Stroke: PT Assessment and 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
Dr. L. Surbala (MPT Neuro)

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

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

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

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

 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

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

 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)

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

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

• 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

• 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)

 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)

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

 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

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

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

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

5. Abnormal synergy

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

Hemispheric Behavioral Differences.

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.

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

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

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

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) aphasiaDr. L. Surbala (MPT Neuro)

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?

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.

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

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

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

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

 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

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

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

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

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

A sling for Glenohumeral support
AFO
Cane

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

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

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

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

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

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

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

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

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

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

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

 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

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

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)

 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

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

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

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

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

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

 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

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

• 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

 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

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

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

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

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.

Stroke: PT Assessment and Management

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