DEFINITION

Is the sudden loss of neurological function caused by an interruption of the blood flow to the brain. The term cerebrovascular (CVA) is used interchangeably with stroke to

refer to the vascular conditions of the brain.

EPIDEMIOLOGY
3rd leading cause of death and the most common

cause of disability among adults in the U.S. > in males than in females Compared to whites, African-Americans have twice the risk factor, also higher in MexicanAmericans, American Indians, and Alaska Natives. Increases incidence with risk factors Hemorrhagic stroke account for the largest number of deaths, with mortality rates of 3738% at 1 month.

 Ischemic stroke have mortality rate of

only 8-12 % at 1 month. The most common cause of chronic disability Of survivors, an estimated 1/3 will be functionally dependent after 1 yr. experiencing difficulty with ADL, ambulation, speech, and so forth.

ETIOLOGY
Atherosclerosis Schemic stroke Cerebral thrombosis Cerebral embolus (CE) Intracerebral hemorrhage Cerebral hemorrhage Subaracchnoid hemorrhage Arteriovenous malformation (AVM)

RISK FACTORS
HPN the most treatable
Diabetes mellitus Hyperlipidemia

Cigarette smoking
Cardiac disease Heavy alcohol consumption

Family hx of stroke
Previous stroke

DIFF. PATHOGENESIS OF STROKE

CRITERIA Incidence THROMBOTIC 40% EMBOLIC 30% LACUNAR 20% Similar to thrombosis; small infarcts Chronic process; gradual onset HEMORRHAGIC 10% HPN rupture of penetrating arterioles leading hemorrhage Sudden Mechanism Atherosclerotic Cholesterol hematogenous stenosis or occlusion of large materials blood vessel Onset & Progressi on Gradual, slow stepwise progression of symptoms, may be hours to days (+) warning signs; commonly occurs at night > 50% w/ TIA abrupt

Scenario

Most occur in setting of MI

DIFF. PATHOGENESIS OF STROKE (CONT.)

CRITERIA Sites THROMBOTIC Internal carotid Artery or MCA EMBOLIC Cortical small vessels Cortical deficits (hallmark) LACUNAR Small, perforating arterioles Discrete & specific subcortical deficits HEMORRHAGIC Sites of lacunes

Clinical Manifestations

Aphasia; Visual fields cuts hemiparesis hemisensory

Inc. Intracerebral perfusion Subcortical Deficits (more extensive)

Prognosis

Severe impairment

Repeated stroke in same vascular territory

Excellent; 85% w/ very good recovery

Poor; initial MR= 50-70% vs. if blood is reabsorbed mild deficits

CLASSIFICATION OF STROKE
A.TEMPORAL CLASSIFICATION
B.PATHOPHYSIOLOGICAL

CLASSIFICATION C.NEUROANATOMICAL CLASSICATION

TEMPORAL CLASSIFICATION
1. Transient ischemic attack (TIA)

focal neurologic attack with complete recovery within 24 hrs - Temporary interruption of blood supply to the brain - No neurologic dysfunction 2. Reversible ischemic neurologic deficit (RIND) - focal neurological deficit that lasts longer than 24 hrs. but still with reversible signs and symptoms
-

TEMPORAL CLASSIFICATION
3. Stroke in evolution/ Progressive - characterized by progressive development of more severe neurological impairments 4. Complete stroke - Stable neurologic deficit - No reverse and with no progress

B. PATHOPHYSIOLOGICAL CLASSIFICATION

Ischemic - the result of a thrombus, embolism, or conditions that produce low systemic perfusion a. Thrombotic b. Embolic c. Lacunar Hemorrhagic- Abnormal bleeding into the in

extravascular areas of the brain are the result of rupture of the cerebral vessel or trauma. a. Intracerebral b. Subarachnoid

C. NEURONATOMICAL CLASSIFICATION
(CORTICAL HOMUNCULUS)

NEUROANATOMICAL CLASSIFICATION OF STROKE

CIRCLE OF WILLIS Is a part of the cerebral circulation and is composed of the following: Ant. Cerebral artery (left & right) Internal carotid artery (left & right) Post. Communicating artery (left & right) Post. Cerebral artery (left & right) Basilar artery Middle cerebral artery Ant. Communicating artery (left & right)

CIRCLE OF WILLIS
Was named after Thomas Willis by his

student Richard Lower. Also called Willis Circle, Loop of Willis, Cerebral arterial circle and Willis Polygon. Is a circulatory anastomosis that supplies blood to the brain and surrounding structures.

