STROKE REHABILITATION

INTRODUCTION
I. DEFINITION OF STROKE
Sudden occurrence of permanent damage to an area of brain caused by a blocked
blood vessels bleeding within the brain.
Traumatic injury to the brain, demyelinating lesions, brain tumors, brain abscesses, &
other stroke-like symptoms are not included in this definition.
II. CLASSIFICATION
Ischemic vascular occlusion
Hemorrhagic bleeding within the parenchyma of the brain
*Nonparanchynmal hemorrhage Subarachnoid hemorrhage (SAH) due to a
ruptured intracranial
aneurysm.
III. MANIFESTATION
Focal weakness most common
Sensory loss
Speech
Language disturbance
Visual loss
IV. OBJECTIVE OF STROKE REHABILITATION
Achieve max. level of functional independence
Facilitate neurological recovery
Successful reintegration back into home, family and community
Reestablish meaningful and gratifying life
Educating of the stroke survivor and his family regarding secondary stroke prevention
V. EPIDEMIOLOGY
780,000 Americans suffer, of which 600,000 are an initial event.
Stroke remains 3rd leading cause of death in US, after heart disease and cancer.
Age related- uncommon before age 50, but doubling each decade after 55.
More common in men--young cohorts, but women for over age 85.
VI. RISK FACTORS
Annual risk of 5% after initial stroke, 5-year cumulative risk of 25 %, or as high as 42%.
Hypertension, heart disease, DM

 Heavy alcohol
consumption

VII.

TYPES OF STROKE
1. Transient Ischemic Attacks
Strokelike event that completely resolves within 24 hrs.
Symptoms occurs only a few seconds or minutes followed by apparent resolution.
Despite complete resolution acute infarcts can be present in some MRI results
high risk for further vascular events.
TIA requires thorough investigations.
2. Cerebral Thrombosis
Thrombosis of large extracranial and intracranial vessels as the result of
atherosclerotic CVD
approximately 30% of all cases of stroke.
Common in vessels of Neck and base of brain.
Occlusion of these vessels causes large infarction.
Risk factor of atherosclerosis: HPN, DM, smoking & hyperlipidemia.
It begins subtly and affected individual may have weakness or difficulty to walk or
get out of bed.
It worsens over some hours or days, followed by stabilization and then gradual
improvement.

3. Cerebral Embolism
Responsible for about 30% of all cases
SOURCES OF EMBOLI:

Cardiogenic thrombus at a recent site of MI, area of myocardial

hypokinesis, w/in left atrium in pts with atrial fibrillation, or on diseased or prosthetic valves.

Paradoxical embolism DVT in the pelvis or leg.

Cerebral blood flow and anatomy of the cerebral circulation favor

passage in the middle cerebral artery.
Treatment:
Anticoagulants- for long term secondary prevention of recurrence, but immediate
anticoagulation with heparin can increase risk of symptomatic hemorrhagic conversion.
*That is why anticoagulation therapy is delayed from the acute onset for up to 2 weeks
in individuals with large cardioembolic infarctions.
4. Lacunar Stroke
Approximately 20% of all strokes
Small, circumscribed lesions, 1.5 cm from occlusions in the deep penetrating
branches of the large vessels of subcortical structures.
Highly asso. with HPN, microatheroma or lipohyalinosis.

