The document provides a comprehensive overview of stroke, highlighting its definition as an acute neurological dysfunction resulting from cerebral circulation abnormalities, with lasting deficits. It covers epidemiology, risk factors, types of strokes (hemorrhagic and ischemic), symptoms, pathophysiology, classification, stages of recovery, and rehabilitation considerations. Additionally, it discusses diagnostic methods, prognosis, and a specific patient case study to illustrate the clinical implications.

1. STROKE
Dr. Madhu S M

2. Introduction
Stroke is an acute onset of neurological
dysfunction due to an abnormality in
cerebral circulation with resultant signs
& symptoms which corresponds to
involvement of focal areas of the brain

3. Acc. To who
It is defined as the sudden onset of
neurological deficits due to an
abnormality in cerebral circulation with
the signs and symptoms lasting for more
than 24 hours or longer

4. Transient ischemic attack
It is defined as the sudden onset of
neurological deficits due to an
abnormality in cerebral circulation with
the signs and symptoms lasting for less
than 24 hours

5. Epidemiology
Third leading cause of death
The incidence of stroke is about 1.25
times greater for males than females
Most common cause of disability among
adults

6. Etiology
Atherosclerosis
Cerebral Thrombus
Cerebral embolus
Embolism from the heart (cardiac origin)
Intracranial hemorrhage
Subarachnoid hemorrhage
Intracranial small vessel disease
Arterial aneurysms
Arterio-venous malformation
Haematological disorders (haemoglobinopathies,
leukemia)
Atherothromboembolism

7. Miscellaneous rare causes of
stroke
 Infective endocarditis & HIV infection
 Tumour
 Perioperative stroke (due to hypotension and boundary
zone infarction, trauma to and dissection of neck arteries, paradoxical
embolism, fat embolism, infective endocarditis)
 Migraine
 Chronic meningitis
 Inflammatory bowel disease (ulcerative and Crohn's
colitis)
 Hypoglycemia
 Snake bite, fat embolism

8. Risk factors
NON MODIFIABLE
MODIFIABLE
 Ageing & gender
 Positive family history
 Circadian and seasonal
factors (peaks between 10
am till noon)
 Heart disease
 Diabetes mellitus
 Hypertension
 Peripheral arterial disease
 Blood pathology (increased
haematocrit, clotting
abnormalities, sickle cell
anaemia etc)
 Hyperlipidemia
 TIA
 Smoking
 Obesity
 Lack of physical exercise
or sedentary life style
 Diet & excess alcohol
consumption
 Oral contraceptives
 Infection (meningeal
infection)
 Psychological factors
 Vasectomy

9. warning signs of stroke
 Sudden numbness or weakness of face, arm, or leg, on
one side of body
 Sudden confusion, trouble speaking or understanding
 Sudden blurring of vision
 Sudden onset of dizziness, loss of balance or
coordination
 Sudden, severe headaches with no known cause
 Other important but less common stroke symptoms
include:
• Sudden nausea, fever, & vomiting distinguished from a viral illness
by speed of onset (minutes or hours vs several days)
• Brief loss of consciousness or a period of decreased
consciousness (fainting, confusion, convulsions, or coma)

10. Pathophysiology
 Ischemia results in irreversible cellular
damage with a core area of focal
infarction within minutes
• Transitional area surrounding core is termed
ischemic penumbra & consists of viable but
metabolically lethargic cells
 Ischemia produce cerebral edema, that
begins within minutes of insult & reaches
a maximum by 3 to 4 days.
 Swelling gradually subsides & generally
disappears by 2 to 3 weeks

11. Oedema elevates ICP, leading to
intracranial HT & neurological
deterioration associated with
contralateral & caudal shifts of brain
structures
Cerebral edema is the most frequent
cause of death in acute stroke & is
characteristic of large infarcts involving
MCA & ICA

12. Classification
Depending on the cause
• Haemorrhagic stroke
 Intracranial haemorrhage
 Subarachnoid haemorrhage
 Signs of raised ICP will be evident with a history of a
traumatic accident

13. • Ischemic stroke
 Thrombotic: more common. Usually occurs in the
sleeping hours. Characterised by gradual onset of
symptoms
 Embolic: Occurs in the waking hours of the day.
Sudden onset of symptoms preceded by giddiness in
most conditions

14. Depending on the severity
• Mild stroke: symptoms subside with no deficit
in a week period
• Moderate stroke: symptoms recover in a period
of 3 - 6 months with minimal neurological
deficit
• Severe stroke: there is no complete recovery
of the symptoms even after 1 years. Always
ends up with severe neurological deficit

