Pathology+of+stroke

18,918 views 56 slides May 24, 2010
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“The true measure of a
man is how he treats
someone who does him
absolutely no good.”
– Ann Landers

Pathology of
Cerebro-vascular Disease
(Stroke)
Dr. Venkatesh M. ShashidharDr. Venkatesh M. Shashidhar
Associate Professor of Pathology
Fiji School of Medicine

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Introduction:
Stroke is the third most common cause
of death and the second most common
cause of neurologic disability after
Alzheimer's disease.
Its incidence has decreased in recent
decades, but the decrease appears now
to have leveled off, and it remains the
leading cause of institutionalization for
loss of independence.

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Introduction:
“Stroke” Cerebro Vascular accident (CVA)
Acute neurological deficit ↓ blood supply.
Third leading cause of death. (2/1000/y)
Varying severity, location & types
Global / Focal
Transient Ischemia evolving &
completed.
Low O2 (hypoxia) / Low blood supply.

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Brain Blood Supply Features:
High oxygen requirement.
Brain 2% of body weight - 15% of cardiac output
20% of total body oxygen.
Continuous oxygen requirement
Few minutes of ischemia - irreversible injury.
Neurons - Predominantly aerobic.
Sensitive areas:
Adults -Hippocampus, 3,5
th
& 6
th
layer of cortex,
Purkinje cells. Border zone (watershed areas)
Brain stem nuclei in infants.

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Stroke Types:
Clinical
Transient Ischemic Attack –TIA <24h
Evolving stroke
Completed stroke
Recurrent / multiple stroke.
Pathological
Focal / Global
Ischemic (white/pale) & hemorrhagic (red)
Lacunar infarcts (pale chronic cystic)

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Common Types and Incidence:
Infarction: Incidence 80% - mortality 40%
50% - Thrombotic – atherosclerosis
Large-vessel 30% (carotid, middle cerebral)
Small vessel 20% (lacunar stroke)
30% Embolic (heart dis / atherosclerosis)
Young, rapid, extensive.
Hemorrhage: Incidence 20% - mortality 80%
Intracerebral or subarachnoid.
aneurysm, hypertension/congenital.

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Etiology:
Complication of several disorders
Atherosclerosis – most common.
Hypertension, smoking, diabetes.
Heart disease – Atrial fibrillation.
Other:
Trauma – fat embolism
Tumor, Infection
Caissons disease – Bends *Pacific.

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Risk factors:
Non modifiable
Age
Male sex
Race
Heredity
Modifiable
Hypertension
Diabetes
Smoking
Hyperlipidemia
Excess Alcohol*
Heart disease (AF)
Oral contraceptives
Hypercoagulability.

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Clinical Categories:
Global Ischemia.
Hypoxemic encephalopathy
Hypotension, hypoxemia, anemia.
Focal Ischemia.
Obstruction to blood supply to focal area.
Thrombosis, embolism or hemorrhage.

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Global Ischemia:
Etiology:
Impaired blood supply - Lung & Heart disorders.
Impaired O2 carrying – Anemia/Blood dis.
Morphology:
Laminar necrosis, Hippocampus, Purkinje cells.
Border zone infarcts – “Watershed”
Sickle shaped band of necrosis on cortex.
Clinical Features:
Mild transient confusion state to
Severe irreversible brain death. Flat EEG,
Vegetative state. Coma.

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Causes of hypotension
Myocardial infarction
Septic shock
Internal hemorrhage
Massive GI bleed ruptured varices
bleeding ulcer, carcinoma
Ruptured aortic aneurysm.
Shock, Others

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Watershed/Boundary zone infarcts:

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Focal Ischemia:
Thrombosis:
Progressive, recurrent,
Pale or ischemic infarct.
Eg. Lacunar infarct
Embolism / Hemorrhage:
Sudden.
Red or hemorrhagic infarct.
Atherosclerosis – rupture/embolism

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Embolism formation:

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Local infarction:
Cell death ~ 6min
central infarct area
or umbra,
surrounded by a
penumbra of
ischemic tissue
that may recover

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Haemorrhagic - Arterial embolus

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Infarct Pathogenesis:
Reduced blood supply – hypoxia/anoxia.
Altered metabolism  Na/K pump block.
Glutamate receptor act.  calcium influx.
1-6 min – ischemic injury – vacuolation.
>6 min – cell death.

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Infarct Stages:
Immediate – 6 hours
No Change both gross & micro
Acute stage – 2 days
Oedema, loss of grey/white matter border.
Inflammation, Red neurons, neutrophils
Intermediate stage – 2 weeks.
Demarcation, soft friable tissue, cysts
Macrophages, liquifactive necrosis
Late stage – After 4 weeks.
Fluid filled cysts with dark grey margin (gliosis)
Removal of tissue by macrophages
Gliosis – proliferation of glia, loss of architecture.

