Cerebro vascular

accidents
PRESENTED BY
JOMI JOSEPH E
GIKKU ALIAS BENNY
prayer
Ragadi rogan sathathanu shakthan
Asheshakayaprasruthanasheshan
Outhusukya mohaarathithan jakkana
Yo apoorva vaidya namosthu thasmaii
contents
Definition of CVA
Blood supply of cerebral hemispheres
Classification
Stroke
Ischemia & infarction
Haemorrhages
Stroke in old age
Stroke in children
Examination
Investigation
Differential diagnosis
Management
Conclusion.


definition
A cerebrovascular accident (CVA) is an
ischemic attack of brain tissue or
ultimately an infarction of brain tissue
caused by an interruption in cerebral
blood flow. This results from damage
to an artery supplying blood to the
brain. Ischimia of brain tissue lasting
five minutes or less will cause
permanent damage because neural
tissue is incapable of regeneration
Causes of CVAs
cardiac disease
trauma
infection
neoplasm (tumor)
exogenous toxins
arterio-venous malformations (AVMs)

Blood Supply of Brain
Internal Carotid Arteries :transfer
oxygen- ated blood from the common
carotid arteries of the neck to the circle
of Willis.
Circle of Willis : transfers oxygenated
blood from incoming arteries to deep
internal arteries of the brain.

Vertebral Arteries : transfer oxygen-ated blood
from the subclavian arteries, up through the
transverse foraminae of the cervical vertebrae
and to the basilar artery of the brain.
Basilar Artery : transfers oxygenated blood from
the vertebral arteries to the circle of Willis of
thebrain.
Principle Brain Arteries


aortic arch
external carotid
Posterior cerebral
basilar
vertebral
internal carotid
middle cerebral
anterior cerebral
The major types of
cerebrovascular accident

Stroke
Cerebral ischaemia and infarction
Transient Ischemic Attacks
Atherosclerotic thrombosis
Lacunes
Embolism
Hemorrhage

Definition Of Stroke
Rapidly developed clinical sign of
focal disturbance of cerebral function of
presumed vascular origin and of more
than 24 hours (WHO)
TIA (Transient Ischaemic Attack)
recovery is complete within 24 hours.
10% of patients will go on to have a
stroke.

Sub-types Of Stroke
Ischaemic obstruction to one of major
cerebral arteries, brainstem strokes are
less common.
Haemorrhage 9% are caused by
haemorrhage to the deep parts of the
brain. Patients are usually
hypertensive.

classification
Based on duration
-Stroke
-Transiant ischaemic attack
-Minor stroke
Based on pathology of underlying focal
-brain injury
-Infarction
-Haemorrhage.


Clinical classification
Transient ischemic attack (TIA) :lasting
less than 24hrs.
Evolving stroke:gradual step wise
developmentof stroke.
Reversible ischemic neurological deficit
(RIND):resolve within 1-3 weeks.
Completed stroke:rapid in onset,doesnt
progress beyond 96hrs

Etiology
Complication of several disorders
Atherosclerosis most common.
Hypertension, smoking, diabetes.
Heart disease Atrial fibrillation.
Other:
Trauma fat embolism
Tumor, Infection
Caissons disease
Risk factors
Non modifiable
Age
Male sex
Race
Heredity

Modifiable
Hypertension
Diabetes
Smoking
Hyperlipidemia
Excess Alcohol*
Heart disease (AF)
Oral contraceptives
Hypercoagulability
Complications of acute stroke
Chest infection
Epileptic seizures
Deep venous thrombosis
Pulmonary embolisam
Painful sholder
Pressur sores
Urinary infection
Constipation
Depression & anxiety

Stroke: Ischemia
Insufficiency of blood supply
Glucose & O2 deprivation, build-up of
wastes
NOT synonymous Anoxia:
O2 deprivation only
Few seconds: little or no damage
6-8 minutes ---> Infarction
neurons & other cells die
A consequence of ischemia. Acute right
hemispheric infarction with
swelling leading to uncal herniation. This
picture of the base of the


A consequence of ischemia. Acute right hemispheric infarction with
swelling leading to uncal herniation. This picture of the base of the
brain shows the necrotic, herniated mesial temporal lobe
(arrowhead).

Cerebral ischaemia and
infarction
The principal pathological process
under consideration here is the
occlusion of arteries supplying the
brain. The two internal carotid arteries
and the basilar artery form the Circle of
Willis at the base of the brain, which
acts as an efficient anatomotic device in
the event of occlusion of arteries
proximal to it.
Occlusion leads to sudden severe ischaemia in the area
of brain tissue supplied by the occluded artery, and
recovery depends upon rapid lysis or fragmentation of
the occluding material:
Reversal of neurological function within minutes or
hours gives rise to the clinical picture of a transient
ischaemic attack.
When the neurological deficit lasts longer than 24
hours, it may be called a reversible ischaemic
neurological deficit ( RIND ) if it recovers completely in
a few days,
or a completed stroke if there is a persistent deficit.
Sometimes recovery is very slow and incomplete.