5. Cerebral Hemorrhage
Approx. 11% of cases
HPN- most common cause- at the site of small, deep , penetrating arteries.
Occurs through rupture of microaneurysms (Charcot-bouchard aneurysms)
Majority of lesions occurs in the putamen or thalamus, and about 10% occurs in
cerebellum.
Cerebral amyloid angiopathy- another cause of cerebral hemorrhage- about 520% cases.
Clinical onset is often dramatic with severe headache and rapidly progressive
neurologic deficits.
Well-recognized complication of anticoagulant therapy
Other causes : trauma, vasculitis and bleeding into a tumor & pts with bleeding
diasthesis.
Manifestations: sudden headache, inability to stand, n&v, and vertigo
Acute hydrocephalus- caused by large posterior fossa lesions in which edema and
hematoma occludes the 4th ventricle. requires immediate decompression
6. Subarachnoid Hemorrhage
Accounts for 7% of cases
Usually result from rupture of arterial aneurysm at the base of the brain with
bleeding in the subarachnoid space.
Risk of aneurysm rupture increases as the size increases-- intervention is advised
for asymptomatic aneurysm.
Signs and symptoms of rupture:
Sudden severe headache
Nausea and vomiting
Signs of meningeal irritation
Focal signs- complication of arterial vasospasm
Coma- 1/3 of patients die acutely.
Nimodipine- reduce likelihood or severity of vasospasm.
Complication:
Hydrocephalus obstruction of ventricular system or arachnoiditis from blood
in the CSF
SAH may also result from bleeding from an arteriovenous malformation
(AVM) a tangle of dilated blood vessels found on the surface of the brain
parenchyma.
These are congenital abnormalities and tend to bleed in childhood and young
adulthood.
S/sx- seizure or chronic headache
Treatment: surgical excision, proton beam therapy, or neurovascular ablation.

STROKE SYNDROMES
Cluster of signs and symptoms produced due to the occlusion of an artery supplying a
particular region of the brain
Classification:
1.
Large vessel Stroke within the Anterior Circulation
2.
Large vessel Stroke within the Posterior Circulation
3.
Small vessel Disease of either Vascular Bed
CEREBRAL CIRCULATION

1. Anterior Circulation MCA, ACA, and

Anterior Choroidal Artery
2. Posterior Circulation Vertebral Artery,
Basilar Artery and Posterior Cerebral Artery
STROKE WITHIN THE ANTERIOR
CIRCULATION
A. Middle cerebral artery, Anterior cerebral
artery, Anterior choroidal artery
B. Occlusion of the Internal Carotid Artery
and its branches
1. Internal Carotid Artery Syndrome
no observable deficit to catastrophic
good collateral circulation
no neurological consequences
may occur with carotid occlusion
2. Middle cerebral artery is occluded at its origin
cerebral edema that usually accompanies such a large lesion with brain displacement
depressed consciousness
head and eyes deviated to the side of the lesion
Contralateralhemiplegia
decreased sensation
homonymous hemianopia
Dominant hemisphere is involved
aphasia is usually present without weakness, which may be severe if the entire territory of
the MCA is infarcted
Nondominant hemisphere lesions, perceptual deficits and neglect
Patients who survive the acute lesion regain control of head and eye movements, and
normal level of consciousness is restored. However, severe deficits involving motor,
visuospatial, and language function usually persist.
Occlusion of the middle cerebral artery branches, except for the lenticulostriate
-almost always embolic in origin, and the associated infarctions are smaller and more
peripherally located
than those seen after occlusion of the MCA trunk
-dense sensory-motor deficit on the contralateral face, arm, and leg, with less
involvement of the leg.
Recovery:
The patient is usually able to walk with a spastic, hemiparetic gait
Little recovery occurs in motor function of the arm
Small focal infarctions from occlusions of branches of the superior division will produce
more limited deficits
-pure motor weakness of the contralateral arm and face, apraxia, or expressive
aphasia.
Lesions affecting the right hemisphere
- Neglect of the left side of the body.

-Initially, the patient may completely ignore the affected side and even assert that his left
upper extremity
belongs to someone else.
- Such severe neglect often gradually improves but may be followed by a variety of
persisting impairments
such as deficits in attention, constructional apraxia, dressing apraxia, perceptual deficits,
and aprosodia.
Lacunar strokes occur in the distributionof the lenticulostriate branches of MCA
- Internal capsule (most common)
- Causing a pure motor hemiplegia
a. anterior lesion in the internal capsule may cause dysarthria with hand clumsiness
b. lesion of the thalamus or adjacent internal capsule causes a contralateral sensory
loss with or without
weakness
* The neurologic deficits in these lesions often show early and progressive recovery with good
ultimate outcome.
3. Anterior Cerebral Artery Syndromes
Supplies the Median and paramedian regions of the frontal cortex and the strip of the
lateral surface of the hemisphere along its superior border
Occlusions (uncommon)
- contralateral hemiparesis with relative sparing of the hand and face and greater
weakness of the leg
Lesions affecting the left side
Transcortical motor aphasia characterized by diminution of spontaneous speech but
preserved ability to repeat words
Grasp reflex ,sucking reflex and paratonic rigidity (also known as gegenhaltenmuscle
hypertonia presenting as an involuntary variable resistance during passive movement
of a limb)
Urinary incontinence is common
Large lesions of the frontal cortex
-often produce behavioral changes
-lack of spontaneity, distractibility, and tendency to perseverate.
Affected individuals may have diminished reasoning ability.
Bilateral anterior cerebral artery infarctions may cause severe abulia (lack of initiation)

