Chapter 15

STROKE
By: Dr Sameen Arshad PT
M.Phil. Physiotherapy
CHAPTER CONTENTS
 Epidemiology and Etiology

 Risk Factors and Stroke Prevention

 Pathophysiology

 Neurologic complications and associated conditions

 Medical Diagnosis of Stroke

 Medical, pharmacological and surgical management of stroke

 Framework for Rehabilitation

 Examination

 Goals and outcomes

 Physical therapy interventions

 Patient client related instruction

 Discharge planning

 Recovery and outcomes

 Summary
 INTRODUCTION
 Stroke or Cerebrovascular Accident (CVA) is the sudden loss of neurological
function caused by an interruption of the blood flow to the brain.
 Ischemic stroke is the most common type, affecting about 80 percent of
individuals with stroke.
 The term hemiplegia is often used generically to refer to the wide variety of
motor problems that result from stroke.
 Changes in the level of consciousness and impairments of sensory, motor,
cognitive, perceptual, and language functions.
 The location and extent of brain injury, the amount of collateral blood flow,
and early acute care management determine the severity of neurological
deficits in an individual patient.
CLASSIFICATION OF
STROKE

Strokes are classified by:

 Etiological categories (thrombosis, embolus, or hemorrhage)
 Specific vascular territory (anterior cerebral artery syndrome, middle
cerebral artery syndrome, and so forth)
 Management categories (transient ischemic attack, minor stroke, major
stroke, deteriorating stroke, young stroke).
EPIDEMIOLOGY
 Stroke is the fourth leading cause of death and the leading cause of
long-term disability among adults in the United States.
 An estimated 7,000,000 Americans older than 20 years of age have
experienced a stroke.
 Each year approximately 795,000 individuals experience a stroke;
approximately 610,000 are first attacks and 185,000 are recurrent
strokes
 The incidence of stroke is about 1.25 times greater for males than
females.
 The incidence of stroke increases dramatically with age, doubling in the
decade after 65 years of age.
ETIOLOGY
 Thrombosis (atherosclerosis)
 Embolism (dislodged thrombus)
 Hemorrhage (hypertension, aneurysm, Arterio-venous malformation)
 Atherosclerosis is a major contributory factor in cerebrovascular
disease.
 It is characterized by plaque formation with an accumulation of lipids,
fibrin, complex carbohydrates, and calcium deposits on arterial walls
that leads to progressive narrowing of blood vessels.
 Interruption of blood flow by atherosclerotic plaques occurs at certain
sites of predilection.
 These generally include bifurcations, constrictions, dilation, or
angulations of arteries.
 The most common sites for lesions to occur are at the origin of the
common carotid artery or at its transition into the middle cerebral artery,
at the main bifurcation of the middle cerebral artery, and at the junction
of the vertebral arteries with the basilar artery.
 Cerebral thrombosis refers to the formation or development of a blood
clot within the cerebral arteries or their branches.
 It should be noted that lesions of extracranial vessels (carotid or vertebral
arteries) can also produce symptoms of stroke.
 Thrombi lead to ischemia, or occlusion of an artery with resulting cerebral
infarction or tissue death (atherothrombotic brain infarction [ABI]).
 Thrombi can also become dislodged and travel to a more distal site in the
form of an intra-artery embolus.
 Cerebral embolus (CE) is composed of bits of matter (blood clot, plaque)
formed elsewhere and released into the bloodstream, traveling to the
cerebral arteries where they lodge in a vessel, produce occlusion and
infarction.
 The most common source of cerebral embolus is disease of the
cardiovascular system.
 Occasionally systemic disorders may produce septic, fat, or air emboli
that affect the cerebral circulation.
 Ischemic strokes may also result from low systemic perfusion, the
result of cardiac failure or significant blood loss with resulting systemic
hypotension.
 The neurological deficits produced with systemic failure are global in
nature with bilateral neurological deficits.
 Hemorrhagic strokes, with abnormal bleeding into the extravascular
areas of the brain are the result of rupture of a cerebral vessel or trauma.
 Hemorrhage results in increased intracranial pressures with injury to
brain tissues and restriction of distal blood flow.
 Intracerebral hemorrhage (IH) is caused by rupture of a cerebral
vessel with subsequent bleeding into the brain. Primary cerebral
hemorrhage (nontraumatic spontaneous hemorrhage) typically occurs
in small blood vessels weakened by atherosclerosis producing an
aneurysm.
 Subarachnoid hemorrhage (SH) occurs from bleeding into the
subarachnoid space typically from a saccular or berry aneurysm
affecting primarily large blood vessels.
 Congenital defects that produce weakness in the blood vessel wall are
major contributing factors to the formation of an aneurysm.
 Hemorrhage is closely linked to chronic hypertension.
 Sudden and severe cerebral bleeding can result in death within hours,
because intracranial pressures rise rapidly and adjacent cortical tissues
are compressed or displaced as in brainstem herniation.
 RISK FACTORS AND STROKE
PREVENTION
 Hypertension, heart disease, and diabetes.
 In patients with ABI, 70 percent have hypertension, 30 percent
coronary heart disease, 15 percent congestive heart disease, 30
percent peripheral arterial disease, and 15 percent diabetes.
 This coexistence of vascular problems increases significantly with
the age of the patient.
 Stroke risk is increased by four to six times in patients with high
blood pressure (elevated above 160/95 mm Hg).
 Cardiovascular risk is also increased with elevated total blood
cholesterol and low density lipoprotein (LDL) cholesterol and is
