STROKE

1. DISEASE/DISORDER:
Definition
Cerebrovascular disease refers to an abnormality of the brain, resulting from a pathologic process of
the blood vessels. The terms stroke or cerebrovascular accident refer to the abrupt onset of a focal
neurologic deficit caused by cerebrovascular disease.

Etiology
Strokes can be classified as ischemic (85%) or hemorrhagic (15%).

The Trial of Org 10172 in Acute Stroke Treatment (TOAST) classification system 1 for ischemic stroke
is based on the underlying stroke mechanisms:

1. Large artery atherosclerosis: Intracranial, extracranial (carotid, aortic arch)

2. Cardioembolic: Atrial fibrillation, segmental wall akinesis, paradoxical embolus, patent
foramen ovale, and congestive heart failure
3. Small vessel: Lacunar infarction
4. Other: Vessel dissection, venous thrombosis, drugs
5. Cryptogenic

Hemorrhagic strokes are most often caused by hypertension, with lesions typically located in the basal
ganglia, thalamus, pons, and cerebellum. Amyloid angiopathy is the second most common cause, with
lesions more often in cortical locations. Other cause of stroke include medications (either iatrogenic,
e.g., warfarin, novel oral anticoagulant (NOAC) agent, or drugs of abuse, e.g., cocaine), vascular
malformations, cerebral venous thromboses, or tumors.

Epidemiology including risk factors and primary prevention

Stroke is the most common neurologic emergency, and it is the leading cause of disability in the United
States.

Modifiable risk factors include hypertension, hyperlipidemia, poorly controlled diabetes mellitus,
obesity, substance abuse, and atrial fibrillation.

Hypertension is the greatest risk factor for both ischemic and hemorrhagic stroke; the higher the blood
pressure (BP), the greater the risk. This is why even in prehypertensive individuals (systolic BP of 120-
139 mm Hg), lifestyle modifications (diet, exercise) to reduce BP are recommended.

Multiple epidemiologic studies have found an association between hyperlipidemia and an increased
risk of ischemic stroke. Individuals with diabetes have a greater susceptibility to atherosclerosis and
proatherogenic risk factors (hypertension and hyperlipidemia). The presence of hyperglycemia, or
elevated blood sugars, can enlarge eventual stroke size and increase the risk of brain hemorrhage. 2

Obesity is associated with an increased incidence of all listed modifiable risk factors. Excessive alcohol
consumption, tobacco use, and other substance abuse leads to stroke predisposition. Atrial fibrillation is
associated with a 4 to 5-fold increased risk of ischemic stroke because of embolism of stasis-induced
thrombi.

Nonmodifiable risk factors include a family history of cerebrovascular disease, sickle cell disease, or
hypercoaguable states. Ethnic populations, such as African-Americans and Hispanics, are more likely
to have cerebrovascular disease than Caucasians. Advanced age and male sex are also other
nonmodifiable risk factors.

Patho-anatomy/physiology
There are signs and symptoms characteristic of vascular lesions in the various arterial territories of the
brain.1

1. Middle cerebral: Contralateral loss of strength and sensation in the face, upper limb, and to a
lesser extent, the lower limb. Aphasia characterizes dominant hemisphere lesions, while
neglect accompanies nondominant hemisphere lesions.
2. Anterior cerebral: Contralateral loss of strength and sensation in the lower limb and, to a
lesser extent, in the upper limb.
3. Posterior cerebral: Contralateral visual field deficit, possibly confusion and aphasia if present
in the dominant hemisphere.
4. Penetrating branches (lacunar syndrome): Contralateral weakness or sensory loss (usually not
both) in the face, arm, and leg. Dysarthria or ataxia may be present. Aphasia, neglect, or visual
loss are not characteristic of lacunar syndromes.
5. Basilar: Combinations of limb ataxia, dysarthria, dysphagia, facial and limb weakness, and
sensory loss. Pupillary asymmetry, dysconjugate gaze, decreased responsiveness, and visual
field loss may be present.
6. Vertebral (or posterior inferior cerebellar): Truncal ataxia, dysarthria, dysphagia, ipsilateral
sensory loss on the face, and contralateral sensory loss below the neck.

Disease progression including natural history, disease phases or stages,

disease trajectory (clinical features and presentation over time)
Presentation of ischemic strokes varies according to the underlying etiology. 4

Thrombotic/atherosclerotic strokes typically occur with a slow fluctuating clinical course, with deficits
progressing over 24 to 48 hours. Thrombotic strokes are more likely to be preceded by transient
ischemic attacks.

