Stroke - Physiotherapy Treatment - Dr Rohit Bhaskar

©2021 Dr Rohit Bhaskar PT https://www.pt-pedia.com/ 1
STROKE
PHYSIOTHERAPY MANAGEMENT

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

It is defined as the sudden onset of
neurological deficits due to an
with the signs and symptoms lasting
for more than 24 hours or longer

It is defined as the sudden onset of
neurological deficits due to an
with the signs and symptoms lasting
for less than 24 hours
TIA

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
EPIDEMIOLOGY

 Atherosclerosis
©2021 Dr Rohit Bhaskar PT https://www.pt-pedia.com/
 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)
6
ETIOLOGY

 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
colitis)
 Chronic meningitis
 Inflammatory bowel disease (ulcerative and Crohn's
 Hypoglycemia
 Snake bite, fat embolism
7
RARE CAUSES

MODIFIABLE
NON 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
8
RISK FACTORS

 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)
WARNING SIGNS

 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
PATHOPHYSIOLOGY

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

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

• 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

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

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

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

• 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
STAGES OF RECOVERY

• 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

• 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

 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)
MCA

 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)
PCA

 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
ACA

 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
VERT.-BASILAR SYNDROMES

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.

 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
LACUNAR SYNDROMES

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
PRIMARY IMPAIRMENT

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

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

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

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

 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.

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

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

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

 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

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.

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.

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

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.
INDIRECT IMPAIRMENTS

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.

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

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

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.

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

Urine analysis
CBC count
Blood sugar level
Blood cholesterol & lipid
profile
Cardiac evaluation
Lumbar puncture
TESTS

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.

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

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).

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
RECOVER & PROGNOSIS

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

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

 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
A CASE

 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

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?

PT ASSESSMENT

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.
HISTORY

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

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
OBSERVATION

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
VITALS

Expressive and/or receptive aphasia
Attention disorders
Memory deficits, including
declarative and procedural
memory
Executive function deficits
ATTENTION

Visual field deficits
Weakness & sensory loss in
facial musculature
Deficits in laryngeal & pharyngeal
function
Hypoactive gag reflex
Diminished, but perceived,
superficial sensations
CN EXAM

 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
SENSORY EXAM

Glenohumeral subluxation
Shoulder impingement syndrome
Adhesive capsulitis
Complex Regional Pain Syndrome
and Shoulder-Hand Syndrome
JOINT EXAM

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

Synergistic patterns of movement
Hypertonicity
Weakness
Associated movements or synkinesis
Apraxia including motor & verbal
apraxia
MOTOR FUNCTION

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

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
ENDURANCE

Edema may occur in affected limbs
May be associated with shoulder
hand syndrome
LYMPHATIC DRAINAGE

• Decrease Tidal volume & vital
capacity
• Decrease Respiratory muscle
strength
• Ability to cough & strength of cough
is decreases
• Dyspnea during exercise
VENTILATION

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
GAIT & LOCOMOTION

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

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
POSTURE

Using FIM, Barthel index, FMA
There is compromised basic as well
as instrumental ADL
Ambulatory capacity is
compromised
FUNCTIONAL ASSESS.

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

Tonal abnormalities
Muscular weakness
Synergistic pattern
Tightness & contracture
Imbalance &
incoordination
Gait abnormalities
Postural abnormalities
Functional disability
PROBLEM LIST

PT MANAGEMENT

Positioning strategies
Improve respiratory & circulatory
function
Prevent pressure sores
Prevent from deconditioning
ACUTE STAGE

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

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)

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

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

5 days a week for a minimum of 3
hours of active rehabilitation per day
Intensive rehabilitation if vitals are
stable
POST ACUTE STAGE

PT INTERVENTIONS

 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
IMPROVE SENSORY FUNCTION

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
FLEXIBILITY

 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)
IMPROVE STRENGTH

 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
MANAGE SPASTICITY

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
IMPROVE MOVT CONTROL

Suggested exercise
• Rolling
• Supine to sit & sit to supine
• Sitting
• Bridging
• Sit to stand & Sit down
• Modified plantigrade
• Standing
• Transfer
POSTURAL CONTROL

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

• 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
IMPROVE UE FUNCTION

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
MANAGE SHOULDER PAIN

 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
IMPROVE LL FUNCTION

 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
IMPROVE BALANCE

Initial gait training between
parallel bars
Proceed outside bars with aids & then
without aids
Walking forward, backward, sideways
& in cross patterns
PBWSTT with higher speed improve
overall locomotor activity &
overground speed
Proper use of orthotics & wheelchair
IMPROVE LOCOMOTION

• 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
IMPROVE AEROBIC FUNCTION

 Proper head position in chin down position
 Movements of lips, tongue, cheeks, & jaw
 Firm pressure to anterior 3rd oftongue
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
IMPROVE FEEDING

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
IMPROVE MOTOR LEARNING

 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
PATEINT & FAMILY EDU.

 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
DISCHARE

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.
REFERENCES

Stroke - Physiotherapy Treatment - Dr Rohit Bhaskar

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