CEREBROVASCULAR ACCIDENT

I. General Medical Background

A. Definition
- stroke in layman's term
- sudden focal neurologic deficit characterized by loss of motor
control, altered sensation, cognitive or language impairment &
disequilibrium or coma caused by non-traumatic brain injury resulting
from rupture or occlusion of cerebral blood vessels
B. Classification
1. Transient Ischemic Attack (TIA)
- temporary interruption of blood supply to the brain producing
symptoms of focal neurologic deficit, which lasts for a few
minutes to several hours but not > 24 hrs.
2. Reversible Ischemic Neurological Deficit (RIND)
- etiology: unknown
- likely to result from small infarctions of the deep subcortical
gray and white matter, resulting in only temporary impairment
3. Stroke In Evolution (Deteriorating Stroke)
- an unstable ischemic event characterized by progressive
development of more neurologic impairment
- often associated with occlusive thrombosis of major cerebral
artery
4. Completed Stroke
- characterized by presence of stable, usually severe deficits
C. Epidemiology
- the most serious neurological problem in the United States
- 2nd only to head trauma as the leading cause of neurological
disability
- 3rd most common cause of death in the Western world behind heart
disease and cancer
- incidence rises with increasing age; primarily a disease of older
individuals but 25% occurs in persons younger than 65 years old
- men > women
D. Etiology
1. Extrinsic Causes problem is from outside the brain
1.1 Emboli
- comprises 30% of all stroke cases
- sudden in onset and usually lodges on small caliber
distal arteries in the brain
1.2 Decreased perfusion pressure or increased blood viscosity
with inadequate cerebral blood flow (CBF)
1.3 Trauma that interrupts the blood flow to the brain
2. Intrinsic Causes problem originates from the blood vessels of the
brain or from the brain itself
2.1 Thrombosis
- most common cause of stroke
- blood clot on the walls within the cerebral arteries and
their branches
2.2 Lipohyalinosis
- chronic process resulting from severe hypertension
- small arteries become damaged in the process and
become thickened, hyalinized and thrombosed, making
the vessel thick and narrow
2.3 Bleeding in the CNS (hemorrhage)
- intracranial hemorrhage
a. arterial dissection weak walls of blood vessel
b. aneurysm abnormal out pouching of the blood vessel
c. arteriovenous malformation abnormal connection
arteries
RISK FACTORS:
A. Modifiable
1. By lifestyle changes
1.1 cigarette smoking
1.2 hypercholesterolemia
1.3 obesity
1.4 heart disease
2. By medical means
2.1 transient ischemic attack
- approximately 35% in persons with TIA
will have a stroke within 5 years

between veins and

- considered as physical warning signs of

an impending stroke
2.2 asymptomatic carotid bruit secondary to carotid
stenosis
2.3 diabetes mellitus increase relative risk of ischemic
stroke to 2-3x that of the general population
2.4 hematocrit and serum fibrinogen increase blood
viscosity
B. Non-modifiable: age, sex, race, and previous stroke
C. Major risk factors
1. Age main risk factor
55 years old doubles the risk
2. Hypertension greatest treatable risk factor for ischemic as well as hemorrhagic
cerebrovascular accident
3. Diabetes mellitus 2x > non-diabetics
4. Previous stroke or TIA up to 50% of all CVA in patients
with TIA
E. Pathophysiology
CVA

INFARCTION

BLEEDS

INTRACEREBRAL

HYPERTENSIVE

1.
2.
3.
4.
5.
6.

NON-HYPERTENSIVE

Putamonal
Lobar
Thalamic
Pontine
Cerebellar
Intraventricular
TYPES
1.
2.
3.
4.