STROKE WITHIN THE POSTERIOR

CIRCULATION
A. Paired Vertebral Arteries
B. Basilar Artery
C. Paired Posterior Cerebral
Arteries
1. Vertebrobasilar Syndromes
The two vertebral arteries join
at the junction of the medulla
and pons to form the basilar
artery.
They supply the brainstem by
paramedian and short
circumferential branches and
supply the cerebellum by long
circumferential branches
When motor impairments are
present, they are often
bilateral, with asymmetric corticospinal signs, and they are frequently accompanied
by cerebellar signs
Cranial nerve lesions are very frequent and occur ipsilateral to the main lesion
There may be dissociated sensory loss (involvement of the spinothalamic pathway with
preservation of the dorsal column pathway or vice versa), dysarthria, dysphagia,
disequilibrium and vertigo, and Horners syndrome
a. Lacunar infarcts
occlusion of small penetrating branches of the basilar artery or posterior cerebral
artery
b. Brainstem lacunes
symptomatic
c. Pontine lacunar infarcts
pure motor hemiparesis
d. Lateral medullary syndrome (Wallenbergs syndrome)
infarction in the lateral wedge of the medulla
It may occur as an occlusion of the vertebral artery or the posterior inferior
cerebellar artery
e. Basilar Artery Occlusion
May result in severe deficit with complete motor and sensory loss and cranial
nerve signs from which patients do not recover
f. Locked-in syndrome
is an uncommon but devastating stroke syndrome involving the brainstem
affects the upper ventral pons, involving the bilateral corticospinal and
corticobulbar pathways but sparing the reticular activating system and ascending
sensory pathways
g. Focal infarctions may occur in the midbrain and affect the descending corticospinal
pathway
sometimes also involving the third cranial nerve nucleus (Webers syndrome)
resulting in ipsilateral third nerve palsy and paralysis of the contralateral arm and
leg.
h. Occipital lobe infarction

 partial or complete contralateral hemianopia, and when these visual deficits

involve the dominant hemisphere, there may be associated difficulty in reading or
in naming objects
2. Thalamus is involved
There is contralateral hemisensory loss
o contralateral hemianesthesia and central pain (25 %) (brainstem and parietal
lobe)
Thalamic syndrome
o patients report unremitting, unpleasant, burning pain affecting the opposite side
of the body
Evaluation of the Stroke Etiology
Mostly, stroke represents only one facet of systemic atherosclerotic vascular disease
- hypertension, diabetes, and smoking. Stroke, however, can occur in the absence of
common risk factors or
atherosclerosis
Basic evaluation of stroke cause
-thorough physical and neurological examination
-cerebral imaging (CT or preferably MRI)
-an electrocardiogram
- noninvasive carotid studies
-echocardiogram
Possible cardiogenic embolism, a 24-hour Holter monitor is appropriate
CT or MR angiography
When concerns regarding large vessel occlusion, stenosis, or dissection are present
Conventional angiography reserved for use during intravascular interventions.
STROKE IN CHILDREN AND YOUNG ADULTS
40% to 50%, no obvious risk factors such as
sources of cardiogenic emboli and
atherosclerosis are found.
Acute Stroke Management
Goals :
(a) to limit or reverse neurologic damage through
thrombolysis or neuroprotection
(b) to monitor and prevent secondary stroke
complications such as elevated intracranial pressure
a. Intravenous thrombolysis with recombinant
tissue plasminogen activator
-known to be effective when administered to
appropriate individuals within 3 hours of
symptom onset since the mid-1990s
b. Thrombolysis (recent)
-safe as late as 4.5 hourspoststroke in a
selected population, it is clear that this interventionnis most effective when given as
early as possible

