STROKE

 Definition:
 A stroke is the sudden death of a portion of the brain
cells due to a lack of oxygen. A stroke occurs when
blood flow to the brain is damage resulting in
abnormal function of brain. It causes by blockage or
rupture of an artery to the brain.
Types of stroke:
Ischemic(80%)
Hemorrhagic strokes(20%) and venous
occlusions.
Ischemic Stroke

The most common type of stroke --

accounting for almost 80% of all strokes --
is caused by a clot or other blockage
within an artery leading to the brain.
PATHOPHSIOLOGY OF INFARCT:
CERBRAL ISCHEMIA is significantly reduced
blood flow to all r selected parts f brain.It is a
dynamic process in which location and
degree of infarction changes with time and
manifestaions are predicted by
location,duration and tissue volume involved.
When an infarct occurs there is a dense
ischemic focus and a less dense ischemic
penumbra.Cells in d dense ischemic area are
irreversibly damaged.Cells widin d penumbra
remain viable but at risk for few hours.
Ischemia produces energy depletion in the
affected cells.loss of homeostasis,accumulation
of Ca,Na and Cl ions along with water,anerobic
glucolysis with production of intra and
extracellular acidosis occur.
Ischemic injury also leads to accumulation of
extracellar glutamate and free radicals occurs.
All these changes are part of the ISCHEMIC
CASCADE,that leads to cell membrane
dysfunction and loss of integrity with
subsequent cell death.
INFARCTION ETIOLOGY-
1)Large vessel occlusions 40-50%
2)Small vessel occlusions 25%
3)Cardiac emboli 15%
4)Blood disorders 5%
5)Nonatheromatous occlusions 5%
(vasculitis,vasculopathy)
The primary risk factor for ischemic
stroke is age(elderly due to
atherosclerosis).
HYPERTENSION and HEART diseases are
also major risk factors.
Presentation of Ischemic Stroke
TIA
– complete recovery of symptoms in 24hr
usually lasts 5-20 minutes.
Stroke
– persisting neurologic deficit after 24hrs
– infarct on CT or MRI
Cerebral infarction imaging:
CT Findings

HYPERACUTE INFARCT(<12HRS)
Normal(50-60% cases).
Hyperdense artery(25%).
Obscuration of lentiform nuclei.

ACUTE(12 TO 24HRS)
Low density basal ganglia.
Loss of gray-white matter interfaces(insular ribbon
sign).
Sulcal effacement and hypo attenuating brain tissue.
Hyperdense mca
sign
Obscuration of
lentiform nuclei
Loss of gray-white matter
interfaces(insular ribbon sign)
1-3 days(Subacute)
Increasing mass effect.
Low density area that involves both white and gray
matter.
Hemorrhagic transformation can occur.

4-7 days
Gyral enhancement.
Mass effect,edema persists.
Hypo attenuating brain tissue
Hemorrhagic transformation
MASS
EFFECT
1-8 weeks
Mass effect,edema may persist.
Transient calcifications may occur(pediatric
strokes)

Months to years(Chronic)
Encephalomalacia changes,volume loss.
Calcification rare.
CALCIFICATIONS
CEREBRAL INFARCTION:MR FINDINGS
IMMEDIATE
Absence of normal “flow void”.
Intravascular contrast enhancement.
Low on ADC.
Perfusion alterations.

<12hrs
Anatomic alterations on T1w.
Sulcal effacement.
Gyral edema.
Loss of gray-white interface.
12-24 hours
Hyperintensity on T2w images develops.
Meningeal enhancement adjacent to infarct.
Mass effect.

1-3 days
Intravascular,meningeal enhancement begin decreasing.
Early parenchymal contrast enhancement.
Signal abnormalties striking T1w,T2w.
Hemorrhagic transformations become evident.
HYPERINTENSITIES IN BRAIN
MASS EFFECT
4-7 days
Striking parenchymal enhancement.
Hemorrhage apparent in 25%.
Mass effect,edema begin diminishing.

1-8 weeks
Mass effect resolves
Decrease in abnormal signal on T2w sometimes(fogging).
H’ic changes become chronic

Months to years
Encephalomalacic changes,volume loss in affected vascular
distribution
Hemorrhagic residua(hemosiderin/ferritin)
HEMORRHAGIC INFARCTS ON MR
RESTRICTION ON DWI
ENCEPHALOMALCIC
CHANGES
Lacunar infarcts
These are small deep cerebral infarcts located typically
in basal ganglia and thalamus.
These are usually embolic,thrombotic lesions in the
single penetrating end arterioles.
Imaging:
Because of their small size some of the infarcts may not
be visible on CT.
On MR they may appear as rounded or slit like lesions
hypo in T1w.
Hyperintense areas on T2w.

D/D Enlarged perivascular spaces(Virchow-Robins)

LACUNAR INFARCTS
HYPOXIC-ISCHEMIC ENCEPHALOPATHY
It occurs as a result of global perfusion or oxygenation
injury rather than focal infarction injury.
Causes are severe prolonged hypotension,cardiac arrest
with successful resuscitation, profound neonatal
asphyxia and carbon monoxide inhalation.
Basal Ganglia are also the common site for HIE.
In Premature infants the border zone is in the deep
periventricular white matter and HIE manifestations are
periventricular leukomalcia.
2 patterns are seen in HIE Arterial or border zone
infarcts and Generalised cortical(pseudolaminar)
necrosis.
The most frequently and severly affected area
parietooccipital region at the confluence b/w
ACA,MCA and PCA.
Parasagittal cortex
and subcortical white matter
brain injury in a term infant.
IMAGING:

NECT-Low density band noted at the interface between

major vascular teritories.The basal ganglia and
parasaggital areas are the most frequent sites.