1. Aneurysm
- blooming of the
vessel
2. AV malformation
3. HPN

1. Blood-Dyscrasia
2. Leukemia
3. Dengue
4. Amphetamine
5. Infection
OUTCOMES

Thrombotic
Embolic
Lacunar
Venous

F. Clinical Manifestation
BASED ON ETIOLOGY
Pathogenesis of Stroke
CRITERIA
THROMBOTIC
Incidence
40%
Mechanism
Atherosclerosis
Occlusion of a
large blood
vessel
Onset of
Gradual, slow
Progression
stepwise
Progression of
six-hrs to days
Scenario
(+) warning
signs
Commonly
occurs at night
Sites
Int. carotid art or
MCA
Clinical
Manifestation

SUB-ARACHNOID
HEMORRHAGE

Aphasia, Visual
Field Cuts,

TIA
RIND
Completed Stroke

EMBOLIC
30%
Cholesterol
Hematoma
materials

LACUNAR
20%
Similar to
thrombosis
Small
infarcts
Chronic
process,
Gradual
onset

HEMORRHAGIC
10%
HTN rupture of
penetrating
arterioles

Cortical small
vessels

Small
perforating
arterioles

Cortical
deficits,

Discrete &
Specific

Sites of lacunae,
Brainstem, Basal
Ganglia, Int.
Capsule
Increase ICP,
Subcortical Deficits

Abrupt

Sudden

Commonly
occurs in
settings of MI

Prognosis

Hemiparesis,
Hemisensory

Seizures,
Aphasia,
Neglect

Sever
impairment

Repeated
stroke in
same
vascular
territory

Subcortical
Deficits,
Pure Motor
Stroke, Pure
Sensory
Stroke
Excellent
85% with
good
recovery

more extensive,
Hemiplegia,
Hemisensory loss,
Visual Field
Defects
Poor initial
Mortality rate 5070%; if blood
reabsorbed mild
deficits

BASED ON ARTERY INVOLVED

1. Middle Cerebral Artery Stroke
most common site of stroke
Supplies: lateral aspect of the cerebral hemisphere, subcortical structures
IMPAIRMENTS:
Upper Division: dysphagia, head/eye turning toward lesion
: contralateral hemiplegia
: contralateral hemianesthesia
: contralateral hemianopsia
: uninhibited neurogenic bladder
Dominant hemisphere Broca (motor) aphasia, apraxia
Nondominant hemisphere aprosody, visual deficit,
neglect syndrome
Lower Division: contralateral hemianopsia
Dominant hemisphere Wernicke aphasia
Nondominant hemisphere affective agnosia
2. Anterior Cerebral Artery Stroke
supplies the medial aspect of the cerebral hemisphere & subcortial structures
IMPAIRMENTS:
Contralateral hemiplegia
Contralateral hemianesthesia
Grasp reflex-groping
Disconnection apraxia
Akinetic mutism (abulia)
Head/eye turning toward lesion
3. Posterior Cerebral Artery Stroke
supplies the corresponding occipital, medial & inferior temporal lobe upper brainstem, midbrain
& post. Diencephalons
IMPAIRMENTS:
Hemisensory deficits
Visual agnosia
Visual impairment
Prospopagnosia
Alexia without agraphia
Dyschromatopsia
Memory deficits
4. BRAINSTEM STROKE SYNDROMES
UNILATERAL BRAINSTEM STROKE loss of cranial nerve function
ipsilaterally and sensorimotor dysfunction contralaterally
Brainstem Strokes ipsilateral, contralateral or bilateral limb ataxia
Cerebellar Strokes ipsilateral ataxia
STRUCTURAL
SYNDROME
LOCATION
INJURY
CHARACTERISTICS
Weber
Medial basal
CN III Corticospinal
3rd nerve ipsilat. Palsy
membrane
tract
contralat. Hemiplegia
Benedicts
Tegmentum of
CN III Spinothalamic Contralateral loss of joint
membrane
tract
poisition. Contralateral
Medial lemniscus
loss of pain & temperature
sensation.
Locked-in
Bilateral basal
Corticospinal tract
Bilateral hemiplegia
pons
Corticobulbar tract
Bilateral CN palsy (upward
gaze spared)
Millard-Gubler
Lateral pons
CN VI
Ipsilateral 6th nerve palsy
CN VII
Ipsilateral facial weakness
Corticospinal tract
Contralateral hemiplegia
Wallenbergs
Lateral medulla Spinocerebellar
Ipsilateral hemiataxia
tract
Ipsilateral loss of facial
CN V
pain & temperature
Spinothalamic tract
sensation
Vestibular nuclei
Contralateral loss of body
Sympathetic tract
pain & temperature