c. Clot removal devices

-e.g.Merci device, have been studied but are not
yet in routine clinical use
d. Control of blood pressure, fever, and hyperglycemia
- improve outcome in acute stroke
e. Brain cooling
-remain under investigation
Secondary Stroke Prevention
-involves a multipronged effort at risk factor reduction, which may involve behavioral
change
-smoking cessation, aerobic exercise, and dietary modifications in addition to optimizing
treatment of associated medical risk factors, such as hypertension and diabetes
Specific Medications for Stroke Prevention
A. Antiplatelet medications are appropriate for the majority of patients for secondary
prevention of ischemic stroke
1. Aspirin 50 to 325 mg provides a reduction in stroke of approximately 25%
S.E: Gastrointestinal toxicity & Allergy
2. Clopidogrel (more costly) same as Aspirin (efficacy)
3. Ticlopidine is a related drug, with similar efficacy. It has largely fallen out of use due to
concerns regarding neutropenia
4. Dipyridamole, has some efficacy when taken alone but is generally prescribed as part
of a fixed dose combination with aspirin (Aggrenox).
5. Warfarin use for stroke prevention is generally restricted to patients with atrial
fibrillation or other known cardiac or other embolic
source
B. Carotid endarterectomy
- reduces the risk of stroke in those patients with
single or multiple TIAs and with 70% or greater
stenosis of the ipsilateral internal carotid artery
C. Carotid stenting
-has been studied as an alternative to
carotid endarterectomy, particularly in
patients who may be at poor surgical
risks

 REHABILITATION DURING ACUTE PHASE

In US, acute stroke care is often transitioned rapidly to rehab care, often within matter
of days.
Should not be considered a separate phase of care, that only begins after acute
medical intervention, rather it is integral part of medical management.
FOCUS OF REHABILITIVE CARE
Pressure Ulcers
among pts with hemiplegia, lethargy, and incontinent
Management:
protection of skin from excessive moisture
use of heel protecting splints
maintenance of proper position with frequent turning
Daily inspection
Routine cleaning
Aspiration and Pneumonia
Among patients with dysphagia
Among able-bodied- aspiration usually results from vigorous coughing
Management:
Avoiding oral feeding among patients who are not alert
Assessment of ability to swallow even in alert pts
Swallowing videofluoroscopy or flexible endoscopic evaluation of swallowing (FEES)
may be performed
NGT feeding or gastrostomy may be necessary
Keep head of the bed elevated
Impairment Of Bladder Control
Initially cause a hypotonic bladder with overflow incontinence
If indwelling catheter- should be removed as soon as possible then reassessment.
Regular intermittent catheterization is preferable than indwelling catheter.
Contractures
May result when spasticity is present
Management:
Regular passive stretching
Moving the joints thru ROM
Deep Vein Thrombosis
High especially in pts with hemiplegia
Management:
Mobilization
Useful to prevent:
DVT
Deconditioning
Gastrophageal regurgitation and aspiration pneumonia
Contracture formation

 Skin breakdown
Orthostatic intolerance
o

Specific task: (gen. begins w/in 24-48 hrs)

Turning from side to side
Sitting up in bed
Transferring to a wheelchair
Standing and walking

