Pathology of Stroke & CVA

“The true measure of a man is
how he treats someone who
does him absolutely no good...”
– Ann Landers

True beauty lies in the Heart….!

CPC 4.3.5 – Robert
• Robert is a 62 year old recently retired from QLD
railways.
• He lives in Cairns with his wife Rose and their
son Aiden who is 40 yrs old with Downs
syndrome.
• He has fallen from a ladder whilst picking
mangoes.
• His wife found him unconscious in the back yard.
• On arrival at the A&E department he is
conscious but appears confused. He is
complaining of a pain in his L arm.

• What happened:Patient is unable to talk
• Collateral History: wife,son, neighbours,
paramedics.
• What happened? Neighbour saw him at top of
ladder veer to the left and fall 2.5 m landing on his
head. She called out to his wife who attended the
scene. Wife says that he did not seem to hear her
and his left arm was shaking. The shaking lasted
for about 2minutes. He did not seem to regain
consciousness until he was administered oxygen
by the paramedics about 10 minutes later. He then
seemed to come around but appeared confused .
He was unable to move his Left arm, R arm and
Right leg. Wife says he was well prior to going out
to pick mangoes.

• PMH: Hypertension diagnosed in 2000. a bit
forgetful taking medication.
• PSH: 1968 appendicectomy.
• SH married for 40 years to Rose, they had 2
children. Their oldest Aiden was born with downs
syndrome and has lived with them all his life;
alcohol 2 beers x2/week, non smoker.
• FH mother: breast ca age 72 years; well age 85yr
• Father died CVA aged 71
• Brother has hypertension and type 2 DM
• Allergies: aspirin
• Immunisation Fluvax 4.06, Pneumovax 2004
• Medication Ramipril 2.5mg OD [when remembers
it]

• T 36.4 C rr 16/min BP 168/98 mmHg pulse
110 bpm irregular, O2 sats RA 92% (on mask
O2 4l/min) BMI 31 BGL 16m/mol
• General appearance : confused to place and
time; no memory of fall or period preceding
fall; drooping R side face and R side of body
• EMST cervical collar ABCDE
• Peripheries : no clubbing. CRT<2 secs
• CVS Irregular HR no murmurs, no carotid
Bruits
• CNS GCS 13 Pupils R>L sluggish
response[AVPU];

• Boggy Haematoma L temporo parietal area.
• Gross dysphasia, drooping R side of face,
• Flaccidity R side of body, brisk reflexes with
equivocal plantar reflex
• Painful swelling with bruising lower L arm just
distal to elbow, unable to test L power, tone or
reflexes due to pain when moving L arm
• Power/reflexes/tone normal L leg
• Sensation : responds to pain
• Resp., GI, Renal: all normal

• Head injury
– Contusion, Concussion
– Epidural hematoma
– Subdural hematoma
• Cerebrovascular accident (stroke)
– CVA: embolic
– CVA: haemorrhagic
– Metabolic cause
– Seizure ? cause
• Trauma to L arm ?# radius / ulna

Education must award self-
confidence, the courage to depend
on one’s own strength.
- Baba

Pathology of
Cerebro-Vascular Disease
(Stroke)

Dr. Shashidhar Venkatesh Murthy
Associate Professor & Head of Pathology

Introduction:
• “Stroke” Acute neurological deficit – clinical.
• Cerebro Vascular accident (CVA) – Pathology.
• Low O2 (hypoxia) / Low blood supply.
• Varying severity, location & types
• Transient, evolving & completed.
• Global / Focal, arterial / venous
• Ischemic / hemorrhagic.

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.

Brain Blood Supply Features:
• High oxygen requirement.
– Brain 2% of body weight - 15% of cardiac output
– 20% of total body oxygen
– Continuous oxygen requirement – no change with BP
– Few minutes of ischemia - irreversible injury.
• Neurons - Predominantly aerobic.
• Sensitive areas:
– Adults - Hippocampus,
3,5th & 6th layer of cortex,
Purkinje cells - cerebellum
Border zone (watershed areas)
– Brain stem nuclei in infants.

