physically therapy

1. Stroke Rehabilitation
Prepared by
Dr/Mohammed Alshehari

2. Topics
• EPIDEMIOLOGY AND ETIOLOGY
• RISK FACTORS AND STROKE PREVENTION
• PATHOPHYSIOLOGY
• CLINICAL MANIFESTATIONS OF STROKE.
• NEUROLOGICAL COMPLICATIONS AND
ASSOCIATED CONDITIONS
• PHYSICAL THERAPY INTERVENTIONS

3. • Stroke (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% of individuals with stroke, and results
when a clot blocks or impairs blood flow, depriving the brain
of essential oxygen and nutrients. Hemorrhagic stroke occurs
when blood vessels rupture, causing leakage of blood in or
around the brain.

4. EPIDEMIOLOGY AND ETIOLOGY
• Stroke is the fourth leading cause of death and the leading
cause of long-term disability among adults in the United
States. The incidence of stroke increases dramatically with
age, doubling in the decade after 65 years of age. Twenty-
eight percent of strokes occur in individuals younger than 65
years of age. hemorrhagic stroke accounts for the largest
number of deaths, with mortality rates of 37% to 38% at
1month ischemic strokes have a mortality rate of only 8% to
12% at 1 month.

5. EPIDEMIOLOGY AND ETIOLOGY (con’t)
• Atherosclerosis
• Cerebral thrombosis
• cerebral infarction
• Cerebral embolus (CE)
• Intracerebral hemorrhage (IH)
• cerebral hemorrhage
• Aneurysm
• Subarachnoid hemorrhage
• Arteriovenous malformation (AVM)

6. RISK FACTORS AND STROKE
PREVENTION
• Cardiovascular diseases
• hypertension,
• heart disease (HD),
• disorders of heart rhythm,
• diabetes mellitus (DM).
• (hypercholesterolemia) low-density lipoprotein (LDL [“bad”])
• 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.

7. RISK FACTORS AND STROKE
PREVENTION (con’t)
• Modifiable risk factors include cigarette smoking, physical
inactivity, obesity, and diet.
• Lifestyle changes can greatly reduce the risk of stroke
• Recommendations include controlling BP, diet (cholesterol
and lipids), weight loss, quitting smoking, and
• increasing physical activity, as well as effective disease
management

8. PATHOPHYSIOLOGY
• Sudden cessation of cerebral blood flow and oxygen glucose
deprivation sets in motion a series of pathological events.
Within minutes neurons die within the ischemic core tissue,
while the majority of neurons in the surrounding penumbra
survive for a slightly longer time. Cell survival depends
largely on the severity and the duration of the ischemic
episode. The release of excess neurotransmitters (e.g.,
glutamate and aspartate) produces a progressive
disturbance of energy metabolism and anoxic depolarization

9. PATHOPHYSIOLOGY (con’t)
• This results in an inability of brain cells to produce energy,
particularly adenosine triphosphate (ATP). This results in an
inability of brain cells to produce energy, particularly
adenosine triphosphate (ATP). This is followed by excess
influx of calcium ions and pump failure of the neuronal
membrane

10. PATHOPHYSIOLOGY (con’t)
• 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 fluid from the blood into brain tissues.
The swelling gradually subsides and generally disappears by
2 to 3 weeks

11. PATHOPHYSIOLOGY (con’t)
• 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 pressure (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.

12. Clinical Manifestations of Anterior
Cerebral Artery Syndrome
 Contralateral hemiparesis involving mainly the LE (UE is
more spared)
 Contralateral hemisensory loss involving mainly the LE (UE is
more spared)
 Urinary incontinence
 Problems with imitation and bimanual tasks, apraxia
 Abulia (akinetic mutism), slowness, delay, lack of
spontaneity, motor inaction
 Contralateral grasp reflex, sucking reflex Can be
asymptomatic if circle of Willis is competent