Evaluation for Rehabilitation Program

1. Patients with premorbid conditions such as dementia- subacute rehabilitation
program may be appropriate
2. Less intense rehab program with a lesser degree of medical supervision over a longer
period of time.
3. Some individuals needs complete period of intensive acute rehabilitation
followed by subacute rehabilitation, before returning home.
4. Outpatient basis and homecare agency- patients with partial aphasia, visual loss or
monoparesis
Criteria For Admission To A Comprehensive Rehab Program
Stable neurologic status
Significant persisting neuro deficit
Identified disability affecting atleast 2 of the ff: mobility, self care activities,
communication, bowel or bladder control, or swallowing
Sufficient cognitive function to learn
Sufficient communicative ability to engage with the therapist
Physical ability to tolerate the active program (atleast 3hrs/day)
Achievable therapeutic goals
Hemiparesis
Arm is more involved than leg
most importantly because greater number of stroke involves Middle cerebral artery
than Anterior cerebral artery
Very distinct functional demands placed on upper limbs than lower limbs
Poor prognosis --complete arm paralysis at onset or no measurable grasp strength by 4
weeks.
For patients with motor recovery by 4 weeks 70% will make a full or good recovery.
Poor prognosis no initial motion w/in 3weeks or if motion in a second segment is not
followed within a week.
Aphasia
Time course of recovery is usually slower and more prolonged than motor abilities, with
improvement continuing more than a year.
Brocas (nonfluent) aphasia :
a. With large lesions- little recovery
b. Smaller lesions- milder aphasia with anomia and word-finding difficulty
Global aphasia-tend to progress slowly , with comprehension often improving more
than expressive ability.
Visual impairment

 Generally , visual improvement is modest, if the field defect persists beyond a few
weeks, late recovery is less likely.
Tools that can be used to assess mental status:
Mini-Mental State Examination (MMSE)- screens variety of mental demands and gives a
well- validated of overall mental function.
NIH stroke scale(NIHSS)- includes some elements of cognitive and language ability.
Specific Stroke Impairment & their rehabilitation
Dementia usually there is premorbid cognitive decline already, undiagnosed
Delirium- early treatment of underlying cause such as F&E disturbances, infection,
sleep disruption, or medication side effects.
Consciousness- stimulants ( dextroamphetamine or methylphenidate) as well as
modafinil.
Visual neglect- letter cancellation tasks or line bisection
Hemispatial neglect- visual and/or verbal cuing or fresnel prism applied to eyeglasses.
Construction ability( unable to copy or draw simple figures)
Others impairment of preceptual function: failure to recognize palm writing
( graphestesia), unable to identify objects in hand(astereognosis), and extinction of
simultaneous bilateral stimulation.
Anosognosia- inability to recognize disability
Apraxia- inability to execute an intended movement with motor ans sensory function
Behavioral changes- usually involves frontal lobe damage; apathy is common
Deficits in attention and executive function- commonly mistaken for memory
impairment
Emotional Lability
more common in right hemisphere lesions.
Unable to control or suppress emotional response to stimuli
May cry or laugh very easily though they recognize it as inappropriate
Often mistaken for depression
May respond to TCA or SSRI antidepressants

VISUAL DEFICITS, DYSPHAGIA, MOTOR IMPAIRMENT,

SENSORY IMPAIRMENT AND CENTRAL PAIN
VISUAL DEFICITS

VISUAL FIELD DEFICITS

common among patients with strokes in the middle cerebral artery or
posterior cerebral artery distributions.
Bedside testing of visual fields, including examination for extinction with
simultaneous stimulation
More formal visual field testing
Patients with isolated visual field deficits, but without concomitant
hemispatial neglect, generally learn to compensate effectively.
Improving size of visual fields:
therapist-directed and computer-based training (e.g., Vision Restoration
Therapy, Novavision, Inc.)

EXTRAOCULAR PALSIES AND ASSOCIATED DIPLOPIA

Stroke in the brainstem
Patching is often useful to prevent diplopia
alternated between eyes