Stroke Types:
• Clinical
– Transient Ischemic Attack –TIA - resolve <24h
– Evolving stroke – increasing >24h. – Thromb.
• Recurrent / multiple stroke – sec. factors.
– Completed stroke – no change… embolic.
• Pathological
– Focal / Global
– Ischemic (Embolic/Thrombotic), Hemorrhagic.
– Venous infarcts. (young, infections)

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.
– Venous thromboembolism (rare)
• Hemorrhage: Incidence 20% - mortality 80%
– Berry aneurysm, Microaneurysm, Atheroma.
– Intracerebral or subarachnoid.

Stroke location and incidence:

Clinical 30day
Cause % presentation mort(%) Pathogenesis
Cerebral 85 Slowly / sudden 15-45 Cerebral
infarction evolving signs and hypoperfusion
symptoms Embolism
Thrombosis

Intracerebral 10 Sudden onset of 80 Rupture of micro-
hem. stroke with raised aneurysm or arteriole
intracranial
pressure
Subarachnoid 5 Sudden headache 45 Rupture of saccular
haemorrhage with meningism aneurysm on circle of
Willis

Hypertensive Intracerebral Hem: Sites

1. Putamen-Claustrum 55%

2. Cerebral white matter 15

3. Thalamus 10

4. Pons 10

5. Cerebellum 10

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.

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

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

Global Ischemia:
• Etiology:
– Impaired blood supply - Lung & Heart disorders.
– Impaired O2 carrying – Anemia/Blood dis.
– Impaired O2 utilization – Cyanide poisoning.
• Morphology:
– 3rd, 5th and 6th layers of the cortex, CA1 sector of the
hippocampus and in the Purkinje cells in the cerebellum
– 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.

Morphology in Global Ischemia
1. Watershed zone
(Acute - ACA-MCA)
2. Laminar necrosis -
(chronic- short
penetrating arteries)
3. Sommer sector of
hippocampus.
4. Purkinje cells of
cerebellum.

Watershed/Boundary zone infarcts:

Carotid thrombosis

Lamellar necrosis in global ischemia.

Chronic

Local infarction:

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

Infarct Pathogenesis:
• Reduced blood supply – hypoxia/anoxia.
Hours • Altered metabolism  Na/K pump block.
• Glutamate receptor act.  calcium influx.
• ischemic injury – Red neuron, vacuolation.
• cell death, karyorrhexis.
1-day
3-day • Inflammation – edema.
1 wk.
• Macrophages - > 5d.
• Liquifaction cavity – >1wk
>4wk • Glial proliferation – >1wk. (astrocytes)

Infarct Stages:
• Immediate – <24 hours
– No Change gross, micro  Na/K loss, Ca+ influx.
• Acute stage – < 1week
– Oedema, loss of grey/white matter border.
– Inflammation, Red neurons, necrosis, neutrophils
• Intermediate stage – 1- 4 weeks.
– Clear demarcation, soft friable tissue, cysts
– Macrophages, liquifactive necrosis
• Late stage – > 4 weeks.
– Removal of tissue by macrophages
– Fluid filled cysts with dark grey margin (gliosis)
– Gliosis – proliferation of glia at periphery.

Cerebral Edema: narrow sulci, flat gyri.

Edema - 
Normal - 

Cerebral edema
• Congestion
• Flat gyri
• Narrow sulci

Cerebral Infarction - Late

Cyst + hemosiderin

Normal Cerebral cortex: gray matter.

Yellow 
oligodendrocytes

Orange 
astrocytes,

Blue 
neurons.

Normal Cerebral cortex: white matter.