In contrast, cardioembolic stroke has a sudden onset. Although the neurologic deficits can be severe
with cardioembolism, as the embolus fragments into smaller pieces, these deficits can rapidly resolve.

Hypertensive hemorrhages have a variable progression ranging from minutes to days. Symptoms
include headache, nausea, or vomiting because of increased intracranial pressure.

Specific secondary or associated conditions and complications

The most common neurologic complications of cerebrovascular disease include recurrent stroke, with a
12 to 15% incidence in the first year, followed by hemorrhagic transformation, hydrocephalus, cerebral
edema, and seizure.5 Cardiac complications include arrhythmia, acute coronary syndrome, and heart
failure. Infectious complications include urinary tract infections and aspiration pneumonias.
Thrombotic complications include deep venous thrombosis, pulmonary embolus, and thrombophlebitis.

2. ESSENTIALS OF ASSESSMENT
History
At initial evaluation, patients with ischemic stroke who present within the 0- to 4.5-hour time window
may be eligible for intravenous thrombolysis with tissue plasminogen activator.6,7 Stroke distribution,
type, and etiology should be documented.
For patients with a large vessel occlusion of the anterior circulation (i.e., the M1 branch of the middle
cerebral artery), intra-arterial therapy with a clot retriever device is a second treatment in ischemic
stroke within 6 hours from symptom onset 8,9,10. Used in conjunction with intravenous tissue
plasminogen activator therapy, thrombectomy with a stent retriever in the anterior circulation improved
functional outcomes at 90 days 11.

A significantly higher proportion of patients who received intra-arterial therapy achieved a good
functional outcome compared to medical management alone, without an increase in the incidence of
symptomatic intracranial hemorrhage. In the MR CLEAN study, there were 13.5% absolute risk
difference points in rates of functional independency between patients who received intra-arterial
therapy compared to medical management alone8.

On admission to a rehabilitation unit, acute interventions, such as hemicraniectomy, carotid

revascularization, or ventriculostomy placement should be listed. The patient’s hospital course and
complications should also be reviewed. Medical history should focus on stroke risk factors. A thorough
social history should discuss family support, home environment, and alcohol, tobacco, or drug use.

Physical examination
Vital signs should focus on temperature, pulse, respiratory rate, pulse oximetry with supplemental
oxygen requirements, and blood pressure for the previous 24 hours. The patient’s level of arousal and
responsiveness should always be documented. Head, ears, eyes, nose, and throat examination includes
evaluation of incision sites, extraocular musculature and pupils, and the presence of a nasogastric tube.

Cardiovascular examination includes auscultation for the presence of a murmur, distant heart sounds,
irregular rhythm, and a carotid bruit. The pulmonary examination includes careful auscultation both
anteriorly and at the lung bases. The abdominal examination should document bowel sounds,
abdominal tenderness, and the presence of a percutaneous endoscopic gastrostomy tube and urinary
catheter.

A careful neurologic examination can often localize the region of brain dysfunction. The exam includes
evaluation of mental status, cranial nerve, motor, cerebellar, and sensory function. Motor control,
strength, balance, coordination, and gait should be evaluated. Examination of cortical function includes
testing for aphasia, apraxia, neglect, and cortical sensation. Presence and severity of spasticity should
be assessed. The extremity examination should include check for distal pulses, edema, color changes,
and calf pain.

Functional assessment
The functional history documents the patient’s prestroke baseline and current status in order to aid in
determining the prognosis.

This includes the prestroke ability to perform basic activities of daily living, ambulatory status, and use
of durable medical equipment. Physical therapy and occupational therapy assessments are valuable for
poststroke functional status.

Premorbid cognitive impairments, such as psychiatric disease, dementia, and learning disability, should
be documented.

Speech/language pathologists can provide valuable input when managing any cognitive and
communication deficits after stroke. A swallow assessment may include a bedside swallow evaluation,
in addition to either a modified barium swallow or a fiberoptic endoscopic evaluation of swallow to
evaluate dysphagia and to screen for aspiration risk.

If caregiver services were required prior to admission for either physical or cognitive impairments, the
duration and frequency of this level of care should be documented.
Laboratory studies
Laboratory studies focus on both identification of stroke etiology and evaluation for acute treatments.3
Serum electrolytes, cholesterol panel, liver function tests, complete blood count, and hemoglobin A1c
are a part of standard practice.