Neurological symptoms and
signs

The loss of function that the patient
notices, and which may be apparent on
examination, entirely depends on the
area of brain tissue involved in the
ischaemic process
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.
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.

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


Transient Ischemic
Attacks(TIA)

Definition of term

Current opinion holds that TIAs are
brief, reversible episodes of focal,
nonconvulsive ischaemic neurologic
disturbance, Consensus has been that
their duration should be less than 24 h.


Pathogenesis
Pathogenesis of Ischemic neuronal
death
Ischemia

Excitatory amino acid receptors

Borderzone or penumbra

Programmed cell death

Different types of TIA
LOW FLOW TIA- Brief,
recurrent,sterrotyped associated with
atheroscleroticlesion at ICA,MCA
STEM junction of veretabral &basilar
arteries.
embolicTIA-discrete,single,prolonged,it
lasts for less than 24 hrs,it idicates
infarct has occuered.
Lacunar/penetrating vessel TIA-
occlusion of small vessels as a result of
lipohyalinosis in response to HTN
Clinical picture
Transient Ischaemic Attacks can reflect
the involvement of any cerebral artery.
The loss of function entirely depends on
the influenced artery.
It may last a few seconds or up to 12 to
24 h, Most of them last 2 to 15 min.
There are only a few attacks or several
hundred.
Between attacks, the neurologic
examination may disclose no
abnormalities.
A stroke may occur after numerous
attacks have occurred over a period of
weeks or months.


Brain infarction
Blood supply to brain is interupted
For 30 sec. Brain metabolism altered
For 1 mte neuronal function may cease
For 5 mte anoxia initiates.






local vaso dilation

stasis of blood colum

segmentation of blood cells

oedema

necrosis of brain tissue
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.

Causes of infarcts
Thrombosis/occlusion
Decreased blood flow:
- hypotension
- vascular stenosis
- increase in vascular permeability
Emboli
- artery to artery ( arterial territory )
- cardioembolic
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
types
Atherosclerottic infarction
Cardiac embolisam
Small vessel lacunar infarction
Cryptogenic infarction.
Atherosclerotic infarction
Atherosclerotic plaque at the
bifurcation or curve in one of the large
vessels
Leads to progressive stenosis with final
large artery occlusion
Caused by trombosis of narrowed
lumen.
Embolic infarction
This is one of the most common cause
of stroke. In most cases of cerebral
embolism, the embolic material consists
of a fragment that has broken away
from a thrombus within the heart.
Embolism due to fat, tumor cells,
fibrocartilage, amniotic fluid, or air is a
rare occurrence and seldom enters into
the differential diagnosis of stroke.



Clinical Picture
Of all strokes, those due to cerebral
embolism develop most rapidly.
The embolus strikes at any time of the
day or night. Getting up to go to the
bathroom is a time of danger.
The neurologic picture will depend on
the artery involved and the site of
obstruction.
It is important to repeat that an embolus
may produce a severe neurologic deficit that
is only temporary; symptoms disappear as the
embolus fragments. In other words ,
embolism is a common cause of a single
evanescent stroke that may reasonably be
called a prolonged TIA. Also as already
pointed out, several emboli can give rise to
two or three transient attacks of differing
pattern or , rarely , of almost identical pattern.


Course and prognosis
Most patients survive the initial insult,
and in many the neurologic deficit
may recede relatively rapidly, as
indicated above.
The eventual prognosis is determined
by the occurrence of further emboli
and the gravity of the underlying
illness- cardiac failure myocardial
infarction, bacterial endocarditis and
so on.
Embolism formation
Cerebral thrombosis

Most cerebrovascular disease can be
attributed to atheroscleroses and
chronic hypertension; until ways are
found to prevent or control them,
vascular disease of the brain will
continue to be a major cause of
morbidity
Embolism
Clinical picture
In more than half of patients, the main part
of the stroke is preceded by minor signs or
one or more transient attacks of focal
neurologic dysfunction. The final stroke may
be preceded by one or two attacks or a
hundred or more brief TIAs, and stroke may
follow the onset of the attacks by hours,
weeks, or, rarely, months.
The most occurrence of the thrombotic stroke
is during sleep.The patient awakens
paralyzed. Either during the night or in the
morning.
Unaware of any difficulty, he may arise and
fall helplessly to the floor with the first step
Clinical picture
Associated symptoms