Nucleus ambiguous

sensation
Nystagmus
Ipsilateral Horners
syndrome
Dysphagia & Dysphonia

5. LACUNAR STROKE
Location: deep cerebral white matter, basal ganglia, thalamus and
pons
Result from: occlusion of single, small perforating arteries common &
Present with a variety of neurological and functional
deficits
SYNDROME
ANATOMICAL SITES
Pure motor stroke syndrome
Posterior limb internal capsule basis
pontis
Pure sensory stroke
Thalamus, thalamocortical projections
Sensory-motor stroke
Junction of internal capsule & thalamus
Dysarthria-Clumsy hand
Anterior limb internal capsule, pons
Ataxia hemiparesis
Coronoa radiata, internal capsule, pons,
hemiballismus
thalamus, subthalamic nucleus
SIGNS & SYMPTOMS
SENSATION
- Frequently impaired but rarely absent on the hemiplegic side.
Loss of sensation after stroke can have a significant effect on it
and skin protection and motor control.
MOTOR FUNCTION
Sequential Recovery Stage:
With hemiplegia, weakness and poor control of voluntary movement is present initially, associated
with reduced resting muscle tone.
As voluntary movement returns, nonfunctional mass flexion and extension of the limbs are first
noted. Synergy patterns or mass contraction of multiple muscle groups are seen.
Later movement patterns can be noted to be independent of synergy.
Alteration in Tone:
Flaccidity usually present immediately after the stroke and is generally
shortlived, lasting hours, days or weeks
Spasticity velocity dependent in resistance to muscle stretch that develops
after an upper motor neuron injury
emerges in about 90% of cases; tends to occur in predictable
muscle groups, commonly the antigravity muscles
Synergy patterns stereotyped primitive movement patterns associated with
the presence of spasticity, they may be elicited either reflexly, as associated functions or
as voluntary movement patterns
*strongest components
FLEXION
EXTENSION
Upper
Scapular retraction, elevation,
Shouler protraction, shoulder
Extremity shoulder abduction, external
adduction, internal rotation*,
rotation, elbow flexion*,
elbow extension, forearm
forearm supination, wrist &
pronation, wrist extension,
finger flexion
finger flexion
Lower
Hip flexion*, abduction and
Hip extension, adduction*,
Extremity external rotation, knee flexion,
internal rotation, knee
ankle dorsiflexion, inversion
extension, ankle plantarflexion,
and toe extension
inversion, toe flexion
Reflexes altered and vary according to the stage of recovery
initially, stroke results in hypotonia and areflexia during the middle
stages of recovery when spasticity & synergies are strong,
hyperreflexia emerges
stretch reflexes become hyperactive and patients typically
demonstrate clonus and the clasp-knife reflex
cutaneous reflex (+Babinski) may be present
primitive or tonic reflex patterns may appear in a readily
identifiable reaction consists of abnormal, automatic responses of
the form associated involved limb resulting from action occurring in
some other part of the body
Incoordination can result from cerebellar or basal ganglia involvement from
proprioceptive losses or from motor weakness
Bladder and Bowel dysfunction urinary and bowel incontinence is a frequent
consequence of stroke
Orofacial dysfunction
Dysphagia swallowing dysfunction recurring in 30%
Apraxia an inability to perform purposely movement although there is
no motor impairment
problem exists in performing previously learned movements,

