CEREBROVASCULAR ACCIDENT

1. CEREBROVASCULAR ACCIDENT

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

5. Acute neurological injury which occursas a result of ; • 1—Embolism • 2---Thrombosis • 3---Haemorrhage • 4---Demyelation • 5---SOL { Space occupying lesion}

6. RISK FACTORS • Age—advanced age • Sex—males more than females • Hypertension • DM • Hyperlipidemia • Smoking • Excess alcohol consumption • Polycythemia

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

8. 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

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

10. CVS---valvular heart disease ,AF • Skin---signs of cholesterol embolism+IE • Fundus

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

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

13. 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

17. COMMONCAUSES • Hypertension • Trauma • Bleeding diathesis • Amyloid angiopathy • Illicit drug abuse {amphetamine , cocaine} • Vascular malformation • Rupture of aneurysm • Vasculitis

18. SUBARACHANOID HAEMORRHAGE 1--Bleeding from aneurysm typically located in the anterior half of circle of willis at the base of the brain. 2—2nd commonest causes A/V malformation bleeding diathesis drugs amyloid angiopathy

19. COMPLICATION OF SAH DUE TOANEURYSM • Rebleeding within 10 days • Vasospasm • Systemic complications --hyponatremia --MI --CNS disturbance

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

21. 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 90%mortality

22. 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

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

24. 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

25. 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 >1.5 cm in diameter, surgical evacuation may be life saving

26. 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

27. 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

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

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

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

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

32. CLASSIFCATION ACCORDING TOLOBES FRONTAL LOBE Personality and emotional disorders Expressive dysphasia Contralateral hemiparesis Primitive reflexes

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

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

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

36. LOCALIZING FEATURES OF MOTORLESIONS CEREBRAL CORTEX • Flaccid weakness---flexors+extensors equally affected (globalweakness)

37. 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 )

39. 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

40. l 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

41. 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

42. 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 occluded—cortical blindness (pt is blind but all the pupillary reflexes are intact

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

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

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

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

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

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

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