Seizures accompany the onset of stroke in a
small number of cases (10-50%); in other
instances, they follow the stroke by weeks
to years. The presence of seizures does not
definitively distinguish embolic from
thrombotic strokes, but seizure at the onset
of stroke may be more common with
embolus.
Clinical picture
Associated symptoms
Headache occurs in about 25% of patients
with ischaemic stroke, possibly because of
the acute dilation of collateral vessels.
Course and Prognosis
When the patient is seen early in the
cerebral thrombosis, it is difficult to
give an accurate prognosis.
As for the eventual or long-term
prognosis of the neurologic deficit ,
there are many possibilities.
It must be mentioned that having had
one thrombotic stroke, the patient is at
risk in the ensuing months and years
of having a stroke at the same or
another site, especially if there is
hypertension or diabetes mellitus
Normal blood flow Thrombosis
Artery
Blood supply
Blood clot
Oxygen
starved
brain
tissue
Lacunar infarct
small penetrating branches of the cerebral
arteries may become occluded, and the
resulting infarcts may be so small or so
situated as to cause no symptoms
whatever. As the softened tissue is
removed, it leaves a small cavity, or
lacune.


Lacunar infarct
In our clinical and pathologic material,
there has always been a strong
correlation of the lacunar state with a
combination of hypertension and
atherosclerosis and, to a lesser degree,
with diabetes.
In all the cases of lacunar infarction, the
diagnosis depends essentially on the
occurrence of the certain unique stroke
syndromes of limited proportions.


Lacunar infarct
Recognition of lacunar stroke is
important
Future lacunar stroke can be reduced
by
treating HTN
Anticoagulation is not indicated ( No
evidence)
Aspirin is also of uncertanty

Lacunar Infarct in pons
Cryptogenic infarction
Infarct of undetermind cause.
Cerebral hemorrhage
Neurologic symptoms from mass
effect on neural structures or from toxic
effects of blood itself.
types
Intracranial
Intracerebral
Sub arachnoid

Intracranial Hemorrhage
This is the common, well-known
spontaneous brain hemorrhage. It is
due predominantly to chronic
hypertension and degenerative changes
in cerebral arteries.Hemorrhage may
interfere with cerebral function through
a variety of mechanisms, including
destruction or compression of brain
tissue and compression of vascular
structures, leading to secondary
ischaemia and edema.

Intracranial hemorrhage is classified by its
location as intracerebral, subarachnoid,
subdural, or epidural, all of which- except
subdural hemorrhage- are usually caused by
arterial bleeding.
The bleeding occurs within brain tissue,
and rupture of arteries lying in the
subarachnoid space is practically unknown
apart from aneurysms. The extravasation
forms a roughly circular or oval mass that
disrupts the tissue and grows in volume as
the bleeding continues . Adjacent brain
tissue is distorted and compressed. If the
hemorrhage is large, midline structures are
displaced to the opposite side and reticular
activating and respiratory centers are
compromised, leading to coma and death.
Intraventricular Hemorrhage
Intracerebral Hemorrhage
Of all the cerebrovascular diseases,
brain hemorrhage is the most
dramatic.It has been given its own
name, apoplexy.
Clinical Picture
With smaller hemorrhages, the clinical
picture conforms more closely to the
usual temporal profile of a stroke, i.e, an
abrupt onset of symptoms that evolve
gradually and steadily over minutes,
hours, or a day or two, depending on the
size of the ruptured artery and the speed
of bleeding.
Headache and vomiting are cardinal
features.Very small hemorrhages in
silent regions of the brain may escape
clinical detection.

Clinical Picture
Clinical features vary with the site of
hemorrhage.
Deep cerebral hemorrhage The two most
common sites of hypertensive hemorrhage
are the putamen and the thalamus, which
are separated by the posterior limb of the
internal capsule. This segment of the
internal capsule is traversed by
descending motor fibers and ascending
sensory fibers, including the optic
radiations.

Clinical Picture
Lobar hemorrhage Hypertensive
hemorrhages also occur in subcortical
white matter underlying the frontal,
parietal, temporal, and occipital lobes.
Symptoms and signs vary according to
the location.

Pontine hemorrhage With bleeding into the pons,
coma occurs within seconds to minutes and
usually leads to death within 48 hours. Ocular
findings typically include pinpoint pupils.
Horizontal eye movements are absent or
impaired, but vertical eye movements may be
preserved.
Cerebellar hemorrhage The distinctive symptoms
of cerebellar hemorrhage (headache,
dizziness, vomiting, and the inability to stand
or walk) begin suddenly, within minutes after
onset of bleeding.
Clinical Picture
Of all strokes, those due to cerebral
embolism develop most rapidly.
The embolus strikes at any time of the
day or night. Getting up to go to the
bathroom is a time of danger.
The neurologic picture will depend on
the artery involved and the site of
obstruction.