Yellow  oligodendrocytes
Orange  astrocytes

Cerebral Edema:

Normal Edema

Axonal Injury:

A, Hypoxic/ischemic injury in cerebral cortex - "red neurons." shrunken cell
B, Axonal spheroids at points of axonal disruption
C, Swollen cell body and peripheral dispersion of Nissl substance (chromatolysis)

H&E Stain.

Acute Infarction: Oedema

Edema - Normal

Cerebral Infarction: Macrophages

Infarct : Microscopy

3 days 1 week
>3 week 1 Day

D

A- 3 days: neutrophils. B-10 days: plenty of macrophages
C-old: tissue loss + gliosis. D-1day: Red neurons & axon bulbs

“Where there is love of
Medicine, there is love of
humankind”
-- Hippocrates

Specific focal Infarcts

MCA
ACA
PCA

MCA
ACA
PCA

Specific
focal
Infarcts

MCA Features:
• Paralysis of the contralateral
face, arm and leg
• Sensory impairment over the
contralateral face, arm and leg
• Homonymous hemi or
quadrantonopia
• Paralysis of gaze to the
opposite side
• Aphasia (dominant) and
dysarthria
• Penetrating - contralateral
hemiplegia/paresis, slurred
speech.

MCA stroke.

Wikipedia: GNU Free Documentation license

Major Arteries: MCA

MCA

• Contralateral face & body (arms & leg)
paralyasis + Sensory impairment.
• Homonymous hemi or quadrantonopia.
• Paralysis of gaze to the opposite side.
• Aphasia / Apraxia / Agnosia / Dysarthria (dom)

ACA stroke.
• Paralysis of contralateral foot
and leg
• Sensory loss over toes, foot
and leg
• Impairment of gait and stance
• Abulia (slowness and
prolonged delays to perform
acts)
• Flat affect, lack of spontaneity,
slowness, distractibility
• Cognitive impairment, such as
perseveration and amnesia Wikipedia: GNU Free Documentation license

• Urinary incontinence

PCA stroke.
Peripheral (cortical)
• Homonymous hemianopia
• Memory deficits
• Perseveration (repeat response)
• Several visual deficits (cortical
blindness, lack of depth perception,
hallucinations)
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

Wikipedia: GNU Free Documentation license

Arterial embolic stroke:

Embolic stroke: sudden, pin point hemorrhages over a triangular area.

Cerebral Infarction – Old (>3w)

Hypertensive CVD
• Intraerebral/Subarachnoid Hemorrhage
– Microaneurysm hemorrhages – Basal ganglia.
Putamen(60%), thalamus, ventricles.
– Berry aneurysm hemorrhages – subarachnoid.
• Chronic Hypertension: (dementia)
– Slit hemorrhages. Microhemorrhages heal as slit with
pigment.
– Lacunar infarcts: Brain stem - pale infarcts.
• Hypertensive encephalopathy-Malignant.
– Headache, confusion, vomiting – Raised ICP.

Hypertension Stroke:

Hemorrhagic stroke (new) & Lacunar infarct (old)

Central Pontine Hemorrhage - Herniation

Fusiform
atherosclerotic
aneurysm

Berry
Aneurysm

Incidence

Pathogenesis

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

Diagnosis: Recent cerebral infarction in left MCA distribution.
Left cerebral hemisphere shows swelling with compression of the lateral
ventricle mainly in the frontal area, due to recent infarct in the Middle Cerebral
Artery (MCA) distribution. The brain in the MCA area shows discoloration of
the cortex and also blurring between the cortex and white matter.

Right (Non-dominant) - Hemisphere Stroke:
• 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

CNS AV Malformations:
• Many types:
– AV Malformation *
– Cavernous angioma
– Telangiectasia
– Venous angioma
• Cause of Seizure
disorders & hemorrhage.
• Most common
congenital vascular
malformation.
• Typically located in the
outer cerebral cortex
underlying white matter.

