CEREBROVASCULAR ACCIDENT

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CEREBROVASCULAR ACCIDENT
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• CLASSIFICATION
• Complete stroke
• T.I.A
• R.I.N.D
• Stroke in evolution

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• Acute neurological injury which occurs as a
  result of
• 1Embolism
• 2---Thrombosis
• 3---Haemorrhage
• 4---Demyelation
• 5---SOL Space occupying lesion

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• RISK FACTORS
• Ageadvanced age
• Sexmales more than females
• Hypertension
• DM
• Hyperlipidemia
• Smoking
• Excess alcohol consumption
• Polycythemia

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• O.C. pills
• Vasculitis
• Thrombophillia
• Anticardiolipin antibody
• Homocysteinurea

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MANAGEMENT

• HISTORY
• May be helpful
• Headache vomiting ---favour the Dx of IC hge or
  SAH
  
  
  
  
  
• Abrupt onset of impaired cerebral function
  without focal symptoms suggest SAH

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• EXAMINATION
• BP
• Breathing
• Fever----meningitis
• subdural haematoma
• brain abcess
• infective endocarditis
• Neck---for bruits
• Pulses----in neck and arms

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• CVS---valvular heart disease ,AF
• Skin---signs of cholesterol embolismIE
• Fundus

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• INVESTIGATIONS
• CBC , ESR
• UE, RBS
• LFT, PT, PTT
• CT scan brain or MRI
• Doppler U.S of carotids
• Echo
• Hypercoagguable screen
• Screen for connective tissue disease
• Toxicology screen

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• D/D
• --Migraine
• --Head trauma
• --Brain tumour
• --Systemic infections
• --Toxic metabolic disturbance
• hypoglycemia
• acute renal hepatic failure
• drug intoxication
• Todd,s paralysis

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• HAEMORRHAGE
• Intracranial hge can be caused by
• Intracerebral hge ICH
• also called parenchymal hge which involves
  bleeding directly into brain tissue.
• SAH
• involves bleeding into the CSF that surrounds
  the brain and the spinal cord
• Trauma
• causing subdural or extradural haematomas

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• COMMON CAUSES
• Hypertension
• Trauma
• Bleeding diathesis
• Amyloid angiopathy
• Illicit drug abuse amphetamine , cocaine
• Vascular malformation
• Rupture of aneurysm
• Vasculitis

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• SUBARACHANOID HAEMORRHAGE
• 1--Bleeding from aneurysm typically located
  in the anterior half of circle of willis at the
  base of the brain.
• 22nd commonest causes
• A/V malformation
• bleeding diathesis
• drugs
• amyloid angiopathy

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• COMPLICATION OF SAH DUE TO ANEURYSM
• Rebleeding within 10 days
• Vasospasm
• Systemic complications
• --hyponatremia
• --MI
• --CNS disturbance

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• TREATMENT
• Identify cause
• Prevent rebleeding
• Prevent brain damage due to delayed ischaemia
  related to vasoconstrictionof IC arteries
• --surgical removal
• --Calcium channel blocker -Nimodipine

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• PROGNOSIS
• SAH from intra cranial aneurysm has a mortality
  of 50
• Prognosis is closely related to pts neurological
  condition on hospital arrival
• Pts who are alert and have no major focal defecit
  have a 70-80 chances of survival
• Those who are comatosed have 90mortality

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• INTRACERBRAL HAOMORRHAGE
• Strongly associated with hypertension
• Hypertension leads to fibrinoid necrosis of
  arterioles
• Long standing hypertension leads to hyaline
  changes in the muscular and elastic arterial
  layer-----leads to microaneurysim-----liable to
  rupture
• Middle cerbral artery and the lenticular branches
  are prone to develop these aneurysms
• Majority of ICH occur in the region of the
  internal capsule

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• FIVE COMMON AREAS OF HAEMORRHAGE
• Putamen
• White matter or lobe
• Thalamous
• Pons
• Cerebellum

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• ICH usually presents abruptly when the pt. is
  awake
• Severe headache
• ½ of pts. Present with LOC and fits
• Since internal capsule is involved so there is
  hemiplegia
• Massive bleeding---increase intracranial
  pressure---papilloedema----deep coma

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• GENERAL RULE
• If the bleeding is greater than 80 mls as
  estimated by CT scan, and is associated with deep
  coma------chances of survival are very poor
• ICH of moderate size gt1.5 cm in diameter,
  surgical evacuation may be life saving

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• Bleeding forms localized haematoma
• ---spreads along the white matter
• ---haematoma enlarges and continues to grow
• ---pressure surrounding it increases to limit its
  spread
• OR
• Decompresses itself into the ventricular system
  CSF

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• Any patient with sudden onset of severe headache
  should be considered to have SAH.
• Headache with global impairement of conciousness
  is typical
• Focal neurological signs are rare
• Diplopia cranial nerve lesion may occur
• Neck stiffness
• Subhyloid hge