DYSPHAGIA

affect 40% of patients with a unilateral hemispheric stroke

more severe and persistent in brainstem lesions or bilateral hemispheric strokes
risk factor for pneumonitis and aspiration pneumonia.
favorable prognosis
may affect either or both the oral preparatory pharyngeal phases of swallowing
Bedside evaluation:
observation of the function of the lips, tongue, cheeks, and jaw
elevation of the larynx during swallowing
vocal quality.
oral control, the timeliness of swallowing, presence or absence of a wet vocal
quality, and the presence or absence of coughing
patient swallow a small amount of water (3090 mL) at the bedside
If initial screening examination suggests dysphagia
more extensive bedside evaluation by a speech and language pathologist
A videofluoroscopic swallowing study (VFSS) (also called a modified barium
swallow)
Swallowing mechanism
Direct visualization of aspiration
FEES
More direct visualization of swallowing
Alternative to VFSS
Avoid radiation present with VFSS
Compensatory and recovery strategies are useful for dysphagia.
Modified food consistencies
pureed foods or thickened liquids

physical maneuvers
controlling food bolus size and pacing, or using a chin tuck or
double swallow.

It appears likely that practicing swallowing over time improves

performance and may enhance the process of spontaneous
recovery.
nasogastric, gastrostomy, or jejunostomy
tube
hemispheric stroke
patients who cannot swallow safely
recover good swallowing
NGT short term use
function
Gastrostomy Long term use
brainstem lesions or
Not entirely effective in preventing
bilateral hemisphere
aspiration pneumonia
lesions progress more
MALNUTRITION
Nutritional Supplementation is necessary
If ineffective do tube feeding

slowly some require

indefinite use of a
feeding tube.

MOTOR IMPAIRMENT

Strength, power, motor control and coordination, muscle tone, and balance may all be
affected by stroke
MEDICAL RESEARCH COUNCILS (MRC) 6-POINT SCALE, 0 to 5

most widely used clinical scale

often supplemented by qualifying descriptions (e.g., elbow flexion is 4/5 on MRC
scale in a flexion synergy pattern with moderately reduced motor control).
DYNAMOMETER limited use
BRUNNSTROM
movement patterns are evaluated and motor function is rated according to
stages of motor recover
strength correlates with performance on functional tasks

OTHER TESTS:for Research

FUGL-MEYER SCALE(Fugl-Meyer, et. al)
evaluates strength, reflexes, and coordination, and a composite score is derived
on a scale of 0 to 100.
reliable, and repeat scores reflect motor recovery over time.
WOLF MOTOR FUNCTION TEST
MOTOR ACTIVITY LOG
ARM RESEARCH ACTION TEST
SPASTICITY OR MUSCLE TONE
Abnormal increases in muscle tone are quite commonly seen in hemiparetic limbs, and
patients with more severe spasticity tend to have less well-preserved motor control.
Factors such as posture and limb position can affect spasticity and must be considered
when measuring muscle tone.
ASHWORTH SCALE - most widely used for measuring spasticity
MANAGEMENT:
conservatively with stretching and positioning.
injection therapy (principally botulinum toxin, but previously more commonly
phenol or alcohol injection)
MOTOR RECOVERY
Motor recovery may become evident within hours to days after a stroke
APPROACHES TO FACILITATE AND ENHANCE MOTOR RECOVERY:
Traditional approaches, such as the neurodevelopmental technique advocated
by Bobath
little empiric evidence supporting the use of these techniques (NDT,
Brunnstrom, Rood, PNF)

functionally oriented exercise training (such as practicing transfers and

early ambulation),
increasingly replaces traditional techniques
repetitive task-oriented practice.
Neurodevelopmental (NDT) exercises

NEW TECHNIQUES
Constraint-Induced Movement Training (CIMT)
intensive short course (generally 2 weeks) of upper limb training with
repetitive task-oriented practice and behavioral shaping techniques to
enhance not only motor control of the upper limb but also incorporation
into behavioral repertoires.
MECHANISM: unknown; overcome learned nonuse of the weak limb
Robot-Aided Exercise
used by individuals with more severe paresis after stroke
Upper limb devices, such as the InMotion2 (Interactive Motion
Technologies, Cambridge, MA), have been shown to provide benefit in both
the acute and chronic phases of stroke .
Lower limb robotic systems have been developed for gait training
not proven superior to comparably dosed hands-on therapy
Electrical stimulation of the limb (sometimes termed therapeutic electrical
stimulation or functional neuromuscular stimulation)
treatment for hemiparesis
may be beneficial in restoring motor use to some extent
Biofeedback using electromyogram (EMG) signals
used in an attempt to improve motor control poststroke.
Results of trials have been mixed