Summary:
• Stroke: Ischemic / Thrombotic / Hemorrhagic
– Acute neurological deficit - Clinical
– Cerebro Vascular Accident – Pathology.
• Etiology: Thrombosis, Embolism, Hemorrhage.
• Risk factors: AS, Hypertension, Smoking.
• Global – Systemic Hypoxia – Watershed & lamellar infarct
• Focal – Basal ganglia, Putamen, Int. capsule (MCA)
• Pathogenesis: Infarction  Liquifaction necrosis  Cyst
formation with peripheral gliosis. (loss of neural function)
• Hypertension & CVA:
– Atherosclerosis - Thrombosis
– Haemorrhage (Intra/subarachnoid),
– chronic benign: Lacunar infarcts & slit hemorrhages.
– Hypertensive Encephalopathy,

Cerebral Infarction: Microscopy

Macrophages &
Red Neurons Neutrophil Infil. early Gliosis

Loss of Myelin Gliosis

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

– Martin Luther King Jr.

A 78y male, hypertensive. Sudden headache collapsed
while morning walk. Image shows the lesion. Most likely
cause?

1. Ruptured Berry Aneurysm.
2. Ruptured AV malformation.
3. Hemorrhagic infarct.
4. Lacunar infarct.
5. AS- embolic infarct.
55%
lesion is a hemorrhagic infarct in the
distribution of the RMCA. The basic
35%
mechanism is arterial occlusion,
usually by an embolus, with reperfusion
8%
and leakage through a damaged
2%
0%
capillary bed following lysis of the
1 2 3 4 5 embolus.

This photograph shows a slice through the
cerebral hemispheres. The most likely
pathogenesis is:
1.Cerebral trauma due to
head injury.
2.Hypertensive hemorrhage.
3.MCA Embolism from a
mural thrombosis on a
myocardial infarct.
4.Atheroma and thrombosis
93%
at the carotid bifurcation.
5.Bleeding due to Severe
thrombocytopenia.

5% 2%
0% 0%

1 2 3 4 5

Section of Brain specimen. The lesion is most
likely caused by?
1. Gunshot
2. Coup injury-Contusion
3. Contra coup injury.
4. Ruptured ACA
aneurysm.
5. Hypertensive 69%

narrowing.
31%

0% 0% 0%

1 2 3 4 5

Stroke. Most likely clinical feature?

1. Visual deficit.
2. Hemiparesis – leg
3. Memory deficit.
ACA infarct involving the medial and
4. Aphasia parasagittal aspect of the motor cortex,
5. Emotional disturbance. causing contralateral paralysis of the leg.

65%

30%

4%
0% 0%

1 2 3 4 5

This photograph shows a slice through the
cerebral hemispheres. The most likely cause is,

1. Head injury.
2. Hypertensive hemorrhage.
3. Embolic infarct.
4. Atherosclrerotic narrowing.
5. Severe thrombocytopenia.
96%

4%
0% 0% 0%

1 2 3 4 5

A 67y man with IHD is rushed to ED after collapse.
Brain at autopsy. Most likely Artery involved?
1. External Carotid A.
2. Internal Carotid A.
3. Middle Cerebral A.
4. Sagittal venous sinus.
5. Anterior Cerebral A.

92%

The trifurcation of the middle cerebral artery
is a favored site for lodgment of emboli and
for thrombosis secondary to atherosclerotic
damage. This deprives the parietal cortex of
circulation and produces motor and sensory
6% deficits. When the dominant hemisphere is
0% 0% 2%
involved, these lesions are commonly
1 2 3 4 5
accompanied by aphasia.

Stroke Patient. Most likely Artery involved?
1. PCA
2. ACA.
3. MCA
4. Vertebral
5. Basilar

96%

Infarct involving the ACA distribution.