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• PUTAMEN
• Majority of hgic strokes occur in this area
• Hemiparesis or hemiplegia
• Sensory loss
• Aphasia if on dominant side
• Surgery of questionable value

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• PONS
• Rapid loss of conciousness
• Pin point pupils
• Periodic respiration
• Quadriparesis
• Surgery of no value

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• WHITE MATTER OR LOBE
• Same as putamin hge signs
• Distinguished only by neuroimaging
• Surgical evacuation, if suitable

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• EMBOLIC STROKE
• Usually occur abruptly
• Occasionally present with stuttering fluctuating
  symptoms
• Either the anterior (carotid) or posterior
  (vertibobasilar ) circulation may be involved

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• CLASSIFCATION ACCORDING TO LOBES
• FRONTAL LOBE
• Personality and emotional disorders
• Expressive dysphasia
• Contralateral hemiparesis
• Primitive reflexes

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• PARITAL LOBE
• -Spatial disorientation
• -Apraxia acalculia agraphia alexia
• -Sensory inattention,neglect of non dominant side
  
• -Contralateral hemisensory loss
• -Lower quadrantonopia

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• TEMPORAL LOBE
• -Receptive dysphasia
• -De ja vu phenomena
• -Hallucination of taste and smell
• -Excessive lip smacking
• -Micropsia
• -Upper quandrantonopia

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• OCCIPITAL LOBE
• -Homonymous hemianopia with sparing of the macula
• -Thalamic syndrome

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• LOCALIZING FEATURES OF MOTOR LESIONS
• CEREBRAL CORTEX
• Flaccid weakness---flexorsextensors equally
  affected (global weakness)

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• INTERNAL CAPSULE
• Spastic weakness
• Extensors more than flexors
• Distal muscles affected more than proximal
• Patient looks away from the lesion (paralysis of
  head and eye movement )

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• BRAIN STEM
• --crossed hemiplegia i.e ipsilateral cranial
  nerve palsy with contralateral
• limb palsy
• ROOT AND PERIPHERAL LESION
• --peripheral nerve lesions usually affect both
  motor and sensory function in muscles and skin
  supplied by the nerve

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• LOCALIZING ACCORDING TO BLOOD SUPPly
• MIDDLE CEREBRAL ARTERY
• Supplies majority of the internal capsule, larger
  part of frontal , parietal and temporal lobe)
• Contralateral spastic weakness
• Hemianopia
• May have signs of frontal , temporal or parietal
  lobes

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• ANTRIOR CEREBRAL ARTERY
• (Supplies the frontal lobe , superior portion of
  cerebral cortex and anterior portion of internal
  capsule)
• --Motor dysphasia
• --Cortical flaccid weakness of the opposite leg
• --Cortical sensory loss in opposite leg
• --Frontal lobe signs

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• POSTERIOR CEREBRAL ARTERY
• (supplies occipital lobe, branch to thalamous and
  mid brain)
• --homonomous hemianopia with sparing of the
  macula
• --thalamic syndrome
• --if both cerebral arteries are occludedcortical
  blindness (pt is blind but all the pupillary
  reflexes are intact

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• CNS LOCALIZATION
• HEMIPLEGIA
• CORTICAL
• speech disturbances
• UMNL 7th N palsy
• SUBCORTICAL
• multiple cranial nerve
• palsy

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• SPINAL CORD
• Bilateral pyramidal signs
• Higher function intact
• No cranial nerve palsy apart from occasional 11th
  nerve palsy

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• WEAKNESS OF LOWER LIMBS
• With pyramidal signs
• cord lesion
• MND
• Without pyramidal signs
• neuropathy either sensory or
• motor
• muscle disease

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• CRANIAL NERVES
• Single
• DM or Bell,s palsy
• Multiple
• brain stem , with or without
• long tract signs----SOL
• ----vascular

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• EXTRAPYRAMIDAL
• With pyramidal signs
• vascular like atherosclerosis
• Without pyramidal signs
• degenarative group

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• CEREBELLAR
• Wings
• look for pes cavus
• Tract signs
• SOL (acoustic neuroma)
• PICA
• MUSCLES
• Dystrophies

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• CEREBELLUM
• Headache
• Vertigo
• Atxia
• Lethargy
• No focal weakness
• Surgical evacuation for all except small
• haemorrhages

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• CLASSIFICATION
• Within the cavernous sinus (infraclinoid)
• It may compress structures like 3,4,5 and 6th
  nerve palsy
• ----dilated pupil
• ----facial pain
• ----variable loss of facial sensation

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• Above the cavernous sinus (supraclinoid)
• Most frequently compress the occulomotor nerve ,
  optic tracts and chiasm
• May extend into the frontal lobe

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• 6th year

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