THERAPY FOR MOBILITY

HEMIPLEGIC PATIENTS
intensive gait training when therapy consists of walking on a treadmill with body
weight partially supported (PBWSTT) with a harness
Robotic therapy
proposed as an alternative to PWBSTT training,
Lokomat (Hocoma, Inc.) and the ReoAmbulator (Motorika, Inc
therapist-assisted locomotor training with a treadmill is more effective

SENSORY IMPAIRMENT AND CENTRAL PAIN

Sensory impairment may occur with or without accompanying motor weakness

following a stroke
loss of proprioception generally results in reduced motor performance even in the
absence of weakness

CENTRAL PAIN SYNDROME

Lesions of the thalamus may cause severe contralesional sensory loss and result
in a central pain syndrome
strokes involving the spino-thalamo-cortical pathway
begins a few weeks after stroke onset and becomes intractable to conventional
medications
described as burning in character

PERCEPTUAL IMPAIRMENT
often seen in parietal lobe lesions

Manifestation:
inability to perceive stimulation of the affected side during simultaneous
bilateral stimulation (extinction),
reduced two-point discrimination,
reduced object recognition (stereognosis),
impaired recognition of digits drawn in the palm (graphesthesia).

MANAGEMENT:
Sensory loss few interventions
Central pain
PHARMACOLOGIC:
TRICYCLIC ANTIDEPRESSANTS
Some have inadequate response
Problematic Anticholinergic side effects (-)
Anticonvulsants(gabapentin or lamotrigine)
Some efficacy

OUTCOME AND PROGNOSTICATION IN STROKE

REHABILITATION
Important elements of
prognosis
Prospects of survival
Degree of recovery
Extent of possible residual
disability

Developing accurate prognostic

models
Complex functions of the brain
stroke lesion location and size
Limitation of assessment technique
Impact of baseline factors
Age
Comorbid conditions
Personality and coping
abilities
Social factors

Predicting Survival

Coma following a stroke onset

indicates a poor prognosis

when it occurs in relation to

cerebral infarction, it reflects a
large
lesion with cerebral edema.
Early death following a stroke is usually related to the underlying pathology, the
patients age, and to the severity of the lesion.
First cerebral

Hemorrhagic stroke

infarction
Ag
e

Survival at 30 days
88%- 92%

62%- 63%

88%- 92%

55%

4564
65
I.

Predicting Disability and Functional Status

key outcomes:
1. restoration of function
2. community
reintegration

central purpose:
lessen ultimate disability

prognosis for recovery from

lacunar lesions is usually excellent

large vessel infarctions is related to the

volume of the lesion

54% - 80% walk independently within the first 3

months post stroke

80% independent in mobility

47% and 76% of survivors achieve partial or total

independence in
ADLs
The capacity of individuals to perform these activities is
usually scored on ADL scales, such as the Functional
Independent Measure (FIMR)
Other important variables include age and sitting
balance
The effect of age on outcome may partly be related to more frequent comorbid
diseases and functional impairments

initial ADL assessment

(most commonly, the FIM score)

The single most useful predictor of functional outcome

Post-Stroke Rehabilitation Outcomes Project

better outcomes if admitted into a rehabilitation program early

reduce the likelihood of secondary complications and help patient motivation

II.

Social Variables
long-term institutional care

need maximum physical assistance in ADLs

bowel or bladder incontinence

prestroke family interaction and the presence of an able spouse

The best estimate of prognosis can be made only after a thorough and comprehensive
evaluation of the patients medical, neurologic, functional, and psychosocial statuses.