15. Depending on the duration
• Acute stroke: to a period of one week or until
spasticity develops
• Sub acute stroke: after the development of
spasticity & last for a period of 3-12 months
• Chronic stroke: more than 12 months

16. Depending on the symptoms
• MCA Syndrome
• ACA Syndrome
• PCA syndrome
• Vertebro basilar artery syndrome
 Vertebral artery
 Basilar artery
 Internal carotid artery
• Lacunar syndrome

17. stages of recovery
• Stage 1: recovery occurs in a stereotyped
sequence of events that begins with a period of
flaccidity immediately following acute episode.
No movement of limbs can be elicited
• Stage 2: basic limb synergies or some of their
components may appear as associated reactions.
Minimal voluntary movement may be present.
Spasticity begins to develop

18. • Stage 3: Gains voluntary control of movement
synergy although full range is not developed.
Spasticity has further increased
• Stage 4: some movement combination that do
not follow the synergy are mastered first with
difficulty & later with more ease. Spasticity
begins to decline

19. • Stage 5: more difficult movement are learnt as
the basic limb synergy lose their dominance
over motor roots. Spasticity further declines
• Stage 6: disappearance of spasticity, individual
joint movement become possible & coordination
approaches normal. Normal motor function is
restored

20. mca
 Contralateral hemiplegia (UL & face more
affected than LL)
 Contralateral hemisensory loss (UL & face more
affected than LL)
 Ideomotor apraxia
 Ataxia of contralateral limb
 Contralateral Homonymous hemianopia
 Left hemisphere infarction
• Contralateral neglect
• Possible contralateral visual field deficit
• Aphasia: Broca’s (expressive) or Wernicke’s (receptive)

21. pca
 Coordination disorders such as tremor or ataxia
 Contralateral homonymous field deficit
 Cortical blindness
 Cognitive impairment including memory
impairment
 Contralateral sensory impairment
 Thalamic syndrome (abnormal sensation of severe
pain from light touch or temperature changes)
 Weber’s syndrome (contralateral hemiplegia &
third nerve palsy)

22. aca
Contralateral Hemiplegia or monoplegia of
LL (LL more affected than UL)
Contralateral sensory loss of LL
Urinary incontinence
Problems with imitation & bimanual task
Abulia (akinetic mutism)
Apraxia
Amnesia
Contralateral grasp reflex, sucking reflex

23. Vertibro-Basilar artery syndromes
 Medial medullary syndrome (vertebral artery)
 Lateral medullary (Wallenberg's) syndrome
(PICA)
 Complete basilar artery syndrome (locked-in
syndrome)
 Medial inferior pontine syndrome
 Lateral inferior pontine syndrome (AICA)
 Medial midpontine syndrome
 Lateral midpontine syndrome
 Medial superior pontine syndrome
 Lateral superior pontine syndrome

24. Locked-in syndrome (LIS)
• Acute hemiparesis rapidly progressing to
tetraplegia & lower bulbar paralysis (CN V
through XII are involved)
• Initially patient is dysarthria & dysphonic &
progresses to mutism (anarthria)
• There is preserved consciousness & sensation
• Horizontal eye movements are impaired but
vertical eye movements & blinking remain intact.
• Communication can be established via these eye
movements.

25. Lacunar syndrome
 Caused by small vessel disease of deep white
mater
• Pure motor lacunar stroke: posterior limb of internal
capsule, pons, & pyramids
• Pure sensory lacunar stroke: ventrolateral thalamus or
thalamocortical projections
 Ataxic hemiparesis
 Dysarthria
 Clumsy hand syndrome
 Sensory/motor stroke
 Dystonia/involuntary movements

28. Red flag

29. Primary impairment
1. Altered sensation
• Pain (central pain or thalamic pain syndrome
characterized by constant, severe burning pain
with intermittent sharp pains
• Hyperalgesia
• Loud sound, bright light etc. may trigger pain

30. 2. Vision
• Homonymous hemianopia, a visual field defect,
occurs with lesions involving the optic radiation
(MCA) or to primary visual cortex (PCA)
• Visual neglect & problems with depth
perception, and spatial relationships

31. 3. Weakness
• Usually seen in the contralateral side of the
lesion
• MCA stroke are more common so weakness is
largely seen in the UL in clinical practice
• Distal muscle are more affected than proximal
muscles
• Mild weakness of ipsilateral side

