CARDIOVASCULAR ACCIDENTS

CVA

1. CEREBROVASCULAR ACCIDENTS Dr. AISHWARYA RAI (PT) BPT, Fellow in Regenerative Rehabilitation, CKTP.

2. DEFINITION It is an acute onset of neurological dysfunction due to an abnormality in cerebral circulation with resultant signs and symptoms that correspond to involvement of focal areas of brain. If neurological deficits persist for less than 24 hours- TIA If neurological deficits persist for more than 24 hours- stroke.

3. CLASSIFICATION

4. RISK FACTORS POTENTIALLY MODIFIABLE NOT MODIFIABLE TIA HYPERTENSION DIABETES MELLITUS OBESITY HIGH SERUM CHOLESTEROL CARDIAC DISEASE (ATRIAL FIBRILATION, CHF, LVH, CAD, etc) H/O SMOKING ALCOHOL CONSUMPTION COCAINE USE PRIOR STROKE AGE RACE GENDER FAMILY H/O STROKE

5. PATHOPHYSIOLOGY

6. In the normal brain, cerebral blood flow to a particular part varies depending on the metabolic requirements, i.e. the supply of O2 and glucose is ‘coupled’ to the tissue needs. After infarction, between areas of reduced flow and areas of luxury perfusion, lie areas of relative luxury perfusion where reduced flow exceeds the tissue requirements, i.e. ‘uncoupling’ of flow and metabolism occurs. Progression from reversible ischaemia to infarction depends upon the degree and duration of the reduced blood flow along with presence of collateral circulations. A mismatch between CBF and metabolic demands lead to either electrical failure of lactic acidosis (in case glucose is available). A cascade of events take place that ultimately lead to accumulation of toxic compounds and apoptosis. Interruption in this blood flow hence leads to a series of pathoneurological events that leads to irregular cell damage with a core area of focal infarction within minutes. Ischaemic penumbra- Area surrounding the core that consists of viable but metabolically lethargic cells.

7. CIRCLE OF WILLIS It is an anastomosis formed by the ICA, VA and their branches at the base of brain. Also known as circulus arteriosus

8. The anterior cerebral artery is a branch of the internal carotid and runs above the optic nerve to follow the curve of the corpus callosum . Soon after its origin the vessel is joined by the anterior communicating artery. Deep branches pass to the anterior part of the internal capsule and basal nuclei. Cortical branches supply the medial surface of the hemisphere: 1. Orbital 2. Frontal 3. Parietal ANTERIOR CEREBRAL ARTERY SYNDROME

9. MIDDLE CEREBRAL ARTERY SYNDROME The middle cerebral artery is the largest branch of the internal carotid artery. It gives off (1) deep branches (perforating vessels – Lenticulostriate ) which supply the anterior limb of the internal capsule and part of the basal nuclei. It then passes out to the lateral surface of the cerebral hemisphere at the insula of the lateral sulcus . Here it gives off cortical branches (2) temporal, (3) frontal, (4) parietal.

10. POSTERIOR CEREBRAL ARTERY SYNDROME The posterior cerebral arteries are the terminal branches of the vertebral arteries. Small perforating branches supply midbrain structures, choroid plexus and posterior thalamus. Cortical branches supply the undersurface of the temporal lobe – temporal branch; and occipital and visual cortex – occipital and calcarine branches.

11. INTERNAL CEREBRAL ARTERY SYNDROME In the most extreme cases there may be: Deterioration of conscious level Homonymous hemianopia of the contralateral side Contralateral hemiplegia Contralateral hemisensory disturbance Gaze palsy to the opposite side – eyes deviated to the side of the lesion A partial Horner’s syndrome may develop on the side of the occlusion (involvement of sympathetic fibres on the internal carotid wall). Occlusion of the dominant hemisphere side will result in a global aphasia. Course occlusion can result in herniation , coma and death.

12. VERTEBRO BASILAR ARTERY SYNDROME It supplies the pons , inner ear and cerebellum. A complete occlusion of VA can result be fatal. A progressive lesion often starts with occipital headache, diplopia , hemiplegia , quadriplegia and coma. Complete basilar syndrome affecting pontine nuclei (without affection of reticular system) results in locked in syndrome. Locked in syndrome results in anarthria , quadriplegia with preserved conciousness , alertness and vertical eye movements. Vertebrobasilar artery system occlusion can result in either ipsilateral or contralateral symptoms depending on whether tracts involved are crossed or uncrossed. DROP ATTACK: Sudden loss of tone in LL muscles due to involvement of medullary pyramids. Symptoms include visual loss, diplopia , homonymous hemianopia , facial numbness or weakness, tinnitus, dysarthria or dysphagia .

13. DIAGNOSTIC TESTS Routine and special blood investigations: CBC, TSH, T3, T4, Lipid profile and blood glucose levels, serum electrolytes, Carotid duplex CT Scan ECG Echocardiography MRI MRA Cerebral angiogram PET

14. DIRECT IMPAIRMENTS Motor deficits- flaccidity, spasticity, stage of spontaneous recovery. Sensory deficits Presence of abnormal reflexes- ATNR, STNR, STLR, etc. Presence of associated reactions- Souque’s phenomena, Ramiste’s phenomena, homolateral limb synkinesis . Speech and Language disorders- aphasia Perceptual deficits- apraxia , agnosia Cognitive dysfunction Dysphagia Bladder bowel impairment Sexual dysfunction

15. MOTOR DEFICITS

16. SENSORY DEFICITS

17. SPEECH AND LANGUAGE DISORDERS APHASIA- INABILITY OR DIFFICULTY IN LANGUAGE OR SPEECH IS CALLED APHASIA. CAUSED DUE TO LESION IN THE DOMINANT PARIETAL LOBE.

18. PERCEPTUAL DEFICITS AGNOSIA- INABILITY TO RECOGNISE OR MAKE SENSE OF UPCOMINING INFORMATION DESPITE SENSORY CAPACITIES. APRAXIA- INABILITY TO PERFORM A LEARNED MOVEMENT EVEN THOUGH THE PATIENT HAS GOOD MUSCLE STRENGTH, COORDINATION, INTACT ATTENTION AND SENSES. CAUSED DUE TO LESION OF PARIETAL LOBE OF DOMINANT HEMISPHERE.

19. COGNITIVE DEFICITS

20. BLADDER & BOWEL IMPAIRMENT

21. SEXUAL DYSFUNCTION PROBLEMS WITH: LIBIDO ORGASM SEXUAL DESIRES ERECTION LUBRICATION

22. GAIT

23. INDIRECT IMPAIRMENTS Psychological complications Musculoskeletal complications Circulatory disturbances Cardiac and respiratory deconditioning GIT and renal disturbance

24. MANAGEMENT Medical: Maintain circulation oxygenation, blood pressure, CO , fluid and electrolyte balance. Prevent oedema, seizures and other complications. Pharmacological: Thrombolytic, anticoagulant, antiplatelet , antihypertensives , antispastics , etc. Neurosurgical: AVM management, Carotid endarterectomy , etc. Rehabilitation

25. references 1. NEUROLOGY AND NEUROSURGERY ILLUSTRATED KENNETH W LINDSAY, IAN BONE & GERAINT FULLER 2. PHYSICAL REHABILITATION, ASSESSMENT AND TREATMENT SUSAN B. O’SULLIVAN & THOMAS J. SCHMITZ 3. PHYSIOTHERAPY IN NEUROLOGICAL CONDITIONS WITH ASSESSMENT AND TREATMENT PROTOCOLS. GOWRISHANKAR POTTURI