I.

PRACTICE PATTERNS CVA can be categorized into four physical therapy practice patterns and these are: (1) 5A Primary prevention/risk reduction for loss of balance and falling; (2) 5D - Impaired motor function and sensory integrity with non-progressive disorders of the central nervous systemacquired in adolescence or adulthood; (3) 5I impaired arousal, range of motion, and motor control associated with coma, near coma, or vegetative state; and (4) 6E: Impaired ventilation and respiration/gas exchange associated with ventilator pump dysfunction or failure1,2.

II.

DEFINITION, ETIOLOGY AND RISK FACTORS Definition: Cerebrovascular accident (CVA is commonly known as stroke or brain attack3. It is characterized by a sudden loss of neurologic function and onset of focal neurologic deficits caused by brain infarction or blood flow interruption to the brain3,4,5. Etiology: Neurologic deficits from stroke are generally caused by intracranial hemorrhage and brain ischemia. Intracranial hemorrhage types of stroke are known as hemorrhagic stroke while strokes caused by brain ischemia are known as ischemic strokes secondary to cerebral thrombosis or cerebral embolism. Intracranial hemorrhage accounts for 15% of all type of stroke and is subdivided into intracerebral hemorrhage which accounts for 10% of this type of stroke and subarachnoid hemorrhage which accounts for 5% of this type of stroke6,7. Ischemic stroke on the other hand accounts for the remaining 85% of types of stroke with 40% caused by large vessel thrombosis and 20% by small vessel thrombosis. Cerebral embolism on the other hand, accounts for 20% affectation of this type of stroke6, 7. Risk Factors are divided into two broad categories; modifiable and non-modifiable.

Non-modifiable risk factors are: age, race, sex and previous history of stroke. Moreover, maternal or paternal family history stroke increases the risk of a persons chances to have a stroke8,9. Modifiable risk factors includes: Hypertension with blood pressure greater than 160/96 mmHg, smoking, elevated serum cholesterol with cholesterol level greater than 200mg/dl or low density lipoprotein greater than 160ml/dL, obesity, high alcohol consumption, illicit drug use, genetic or congenital vascular malformations, transient ischemic attack, increased blood viscosity characterized by increased hematocrit and serum fibrinogen, heart disease such as coronary artery disease, left ventricular hypertrophy, cardiac failure and non-valvular atrial fibrillation8,9. III. PATHOLOGY, PATHOGENESIS, PATHOPHYSIOLOGY AND CLINICAL MANIFESTATIONS Ischemic strokes such as thrombotic type are the result of arterial blockage caused by a thrombi formation in the brain arteries or intracranial vessels. This is secondary to an atherosclerosis and inflammatory process that damage arterial walls leading to increased coagulation producing a thrombus. With arterial wall damage, platelets and fibrin adhere to arterial walls and clots formed thereby gradually occluding the artery. Transient ischemic attacks (TIA) is the result of thrombotic particle blocking intermittently the brain arteries or causing brain arterial spasm which results in sudden neurologic deficits which resolves completely in 24 hours10. Embolic type of ischemic stroke on the other hand is caused by a breakage of thrombus fragments formed outside the brain or in the heart, aorta, common carotid or thorax. This embolus lodges in the lumen of brain arteries and blocks it causing ischemia, neuronal infarction and neurologic deficits10. With neuronal infarction or neuronal death the brain blood flow falls below 8-10 mL/100mg/minute of brain tissue producing focal area of neuronal irreversible cellular damage

and ischemic penumbra which consist of viable but metabolically lethargic neuronal cells11,12. With this brain infarction, cerebral edema occurs which increases intracranial pressure (ICP) and brainstem herniation leading to neurologic deficits12. Clinical manifestations of Ischemic stroke: Clinical manifestation of Ischemic strokes varies depending on the type of affected brain artery. The manifestations are grouped according to syndromes which involves a group of impairments as a result of blood flow disruption in specific areas of the brain. The more proximal the artery is affected, the greater is the resulting hypoxia, this is because the brain is supplied by more than one artery13. The following are the findings associated with different types of ischemic stroke syndrome: (1) Middle cerebral Artery Syndrome- contralateral hemiplegia and hemianesthesia, global aphasia, brachial syndrome/weakness of the upper extremity, frontal opercular syndrome or facial weakness with motor aphasia with or without weakness, Wernickes aphasia; (2) Anterior Cerebral Artery Syndrome- contralateral hemiparesis and sensory loss, abulia (delay in verbal and motor response), akinetic mutism; (3) Internal carotid Artery Syndrome- symptoms of both Anterior and Middle cerebral Artery Syndrome; (4) Posterior Cerebral Artery Syndrome-thalamic syndrome (abnormal pain, temperature, proprioception and touch sensation, apathy, amnesia and perseverations and superimposition of unrelated information, dis-inhibition syndromes with personality changes, cognitive dysfunction, loss of self-activation, personality changes, contralateral ataxia, oculomotor palsy, hemiballismus, paresis of upward gaze, drowsiness,c coma, decerebrate rigidity, homonymous hemianopsia, alexia, agnosia (difficulty recognizing faces, objects, symbols, colors), anomia (impaired ability to identify objects by name, visual hallucinations; (5) Vertebral and Posterior Inferior Cerebellar Artery