If coagulopathy is suspected, a coagulation panel, D-dimer, and fibrinogen are performed.

Hypercoaguable testing for arterial thromboses includes antiphospholipid antibody panel, lupus
anticoagulant, Russell viper venom, and hemoglobin electrophoresis. Additional tests for venous
thromboses are protein C and S, antithrombin III, Factor V Leiden, and Factor II G20210A.
Autoimmune testing, such as erythrocyte sedimentation rate, antinuclear antibody, Complement
components 3 and 4, SS-A, SS-B, and high-sensitivity C-reactive protein, should be performed.

In patients with a concern for hereditary stroke, testing for mutations of the Notch 3 gene on
chromosome 19 can help with the diagnosis of Cerebral Autosomal-Dominant Arteriopathy with
Subcortical Infarcts and Leukoencephalopathy (CADASIL) 12.

Imaging
Computed tomography (CT) scan of the brain without contrast will identify a hemorrhagic stroke,
because blood is radiopaque (bright). However, CT may not show obvious changes in patients with
acute ischemic stroke within the first 24 hours. Signs to look for on the CT in patients with ischemic
stroke include loss of grey/white differentiation, sulcal effacement, slit-like ventricles, and midline
shift.

Magnetic resonance imaging of the brain allows for identification of ischemic lesions. A set protocol
includes T1, T2, fluid-attenuated inversion-recovery (FLAIR), diffusion-weighted imaging (DWI), and
apparent-diffusion coefficient sequences. T1 shows possible subtle changes (appears dark) because of a
decreased signal. On T2, ischemic lesions and cerebral edema appear white. With FLAIR, ischemic
lesions appear white; the suppression of the cerebrospinal fluid (CSF) (dark) makes it easier to find
pathology at the CSF/brain junction.

Ischemic lesions with DWI appear white, with maximal intensity at 40 hours 13. On apparent diffusion
coefficient, ischemic lesions appear dark where the DWI is bright. It is maximally dark at 28 hours.

Supplemental assessment tools

Magnetic resonance angiography (MRA) evaluates the intracranial vessels and the extracranial vessels
of the neck. MRA can detect arterial stenosis, aneurysms, and arteriovenous malformations.

Magnetic resonance venography can be used to identify venous sinus thrombosis. It can also detect
atypical hemorrhagic infarcts located high in the convexity, with more associated edema.

Transcranial Doppler ultrasound detects left to right shunt (most common is the patent foramen ovale),
emboli monitoring, diagnosis of intracranial stenosis or acute occlusion, and monitoring of acute
thrombolytic therapy14.

Early predictions of outcomes

Risk factors for disability after stroke include severe stroke with minimal motor recovery at 4 weeks,
evidenced by either a prolonged flaccidity, or a late return of the proprioceptive facilitation (>9d) of the
proximal traction response in the arm (>13d). Other risk factors are bilateral lesions, low level of
consciousness, previous stroke or functional disability, poor sitting balance, severe neglect, sensory and
visual deficits, global aphasia, urinary or fecal incontinence (lasting >1-2wk), and delay in medical
care.
Environmental
Environmental factors can significantly impact morbidity. In patients with limited bed mobility, a stage
I pressure ulcer can form in as little as 2 hours. Turning/positioning schedules are integral to maintain
skin integrity.

Orientation cues are important for patients with confusion or neglect. Dry-erase boards that are updated
daily with the day, month, and year, as well as names of the care providers and scheduled
test/procedures provide additional environmental support.

Social role and social support system

After a cerebrovascular event, it is common to see changes to the patient’s social role, both at home
and in their community. There is a sense of loss, and it is appropriate for patients to grieve this loss.
During this time, the support of family and friends is extremely important.

Professional Issues
The goal of providing acute stroke treatment and stroke rehabilitation is to restore as much
independence as possible by improving physical, mental, and emotional function. This must be done in
a way that preserves the dignity of the patient and motivates the patient to adjust and regain functional
abilities.