gestures, and sequences of movements

2 categories of apraxia:
Ideomotor movement is not possible upon command but may
occur automatically
Ideational purposeful movement is not possible either
automatically of upon command
Functional abilities impaired or absent
rolling, sitting up, transfers, standing up and walking
pose significant problems for moderate to severely
involved patients with acute stroke
Speech and language disorder seen in patients with lesions in the parieto-occipital cortex of the
dominant hemisphere (usually left)
Aphasia term used to describe an acquired communication disorder caused by brain damage
and is seen as an impairment of language, comprehension, and use
a) wernickes aphasia
b) Brocas aphasia
c) Global aphasia
G. Complications
1. Pneumonia of Pulmonary Embolism management includes measure to preserve good airway,
assistance in clearing up
2. Intellectual Regression most common complication due to sensory
deprivation
3. Physiological Deconditioning secondary to weakness and immobilization;
problems of fatigue, orthostatic hypotension, lack of motivation, depression, and poor
exercise tolerance
4. Depression common between 6 months to 2 years after CVA
5. Bladder Incontinence may be due to the presence of a flaccid, distended
bladder
6. Bowel Dysfunction often accompanies bladder problems
7. Contractures second most common complication
8. Reflex Sympathetic Dystrophy also called shoulder hand syndrome
9. Falls prevention approaches are cognitive training, balance training, getting of environmental
hazards, and use of assistive devices
10. Urinary Sepsis due to the use of indwelling catheter; increase risk of UTI
11. Deep Vein Thrombosis marked by edema, tenderness, venous distention
high risk of pulmonary embolism
12. Heterotropic Ossification affects shoulder and the elbow
13. Frozen Shoulder due to weakness of rotator cuff muscles
H. Differential Diagnosis
Symptoms seldom due to cerebrovascular disease:
Vertigo alone
Confusion
Dysarthria alone
Memory loss
Dysphagia alone
Delirium
Diplopia alone
Coma
Headache
Syncope
Tremor
Incontinence
Tonic/clonic motor activity
Tinnitus
Conditions most frequently mistaken for stroke:
Seizures
Peripheral neuropathy
Metabolic encephalopathy
Multiple sclerosis
Cerebral tumor
Hypoglycemia
Subdural hematoma
Encephalitis
Cerebral abscess
Migraine
Vertigo, Menieres disease
Psychogenic disorders
ANATOMY OF THE CEREBRAL VASCULATURE
The brain is supplied mainly by the two arterial systems:
1. Internal Carotid System (anterior circulation)
2. Vertebrobasilar System (posterior circulation)
The two systems are almost completely separate from each other
functionally and yet the connections between them exist at the Circle of Willis anatomically.
I. Anterior Circulation
The anterior circulation supplies 80% of the cerebral cortexfrontal, middle, temporal lobes partly and entire blood supply of the
eyes. It originates from the common carotid arteries, which bifurcates
into Internal Carotid and External Carotid arteries. The internal carotid
ascends medially and enters the skull thru the canal in the petrous part
of the temporal bone. It further rises and pierces the dura mater
Ophthalmic artery, Posterior Communicating artery, and the Anterior
Choroidal artery is the first branch. The artery branches out further
into Anterior Cerebral artery (ACA) and Middle Cerebral artery (MCA).
II. Posterior Circulation
The posterior circulation supplies: basal ganglia, brainstem,
internal capsule, cerebellum, and occipital lobe. The basilar artery

bifurcates into two posterior cerebral branches as it continues upward.

It joins the Posterior Communicating arteries thus completing the Circle
of Willis.
The union of the vertebral and spinal arteries made up the
Vertebrobasilar arterial system. The vertebral artery passes the neck
thru the transverse foramina at the level of C6. It rises up into the
second vertebra and enters the cranium by piercing the atlantooccipital membrane and dura mater thru the foramen maghum. As the
left and right vertebral artery merges, the Anterior Basilar artery is
formed at the pontomedullary junction. The Posterior Spinal arteries
are actually branches of the vertebral artery that supplies the anterior
and posterior parts of the spinal cord. The main branches of these
arteries are joined at the level of the medulla before it forms the basilar
artery.