Syndrome- Wallenberg syndrome (characterized by vertigo, nausea, hoarseness and dysphagia, ipsilateral ataxia, ptosis, loss of joint position, ipsilateral tongue weakness, sensory impairment of ipsilateral face and contralateral trunk and extremities, gait unsteadiness, dizziness, nausea and vomiting; (6) basilar Artery Syndrome- bilateral brainstem syndrome manifestation or unilateral sensory and motor aspect of cranial nerve symptoms; (7) Superior cerebellar Artery Syndrome-ipsilateral ataxia, cerebellar ataxia, nausea and vomiting, dysarthria; (8) Anterior Inferior Cerebellar Artery Syndrome-ipsilateral deafness, facial weakness, vertigo, nausea and vomiting, nystagmus and ataxia, horners syndrome (ptosis, miosis or pupil constriction, loss of sweating over ipsilateral side of the face may occur, paresis of lateral gaze may also be evident, pain and sensation of contralateral side of the body are lost; (9) Lacunar Syndrome are small infracts of end arteries in the basal ganglia, internal capsule and pons will present with pure motor deficit or weakness of face and dysarthria, pure sensory stroke, ataxia, clumsiness and weakness13. General Stroke related manifestations and impairments as it relate to ICF model: Depending on the degree of ischemia and brain arteries affected on ischemic subtype of stroke and part of the brain affected by hemorrhagic type of stroke the following stroke related impairments are: (1) dysphagia due to the affectation of unilateral or bilateral brain hemisphere and brainstem, patient will have problems or difficulty with swallowing which impairs his ability to eat thereby affecting his nutritional aspect of his health; (2) Apraxia usually due to the affectation of left hemisphere of the brain, disconnection of right cortical motor association area from left hemisphere due to the injury of the anterior callosal fibers. Patient will have difficulty doing simple functional activities when asked even though the patient understood the instructions given. This will impairs patients ability to dress his self or copying a figure; (3) language and

communication problem due to the affectation of left hemisphere of the brain. Patient will have impairment in speech and communication with other people; (4) Hemiparesis/Hemiplegia, patient will have paralysis or severe weakness of the other half of his body which will impair his ability to perform activities of daily living (ADL), do transfers and ambulation, maintain his sitting/standing balance. Homonymous visual filed defect can also occur with cortical or subcortical hemispheric lesion which will impair patients visual field thereby affecting his mobility, ability to perform ADL, or neglect his other side of his body; (5) Hemisensory loss due to parietal lobe lesions either the cortex or subjacent white matter. This will result to hemineglect. hemi-in-attention and tendency not to use the contralateral arm and leg17. Further complication of stroke impairments are: Falls, musculoskeletal problems such as subluxation, rotator cuff tears, frozen shoulder, bowel and bladder incontinence, physiologic deconditioning, contracture, pressure sore, depression, spasticity17. All of these will affect patients ability to participate and interact in household and community functional activities. 3. MEDICAL AND PHYSICAL THERAPY DIAGNOSTIC PROCEDURES AND TREATMENT/INTERVENTION Medical Management: Medical Diagnosis begins by getting the detailed neurologic history of the patient from the patients family relatives to determine the onset and how it started and progresses. Past medical history important to determine if there was TIA incident, presence of risk factors mentioned earlier. General Physical Examination is performed with neurological examination such as neurovascular tests. Some laboratory test maybe performed depending on the relevance such as: urinalysis, blood analysis, Fasting blood glucose level, blood chemistry profile, blood cholesterol and lipid profile, thyroid function test, full cardiac evaluation, echocardiography, lumbar