decreased with higher levels of high-density lipoprotein (HDL)
cholesterol.
 Cardiac disorders such as rheumatic heart valvular disease, endocarditis,
or cardiac surgery (e.g., coronary artery bypass graft [CABG]) increase
the risk of embolic stroke.
 Atrial fibrillation is an independent risk factor with five times an
increased risk of stroke.
 About 10 percent of individuals with TIA will go on to have a major
stroke within 90 days; 5 percent will have a major stroke within 2 days.
 Stroke is largely preventable.
 Potentially modifiable risk factors include smoking, obesity, lack of
exercise, diet, and excess alcohol consumption.
 Dietary recommendations include control of cholesterol and lipids.
 Cessation of cigarette smoking significantly decreases risk as does
reducing obesity and increasing physical activity.
 Control of associated diseases, especially diabetes, hypertension,
and heart disease, is essential.
 As with a cardiac risk profile, the more risk factors present or the
greater the degree of abnormality of any one factor, the greater the
risk of stroke.
 Non modifiable stroke risk factors include age (for adults older than 55
the lifetime risk is 1 in 6), gender (the rate for women is slightly higher
due to the fact that women live longer), race (African-American), and
family history.
 Effective stroke prevention also depends on improving public awareness
concerning the early warning signs of stroke.
 The significance of recognizing early warning signs rests with prompt
initiation of emergency care under the rule that “time is brain.”
 Early computed tomography (CT) is used to differentiate between
atherothrombotic stroke and hemorrhagic stroke.
 If the stroke is atherothrombotic, clot-dissolving enzymes (tissue
plasminogen activator [t-PA], urokinase, or prourokinase) can be
administered.
 To be effective, thrombolytic therapy such as t-PA must be given within
3 hours of the onset of symptoms and cannot be given with hemorrhagic
stroke because the drug may worsen bleeding.
PATHOPHYSIOLOGY
 Interruption of blood flow for only a few minutes sets in motion a series
of pathological events.
 Complete cerebral circulatory arrest results in irreversible cellular
damage with a core area of focal infarction within minutes.
 The transitional area surrounding the core is termed the ischemic
penumbra and consists of viable but metabolically lethargic cells.
 Ischemia triggers a number of damaging and potentially reversible
events, termed ischemic cascade.
 This is followed by excess formation of free radicals.
 The release of excess neurotransmitters (glutamate and aspartate)
produces a progressive disturbance of energy metabolism and anoxic
depolarization.
 This results in an inability of brain cells to produce energy, particularly
adenosine triphosphate (ATP).
 Calcium influx also stimulates the release of nitric oxide and
cytokines.
 Both mechanisms further damage brain cells.
 The extension of the infarction into the penumbra area generally takes
place over a period of 3 to 4 hours.
 Research efforts are ongoing toward development of drugs that might
restore blood supply and reverse the metabolic changes of the ischemic
penumbra area.
 Ischemic strokes produce cerebral edema, an accumulation of fluids
within the brain that begins within minutes of the insult and reaches a
maximum by 3 to 4 days.
 It is the result of tissue necrosis and widespread rupture of cell
membranes with movement of water from the blood into brain tissues.
 The swelling gradually subsides and generally disappears by 2 to 3
weeks.
 Significant edema can elevate intracranial pressures, leading to
intracranial hypertension and neurological deterioration associated with
contralateral and caudal shifts of brain structures (brainstem
herniation).
 Clinical signs of elevating intracranial pressures (ICP) include
decreasing level of consciousness (stupor and coma), widened pulse
pressure, increased heart rate, irregular respirations (Cheyne-Stokes
respirations), vomiting, unreacting pupils (cranial nerve [CN] III signs),
and papilledema.
 Cerebral edema is the most frequent cause of death in acute stroke and
is characteristic of large infarcts involving the middle cerebral artery
and the internal carotid artery.
MANAGEMENT CATEGORIES
 Transient ischemic attack (TIA)
 Temporary interruption of blood supply to the brain.
 Symptoms of focal neurological deficit may last for only a few minutes or
for several hours, but do not last longer than 24 hours.
 No residual brain damage or permanent neurological dysfunction.
 TIAs may result from a number of different etiological factors including
occlusive episodes, emboli, reduced cerebral perfusion (arrhythmias,
decreased cardiac output, hypotension, overmedication with
antihypertensive medications, subclavian steal syndrome) or
cerebrovascular spasm.
 The major clinical significance of TIA is as a precursor to susceptibility for
both cerebral infarction and myocardial infarction.
 Patients are classified as having a major stroke in the presence of
stable, usually severe, impairments.
 The term deteriorating stroke is used to refer to the patient whose
neurological status is deteriorating after admission to the hospital.
 This change in status may be due to cerebral or systemic causes (e.g.,
cerebral edema, progressing thrombosis).
 The category of young stroke is used to describe a stroke affecting
persons younger than the age of 45. Younger individuals may have
potential for better recovery.
 The severity and symptoms of stroke are dependent on a number of
factors, including
i. the location of the ischemic process
ii. the size of the ischemic area,
iii. the nature and functions of the structures involved, and
iv. the availability of collateral blood flow.
 Rapidity of the occlusion of a blood vessel