I. Prognosis
Depends on the following factors:
Extent of damage
Age
Health status
Location of affectation
Posterior circulation strokes are better than anterior circulation strokes
Posterior circulation strokes are catastrophic due to the life support
function of the affected part (brainstem)
Anterior circulation strokes are more extensive; has poor prognosis
but less complete
Motivation and psychological status of patient
Complications after onset
Presence of risk factors
Etiologic factor
Thrombotic severe impairment because infarction is extensive
Embolic can trigger repeat stroke in the same area; poor prognosis
Lacunar good prognosis because it involves small area
Hemorrhagic poorest prognosis; often fatal
II. Medical Management
Goals: minimize or avert ischemic brain infarction
prevent stroke recurrence
maximize functional recovery
A. Pharmalogical Treatment
Hyperosmolar agents to reduce edema due to severe ischemia and
hemorrhage (mannitol, glycerol)
Thrombolytic agents achieve recanalization of occluded cranial artery
(streptokinase, RTPA)
Hypoviscosity agents Dextran
Anti-HTN (Calcibloc, Diuretics, Beta Blockers)
Atnicoagulants (Heparin, Warfarin) 3-12 mos. following TIA. Contraindicated
in uncontrolled HTN, peptic ulcer disease, other bleeding disorder
Antiplatelet agents (ASA)
B. Surgical
Endarterectomy, CABG, clot removal only in cerebellar stroke, embolectomy
Control of risk factors: less salt in diet, stabilization of diabetes, cessation of smoking, control of
hypercholesterolemia
III. Physical Therapy Examination, Evaluation, & Diagnosis
A. Points of Emphasis in Examination
The physical examination of the patient includes a general medical examination as well as a
neurological examination. An investigation of vital signs (heart rate, respiratory rate, blood pressure)

and signs of cardiac decompensation is essential. The neurological examination stresses function of the
cerebral hemispheres, cerebellum, cranial nerves, eyes, and sensorimotor system. The presenting
symptoms will help to determine the location of the lesion, and comparison of both sides of the body will
reveal the side of the lesion. Bilateral signs are suggestive of brainstem lesions or massive cerebral
involvement.
B. Physical Therapy Diagnosis
1. Mental Status evaluation of the level of consciousness, immediate
recall, short and long term memory, orientation (to
person, place, and time), and ability to follow
instructions (one, two, and three levels)
2. Sensation should include superficial, proprioceptive, and
combined sensations
comparisons with the intact side should always be
done
3. Communication Ability should include receptive language (word
recognition, auditory comprehension, reading comprehension)
and/or expressive language function (word finding, fluency,
writing, spelling)
4. Perception should include body scheme, body scheme, spatial
relations, agnosia, and apraxia
5. Joint Mobility includes ROM and joint play
problems with spasticity may result in inconsistent
ROM findings
AROM tests may be invalid since synergy
dominance may influence performance
6. Motor Control evaluation of tone, reflexes (primitive, tonic), and
higher level reactions
voluntary movement patterns should be examined
for synergy dominance
total abnormalities (flaccidity or spasticity) are
assessed during both passive and active ROM
7. Gait Bobath assessment stressed qualitative control and balance
reactions
Brunnstrom assesses independence from synergies
based on a normal recovery sequence
Barthel index stresses functional independence and
endurance
8. Functional Assessment includes functional mobility skills (bed
mobility, movement transitions, transfers, locomotion, stairs)
basic ADL skills (home chores) should be assessed
BRUNNSTROMS STAGES OF RECOVERY OF MOVEMENT
U.E.
L.E.
Stage 1
The limbs feel heavy when
Flaccidity
moved passively.
Stage 2
Spasticity is developing but
Minimal voluntary movement
may not be very voluntary.
to the lower limb.
Stage 3
The basic limb synergies are
Hip-knee-ankle flexion in
performed voluntarily and the sitting and standing
flexors of wrist and digits are
likely to exhibit more
spasticity than their
antagonists.
Stage 4
Spasticity begins to decrease
Sitting, knee flexion beyond 90
and some movement
degrees with the foot sliding
combinations or basic limb
backwards on the floor;
synergies become available.
voluntary dorsifelxion of the
Placing the hand behind the
ankle without the lifting of the
body.
foot off the floor
Elevation of the arm to a
forward-horizontal position.
Pronation-supination elbow
extended.
Stage 5
Relative independence of the
Standing, isolated non-weight
basic limb synergies and
bearing knee flexion, hip
spasticity is warning.
extended or nearly extended;
Three (3) movements
standing is isolated
represents stage 5:
dorsiflexion of the ankle, knee
Arm raising to a sideextended heel forward in a
horizontal position
position of a short step
Arm forward and overhead
Pronation-supination elbow
extended
Stage 6
Movements are well
Standing, hip abduction

coordinated appear normal or

near normal. Basic
movements synergies no
longer interfere with the
performance awkwardness
may be observed.

