Stroke: PT Assessment and Management

STROKE

Dr. L. Surbala (MPT Neuro)

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


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


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


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


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


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


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


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)


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


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


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


• 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


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


• 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


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)


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)


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


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


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.


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




Red flag


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


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.


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.


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


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


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.


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).


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


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


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


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


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


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.


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


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


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


Arousal, Attention & Cognition Expressive and/or receptive aphasia Attention disorders Memory deficits, including

declarative and procedural memory Executive function deficits


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


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


Joint Integrity and Mobility Glenohumeral subluxation Shoulder impingement syndrome Adhesive capsulitis Complex Regional Pain Syndrome and

Shoulder-Hand Syndrome


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


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

apraxia


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


Assistive & Adaptive Devices A sling for Glenohumeral support AFO Cane


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


Circulation (Arterial, Venous & Lymphatic)

Edema may occur in affected limbs May be associated with shoulder

hand syndrome


Ventilation & Respiration• Decrease Tidal volume & vital capacity• Decrease Respiratory muscle strength• Ability to cough & strength of cough is

decreases • Dyspnea during exercise


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


Balance Compromised static as well as

dynamic balance Pusher’s syndrome may be present

resulting in fall on the affected side


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


Functional assessment Using FIM, Barthel index, FMA There is compromised basic as well

as instrumental ADL Ambulatory capacity is compromised


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


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

PT management


Acute stage 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


Post acute stage 5 days a week for a minimum of 3

hours of active rehabilitation per day Intensive rehabilitation if vitals are

stable

PT interventions


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


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


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)


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


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


Postural control & functional mobility

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


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


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


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


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


Improve locomotion 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 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


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


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


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


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


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.

Health & Medicine

Stroke: PT Assessment and Management