Subarachnoid Hemorrhage
This is the fourth most frequent
cerebrovascular disorder following
atherothrombosis, embolism, and
primary intracerebral hemorrhage.
Saccular aneurysms are also called berry
aneurysms; actually they take the form of
small, thin-walled blisters protruding
from arteries of the circle of Willis or its
major branches. Their rupture causes a
flooding of the subarachnoid space with
blood under high pressure.
Aneurysms are multiple in 20 percent of
patients

In childhood , rupture of saccular
aneurysms is rare, and they are seldom found
at routine postmortem examination; beyond
childhood, they gradually increase in
frequency to reach their peak incidence
between 35 and 65 years of age.
proximately 90 to 95 percent of saccular
aneurysms lie on the anterior part of the
circle of Willis
WHAT IS A STROKE?
Qureshi, A. I. et al. N Engl J Med 2001;344:1450-1460
Most Common Sites and Sources of Intracerebral
Hemorrhage
Subarachnoid Hemorrhage
Stroke in old age
Incidence:2/3 rd of stroke patients are
aged over 60 yrs
Diagnosis:a clear history to be needed
Thrombolysis:few data avilable.
Carotid endarterectomy:benefits occur
quickly after transiant stroke,it indicates
age alone is nota contra indication.
Cormobiditis:IHD,cardiac
failure,COPD,OA,& visual
impairements.
Contd.
Cognitive impairment : adversely
affects outcome.
Diffuse small vessel CVD: very
common & may present insidiously
with gait abnormalities or significant
memory impairment.
STROKE IN CHILDREN
Stroke in children differs from that of
adult by 3 ways
Predisposing factors:cyanotic heart
disease.
Clinical evaluvation:stroke is often
improved due to collateral cir culation.
Anatomical site:perferal bifurcation of
cerebral arteries.adult-circle of willis
Incidence:252/100000 children.
Cva complications-6-25%with sickle cell
disease
67%untreated sickle cell disease.
General examination of stroke patients
Eyes
Diabetic changes
Hypertensive changes
Retinal emboli
Arcus senilis
Cardiovascular system
Blood pressure
Heart rhythm
Murmurs
Jugular venous pressure
Peripheral pulses and bruits
Respiratory system
Pulmonary oedema
Respiratory infection
Abdomen
Urinary retention
Investigations
Computed Tomographic Scans
Usually demonstrates the lesion, more ever it is very
useful to exclude hemorrhagic lesion.
In ischemic stroke, occasionally CT may be normal in
first 24 hours.
Small posterior fossa or lacunar infarction may be
easily missed by CT.
Other imaging techniques (MRI, angiography, transcranial
doppler) can be applied in selected cases.
Carotid doppler
ECG, echocardiogram in suspected Cardiac emboli
Assessment of the risk factors for stroke: blood sugar,
serum lipids, polycythemia

Investigation of a patient with an acute stroke
Diagnostic question investigation
Is it a vascular lesion? CT/MRI
Is it ischaemic or haemorrhage? CT
Lumbaer puncture
What is the underlying vascular disease? ECG
cardiac ultra sound
MRA
doppler ultra sound
contrast angiography

What are the risk facctors? Blood count
cholesterol
clotting/thrombopenia screen
blood glucose
Differential Diagnosis Of
CVA
Primary cerebral tumours
Metastatic cerebral tumours
Subdural heamatoma
Cerebral abscess
Demylination
Hypoglycemia
Encephalitis
Hysterical conversion
Management
(1) Supportive measures
(2) Antiplatelet agents
(3) Thrombolysis
(4) Anticoagulation
(5) Secondary prevention

Anti-platelet agents
Aspirin 325 mg per day
Contraindicated in associated hemorrhage
Active bleeding lesion (e.g. bleeding peptic
ulcer)
Anticoagulation
Indicated in cardiac emboli in presence of
atrial fibrillation or thrombus in left ventricle
Start with heparin infusion continue with
warfarin .
Complication : hemorrhagic transformation
Thrombolysis
Frequently associated with hemorrhagic
transformation of ischemic stroke
Still can be tried if patients presents within 6
hours of onset, absence of hypertension, when CT
does not show excessive low density, or there are
no other obvious contraindication.
Drugs that can be used are streptokinase and Rt-
PA.
Secondary prevention
Control of risk factors
Antiplatelet agent ( aspirin, ticlopidine,
Dipyridamole, clopidogrel)
conclusion
Thus we have gone through the
basic pathology, clinical features,
investigations and complications of
cerebro -vascular accidents. cerebro -
vascular accidents are those occuring
due to impaired structure and function
of various blood vessels suppling the
brain.even a mild infarct or
haemorrhage can create wide spread
consequnce in the body.they are
medical emergencies.
Thank You