Stage 7

Normal motor function is

restored.

beyond range obtained from

elevation of the pelvis, sitting,
reciprocal action of the inner
and outer hamstring muscle
resulting in inward and
outward rotation of the leg at
the knee, combined with
inversion and eversion of the
ankle.
Normal motor function is
restored.

IV. Physical Therapy Prognosis & Intervention

NEURODEVELOPMENTAL TECHNIQUES
CLASSIC NDT APPROACH
1. Bobath (Neurodevelopmental Treatment Approach)
Treatment Methods:
a. Modify sensory input through handling, positioning reflex,
inhibiting postures and use of key points of control (which
was predominantly proximal)
b. Facilitate movement patterns are integrated into the
developing nervous system
A. Basic Premises
1. Sensation of movements are learned per se.
2. Basic postural and movement patterns are learned and are
later elaborated on to become functional skills.
B. Goals of the Neurodevelopment Approach
1. Decrease the influence of spasticity and abnormal
coordination
2. Improve control of the trunk, arms, and legs
3. Refrain normal functional patterns of movement in the adult
stroke patient
C. Principles
1. Treatment should avoid movement and activities that
increase muscle tone or produce abnormal reflex patterns
on the involved side.
2. Treatment should be directed toward the development of
normal patterns of posture and movement patterns are not
based on the developmental sequence but on patterns
important for function.
3. The hemiplegic side should be incorporated into all treatment
activities to re-establilsh symmetry and increase functional
tone.
4. Treatment should produce a change in the quality of
movement and function performance on the involved side.
2. Roods (Sensorimotor Approach)
- its goal is to activate movement and posture responses at an
automatic level while following the normal developmental sequence
Techniques:
a. Follows the cephalo-caudal or proximo-distal pattern of
motor development
b. Uses 8 key developmental patterns: withdrawal supine,
rolling over, pivots prone, co-contraction neck, on elbows, all
4s, standing, walking
c. Superimposed mobility on stability
d. Uses specific sensory stimuli to facilitate motor responses:
quick stretch, fast brushing, long slow stroking, tapping,
vibration, and joint compression to promote co-contraction of
the proximal joint
A. Basic Premises
1. Motor patterns are developed from fundamental reflex
patterns at birth, which are utilized and gradually modified
through sensory stimulation until the highest level is gained
on the conscious cortical level.
2. Applying the proper atimulus to the appropriate sensory
receptor may elicit motor responses reflexively and may
result in the establishment of motor engrams
B. Components of the Roods
1. controlled sensory stimulation
2. use of the developmental sequence
3. the use of activities to demand purposely response
C. Prinicples of Roods Theory
1. Normalization of the tone and evocation of the desired
muscular response are accompanied through the use of

appropriate sensory stimulus.

