Stroke Presentation PDF

Stroke By Dr. Salwa Essam Introduction Its a heterogenous group of disorders involving sudden, focal interruption of cerebral blood flow that causes neurological deficit. Stroke result from ischemic infarction or bleeding into part of the brain, manifest by rapid onset( eg. seconds- m...

Stroke By Dr. Salwa Essam Introduction Its a heterogenous group of disorders involving sudden, focal interruption of cerebral blood flow that causes neurological deficit. Stroke result from ischemic infarction or bleeding into part of the brain, manifest by rapid onset( eg. seconds- minutes) of focal CNS sign and symptoms(focal neurological defect_ almost always some sort of hemiplegia with /without other neurological signs). Its the major neurological disease of our time. Mortality after 1st stroke : 12% by day56  Classification: Haemorrhage -10_20% resulti from vascular rupture(SAH) Brain Ischemia (Infarct) 80_90%: 1. Thrombus 2. Other type of embolism 3. Systemic hypoperfusion  TIA _Transient Ischaemic Attack; This is a minor stroke , it may present with stroke like symptoms ( limb weakness, dysphagia, visual defects) but the clinical effect will completely resolve within 24hrs.They are usu tlt of micro emboli (80%) but not always.Sometimes a mass lesion may mimic a TIA and other times, they are result of a temporary reduce blood flow eg;with massive postural hypotension, decreased bld flow through stenosed artery Complated stroke : the clinical effects have reached their maximum - usu within 6hrs of the onset. Prognosis: Mortality-20% in 1st 2 months, then roughly 10% year. 65 the biggest risk factor. Gender ; men> women Carotid artery stenosis Family history Cerebral aneurysm ( Haemorrhage) Valvular heart diseases. Risk factors: Modifiable : HTN, cigarette smoking, Dyslipidemia, DM, insuline resistance, abdominal obesity, excess alcohol cosumption,lack of physical actinity, high risk diet, heart disorders,intracranial aneurysms, use of certain drugs, vasculitis Unmodifiable: prior stoke,older age, family history of stoke, genetic factors.  TIA comletely resolve within 24 hrs. 80% due to thromboembolus. site of damage can roughly located from clinical signs: Anterior circulation; likly thrombus from CA most likly affecting cerebral function( aphasia/dysphasia , hemiparesis, Amaurosis fugax,hemi sensory loss, hemianopic visual loss *Amaurosi fugax; sudden loss of vision in 1 eye, caused by an infract in the retinal artery  Posterior Circulation ; likely thrombus from vertbrobasilar system, most likely affecting cerbellar / brainstem function( diplopia, vertigo, vomiting, chocking, dysartheria, hemianopic visual loss , sensory loss ,Transient global amnesia,tetraparesis ,LOC) * Transient global amnesia; episod of emnesia - >65yrs age- compLetely resolve within 24hrs. Diagnosis of TIA: Usually clinical check the following: carotid bruit ECG; for any arrhythmia -AF Valvular HD Recent MI Radial pulse / radial delay  Check for the underline cause/RFs: Atheroma Hypertension Postural hypotension DM Polycythemia Antiphospholipid syndrome. DD for TIA: Mass lesion Epilepsy Migraine PROGNOSIS: 5yrs after TIA _30% of Pts have a stroke( of these 30% occure within 1st year), 15% have MI. Investigation and management: Resolve after 24 hrs , if not or we suspect something serious, then follow the protocolas for stroke. Otherwise, patients are often admitted to hospital on the basis of their ABCD2 score. This score preddicts the likelihood of further CVA event.  A patient with score of >4 should be admitted to the hospital and investigation within 24 hrs. A patient with score of