MR-show borderzone hyperintenisties on

T2w.Enhancement may be noted on contrast
enhancement.
Because of cortical laminar necrosis is often
hemorrhagic,MR may show serpentine,gyriform foci that
are high on T1w.BG hyperintensities may also be seen.
Term infants suffering from HIE may show normal or
minimally abnormal ct.
Periventricular leukomalacia in a premature
infant
Severe generalised cerebral edema ensues over
24-48 hrs and is seen as diffusely low density
brain often with a “reversal” sign or white
cerebellum sign.
H’gic cortical necrosis with secondary
calcifications can often be observed within few
days.
MR may show high signal on T1w in BG.
Midbrain tegmentum and lat geniculate nuceli are
commonly affected.
Multicystic encephalomalacia is seen in severe
cases
Reversal sign or
White cerebellum
sign
CLINICAL FEATURES IN STROKE

Ischemic Stroke Syndrome

 Transient Ischemic Attack (TIA)
◦ Neurologic deficit that resolves within 24 hours
 Most TIAs resolve < 30 minutes
 Approx. 10% of patients will have a stroke in 90 days
 Half of these in just 2 days
Thalamic stroke:

-Loss of consciousness at the

onset followed by
consiousness and fluctuating
hypersomnia.
-Senosry loss may precede
development of motor signs.
-Aphasia
-Visual field defects
Caudate nucleus stroke:
Motor deficits
facial and upper extremities
muscle weakness with increased
deep tendon reflexes

Behavioural changes
phsycic
akinesia,apathy,dysarthria and
apathy
Lentiform nucleus lesions:
Special motor disorders like
Dystonia
Dysphasia
Acute short term memory dysfunction

Most commonly occurs in hypertensive or diabetic

arteriolopathy and by embolic heart disease
INTERNAL and EXTERNAL CAPSULE
LESIONS:
The typical features of an internal capsule
lesion are: arm and leg affected equally.
i.e hemiplegia/hemiparesis is noted.
Brain stem lesions
Midbrain
CN 3 –ipsilateral paresis/dilated pupil.

Pons
CN 5,6 and 7 causing facial numbness,weakness of jaw
movements,lateral rectus palsy(double vision) and facial
palsy.Pure hemiparesis/plegia

Meduallry infartcs
CN 8,9,10 and 12th are involved causing vertigo,hearing
loss,dysphagia and tongue weakness.Contralateral facial
sensory symptoms loss.
Cerbellar stroke
(often associated with brainstem strokes)

Vertigo
Nystagmus
Gait ataxia
Trunkal ataxia
Dysmetria
Dysarthria
CLINICAL FEATURES OF ACA STROKE
• Paralysis of contralateral foot and leg.
• Sensory loss over toes, foot and leg.
• Impairment of gait and stance.
• Flat affect, lack of spontaneity, slowness,
distractibility
• Cognitive impairment, such as perseveration
and amnesia
• Urinary incontinence
CLINICAL FEATURES OF MCA STROKE

• Paralysis of the contralateral face, arm and leg

• Sensory impairment over the contralateral face, arm
and leg.
• Homonymous hemi or quadrantonopia.
• Aphasia (dominant) and dysarthria.
• Unilateral neglect, apraxia and agnosia.
• Penetrating - contralateral hemiplegia/paresis,
slurred speech.
CLINICAL FEATURES OF PCA STROKE
Peripheral (cortical)
• Homonymous hemianopia(Unilateral infarction)
when B/L varying degrees of cortical blindness can be noted.
• Several visual deficits (cortical blindness, lack of depth perception,
hallucinations)
• Memory deficits.
• Perseveration

Central (penetrating)
• Thalamus - contralateral sensory loss, spontaneous pain, mild hemi
• Cerebral peduncle - CN III palsy with contralateral hemiplegia
• Brain stem - CN palsies, nystagmus, pupillary abnormalities
Lesions in the Vertebral and Basillar art territories
could result in
1)Quadraplegia.
2)locked in’syndrome(complete muscle paralysis
except for upward gaze)
3)diplopia, ataxia, dizziness, vertigo, nystagmus.
4)weakness of facial, lingual and pharyngeal muscles.
5)dysarthria, dysphagia, unconsciousness.

HALLMARK: Crossed neurological deficits: ipsilateral

CN deficits with contralateral motor weakness.
Locked-In syndrome is a condition in which a
patient is aware and awake, but cannot move or
communicate due to complete paralysis of
nearly all voluntary muscles in the body.
It is the result of a brain stem lesion in which
the ventral part of the pons is damaged.
It also known as Cerebromedullospinal
Disconnection, Pseudocoma,and ventral pontine
syndrome.
When only the distal basilar artery is
occluded,the result is so called “TOP of THE
BASILAR SYNDROME”.
Here the predominant lesions are found in the
thalami,posterior limb of internal capsule,pons
and posterior temporal and occipital lobes.
Lateral Medullary (Wallenburg) Syndrome
Specific post. Circulation infarct involving
vertebrobasilar and/or Post Inferior cerebellar Art.
Signs:
-Ipsilateral loss of facial pain and temperature with
contralateral loss of these senses over the body
-Gait and limb ataxia
-Partial ipsilateral loss of CN V, IX, X, and XI
-Ipsilateral Horner Syndrome may be present
Weber's Syndrome (superior alternating
hemiplegia) is characterized by the presence of
an oculomotor nerve palsy and contralateral
hemiparesis or hemiplegia.

It is caused by midbrain infarction as a result of

occlusion of the paramedian branches of the
posterior cerebral artery.
Benedikt's Syndrome is a posterior
circulation stroke of the brain.

It is characterized by the presence of an

oculomotor nerve palsy and contralateral
ataxia.

It is caused by cerebellar infarction as a result

of occlusion of the posterior cerebral artery.