2. Sensorimotor control is developmentally based.
3. Movement is purposeful.
4. Repetition of sensorimotor responses is necessary for
learning.
3. Proprioceptive Neuromuscular Preparation (PNF)
- a method of promoting or hastening the response of the
neuromuscular mechanism through stimulation of the receptors
- may also be used in both children and adults
- goal: facilitate movements that have functional relevance
- its uses range from the basic acquisition of motor control to the
utilization of these movement patterns and basic postural adaptation
- developmental activities are utilized because they allow focus on
specific areas of the body for control
Techniques:
a. Uses spiral and diagonal components of movement rather
than traditional cardinal planes
b. Activities are developmentally sequenced
c. Sensory stimulation such as proprioception, touch, stretch,
pressure, and auditory stimuli are used to elicit desired
responses
d. Uses of resistance during movement to facilitate irradiation of
impulses to other body parts
A. Basic Premises
1. re-establishment of motor control
2. re-establishment of isometric before isotonic control
3. re-establishment of eccentric before concentric control
4. re-establishment of symmetric before asymmetric movement
patterns
5. re-establishment of discrete before continuous movement
sequence
6. motor learning is achieved through constant repetition
B. Principles
1. All human beings have potentials that are not fully.
developed. PNF uses the the patients stronger movement
patterns to strengthen the weaker motions.
2. Normal motor development proceeds in a cephalocaudal and
proximodistal direction.
3. Early motor behavior is dominated by reflex activity.
4. The growth of motor behavior has cyclist trends as
evidenced by shifts between balances of antagonists is
sought.
5. Goal-direction activity is made up of reversing movement.
6. Normal movement and postures are dependent upon
synergy and a balance interaction of antagonists.
7. Developing motor behavior is expressed in an orderly
sequenced of total patterns or movement and posture.
8. Normal motor development has an orderly sequence but
lacks a step-by-step quality.
9. Improvement of motor ability depends on motor learning.
10. Frequency of stimulation and repetition of activity are used
to promote and improve retention of motor learning and for
the development of strength and endurance.
11. Goal-directed activities, coupled with techniques of
facilitation, are used to hasten learning of total patterns of
walking and self-care activities.
ACUTE STROKE REHABILITATION
Rehabilitation during the acute stage can begin as soon as possible as
patient is medically stabilized within 72 hrs. goals include:
1. maintain ROM
2. promote awareness of active movement and use of affected
side
3. improve trunk control, balance, and symmetry
4. improve functional ability
5. initiate self-care activities
I. POSITIONING first consideration in early stage. The posture which is
desirable to the patient should be avoided because it can
lead to contractures and ulceration.
turning every 2-3 hrs.
sitting and standing are promoted as soon as possible
II. MOBILITY helping the patient to use the less involved arm and leg to
move about in bed
in ROM exercises, careful attention has to be focused to
shoulder to avoid impingement