32. 4. Alteration of tone
• Flaccidity (hypotonicity) is present immediately
after stroke
• Spasticity (hypertonicity) emerges in about 90
percent of cases

33. 5. Abnormal synergy

34. Muscles not involved in either synergy
• Latissimus dorsi
• Teres major
• Serratus anterior
• Finger extensors
• Ankle evertors

35. 6. Abnormal reflexes
• Initially, hyporeflexia with flaccidity & later
hyperreflexia
• May demonstrate clonus, & +ve Babinski
• Movement of head or position of body may elicit a
change in tone or movement of extremities
 The most commonly seen is asymmetric tonic neck reflex
(ATNR)
• Associated reactions are also present in patients who
exhibit strong spasticity and synergies
 unintentional movements of hemiparetic limb caused by
voluntary action of another limb
 by stimulation of yawning, sneezing, or coughing.

36. 7. Altered co ordination
• Proprioceptive losses can result in sensory
ataxia
• Strokes affecting cerebellum typically produce
cerebellar ataxia (e.g.basilar artery syndrome,
pontine syndromes) & motor weakness.
• Basal ganglia involvement (PCA syndrome) may
lead to bradykinesia or involuntary movements

37. 8. Altered motor programing
• Motor praxis is ability to plan & execute
coordinated movement
• Lesions of premotor frontal cortex of either
hemisphere, left inferior parietal lobe, & corpus
callosum can produce apraxia.
• Apraxia is more evident with left hemisphere
damage than right and is commonly seen with
aphasia.
 Ideational apraxia
 Ideomotor apraxia

38. 9. Postural Control & Balance
• Impairments in steadiness, symmetry, & dynamic
stability
• Problems may exist when reacting to a
destabilizing external force (reactive postural
control) or during self-initiated movements
(anticipatory postural control).
• Pusher syndrome: characterized by active pushing
with stronger extremities toward affected side,
leading to lateral postural imbalance

39. 10. Speech, Language, and Swallowing
• Lesions involving cortex of dominant hemisphere
• Aphasia: impairment of language comprehension,
formulation, and use.
• Dysarthria: motor speech disorders caused by
lesions of CNS or PNS that mediate speech
production.
• Dysphagia, occurs with lesions affecting medullary
brainstem (CN IX and X), large vessel pontine
lesions, as well as in acute MCA and PCA lesion

40. 11. Perception and Cognition
• They are the result of lesions in right parietal
cortex & seen more with left hemiplegia than
right.
• These may include disorders of body
scheme/body image, spatial relations, and
agnosias.

41. 12. Emotional Status
• Lesions of brain affecting frontal lobe,
hypothalamus, & limbic system
• May demonstrate pseudobulbar affect (PBA),
also known as emotional lability or emotional
dysregulation syndrome.
 emotional outbursts of uncontrolled or exaggerated
laughing or crying that are inconsistent with mood.
• Depression is extremely common
 persistent feelings of sadness,feelings of
hopelessness, worthlessness or helplessness.

42. 13. Bladder and Bowel Function
• Disturbances of bladder function are common
during acute phase
• Urinary incontinence can result from bladder
hyperreflexia or hyporeflexia, disturbances of
sphincter control, or sensory loss.
• Disturbances of bowel function can include
incontinence & diarrhea or constipation

43. Hemispheric Behavioral Differences.

44. Indirect Impairments
1. Musculoskeletal changes
• Loss of voluntary movement and immobility can
result in loss of ROM & contractures.
 Contractures are apparent in spastic muscles of
paretic limbs
• Disuse atrophy & muscle weakness results from
inactivity and immobility
• Osteoporosis, results from decreased physical
activity, changes in protein nutrition, hormonal
deficiency, & calcium deficiency.

45. 2. Neurological signs
• Seizures occur in a small % of patients - more
common in occlusive carotid disease than in
MCA disease
• Hydrocephalus is rare but can occur with
subarachnoid or intracerebral hemorrhage.

46. 3. Thrombophlebitis & deep venous
thrombosis (DVT)
• complications for all immobilized patients.

47. 4. Cardiac Function
• Stroke as a result of underlying coronary
artery disease (CAD) may demonstrate
impaired CO, cardiac decompensation, & rhythm
disorders.
• If these problems persist, they can alter
cerebral perfusion & produce additional focal
signs (e.g., mental confusion).
• Cardiac limitations in exercise tolerance

48. 5. Pulmonary Function
• Decreased lung volume, decreased pulmonary
perfusion & vital capacity & altered chest wall
excursion
• Aspiration, occurs in about one third of
patients with dysphagia.