13. Clinical Manifestations of Middle
Cerebral Artery Syndrome
 Contralateral hemiparesis involving mainly the UE and face (LE is more
spared)
 Contralateral hemisensory loss involving mainly the UE and face (LE is
more spared)
 Motor speech impairment: Broca’s or nonfluent aphasia with limited
vocabulary and slow, hesitant speech
 Receptive speech impairment: Wernicke’s or fluent aphasia with
impaired auditory comprehension and fluent speech with normal rate
and melody Global aphasia: nonfluent speech with poor comprehension
 Perceptual deficits: unilateral neglect, depth perception, spatial
relations, agnosia Limb-kinetic apraxia
 Contralateral homonymous hemianopsia Loss of conjugate gaze to the
opposite side
 Ataxia of contralateral limb(s) (sensory ataxia) Pure motor hemiplegia
(lacunar stroke)

14. Clinical Manifestations of Posterior
Cerebral Artery Syndrome
• Contralateral homonymous Hemianopsia
 Visual agnosia
 Prosopagnosia (difficulty naming people on sight) Dyslexia
(difficulty reading) without agraphia (difficulty writing),
color naming (anomia), and color discrimination problems
 Memory defect
 Contralateral hemiplegia
 Oculomotor nerve palsy

15. Clinical Manifestations of
Vertebrobasilar Artery Syndrome
• Medial medullary syndrome :
 Ipsilateral to lesion Paralysis with atrophy of half the tongue
with deviation to the paralyzed side when tongue is
protrudeddrome .
 Contralateral to lesion :Paralysis of UE and LE
 Impaired tactile and proprioceptive sense

16.  Complete basilar artery syndrome (locked-in syndrome) :
 Tetraplegia (quadriplegia)
 Bilateral cranial nerve palsy: upward gaze is spared
 Coma
 Cognition is spared

17. Neurological complications and associations
conditions
• Altered Consciousness(coma, decreased arousal levels)
• Disorders of Speech and Language
• Dysphagia
• Cognitive Dysfunction
• Multi-infarct dementia
• Delirium
• Altered Emotional Status

18. • Hemispheric Behavioral Differences
• Perceptual Dysfunction
• Bladder and Bowel Dysfunction
• Cardiovascular and Pulmonary Dysfunction
• Seizures
• Deep Venous hrombosis and
• Pulmonary Embolus

19. Physical therapy interventions
• Strategies to improve motor learning
 Mental practice or mental rehearsal is the systematic
application of imagery techniques for improving
performance and learning.( During early motor learning the
therapist provides extrinsic feedback (e.g., verbal cueing,
manual cueing), and manual guidance to shape
performance)
 Mirror therapy (MT) is a therapeutic intervention that
focuses on moving the less impaired limb while watching its
mirror reflection

20. • Interventions to improve sensory
 Mirror therapy for improving detection of light touch,
pressure, and temperature pain
 Thermal stimulation intervention for improving rate of
recovery of sensation
 Intermittent pneumatic compression for improving tactile
and kinesthetic sensation

21. • Interventions to improve hemianopsia and
unilateral neglect
 visual, verbal, or motor cues
 Imagine you are a lighthouse beam; use your beam to sweep
and scan the floor from one side to the other reaching
 activities or PNF chop or lift patterns

22. • Interventions to improve flexibility and joint
integrity:
 Soft tissue/joint mobilization and ROM exercises
 Positioning strategies are also important in maintaining soft
tissue length

23. • Interventions to improve strength:
• Progressive resistive strength training
• Combining resistance training

24. • Interventions to manage spasticity:
 early mobilization and daily stretching to maintain the
length of spastic muscles and soft tissues and promote
optimal positioning
 Modalities can be used to treat spasticity. These include the
application of cold, massage, and electrical stimulation.
 Orthotic devices

25. • Interventions to improve movement control:
 voluntary movement control
 postural control,

26. • Interventions to improve functional status:
 Bed Mobility
 Sitting
 Sit-to-Stand and Sit-Down
 Transfers
 Standing Transfers

27. • Interventions to improve gait
and locomotion:
walkers, hemi walkers, quad canes
Walking forward
Walking backward
Side stepping
Crossed stepping
Step-up/step-down activities;
 lateral step-ups.