III. RESPIRATORY AND OROMOTOR ACTIVITIES

- to normalize respiratory, facial, swallowing and chewing function
- stress diaphragmatic, basal and lateral costal expansion
- respiratory activities combined with movement pattern (avoid
Valsalva maneuver)
- facial exercises with mirror
- oromotor retraining is important to reduce incidence of aspiration
- retrain muscles for jaw closing and opening via facilitatory techniques
V. Physical Therapy Rehabilitation
PRINCIPLES OF STROKE REHABILITATION
1. There is a clear need for committed medical direction. The role of the
physician includes the provision of medical care.
2. The multiple problems of a patient require the active participation of a
team of professionals.
3. Each of the professional therapists on the team should be knowledgeable
about the appropriate interventions within his discipline.
4. The interventions should be directed at achieving specific therapeutic
goals to be reached by discharge.
5. The early initiation of therapy favorably influences the outcome.
6. Therapy should be directed at specific training of skills and functional
training.
7. Planning for discharge from the in-patient rehabilitation program should
begin on admission.
8. Influence of spouse, family and patients own psychological coping
mechanisms determines ultimate outcome.
9. There should be emphasis on patient and family education about stroke,
risk factor reduction and strategies to maximize functional independence.
10. Rehabilitation requires a functional approach. When impairments cannot
be altered, every effort should be made to compensate for deficits.
REHABILITATION MANAGEMENT
Therapy for Hemiplegia
Early Phase
In the early post stroke phase, the hemiplegic limbs are often paralyzed and flaccid. At this
stage, which may last for a few hours or days, the limbs and joints are prone to development of
contractures.
Therapy during this early phase should consist of proper positioning of the patient in bed and
support of the arm in a wheelchair trough when sitting. Traction on the arm should be avoided when the
patient is moved in bed or transferred to a wheelchair. All joints of the affected limbs should be
passively moved through a full ROM at least once daily. Within hours or a few days, muscle tone returns
to the paralyzed limbs, and spasticity progressively increases. Different approaches are used by
therapists during this phase of motor recovery. The most widely accepted method, the NDT, stresses
exercises that tend to normalize muscle tone and prevent excessive spasticity.
Development of Motor Control
Conventional method of rehabilitation to regain motor control consist of stretching and
strengthening, attempting to retrain weak muscle through re-education. Use of sensory feedback is
often stressed to facilitate muscle activation (sudden stretching of the muscle and vibration). The
system developed by Rood, Brunnstrom, and Kabat emphasize these.
Therapy for the Hemiparetic Arm
Early intervention is important to support the arm, preserve joint ROM, and maintain shoulder
integrity. If the arm becomes spastic, frequent slow stretching can help to reduce the tone. Spasticity
dominates in the flexors. A static wrist hand orthosis is helpful in maintaining this joint sin a functional
position.
The challenge of poor function in ahemiparetic arm has prompted therapist to develop new forms
of therapy. One approach is focused neuromuscular re-education supplemented by EMG biofeedback.
This involves recording surface EMG from the test muscle and using auditory and/or visual display of the
EMG signal as feedback to the patient on the ongoing activity status of the muscle. Another form of
therapy uses ES to provide sensory-motor re-education. When severe weakness of the hemiparetic arm
persists, attention is directed towards functional re-training, using the unaffected limb to achieve
independence in self-care skills, etc. Forcing patient to use the weak limb by repeated encouragement
produces measurable improvement in function in the weakened hand.
Therapy for Mobility
An important rehabilitation goal for a hemiplegic patient is to achieve independent ambulation.
In the early stages of recovery, or the recover is limited to weak synergy patterns only, walking would
not be possible because of poor upright trunk control, inability to achieve single-limb support during
stance, inability to advance the leg during the swing phase. Patient should receive initial therapy to
develop gross trunk control and training in pre-gait activities such as posture, balance and weight
transfer to the hemiparetic limb.
Communication Therapy
In the early stages of rehabilitation, it is important for the therapist to help patient establish a
reliable means for basic yes/no communication. Speech therapy plays an important role in minimizing
patient isolation and encouraging the patient to actively engage in the program. Simple childish
phrases or tasks should be avoided, as patients perceive them as infantile and may withdraw.
Disorder of Cognitive and Behavior

Unilateral Neglect
Many patients with non-dominant parietal lobe lesion have
neglect and ignore the opposite side of the body. Therapy is directed
at re-training, with repetitive exercises or use compensatory
techniques, to teach new methods of task completion. These
therapies include training patient to visually stand from side-to-side.
Depression
Many patients respond to drug therapy. Anti-depressants
improve depression.
Sexuality
Most patients require supportive psychotherapy to provide them
with better mechanism to cope with the sequelae of the stroke. Health
care professionals should be sensitive to the relationship issues and
be prepared to ask questions about intimacy, secual attitudes, needs
and behavior.
Psychosocial Aspects
The psychological, social and family aspects of stroke
rehabilitation are extremely important. The stroke patient fears loss of
independence, and the disabilities reduce self-esteem and self-worth.
All members of the rehab team should contribute to a positive and
supportive milieu to promote coping strategies on the part of the
patient and to assist the patient and family to prepare for discharge
and re-integration into the home and community.
Late Rehabilitation Issues
There are important issues that make post discharge
mandatory. From a medical perspective, the majority of patients with
ongoing medical problems requiring monitoring and therapeutic
intervention such as HTN, heart disease, diabetes, etc. A seizure
disorder develops in about 8% of stroke survivors, and this requires
conventional monitoring and treatment.
The rehabilitation program does not finish when the patient
leaves the hospital, and almost all patients benefit in continued
therapy. Specific problems may become prominent following
discharge include: depression, reduced sexuality, poor role adjustment
in the home and family, equipment needs in transportation and driving,
and secondary physical problems such as excessive spasticity in the
arm, RSD, changing pattern of ambulation. Dantrolene has been used
for many years of pharmacologic treatment of spasticity caused by
stroke. A small number of patients are bothered by spontaneous
spasms at night. These can be controlled by small doses of Diazepam
before bedtime.