischemic detecting acute blood.
from hemorrhagic infarct may  DW imaging is more sensitive
not be seen reliably for 24-48h. for early brain infarction
 Limited sensitivity to acute  MRIP brain regions showing
ischemic changes 40-60% in poor perfusion but no
the first 6hrs abnormality in diffusion are
 Remains the best method for considered equivalent to
detection of ICH ischemic penumbra.
 Contrast enhanced CT add Spf  MRAngiography highly
by showing contrast sensitive for a stenosis of extra
enhancement of sub acute cranial ICA
infarcts. 29
CT SCAN; Ischemia 30
Lab con
Cerebral angiography:
Gold standard for identifying and
quantifying athesc stenosis of the cerebral
Carotid duplex u/s to identify and quantify
a stenosis at the origin of ICA 31
• Most common type of ICH
• Account for about 10% of all stokes
• Associated with 50% of case fatality
• Incidence higher in Asian & AM
 advanced age
 heavy alcohol consumption
 cocaine use 32
• Results from spontaneous rupture of a small penetrating
artery deep in the brain
• Most common sites:
 basal ganglia
 deep cerebellum
 pons
• Most hypertensive IPH develop within 30-90\min 33
• Almost always in awake & some times
stressed pt
• Abrupt onset of focal neurologic deficit
typically worsen over 30-90\min
• Diminished level of consciousness
• Headache & vomiting
• Seizure uncommon 34
• Putamen: contralateral hemiparesis
• Thalamic: contralateral hemiplegia ,prominent
sensory deficit ,typical ocular disturbances
• Pontine: deep coma with quadriplegia ,pin point
• Cerebellar: develop over several hours occipital
headache ,repeated vomiting, ataxia of gait &
dizziness or vertigo 35
• CT
– the most reliable
– after 2 wks value decreases → mimic infarct
• MRI ,CT angiog:
– when the cause of ICH is uncertain
– if pts presented >1-2wks after onset
– younger non hypertensive
– hematoma is unusual site for HTN 36
hemorrhage 37
Subarachnoid Hemorrhage
• Characterized by extravasations of blood into the spaces
covering the CNS that are filled with CSF
• common cause of SAH:
– head trauma
– rupture of saccular aneurysm ~ 80% of cases
– vascular anomaly and extension from 10 ICH
• Incidence accounts for 2-5% of all new strokes
• Affects 21000-33000 popn each yr in US
• Aggregate world wide incidence is ~ 10.5 cases/100,000
persons/yr 38
• . 39
• Incidence increases with age:
– mean age at presentation is 55yrs
• Risk for women is 1.6x that of men
• Risk for blacks is 2.1 x that of whites
• Average case fatality rate is 51% and
accounts for 5% of deaths from stroke
• Most deaths occur within 2wks after the
ictus, 10% before pt receives medical
attention, 24% within 24 hrs after the event 40
Forms of Aneurysm
1. Saccular aneurysm :
 3 most common locations are the terminal ICA, MCA bifurcation
and top of basilar artery
Annual risk of rupture for aneurysm
 < 10mm in size ~ 0.1%
 > 10mm 0.5-1%
 Risk of rupture ~ 6% in the 1st yr after identification
2. Mycotic aneurysm :
 Located distal to the 1st bifurcation of major arteries of the circle
of Willis
 Most result from infected emboli due to bacterial endocarditis
3. Atherosclerotic aneurysm: rarely rupture 41
• Aneurysm size and sites are important in
predicting risk of rupture:
– those > 7mm in diameter
– those at top of Basilar artery and
– at origin of Post. Communicating artery are at high
risk of rupture.
• Major modifiable risk factors
– Cigarette smoking
– Cocaine use
– Heavy alcohol use 42
Clinical Manifestation
• Sudden transient loss of consciousness: ~½ pts
• Severe headache: ~ 45% pts
• Nausea, vomiting, neck pain and photophobia
• P/E
– Retinal hage
– Meningismus
– Focal neurologic deficit 43
– a good quality CT will reveal SAH in 100% of cases within 12 hr
after onset of Sxs and in > 93% within 24 hr
– Can also demonstrate intraparenchymal hematoma,
hydrocephalus and cerebral edema
– Can locate the underlying aneurysm
– Most reliable test for predicting cerebral vasospasm and poor
– Sensitivity drops to 50% at 7days 44
– should be performed in any pt with suspected SAH and
negative or equivocal results on CT
– the CSF should be collected in 4 consecutive tubes
The findings:
─ increased OP, increased RBC count that doesn’t diminish from
tube 1 to tube 4
 > 12 hr to develop
Cerebral angiography or CT angiography:
– localize and define the anatomic details of the aneurysm
• Electrolytes 45
1. Rebleeding :
• Incidence ~ 30% in un Rxed SAH
• Peak in 1st 7days
• Associated with 60% of mortality
• Can be prevented with early Rx
2. Hydrocephalus
• Complicates 20% of pts
• Develops insidiously
• Caused by decreased absorption of CSF
3. Vasospasm
• Sxic vasospasm in ~ 30- 46%
• an inflammatory rxn in the blood vessel wall
• Develops b/n 4 and 12 days after SAH
• The best predictor for vasospasm is the amount of blood seen in the
initial CT 46
4. Hyponatremia
• Seen in 1/3rd of pts
• Develops in the 1st 2wks ff SAH
• Results from inappropriate secretion of vasopressin and
secretion of atrial and brain natriuretic factors which produce
5. Seizure
• Seen in up to 1/3rd of pts
• May lead to rebleeding
• Prophylactic anticonvulsant mandatory 47
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