STROKEAND

MULTIPLE SCLEROSISLAXMI THAPABSC 3RD YEAR

COMS-TH

STROKE• It is a cerebrovascular disorder also known as

cerebrovascular accident• Occurs when there is obstruction in vessels

which impedes blood flow to a part of the brain or haemorrhage into brain

• Results in death of brain cells

RISK FACTORSNON MODIFIABLEAgeGenderFamilyMODIFIABLEHypertensionHeart diseasessmoking

ObesitySleep apneaMetabolic syndromeLack of physical exercises

TYPES1. ISCHEMIC STROKEAn ischemic stroke results from inadequate blood flow to the brain from partial or complete occlusion of an atery

It divides into thrombotic and embolic

a) THROMBOTIC STROKEIt occurs from injury to a vessels wall and formation of blood clot

B) EMBOLIC STROKEIt occurs when an embolus lodge in and occludes a cerebral artery

2. HEMORRHAGIC STROKEIt is caused by bleeding into the brain tissue, the ventricles or subarachnoid space

-primary intracerebral haemorrhage-secondary intracerebral haemorrhage

PATHO-PHYSIOLOGYDue to various etiological factors persisting for a long time

There is disruption of the cerebral blood flow due to obstruction of a blood vessels

Due to the obstruction of blood vessels, initially there is abnormal infiltration of lipid in the intimal layer of the artery

This fatty streaks further develops into the plague

This formation of the palgue may rupture which may travel and occlude the vessels thus limiting the blood flow causing cerebal ischemia

The ischemic cascade begins when cerebral blood flow falls to less than 25ml/ 100 g/min

Due to the cerebral hypoxia, neurons cannot longer maintain aerobic respiration

The mitochondria then switch to anaerobic respiration, which generates large amount of lactic acid

Initiation of anaerobic respiration

Neurons incapable of producing sufficient quantities of adenosine triphosphate (ATP) to fuel the depolarization processes of brain tissue

Maintenance of electrolyte balances begin to fall and cell function ceases

Manifest features like syncope, hemiperesis, weakness of the limb

CLINICAL FEATURES ISCHEMIC STROKEGENERAL Numbness or weakness of face Visual disturbance Sudden severe headache ConfusionMOTOR LOSS Hemiplegia Hemiparesis

Flaccid paralysisCOMMUNICATION LOSS Dysarthria Dysphasia ApraxiaPERCEPTUAL DISTURBANCES Headache Pain and rigidity Visual disturbances Tinnitus, dizziness and hemiparesis

DIAGNOSTIC EVALUATIONCareful history and a complete physical and

neurologic examinationCT ScanMRICerebral angiographyCarotid duplexLumbar puncture for evidence of red blood

cells in cerebrospinal fluid

PREVENTIONControl of hypertensionControl of DMTreatment of underlying cardiac problemAvoid smokingLimiting alcohol intake

MANAGEMENTDRUG THERAPY Recombinant tissue plasminogen activator for

administered IV is used for re-establish blood flow through a blocked artery to prevent cell death

Acetylsalicylic acid is used within 48hrs Platelet inhibitors and anti-coagulant e.g.

aspirin, warfarin

Calcium channel blockers e.g. nimodipine in patient with subarachnoid hemorrhage

Temperature elevation e.g.acetoaminophen Phenytoin for seizures

SURGICAL TREATMENTEvacuation of aneurysm induced hematomas

or cerebral hematomas larger than 3cmAneurysm involves clipping wrapping or

coiling the aneurysm to prevent right bleedingMerei Retriver removes blood clots in patient

who are experiencing ischemic stroke

MULTIPLE SCLEROSIS• It is defined as an auto-immune disease that

affects the CNS and is characterized by the loss/or damage of myelin sheath

TYPES1. RELAPSING/ REMITTING MULTIPLE SCLEROSIS

(RRMS) Characterized by periods of flaretips and

remission2. PRIMARY PROGRESSIVE MULTIPLE SCLEROSIS This type of multiple sclerosis is usually slow

continuous, periodically progressive and results in worsening of disease in a period of time

3. SECONDARY PROGRESSIVE MULTIPLE SCLEROSIS (SPMS):This types is initially diagnosed and disappear but relapse in over a time period (approximately within 10 years) and then becomes steady and disease worsening develops

4. PROGRESSIVE RELAPSING MULTIPLE SCLEROSIS (PRMS)This multiple sclerosis has a steady worsening pattern with acute relapses

ETIOLOGYIdiopathicAging Neuro degenerationPossible precipitating factors: Infection Physical injury Emotional stress Excessive fatigue Pregnancy Poor state of health

PATHO-PHYSIOLOGYDue to various contributing factors (chronic inflammation, viral infestation, injury)

Results in the loss of myelin, disappearance of oligodendrocytes and proliferative astrocytes

Initially myelin sheath of neurons in brain and spinal cord are interfered but nerve fibres are not effected

Changes in the myelin results in plaque formation which will be scattered throughout the CNSLoss of myelin results in noticeable impairment of functionWith the destruction of axons in late stage impulse are totally blocked

Results in permanent loss of nerve function

CLINICAL FEATURESA. MOTOR MANIFESTATION-weakness or paralysis of limbs, trunk & head-diplopia-scanning speech-spasticity of muscles

B.SENSORY MANIFESTATION-numbness and tingling-blurred vision

- Vertigo and tinnitus- Decreased hearing- Chronic neuropathic pain

C.CEREBELLAR- Nystagmus- Ataxia- Dysarthria- dysphagia

D. EMOTIONAL- Anger- Depression- Euphoria

DIAGNOSTIC EVALUATIONA. History collectionB. MRIC. Evoked potential tests (EVPs)D. Cerebrospinal fluid analysis

MANAGEMENT- Corticosteroids to treat acute exacerbation by

reducing edema and inflammation at the site of demyelination

- Immunosuppressive therapy- Antispasmodic- Nutritional therapy