49. 6. Integumentary
• The skin breaks down over bony prominences
from pressure, friction, shearing, and/or
maceration

50. Tests and Measures
Urine analysis
CBC count
Blood sugar level
Blood cholesterol & lipid profile
Cardiac evaluation
Lumbar puncture

51. Imaging
CT Scan
• In acute phase, CT scans are used to rule out
brain lesions such as tumor or abscess & to
identify hemorrhagic stroke
• In sub-acute phase, CT scans can identify
development of cerebral edema (within 3 days)
& cerebral infarction (within 3 to 5 days) by
showing areas of decreased density.

52. Magnetic Resonance Imaging (MRI).
• MRI is more sensitive in diagnosis of acute
strokes, allowing detection of cerebral
infarction within 2 to 6 hours after stroke.
• It is also able to detail extent of infarction or
hemorrhage & can detect smaller lesions

53. Cerebral Angiography.
• Involves injection of radiopaque dye into blood
vessels with subsequent radiography.
• It provides visualization of vascular system and
used when surgery is considered (carotid
stenosis, AVM).

54. Recovery and Prognosis
Fastest in first weeks after onset
Measurable neurological & functional
recovery occurring in first month after
stroke.
Continue to make measurable functional
gains for months or years after insult

55. Late recovery of function is also seen in
patients with chronic stroke who
undergo extensive functional training
• These changes are due to function-induced
plasticity

56. Variation of recovery
Recovery also depends on severity of
stroke
Depends on type of stroke –
hemorrhagic or ischemic
Varies from individual to individual
Depends on intensity of therapy
Depends on age of the patient

57. A case
A male patient with a known case of
hypertension came to emergency
department with history of sudden
collapse & LOC
On examination there is decrease DTR
on right side of body with +ve Babinski’s
sign
There is gradual regain of consciousness
but seems to be confused

58. After a few days in hospital he regain
some of his LL movement but less
improvement in UL
On careful examination he has right
Homonymous hemianopia & sensory loss
including two-point discrimination,
texture, & sense of weight
He also has unilateral neglect & Broca’s
(expressive) aphasia

59. What is the condition?
What may be the cause?
What emergency investigation is called
for ?
Which artery may be involved?
Which areas of the brain is involved?

60. PT assessment

61. History
Abrupt onset with rapid coma is
suggestive of cerebral hemorrhage.
Severe headache typically precedes LOC
Embolus also occurs rapidly, with no
warning, & is frequently associated with
heart disease or heart complications.
Uneven onset is typical with thrombosis.

62. Past history include TIAs or head
trauma, presence of major or minor risk
factors, medications, positive family
history, & recent alterations in patient
function

63. Observation
May have abnormal posturing of limbs
Synergistic patterns in the UL & LL
Facial asymmetry
May use a walking aid E.g. cane
Abnormal gait pattern may also be
observed

64. Vitals
May present with hypertension
Pain
 Shoulder pain, secondary to subluxation, is a common
issue
 Shoulder-hand syndrome involves swelling &
tenderness in hand and pain in entire limb
 Complex Regional Pain Syndrome involves pain &
swelling of hand

65. Arousal, Attention & Cognition
Expressive and/or receptive aphasia
Attention disorders
Memory deficits, including declarative
and procedural memory
Executive function deficits

66. Cranial Nerve Integrity
Visual field deficits
Weakness & sensory loss in facial
musculature
Deficits in laryngeal & pharyngeal function
Hypoactive gag reflex
Diminished, but perceived, superficial
sensations

67. Sensory integrity
 Hemi sensory loss (dysesthesia, or hyperesthesia,
joint position & movement sense)
 May be able to identify sensations but difficulty in
localizing
 Cortical sensations s/a 2 point discrimination,
stereognosis & graphaesthesia are affected
secondary to loss of grip function
 Agnosia
 Perceptual problems
 Unilateral spatial neglect
 Pusher syndrome

68. Joint Integrity and Mobility
Glenohumeral subluxation
Shoulder impingement syndrome
Adhesive capsulitis
Complex Regional Pain Syndrome and
Shoulder-Hand Syndrome

69. Range of Motion
Soft tissue shortening and contractures
Increased muscle stiffness
Joint immobility
Disuse-provoked soft tissue changes
Over extensibility of capsular
structures of Glenohumeral joint