0% 2% 0% 2%

1 2 3 4 5

28y M, Fever 7d, presents acute hemiparesis &
ipsilateral pupillary dilatation. Image cerebellum &
pons. ? Diagnosis
1. Stroke posterior Cer. Art.
2. Bacterial Meningitis.
3. Cerebellar Astrocytoma
4. Glioblastoma multiforme
5. Transtentorial herniation
100%

0% 0% 0% 0%

1 2 3 4 5

85y M, Diabetes, dementia, recent MI, dies of
multiorgan failure. Brain at autopsy (aneurysm of
PCA) . ? Most common complication
1. Dissection.
2. Haemorrhage.
3. Infection.
4. Thrombosis.
5. Recanalization.
41% 41%

17%

0% 0%

1 2 3 4 5

78y M, Hypertensive presents with progressive dementia.
Image shows section of brain. ? Diagnosis

1. Old embolic infarct.
3. Lacunar infarct
4. Recent embolic infarct.
5. Atherosclerotic block.

94%

6%
0% 0% 0%

1 2 3 4 5

A 72y woman, 1 year history of declining memory developed
sudden headache and decreased consciousness and
collapsed while washing dishes. Image shows the lesion.
Most likely cause?
1. Ruptured Berry Aneurysm.
2. Ruptured AV malformation.
4. Lacunar infarct.
5. AS- embolic infarct.
88%

13%

0% 0% 0%

1 2 3 4 5

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).

Old & New
ACA
infarction

Coronal section shows the cerebral hemispheres through the anterior portion of third
ventricle, anterior commissure, and the tip of the temporal lobes. This section is not
quite symmetrical because it shows more of the anterior portion on the left side. The
brain shows a recent area of necrosis in the right anterior cerebral artery distribution
near the midline, with fragmentation of the tissue and poorly demarcated cortex and
white matter. Corpus callosum is very thin and there is also an old slit-like lesion in the
distribution of the left anterior cerebral artery. Diagnosis: Recent infarction in right ACA
distribution, and old infarct, left anterior cerebral artery.
Discuss Clinical Presentation? Complications? Cause of death?

Left PCA
Atherosclerosis
with old infarction

This is a view of the cerebral hemispheres after brainstem and cerebellum have
been removed at the level of the midbrain. There is marked atherosclerosis of
the left posterior cerebral artery. The left occipital lobe (right side of the
photograph) shows a collapsed pigmented area in the distribution of the posterior
cerebral artery. Diagnosis Atherosclerosis of the left posterior cerebral artery with
Old infarction in the area of distribution.

Recent right
infarction MCA
territory with
hemorrhagic
transformation

Axial view showing (Left: superior section Right: inferior portion). The inferior
portion is through the upper portion of the caudate nuclei and the thalami.
The brain shows fragmentation, necrosis, and discoloration in the right MCA
distribution. There is mass effect with compression of the ventricular system. Dark
brown discoloration in the lesion represents early hemorhage.
Diagnosis: Recent infarction in the Right MCA territory with hemorrhage.

Old cystic infarct in the distribution of the left MCA

Coronal sections of cerebral hemispheres . One is anterior and through the optic
chiasm and the posterior section is through the thalami. The left hemisphere (on
the left side of the photograph) is smaller than the right hemisphere. The small
size of the left hemisphere is due to a large cystic lesion that includes the
external portion of the putamen, internal capsule, inferior portion of the frontal
lobe and parts of the temporal lobe. Diagnosis: Old cystic infarct in the
distribution of the left MCA.

Hypertension:
Ruptured anterior
communicating or
anterior cerebral

artery aneurysm

Coronal sections of the cerebral hemispheres through the frontal lobes
and at the level of the genu of the corpus callosum. A hematoma has
destroyed the area around the corpus callosum and inferior frontal gyri.
Hematoma has ruptured into both lateral ventricles. The location of the
hematoma is characteristic of a ruptured anterior communicating or
anterior cerebral artery aneurysm due to hypertension
Note: flat gyri, narrow sulci, herniations.

Spontaneous
hypertensive
thalamic
hemorrhage
with
intraventricular
extension

Coronal section of the cerebral hemispheres through the pulvinar and
quadrigeminal plate. The section shows a hematoma that has destroyed
part of the thalamus on the left side. The hematoma has ruptured into the
lateral ventricle and has compressed the quadrigeminal plate on the left
side. Diagnosis: Spontaneous hypertensive thalamic hemorrhage with
intraventricular extension.

