Stroke

cerebrovascular accident/ stroke

1. Stroke / Cerebro -Vascular Accident (CVA) By, Ms. Ekta S Patel Assistant Professor

2. Introduction: Cerebrovascular accident: The sudden death of some brain cells due to lack of oxygen when the blood flow to the brain is impaired by blockage or rupture of an artery to the brain. A CVA is also referred to as a stroke.

3. Definition:

4. “Focal neurological deficit due to a local disturbance in blood supply to the brain. Its onset is usually abrupt, but may extend over a few hours or longer.” WHO, 1971

5. Its an focal neurological deficit resulting from cerebrovascular disease and lasting more than 24 hours or causing earlier death.

6. Stroke is not diagnosis, but a clinical syndrome with numerous causes.

7. Classification:

8. Etiology: Smoking  High blood pressure (hypertension) Obesity High cholesterol levels Diabetes Excessive alcohol intake Atrial fibrillation. Ischemic stroke

9. Being overweight Drinking excessive amounts of alcohol  Smoking A lack of exercise  Stress Brain aneurysm Hemorrhagic stroke

10. Pathophysiology

11. Common sites of hemorrhagic stroke:

12. Putamen : 35 % - 50% Subcortical white matter 30% Thalamus: 10%-15% Pons 5%-12% Cerebellar white matter <5%

13. Common sites of ischemic stroke

14. Clinical Manifestation Of Specific Cerebral Artery Involvement

15. Middle cerebral artery involvement: Contra lateral paralysis ( hemiplegia ) Contralateral anesthesia loss of proprioception , fine tough, localization ( hemiperesis .) Aphasia (Difficulty in communication ) Dysmetria (difficulty in coordination) Conjugate gaze paralysis (inability to move eyeball in some direction)

16. Anterior cerebral artery involvement 1. occlusion of stem 2. occlusion of distal anterior communicating artery: Contralateral sensory and motor deficit of foot and leg Contralateral weakness of proximal upper extremities Urinary incontinence Apraxia (difficulty in movement on command)

17. Personality changes: flat affect, loss of spontaneity and distractibility Possible cognitive impairment

18. Posterior cerebral artery involvement 1. Thalamogeniculate branch occlusion Contralateral sensory loss Temporary hemiparesis Homonymous hemianopsia 2. paramedin branch occlusion: central midbrain and thalamus: Webber’s syndrome Contralateral hemiplegia

19. Incomplete homonymous heminopsia Dysphasia (Difficulty in generation of speech) Disorientation Visual disturbances Dyscalculia: objects and inability to count Possible memory loss

20. Vertebrobasilar artery involvement Bilateral motor and sensory deficit of all extermities Ipsilateral Horner’s syndrome: miosis , ptosis , decrease sweating Hoarsness Dysphagia Nystagmus , diplopia , blindness Nausea and vomiting Ataxia

21. Common symptoms

22. Motor Hemiparesis Hemiplagia Dysphagia Dysarthria (slurred speech)

23. Bowel and bladder Frequency, urgency, urinary incontnance Constipation

24. Language Non fluent aphasia (motor /expressive aphasia) Fluent aphasia (sensory/ receptive aphasia) Alexia: inability to understand written words Agraphia : inability to express self in written

25. Sensory perceptual Diminished response to superficial sensation : touch, pain, hot, cold Diminished proprioseption : knowledge of body parts in environment Visual defects

26. Perceptual deficit: Unilateral neglect syndrome: fail to report, respond or orient to meaningful stimuli. Apraxia : inability to perform learned or familiar movement on commands Agnosia : loss of ability to identify objects or people Anosognosia : unaware of existance .

27. Depression Memory loss Short attention of span Early distractibility Loss of reasoning, judgment and abstract thinking ability.

28. Diagnostic Evaluation:

29. Physical examination Neurological examination Detailed history collection

30. CT MRI MRA- MR Angiography Carotid ultrasound Transcranial doppler Cerebral angiography Transthoracic echocardiography Transesophageal echocardiography ECG Ambulatory ECG monitoring Prothombotic states

31. Medical managemet Hypervolemic - hemodilution therapy: The therapy is designed to decrease the hematocrit and the viscosity of blood, subsequently increasing CBF. The patient must have a documented SAH and have a baseline neurologic status compatible with aggressive intervention to qualify for the therapy.

32. The infusion technique is begun with 5% albumin and continued for 3 to 7 days The dosage is gradually tapered before discontinuation. Effectiveness of the therapy is measured through improvement in neurologic function and regional CBF measurements.

33. Thrombolytic: ( reteplase , urokinase , rt -PA) recombinant tissue plasminogen activator: ( rt -PA) Treated within 3 hours of stroke symptoms onset 0.9 mg/kg Initial 10% given IV bolus over 1minute remaining infused over 60 min.

34. Anticoagulant or aspirin should not be given in first 24hours after rt -PA treatment.

35. Antiplatelet Anticoagulant Antihypertensive

36. Surgical management Carotid endarterectomy

37. Superficial temporal artery – middle temporal artery anastomosis

38. Clot extraction (MERCI) Mechanical embolus removal in cerebral embolism

39. aneurysm clipping and coiling

40. Thank You