3. REHABILITATION MANAGEMENT AND

TREATMENTS
C urrent treatment guidelines
The American Heart Association (AHA) & American Stroke Association have published guidelines for
the management and rehabilitation of stroke.1-6

Acute stroke management:

 Emergency computerized tomography (CT) scan of the head is performed

to differentiate between ischemic and hemorrhagic stroke.
 Intravenous thrombolysis with recombinant tissue plasminogen activator
(rTPA) is indicated for adults with diagnosis of ischemic stroke in the
absence of contraindications, provided it can be administered within 3 to
4.5 hours of symptom onset.1
 Endovascular techniques (e.g., thrombectomy or intra-arterial
fibrinolysis) are recommended for selected patients.1,6,7 rTPA should still
be administered in eligible patients.1,6 Noninvasive intracranial vascular
imaging (CT angiogram) is recommended if endovascular therapy is
contemplated.6
 Initiation of aspirin within 24-48 hours is indicated for ischemic strokes.1
 Initial management of intracerebral hemorrhage (ICH) includes reversal
of any identified coagulopathy and monitoring/lowering of intracranial
pressure, if increased. Surgical evacuation is generally not indicated for
supratentorial hemorrhage, but is recommended for cerebellar ICH with
brainstem compression or hydrocephalus.2
  Comprehensive stroke centers and stroke systems of care improve
outcomes through prevention and treatment of stroke, as well as post-
stroke rehabilitation.1

Acute and post-acute stroke management and rehabilitation3:

Early initiation of rehabilitation after acute stroke is associated with improved functional outcome at
discharge and shorter rehabilitation length of stay.24

The primary goal of rehabilitation is to prevent complications, minimize impairments, and maximize
function. Initial rehabilitation efforts should start as soon as possible in the acute care setting then
transition to the inpatient rehabilitation setting. Other levels of post-acute care include sub-acute
inpatient rehabilitation, day rehabilitation programs, outpatient programs, and home therapy programs.

Rehabilitation involves a multidisciplinary team, often led by a rehabilitation physician. Depending on

impairments and functional deficits, the team often includes:

 Physical therapy: rehabilitation efforts including stretching, range of

motion, strengthening, balance, endurance, transfers, standing, and
ambulation
 Occupational therapy: rehabilitation efforts include treatment of
impairments related to activities of daily living and upper extremity
impairments
 Speech and language pathology: evaluation and rehabilitation of
cognitive, language, and swallowing impairments
 Neuropsychology: Psychological support and cognitive assessment and
interventions
 Nursing: Assistance with bed mobility and positioning, bowel and
bladder management, skin care, education
 Recreational therapy: community integration, functional cognitive tasks
(games, music, social interaction, etc)
 Social work/Case management: Discharge planning, resource and
benefits counseling, and guidance/education
 Other disciplines: vocational rehabilitation specialist, dietician,
pharmacist

The rehabilitation physician and team play a significant role in minimizing complications:

 Early mobilization: Minimize deconditioning and its associated effects

on fatigue, orthostatic hypotension, and endurance.
 Evaluation and treatment of dysphagia: Dysphagia is common and is a
risk factor for pneumonia. A formal swallowing assessment is essential
for determination of appropriate diet to minimize risk of aspiration;
aspiration is missed on bedside swallow study in 40-60% of patients.
Screening should be performed before any oral intake. Dynamic
instrumental assessment with a videofluoroscopy swallowing study
(VFSS) or fiberoptic endoscopic evaluation of swallowing (FEES) can help
guide rehabilitative techniques.
 Nutrition status: Adequate nutritional status, including adequate
hydration, should be ensured by monitoring daily intake assessment,
 body weight, calorie count, and laboratory tests, such as albumin or
prealbumin.
 Blood glucose levels: Monitor for at least 72 hours post-stroke.
Hyperglycemia or hypoglycemia should be treated adequately. Blood
glucose should be maintained between 110-180 mg/dl with a mean of
140 mg/dl.
 Blood pressure management1,12,13: There is controversy about optimal
blood pressure levels in the acute stage and concern about adverse effect
on collateral circulation in the brain with excessive, rapid lowering of
blood pressure. Malignant hypertension needs to be treated.
 Spasticity: Prevention and early detection are important. Prevention
measures include early mobilization, range of motion, proper positioning,
and use of braces, if needed. Medications include tizanidine, dantrolene,
and baclofen. Botulinum toxin or intrathecal baclofen should be
considered for selected patients. Contractures can be treated using
splinting, serial casting, or surgical correction. Diazepam and other
benzodiazepines should be avoided during the stroke recovery period
because their cerebral effect may delay recovery.
 Deep vein thrombosis (DVT) prophylaxis: Preventative measures
include early mobilization, pharmacological prophylaxis with
subcutaneous heparin or low molecular weight heparin (unless
contraindicated), and pneumatic compression devices or graduated
compression stockings. An inferior vena cava filter may be considered in
patients at risk for pulmonary embolism if anticoagulation is
contraindicated.
 Shoulder pain: Prevention of post-stroke shoulder pain and subluxation
is done through careful monitoring, proper positioning, shoulder
harness/sling or taping, trauma prevention, avoidance of uncontrolled
abduction and overhead pulley use, and precautions during transfers.
Shoulder subluxation and pain may be treated with oral medications,
intra-articular steroid injections, shoulder support, arm trough or lap
tray, stretching, thermal modalities, and functional electrical stimulus.
 Bladder management: Urinary incontinence is a common post-stroke
complication but often resolves over time. Accurate measurement of
intake and output is important. Urinary retention can be assessed with
use of a bladder scanner or an in-and-out catheterization. Timed voids
and temporary use of external or intermittent catheterization may be
helpful. Indwelling catheters increase risk of urinary infection and
prolonged use should be avoided whenever feasible.
 Bowel management: Incontinence is less common than constipation or
fecal impaction. A bowel regimen involving the use of laxatives, stool
softeners, and bowel training should be initiated.
 Skin: Skin integrity should be assessed on admission and monitored
daily. Skin breakdown risk may be assessed with standardized tools, such
as the Braden Scale. Preventative interventions include special
mattresses, frequent turning, proper positioning, transfers, lubricants,
barrier sprays, and protective dressings.
 Medication considerations: Central nervous system (CNS) depressants,
such as neuroleptics, benzodiazepines, and barbiturates, may be
 associated with poorer outcomes and should be avoided whenever
feasible.
 Post-stroke depression: Early diagnosis and treatment is recommended.
Approximately 40% of stroke patients experience depression; depression
may be related to neurotransmitter depletion from stroke lesions and/or
psychological response to physical/personal losses associated with
stroke. Selective serotonin reuptake inhibitors are the preferred
medications. Several studies suggest neural mechanisms of recovery may
be facilitated by certain antidepressants26. Other emerging treatment
approaches include electroconvulsive therapy, acupuncture, music
therapy, and nutraceuticals27. Further studies are needed in these
emerging areas.
 Fall risk: Fall risk should be assessed using established tools and
prevention strategies utilized. Strategies include low beds, bed alarms,
wheelchair belts, and patient/caregiver education.
 Infection: Fever should be reduced promptly. Pneumonia and urinary
tract infections should be prevented and promptly identified and treated
if they occur.

 Specific rehabilitation interventions: Rehabilitation interventions are

based on comprehensive, standardized assessments for impairments
(motor, sensory, cognitive, communication, swallowing, psychological,
and safety awareness) and prior/current functional status (e.g. with
Functional Independence Measures – FIM).
o Motor assessment should be at both the impairment and
functional level. Components should include strength, active and
passive range of motion, tone, gross and fine motor coordination,
balance, apraxia, and mobility. Motor function is addressed with
strengthening, balance and gait training, orthoses, transcutaneous
electrical nerve stimulation (TENS), robot-assisted movement
therapy, constraint-induced movement therapy, and body-weight-
supported treadmill training, and upper extremity interventions in
order to improve activities of daily living.5 Functional electrical
stimulation may help facilitate movement or compensate for lack
of voluntary movement.
o Sensory assessment should include an evaluation of different
sensations (sharp/dull, temperature, light touch, vibratory and
position), a vision exam, and a hearing exam if hearing impairment
is suspected. Compensatory techniques for sensory impairments
should be included in the stroke patient’s individualized
rehabilitation program.
o Cognitive assessment should address arousal, attention, visual
neglect, learning, memory, executive function, and problem
solving.
o Psychosocial assessments should be made of psychological factors
(e.g., pre-morbid personality, level of insight, loss of identity
concerns, sexuality), psychiatric illnesses, available resources,
 social support, patient goals, life situation, and social roles. A home
assessment may be needed.
o Management of dysphagia includes postural changes, increased
sensory input, modified swallowing maneuvers, active exercise
programs, and diet modifications. Non-oral feeding may be
required in some instances, including consideration of
percutaneous endoscopic gastrostomy feeding.3
o Aphasia management includes efforts to increase gains during
spontaneous recovery and use of compensatory techniques for
persistent communication problems. Dysarthria treatments
include interventions to improve articulation, fluency, resonance,
and phonation, compensatory techniques, and use of
alternate/augmentative communication (AAC) devices.
o Cognitive deficits are common. Memory deficits can be managed
through teaching compensatory strategies. Measures to address
visual and spatial neglect should be integrated with other
therapies, and may include prism glasses, increased awareness of
deficits, and compensatory techniques. Neuropsychiatric sequlae
should be identified and treated. Acetylcholinesterase inhibitors or
the NMDA receptor inhibitor, Memantine, can be considered for
patients with vascular dementia or vascular cognitive
impairment.3Amphetamines are not recommended to enhance
motor recovery.3
o Patient, family, and caregiver education is an integral part of
rehabilitation, as are appropriate advocacy and identification and
help with securing of available support and resources. Assessment
findings and expected outcomes should be discussed with the
patient and family/caregivers.

