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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:
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
-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)
Skin breakdown
Orthostatic intolerance
o
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
DYSPHAGIA
physical maneuvers
controlling food bolus size and pacing, or using a chin tuck or
double swallow.
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
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
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
Predicting Survival
Hemorrhagic stroke
infarction
Ag
e
Survival at 30 days
88%- 92%
62%- 63%
88%- 92%
55%
4564
65
I.
central purpose:
lessen ultimate disability
II.
Social Variables
long-term institutional care
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
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
external pneumatic compression devices
preventive measures for upper limb
venous duplex ultrasound imaging
newly diagnosed DVT should immediately receivecomplex regional pain syndrome
desensitization with
therapeutic INR (between 2 and 3)
massage
Acute DVT - bed rest for 24 hours
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