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Cerebral edema

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Edema, loss of demarcation:

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Acute Infarction: Oedema

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Cerebral Infarct : Red Neurons

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Cerebral Infarct - 1 Week

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Cerebral Infarct - 2 Weeks

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Cerebral Infarction: Macrophages

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Cerebral Infarct - Cyst formation

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Infarct with Punctate hemorrhage

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Cerebral Infarction - Late

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C. Infarct - Cyst formation

’’Smile’ at each other, smile at Smile’ at each other, smile at
your friends, smile at your your friends, smile at your
partner, smile at strangers - it partner, smile at strangers - it
doesn't matter who it is – This doesn't matter who it is – This
will help you to grow up in will help you to grow up in
greater love for each other.greater love for each other.
Mother Teresa
1910-1997, Roman Catholic Missionary

Shashi-05/24/10
Intracranial Hemorrhage:
TRAUMA:
Epidural
Subdural
VASCULAR & TRAUMA
Intracerebral
Subarachnoid
Mixed cerebral-subarachnoid
•Intracerebral - Hypertension
•Subarachnoid - Berry aneurysm + Hptn.
•Mixed cerebral – Vascular malformations.

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Hypertensive CVD
Massive Intracerebral Hemorrhage
Ganglionic & Lobar hemorrhages
Putamen(60%), thalamus, ventricles.
Slit hemorrhages.
Microhemorrhages heal as slit spaces.
Lacunar infarcts
Brain stem pale infarcts – arteriolar sclerosis
Hypertensive encephalopathy
Headache, confusion, vomiting – raised ICP.

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Subarachnoid Hemorrhage:

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Ruptured Berry Aneurism

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Intraventricular Hemorrhage:

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Cerebral
Infarction

hemorrhage

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Cerebral
Infarction

hemorrhage

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Lacunar Infarct in pons

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Summary:
Stroke: Acute neurological deficit - Clinical
Cerebrovascular Accident – pathology.
Ischemic/Hemorrhagic
Thrombosis, Embolism/Hemorrhage
Atherosclerosis, Hypertension, Heart Disease.
Global – Systemic Hypoxia – Watershed infarct
Focal – Thrombosis, Embolism or Hemorrhage
Liquifaction necrosis  Cyst formation, gliosis.
Hypertension – Pale, Lacunar infarcts, slit hem.

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Ischemic penumbra:

““The ultimate measure of a The ultimate measure of a
man is not where he stands man is not where he stands
in moments of comfort, but in moments of comfort, but
where he stands in time of where he stands in time of
challenge and controversy” challenge and controversy”

– Martin Luther King Jr.

Anatomy – Stroke.

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Left (Dominant) Hemisphere Stroke:
Common Pattern
Aphasia
Right hemiparesis
Right-sided sensory loss
Right visual field defect
Poor right conjugate gaze
Dysarthria
Difficulty reading, writing, or calculating

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Right (Non-dominant) Hemisphere
Stroke: Common Pattern
Defect of left visual field
Extinction of left-sided stimuli
Left hemiparesis
Left-sided sensory loss
Left visual field defect
Poor left conjugate gaze
Dysarthria
Spatial disorientation

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Brain Stem Stroke: Common Pattern
Pure Motor - Weakness of face and
limbs on one side of the body without
abnormalities of higher brain function,
sensation, or vision (MCA/ACA)
Pure Sensory - Decreased sensation of
face and limbs on one side of the body
without abnormalities of higher brain
function, motor function, or vision
(PCA).

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Brain Stem / Cerebellum / Post
Hemisp. Patterns.
Motor or sensory loss in all four limbs
Crossed signs
Limb or gait ataxia
Dysarthria
Dysconjugate gaze
Nystagmus
Amnesia
Bilateral visual field defects

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Investigations:
CT of the brain without contrast – location/ext.
Electrocardiogram - heart
Chest x-ray - heart
complete blood count, platelet count – hemat.
PT, aPTT – coagulation.
Serum electrolytes – complications.
Blood glucose - DM
Renal and hepatic chemical analyses – status.
National Institutes of Health Scale (NIHSS)
score – clinical/prognosis ?

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“We must all suffer from one of two
pains: the pain of discipline or the
pain of regret” The difference is
Discipline weighs ounces.. while regret
weighs ton’s..!
Jim Rohn

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Hypertensive Intracerebral Hem:
Sites
1. Putamen-Claustrum
2. Cerebral white matter
3. Thalamus
4. Pons
5. Cerebellum
55%
15
10
10
10

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Stroke types and incidence:

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Anatomy – Stroke.
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