puncture. Imaging is also important to determine ischemia or hemorrhage on the brain tissue and these are computerized tomography (CT), magnetic resonance imaging (MRI), positron emission tomography (PET), transcranial and carotid doppler and cerebral angiography. Pharmacological interventions include using anticoagulant therapy (warfarin, Coumadin), antiplatelet therapy (aspirin and anti-hypertensive drugs). Neurosurgical procedures is considered if necessary and these are endarterectomy, surgical repair of superficial ruptured aneurysm or AVM and evacuate clot or hematoma and surgery to remove superficial unruptured AVM when there is a high risk of rupture in the future18. Physical therapy Management: Physical therapy goals for stroke survivors are basically directed on remaining abilities of the patient, train the patient to develop functional skills and enhance it, facilitate psychological coping and adaptation, promote community reintegration and improve quality of life19. Physical Therapy assessment begins with getting the past and present medical history of the patient, review of systems and performing test and measures evaluating the level of consciousness, monitoring vital signs, assessing cardiovascular/pulmonary status, ADL impairments, range of motion, integumentary status, muscle tone and reflexes, mobility of the patient in the bed, sitting, standing, gait, coordination of the patient, needs for assistive devices or orthosis, community support needs20. Physical therapy treatment includes for the patient in this case study includes: (1) therapeutic exercises such as range of motion exercises, muscle and stretching and strengthening, muscle inhibition and facilitation techniques, mobilization and compensatory training techniques; (2) neuromuscular re-education like Brunnstrom, Rood, Bobath, Kabat, knott and Voss; (3) Biofeedback therapy; (4) Functional Electrical Stimulation21; (5) ADL training with the

involvement of family members and patient with community re-integration; (6) mobility training such as bed mobility, transfers and gait training; and (7) Assistive device and/or orthotic training of the patient.

References: 1) OSullivan, Susan B. Schmitz, Thomas J. Physical Rehabilitation. Philadelphia, PA: F.A. Davis Company, 2007:25. 2) Guide to physical therapists practice. Alexandria, Virginia: 2003:357-358, 447-448. 3) OSullivan, Susan B. Schmitz, Thomas J. Physical Rehabilitation. Philadelphia, PA: F.A. Davis Company, 2007:705. 4) Goodman, C C Fuller, Kenda S. OShea, Roberta Kuchler. Pathology for the Physical Therapist Assistant. St Louis, Missouri: Elsevier Saunders, 2012:791. 5) Pablo-Santos, Ramona L. PT-OT Reviewer. San Juan, Metro Manila: C & A Publishing, 2002:267. 6) Goodman, C C Fuller, Kenda S. OShea, Roberta Kuchler. Pathology for the Physical Therapist Assistant. St Louis, Missouri: Elsevier Saunders, 2012:793. 7) Pablo-Santos, Ramona L. PT-OT Reviewer. San Juan, Metro Manila: C & A Publishing, 2002:268. 8) Goodman, C C Fuller, Kenda S. OShea, Roberta Kuchler. Pathology for the Physical Therapist Assistant. St Louis, Missouri: Elsevier Saunders, 2012:791-794. 9) Pablo-Santos, Ramona L. PT-OT Reviewer. San Juan, Metro Manila: C & A Publishing, 2002:269-271. 10) McCance, Kathryn L. Huether, Sue E. Pathophysiology. The biologic basis for disease in Adults and Children. St. Louis, Missouri: 2006:566. 11) Goodman, C C Fuller, Kenda S. OShea, Roberta Kuchler. Pathology for the Physical Therapist Assistant. St Louis, Missouri: Elsevier Saunders, 2012:795. 12) OSullivan, Susan B. Schmitz, Thomas J. Physical Rehabilitation. Philadelphia, PA: F.A. Davis Company, 2007:708. 13) Goodman, C C Fuller, Kenda S. OShea, Roberta Kuchler. Pathology for the Physical Therapist Assistant. St Louis, Missouri: Elsevier Saunders, 2012:796-799. 14) Goodman, C C Fuller, Kenda S. OShea, Roberta Kuchler. Pathology for the Physical Therapist Assistant. St Louis, Missouri: Elsevier Saunders, 2012:803. (15) McCance, Kathryn L. Huether, Sue E. Pathophysiology. The biologic basis for disease in Adults and Children. St. Louis, Missouri: 2006:567.

16) Goodman, C C Fuller, Kenda S. OShea, Roberta Kuchler. Pathology for the Physical Therapist Assistant. St Louis, Missouri: Elsevier Saunders, 2012:804-805. 17) Pablo-Santos, Ramona L. PT-OT Reviewer. San Juan, Metro Manila: C & A Publishing, 2002:284-285. 18) OSullivan, Susan B. Schmitz, Thomas J. Physical Rehabilitation. Philadelphia, PA: F.A. Davis Company, 2007:713-718. 19) Pablo-Santos, Ramona L. PT-OT Reviewer. San Juan, Metro Manila: C & A Publishing, 2002:288-289. 20) OSullivan, Susan B. Schmitz, Thomas J. Physical Rehabilitation. Philadelphia, PA: F.A. Davis Company, 2007:730. 21) Pablo-Santos, Ramona L. PT-OT Reviewer. San Juan, Metro Manila: C & A Publishing, 2002:289.