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Presented by :-RAHUL RAVISHB.Sc-final yr.
Roll no. 71704
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It is a non-traumatic brain injury caused
by occlusion or rupture of cerebral blood
vessels that results in sudden
neurological deficit.
It is also denoted by cerebrovascularaccident(CVA).
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1) Intracranial haemorrhage
(15%) of all stroke:-
Intracerebral haemorrhage (10%)Subarachnoid haemorrhage(5%)
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2)Ischemic brain injury(85%):-Large vessels(20%)
Small vessels(20%)
Cerebral vessels(20%)
Less common cause such as cerebral
vasculitis or cerebralhypotension(5%)
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It occurs due to:-
Rupture of weakend vessels within brain
parenchyma as a result of hypertension. Arteriovenous malformation.
Tumour .
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It occurs due to rupture of a
cerebral artery.
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Modifiable risk factors:-1) Hypertension- it is defined as
SBP>165mmhg or DBP >95mmhg.HTincrease the risk of stroke 6 times.
Among stroke survivours,67% have
chronic HT.
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. Reduction of DBP is associated with
reduction in stroke.
. Isolated systolic HT is more commonamong individuals older than 60yrs.
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It is associated with an increased risk of
atherothrombotic stroke and
haemorrhagic stroke.3) Hypercholesterolemia indicatesindirect risk factor for stroke; is
responsible for CAD & atherosclerosis.
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4)Obesity
5) Heart diseases increases stroke risk
by 2 to 6 times normal.
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1) Age- in younger age group cause ispolycythemia ,whereas in older agegroup HT,CAD etc.
2) Sex 30% more in males.3) Race - seen commonly in blacks andpeople of asian origin.
4) Socio cultural factors- example dietaryrestrictions , various social
taboos,increased salt intake etc.5) Family history of premature vascular
diseases.
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ACA Stroke
MCA Stroke
PCA Stroke
ICA Stroke
VBA Stroke
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Brain is supplied by four major arteries:- Two rt. & lt. ICA. Two rt. & lt. vertebral artery.
Internal carotid artery:- Begins at bifurcation of common carotid artery andascend into deep portions of neck till carotid canal.
It pierces dura mater & gives off branches-- ophthalmic artery- anterior choroidal artery.
It terminates as bifurcation into middle & ant.Cerebral artery.
Ant . Communicating artery communicates withrt./ lt. ACA.
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It Begins as a branch of subclavian artery.
It enters the vertebral foramen of 6th
cervical vertebra and travels up throughforamina of transverse process of C6 to
C1 to foramen magnum & finally into
brain.
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It travels in posterior cerebral fossa ,ventrally medially & unites with oppositeside vertebral artery & forms basilar
artery at upper border of medulla.At upper border of pons ,basilar artery
bifurcates to form posterior cerebralartery.
Posterior communicating artery connectsposterior cerebral artery with internalcarotid artery to form circle of willis.
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Interruptions of bloodflow
Cerebral circulatoryarrest
Irreversible cellulardamage
Focal infarction within
minutes
Transtitional areasurrounding the core
causes Ischm. Penumbra
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Triggers damaging &potentially reversibleevents causes Isch.Cascad
Neurotransmittersglutamate , aspartatereleased
Disturbance of energymetabolism & anoxicdepolarization
Inability of brain cells toproduce energy
Reacts with intracellular
phospholipids
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Free radicals formed
Release of nitric oxide &cytokines
ama e rain cells.eriod: - rs
Causin cere ral dama e.
Max. - days
Swellin su sides.
Wit in 2- weeks
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If there is left sided lesions there is rt. Sidehemiplegia,rt.side sensory loss i.e.hemianaesthesia & speech impairment
asspeech is controlled by lt. side ofbrain(Brocas motor speech area).
If rt.side lesion than hemiplegia &hemianaesthesia of lt. side along with
visuaospatial neglect that meansdisorientation about person,time,place,hisdressing sense etc.
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RAHUL