70. Motor Function
Synergistic patterns of movement
Hypertonicity
Weakness
Associated movements or synkinesis
Apraxia including motor & verbal apraxia

71. Reflex Integrity
Exaggerated deep tendon reflexes
Diminished superficial reflexes
Positive Babinski’s reflex
Impaired Righting, equilibrium, and
protective reactions
Abnormal primitive reflex (ATNR) may
be present

72. Assistive & Adaptive Devices
A sling for Glenohumeral support
AFO
Cane

73. Aerobic Capacity/Endurance
BP, RR, & HR at rest & during exercise
may have a sudden rise
Review pulse oximetry, blood gas, tidal
volume, & vital capacity
Administer a 2 or 6-minute walk test
Administer Borg RPE after walk test or
other physical activity

74. Circulation (Arterial, Venous &
Lymphatic)
Edema may occur in affected limbs
May be associated with shoulder hand
syndrome

75. Ventilation & Respiration
• Decrease Tidal volume & vital capacity
• Decrease Respiratory muscle strength
• Ability to cough & strength of cough is
decreases
• Dyspnea during exercise

76. Gait & Locomotion
Decreased extension of hip &
hyperextension of knee
Decreased flexion of knee & hip during
swing phase
Decreased ankle DF at initial contact &
during stance resulting in hip
circumduction
Trendelenburg

77. Balance
Compromised static as well as dynamic
balance
Pusher’s syndrome may be present
resulting in fall on the affected side

78. Posture
Spastic patterns can involve flexion &
abduction of arm, flexion of elbow, &
supination of elbow with finger flexion
Hip & knee extension with ankle
plantarflexion & inversion
Protracted & depressed shoulder,
scoliosis & hip hiking

79. Functional assessment
Using FIM, Barthel index, FMA
There is compromised basic as well as
instrumental ADL
Ambulatory capacity is compromised

80. Bowel & bladder
Flaccid bowel & bladder during the acute
stage
Bowel & bladder function gradually
regains
Uninhibited bladder if frontal lobe is
involved
Constipation is frequently seen

81. Problem list
Tonal abnormalities
Muscular weakness
Synergistic pattern
Tightness & contracture
Imbalance & incoordination
Gait abnormalities
Postural abnormalities
Functional disability

82. PT management

83. Acute stage
Positioning strategies
Improve respiratory & circulatory
function
Prevent pressure sores
Prevent from deconditioning

84. Positioning strategies
• In supine
• In side lying on normal side
• In side lying on affected side

86. Improve respiratory & circulatory
function
• Breathing exercise
• Chest expansion exercise
• Postural drainage
• Huffing & Coughing techniques
• Passive & active ankle & toe exercise
 (after careful & thorough examination of
cardiopulmonary system)

87. Prevent pressure sores
• Proper positioning
• Relieve pressure points by padding & cushion
• Frequent turning & changing position
• Prevent from moisture
• Use cotton clothing
• Tight fitting cloth is prevented
• Use of water bed, air bed & foam mattress

88. Prevent from deconditioning
• Early mobilization in the bed (active turning,
supine to sit, sit to supine, sitting, sit to stand)
• Pelvic bridging exercise
• Early propped up positioning, sitting & then
later to standing
• Moving around the bed
• Facilitate movement of functioning limbs

89. Post acute stage
5 days a week for a minimum of 3 hours
of active rehabilitation per day
Intensive rehabilitation if vitals are
stable

90. Improve sensory function
 Positioning hemiplegic side towards door or main
part of room
 Presentation of repeated sensory stimuli
 Stretching, stroking, superficial & deep pressure,
iceing, vibration etc.
 Wt bearing ex & Joint approximation tech
 Stoking with different texture fabrics
 Pressure application
 Improve other senses like use of visual & auditory
 PNF tech., use of bilateral UE

91. Flexibility & joint integrity
Soft tissue, joint mobilization & ROM
exercise
AROM & PROM with end range stretch
Effective positioning & edema reduction
Stretching program & splinting
Suggested activities
• Arm cradling
• Table top polishing
• Self overhead activities in supine & sitting &
reaching to the floor

92. Improve strength
Strengthening of agonist & antagonistic
muscle
Graded ex program using free weights,
therabands, sand bags & isokinetic devices
For weak patients (<3/5), gravity-
eliminated ex using powder boards, sling
suspension, or aquatic ex is indicated
Gravity-resisted active movts are
indicated (>3/5 strength)