Spontaneous
hypertensive
hemorrhage of the
left putamen

Axial section of the brain through the level of the putamen and the upper
portion of the thalami. The left hemisphere shows a localized hematoma
that involves the putamen and part of the anterior limb of the internal
capsule. The hematoma has not ruptured into the ventricle and has
spared the insular cortex. Diagnosis: Spontaneous hypertensive
hemorrhage of the left putamen.

Spontaneous
hypertensive right
cerebellar hemisphere
hemorrhage & Acute
hydrocephalus

This is an axial section of the brain, brainstem and cerebellum. The section goes through the
caudate nuclei, part of the anterior commissure, the midbrain and the upper portion of the
fourth ventricle and cerebellar hemispheres. The brain shows hydrocephalus with dilatation of
both anterior portions of the lateral ventricles and the temporal horns. The right cerebellar
hemisphere is enlarged by a hematoma that has originated near the dentate nucleus and has
destroyed part of the white matter of the cerebellar hemisphere and the folia.The fourth
ventricle is compressed to the left side anteriorly. Diagnosis: Spontaneous hypertensive right
cerebellar hemisphere hemorrhage & Acute hydrocephalus.

Old hypertensive
spontaneous
hemorrhage left
putamen

An axial section of the cerebral hemispheres. Shows a pigmented
slit- like lesion in the left putamen. This pigmentation is rusty brown
and within the cavity there is some old blood. The sulci in the insula
are prominent (atrophy). Diagnosis: Old hypertensive spontaneous
hemorrhage left putamen.

Central pontine
hemorrhage
( ICP  herniation)

This is a transverse section of the pons and cerebellum. The pons is
almost completely destroyed by a hematoma that has replaced the
tegmentum and most of the basis pontis . The hematoma has
ruptured into the fourth ventricle which is obscured by this lesion. The
cerebellum is normal . Diagnosis: Central pontine hemorrhage
secondary to cerebral herniation – following increased intracranial
pressure.

Hemorrhagic
Cerebral
Infarction

CT-Scan

Cerebral
Infarction

hemorrhage

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

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 ?

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

Frontal Lobe Functions:
• High level cognitive functions. i.e reasoning,
abstraction, concentration
• Storage of information – memory
• Control of voluntary eye movement
• Motor control of speech in the dominant
hemisphere.
• Motor Cortex – Motor control of the contralateral
side of the body
• Urinary continence
• Emotion and personality

Parietal Lobe Functions:
• Sensory cortex – sensory input is interpreted to define
size, weight, texture and consistency (contralateral)
• Sensation is localised, and modalities of touch, pressure
and position are identified.
• Awareness of the parts of body
• Non-dominant – processes visuospatial information and
• controls spatial orientation
• Dominant is involved in ideomotor praxis (ability to
perform learned motor tasks

Temporal Lobe Functions:
• Primary auditory receptive areas
• In dominant ability to comprehend speech (wernicke’s) –
reception
• Interpretive area – area at the junction of the temporal,
parietal and occipital lobes.
• Plays an important role in visual, auditory and olfactory
perception
• Important role in learning; memory and emotional affect.

Occipital Lobe Functions:
• Primary visual cortex
• Visual association areas
• Visual perception
• Some visual reflexes (i.e. visual fixation)
• Involuntary smooth eye movement

Diencephalon Functions:
• Brain Stem:
– Midbrain, Pons & Medulla
– 10 of the 12 ranial nerves arise from the brainstem
(ipsilateral signs)
– Cortical pathway decussation contralateral signs.
– Some major functions: eye movement, swallowing,
breathing, blood pressure, heat beat, consciousness
• Cerebellum:
– movement – Balance & coordination

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

Pathology of Stroke & CVA

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