Chronic stroke management:

 Rehabilitation team members should provide adequate support as the

patient transitions from inpatient rehabilitation to home. Team can
provide assistance with ordering functionally appropriate durable
medical equipment (DME), instructions for home exercise programs,
arranging for home health or outpatient therapy services, scheduling
follow up medical appointments, and providing information on local
stroke support groups.
 Ongoing management may include a regular exercise program, walking
aids and/or wheelchair, adaptive devices for activities of daily living,
home modifications, addressing return to work, driving, sexual
dysfunction, and ongoing management of stroke risk factors and
comorbid conditions. Appropriate safety measures (e.g., fall prevention)
should be instituted.9
 Secondary prevention of stroke3,4: Appropriate treatment of
hypertension, anticoagulation for atrial fibrillation thrombo-embolic
prophylaxis, use of antiplatelet therapy in cerebral ischemia, prevention
of coronary heart disease, lipid lowering therapy, exercise, and smoking
cessation are all important. Blood sugar maintenance of near-
 normoglycemic levels (80-140 mg/dl) is recommended for long-term
prevention of microvascular and macrovascular complications.

Coordination of care:
Coordination of treatment care plans should include all involved medical specialists, home care
services, outpatient therapists, as well as the patient and their families. A multidisciplinary team is
essential for success.

Patient & family education:

Education must focus on management of risk factors, maintenance of rehabilitation gains, preventing
complications, community support and resources, home modifications, and community reintegration.

Key topics for stroke prevention education (also see “Secondary prevention of stroke” section above):

 Modifiable risk factors include: hypertension, heart disease, diabetes,

obesity or being overweight.
 Recommend: smoking cessation, avoiding excess alcohol consumption,
having a balanced diet, and exercise participation.

Key topics for post stroke complication education and prevention:

 Maintain regular follow up with a primary care physician, who can help
prevent and monitor for complications.
 Monitor for signs and symptoms of post stroke complications: depression,
spasticity or contractures, shoulder pain/subluxation, DVTs, pressure
ulcers, pneumonias, seizures, osteoporosis, UTIs and/or bladder control.
 The following treatment or preventative techniques may be employed:
o Counseling, psychotherapy, local stroke support groups, and
antidepressant medications may be utilized for depression.
o Range of motion exercises and physical therapies can help prevent
limb contractures and shoulder pain.
o Good nutrition and frequent pressure relief, including turning
while in bed, will help prevent pressure ulcers.
o Swallowing exercises and precautions, deep breathing exercises,
and respiratory therapy can minimize risk of pneumonia.
o Bladder training programs may be helpful for poor bladder
function control.

Outcome Measures:
Number of hospital readmissions, functional status, community dwelling, and mortality are important
indicators to measure in the post-discharge period.

Common scales:

 Functional Independence Measure Scale (FIM): Assesses physical and

cognitive function focusing on burden of care. There are a total of 13
motor items and 5 social-cognitive items. Each item is scored from 1-7,
with 7 indicating complete independence.
  Modified Rankin Scale: A global outcome scale that runs from 0-6, with
0 being perfect health without symptoms, and 6 being death. It is
commonly used for measuring the degree of disability, or dependence,
and has become a widely used clinical outcome measure for stroke
clinical trials.

4.CUTTING EDGE/EMERGING AND UNIQUE

CONCEPTS AND PRACTICE
See Cerebrovascular Disorders Part 2.

5. GAPS IN THE EVIDENCE-BASED

KNOWLEDGE
See Cerebrovascular Disorders Part 2.