MEDICAL MANAGEMENT DURING

REHABILITATION
There is a high incidence of comorbid
medical disorders among patients
recovering from stroke, reflecting the
of the patient population and the fact
cerebrovascular disease is often part
generalized disease process

medical complications frequently

occur during the postacute phase of
rehabilitation
I.
Cardiac Disease
a stroke is an acute event in the
course of a systemic disease

age
that
of a

embolic stroke
o
Atherosclerosis
o
hypertensive vascular disease
Common problems:
o
cardiac disease
Angina
75% evidence of coexisting cardiovascular disease
uncontrolled hypertension
o
hypertension (50% to 84%)
Hypotension
o
coronary artery disease (65%)

myocardial infarction
cardiogenic cerebral embolism
congestive heart failure
o
atrial fibrillation
atrial fibrillation
o
arrhythmias from multiple causes
ventricular arrhythmias
o
valvular disease
o
cardiomyopathy
o
endocarditis
o
recent myocardial infarction
Concomitant heart disease has a negative impact on short-term and long-term survival
and probably on functional outcome of stroke patients
Acute exacerbations of heart disease occur frequently during postacute stroke
rehabilitation
Congestive heart failure and angina decrease exercise tolerance

II.

Urinary Tract
o Urinary function can be affected in
Acute management:
ways by stroke, including urinary
Catheterization
infection, urinary retention, and urge
Anticholinergic
incontinence.
medications
acute stroke
oxybutynin
o
urinary retention due to altered
chloride
status
(Ditropan)
o
direct effects of the stroke on the

tolterodine
neurological control of micturition
(Detrol)
Men:
Premorbid voiding
dysfunction
Women: stress incontinence
Disinhibition of the bladder detrusor urinary frequency and urgency
Noninvasive measurement of bladder volume using ultrasound

several

mental

MUSCULOSKELETAL PAIN AND COMPLEX REGIONAL PAIN SYNDROME

develop several weeks to 6 months postonset

more intensive and earlier rehabilitation programs incorporating range-of-motion

exercises
pain in most patients with hemiplegia
glenohumeral subluxation *- most common cause
Preventative measures for

spasticity
shoulder pain
Contracture

Proper positioning
Supporting the arm
VENUS THROMBOEMBOLISM
avoiding traction
-All patients with significant immobility related to stroke should
Spasticity
receive DVT prophylaxis
botulinum toxin
DVT prophylaxis
phenol injections

Low dose subcutaneous heparin

Low molecular weight heparin


external pneumatic compression devices
preventive measures for upper limb
venous duplex ultrasound imaging
newly diagnosed DVT should immediately receivecomplex regional pain syndrome

Frequent passive range of

full-dose anticoagulation with low molecular weight
motion
heparin

desensitization with
therapeutic INR (between 2 and 3)
massage
Acute DVT - bed rest for 24 hours

Inferior vena cava filter to prevent pulmonary embolism

active incorporation of the

cannot safely receive anticoagulation

paretic upper limb
DEPRESSION
relationship between left frontal or bifrontal lesions and major depression
Theories:
stroke may result in brain catecholamine depletion through lesion-induced
damage to the frontal noradrenergic, dopaminergic, and serotonergic projections

Active treatment
reliable indicators:
standard
Persistently depressed
antidepressant
mood
medications

loss of interest in
SSRIs
socialization

stimulant
medication
limited participation in the
(methylphenidate)
SEXUALITY
rehabilitation program
sexual dysfunction
reductions both in libido and sexual performance
psychosocial and medical issues
Stroke is most common in
Older
Hypertension
Diabetics
Prevalence: 57% and 75% after stroke
Fears
most practitioners agree that resuming sexual activity is safe and appropriate
after discharge from the hospital
82% of those who experienced erectile dysfunction after stroke improved
spontaneously within a few months
Iatrogenic
SSRI antidepressants (fluoxetine and paroxetine)
antihypertensives,(b-blockers)
Anticonvulsant
Management
Phosphodiesterase-5 inhibitors
(sildenafil (Viagra)
Late issues
tadalafil (Cialis)
Depression
counseling
Spasticity
Contracture
Ongoing Care
Osteoporosis
continued improvement in motor function is
weight gain
possible in stroke survivors even after years
of
Deconditioning
stable chronic deficits

rehabilitation needs may extend for many years

after the initial even periodic physiatric ass