MCA SYNDROME
Most common seen w/n the inpatient

rehabilitation setting. Is particularly vulnerable to both cardioembolic and thrombotic dse. Than can result in a variety of stroke syndrome.

Characteristics of (R)and (L) Hemiplegia

RIGHT HEMIPLEGIA ( Left Hemisphere) Visuomotor perception and memory intact Visual learning LEFT HEMIPLEGIA (Right Hemisphere) Visuomotor perceptual impairment Loss of visual memory

Behaviors to be learned should be demonstrated step by step , encouraging imitation

Left- sided neglect

Impulse or unorganized in activities of daily living Lack of insight into these problems Safety problems with many fails Lack of insight

Unable to communicate effectively Vocabulary & auditory span reduced Caregivers may assume that the px comprehends much more than he/she does

Characteristics of (R)and (L) Hemiplegia

RIGHT HEMIPLEGIA ( Left Hemisphere) Limit or eliminate words LEFT HEMIPLEGIA (Right Hemisphere) Inability to follow through Cannot be trusted Able to pick up ideas of conversation through body language, tone of voice & facial expression Able to learn from mistakes Able to synthesize parts of the task Will learn from observing others Cautious & unorganized when approaching an unfamiliar situation Neglect is more common than in right hemiplegic Vision Touch Hearing Does not learn from mistakes or observing others

Characteristics of (R)and (L) Hemiplegia

RIGHT HEMIPLEGIA ( Left Hemisphere) Give lots of feedback LEFT HEMIPLEGIA (Right Hemisphere) Learning is impaired Persons performance may not improve Often battles with staff or premature discharge

Visuomotor perceptual impairment Loss of visual memory

Visuomotor perceptive memory provide ways in which learning may proceed

Characteristics of (R)and (L) Hemiplegia

RIGHT HEMIPLEGIA ( Left Hemisphere) Left-sided neglect improves Verbal fluency Impulse/ unorganized in performing ADL Learning is impaired Unable to communicate effectively Behaviors to be learned should visually demonstrated step by step, encouraging imitation Lack of verbal comprehension Learning from mistakes Learning from observing others in the therapy department LEFT HEMIPLEGIA (Right Hemisphere) Vocabulary & auditory retention span are reduced Right sided neglect worsens in response time

CLINICAL MANIFESTATIONS
1. Sensation 2. Motor function Sequential recovery Stages during the early stage of stroke, flaccidity with no voluntary movement is common Usually replaced by the development of spasticity, hyperreflxia & mass patterns movements, termed as Synergies

CLINICAL MANIFESTATION
3. Alteration in tone

4. Synergy pattern upper extremity Lower extremity 5. Reflexes - altered and vary accdg to the stage recovery - Initially : hypotonia and areflexia - Middle stage of recovery : hyperflexia emerges - Clonus and clasp- knife reflex

CLINICAL MANIFESTATIONS
- (+) babinski - STNR - ATNR - STLR - TLR - soques phenomenon - Raimistes Phenomenon

CLINICAL MANIFESTATIONS
6.

Paresis 7. Incoordination 8. Motor Programming Deficits - ideomotor - ideamotor 9. Functional abilities 10. Speech and language disorder

CLINICAL MANIFESTATIONS
TYPES OF APHASIA

Fluent aphasia Non-fluent aphasia Global aphasia

11. Perceptual deficit 12. Cognitive and behavioral changes 13. Bladder and bowel dysfunction 14. Orofacial dysfunction

SECONDARY IMPAIRMENTS
Psychological problems
Decreasing range of movement,

contracture and deformity Deep venous thrombosis Pain Shoulder dysfunction

SPECIFIC PROBLEMS IN STROKE

Shoulder subluxation
Brachial plexus injury Shoulder hand syndrome Heterotopic ossification

MEDICAL COMPLICATIONS DURING POST-ACUTE STROKE REHAB.

PULMONARY ASPIRATION, PNEUMONIA
UTI MUSCULOSKELETAL PAIN FALLS MALNUTRITION

VENOUS THROMBOEMBOLISM
PRESSURE ULCER

TREATMENT/ MANAGEMENT
Gait training
TENS MOBILIZATION

Heat cold prior to stretching

Oral analgesics For perceptual and communication problems

- directions, picture communication

- Train in specific right and left orientation