93. Manage spasticity
 Sustained stretch & slow iceing of spastic muscle
 Rhythmic rotations
 Weight bearing exercise
 Prolonged & firm pressure application
 Slow rocking movement
 Positioning in anti synergistic pattern
 Rhythmic initiation
 Air splints
 Neural warmth
 Electrical stimulation

94. Improve movt control
Dissociation & selection of desired movt
patterns
Select postures that assist desired
movements through optimal biomechanical
stabilization & use of optimal point in
range
Start with assisted movt, followed by
active & resisted movt
Task oriented exercise

95. Postural control & functional
mobility
Suggested exercise
• Rolling
• Supine to sit & sit to supine
• Sitting
• Bridging
• Sit to stand & Sit down
• Modified plantigrade
• Standing
• Transfer

96. In pusher syndrome
• Passive correction often fails
• Use visual stimuli to correct
• Sit on the normal side & ask patient to lean on
you
• Sitting on swiss ball
• Environmental boundary can be used e.g. corner
or doorway

97. Improve ue function
• Early mobilization, ROM, & positioning strategies
• Relearning of movt pattern & retraining of missing
component
• UL weight bearing exercise
• Dynamic stabilization exercise
• Picking up objects, Reaching activities
• Lifting activities
• Manipulation of common objects
• Push up ex. in various position
• Kitchen sink exercise
• Functional movement like hand to mouth & hand to opposite
shoulder
• Advance training – CIMT, biofeedback, NMES, FES

98. Managing shoulder pain
Proper handling & positioning of shoulder
joint
Reducing subluxation, NMES, gentle
mobilization (grade 1 & 2)
Use of supportive devices & slings
Use of overhead pulley is contraindicated
TENS & heat therapy

99. Improve LL function
Strengthening muscles in appropriate
pattern
Suggested activities
• PNF pattern of LL
• Holding against elastic band resistance around
upper thighs in supine or standing positions
• Standing, lateral side-steps
• Exercise to improve pelvic control
Facilitation of DF
Cycling & treadmill training

100. Improve balance
 Facilitate symmetrical wt bearing on both side
 Postural perturbations can be induced in different
positions
 Sit or stand on movable surface to increase
challenge
 Reaching activities
 Dual task training s/a kicking ball in standing,
throwing activities, carrying an object while walking
 Divert attention
 Single limb stance
 Exercise on trampoline

101. Improve locomotion
 Initial gait training between parallel bars
 Proceed outside bars with aids & then
without aids
 Walking forward, backward, sideways & in
cross patterns
 PBWSTT (partial body weight support
treadmill training) with higher speed improve
overall locomotor activity & overground
speed
 Proper use of orthotics & wheelchair

102. Improve aerobic function
• Early mobilization & functional activity
• Treadmill training & cycle ergometer
• Symptom limited graded ex. training
• Ex at 40- 70 % of VO2max, 3 times a week for
20-60 minutes
• Proper rest should be given
• Gradually progressed to 30 minutes continous
program
• Regular ex reduces risk of recurrent stroke

103. Improve feeding & swallowing
 Proper head position in chin down position
 Movements of lips, tongue, cheeks, & jaw
 Firm pressure to anterior 3rd
of tongue with tongue
depressor to stimulate posterior elevation of tongue,
 Puffing, blowing bubbles, & drinking thick liquids
through straw
 Food presentation in proper position
 Texture of food should be smooth
 Tasty food should be given to facilitate swallowing
reflex
 Stroking the neck during swallowing

104. Improve motor learning
Strategy development
• Patient as an active explorer of activity
• Modify strategy of activity in correct patterns
Feedback
• Intrinsic or extrinsic feedback
• Positive & negative feedbacks
Practice
• Repeated practice of functional activity
• Practice in different environment

105. Patient & family education
Give factual information, counsel family
members about patient’s capabilities &
limitations
Give information as much as Pt or family can
assimilate
Provide open discussion & communication
Be supportive, sensitive & maintain a positive
supporting nature
Give psychological support
Refer to help groups

106. Discharge planning
Family member should participate daily
in the therapy session & learn exercises
Home visits should be made prior to
discharge
Architectural modifications, assistive
devices or orthotics should be ready
before discharge
Identify community service & provide
information to the patient

107. References
O’ Sullivan SB, Schmitz TJ. Stroke.
Physical rehabilitation. 5th
ed., New
Delhi: Jaypee Brothers, 2007.
Darcy A. Umphred. Neurological
Rehabilitation, 5th
ed., Mosby Elsevier,
Missouri, 2007.