Anda di halaman 1dari 20


Author(s): Nneka L. Ifejika-Jones, MD MPH

Originally published:7/30/2012
Last updated:4/19/2016



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.


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

The Trial of Org 10172 in Acute Stroke Treatment (TOAST) classification system1 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.


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

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.



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

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.3Serum
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.

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

Ischemic lesions with DWI appear white, with maximal intensity at 40 hours13. 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

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 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

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.


See Cerebrovascular Disorders Part 2.



See Cerebrovascular Disorders Part 2.


See Cerebrovascular Disorders Part 2.

1. Adams HP Jr, Bendixen BH, Kappelle LJ, et al. Classification of subtype of acute ischemic stroke.
Definitions for use in a multicenter clinical trial. TOAST. Trial of Org 10172 in Acute Stroke
Treatment. Stroke. 1993;24:35-41.
2. Guide to Clinical Preventative Services: Report of the U.S. Preventative Servies Task Force. Baltimore,
MD: Williams and Wilkins; 1996.
3. Uchino K, Pary JK, Grotta JC. Acute Stroke Care: A Manual from the University of Texas-Houston Stroke
Tteam. New York, NY: Cambridge University Press; 2007.
4. Garrison SJ. Handbook of Physical Medicine and Rehabilitation. Philadelphia, PA: Lippincott Williams and
Wilkins; 2003.
5. Pendlebury ST, Rothwell PM. Risk of recurrent stroke, other vascular events and dementia after transient
ischaemic attack and stroke. Cerebrovasc Dis. 2009;27 Suppl 3:1-11.
6. Hacke W, Donnan G, Fieschi C. Association of outcome with early stroke treatment: pooled analysis of
ATLANTIS, ECASS and NINDS rt-PA stroke trials. Lancet. 2004;363:768-774.
7. Hacke W, Kaste M, Bluhmki M. Thrombolysis with alteplase 3 to 4.5 hours after acute ischemic stroke. N
Engl J Med. 2008;359:1317-1329.
8. Berkhemer OA, Fransen PS, Beumer D, van den Berg LA, Lingsma HF, Yoo AJ et al; for the MR CLEAN
investigators. A randomized trial of intraarterial treatment for acute ischemic stroke. N Engl J Med. 2015;
9. Goyal M, Demchuk AM, Menon BK, Eesa M, Rempel JL, Thornton J et al; ESCAPE trial
investigators. Randomized assessment of rapid endovascular treatment of ischemic stroke. N Engl J
Med. 2015; 372:1019-1030.
10. Campbell BC, Mitchell PJ, Kleinig TJ, Dewey HM, Churilov L et al; for the EXTEND-IA
investigators. Endovascular Therapy for Ischemic Stroke with Perfusion-Imaging Selection. N Engl J
Med. 2015; 372:1009-1018.
11. Saver JL, Goyal M, Bonafe A, Diener HC, Levy EI, Pereira VM et al; for the SWIFT PRIME
investigators. Stent-Retriever Thrombectomy after Intravenous t-PA vs. t-PA Alone in Stroke. N Engl J
Med. 2015; 372:2285-2295.
12. Meschia JF, Brott TG, Brown RD Jr. Genetics of cerebrovascular disorders. Mayo Clin Proc. 2005; 80:122-
13. Eastwood JD, Engelter ST, MacFall JF, Delong DM, Provenzale JM. Quantitative assessment of the time
course of infarct signal intensity on diffusion-weighted images. AJNR Am J Neuroradiol. 2003;24:680-687.
14. Caplan LR. Diagnosis and treatment of ischemic stroke. JAMA. 1991;266:2413-2418.

Author(s): Rani Haley Lindberg, MD, Mustafa Khan, MD

Originally published:10/3/2012
Last updated:05/05/2016



See Cerebrovascular Disorders Part 1.


See Cerebrovascular Disorders Part 1.



Cutting edge concepts and practice

Constraint-induced movement therapy (CIMT)7,11: This therapy traditionally involves restricting the
unaffected limb for 90% of waking hours for 14 days, while intensively training the use of the affected arm. A
number of studies have shown that CIMT induces a use-dependent increase in cortical reorganization of the
areas of the brain controlling the more affected limb.8,9 Studies have demonstrated significant improvements in
motor and functional outcomes, although there have been mixed results. CIMT is shown to be effective in
patients who have active wrist extension (at least 20 degrees), active finger extension (at least 10
degrees),10 good cognition, limited spasticity, and preserved balance. There are a number of non-standardized
modified versions of CIMT which have arisen in response to critiques of traditional CIMT, including poor
patient tolerance and feasibility in clinics. CIMT has shown effectiveness in improving motor function, but
studies have been limited by small sample sizes.

Bilateral upper extremity training: This training is a recent stroke rehabilitation technique that has been
applied to patients in both acute and chronic post-stroke phases. Investigators have recommended that patients
in the chronic phase poststroke who retain at least a minimal degree of corticospinal integrity (as reflected by,
e.g., active finger movements) should receive unilateral training, and those with little or no distal movement
might benefit more from bilateral training. For those stroke patients without corticospinal tract integrity,
targeting the contralesional hemisphere using bilateral training is expected to be more appropriate, although the
functional gains are expected to be small.5

Body-weight-supported (BWS) therapy21: This modality allows gait impaired stroke patients to safely
participate in task-specific gait training. A harness provides support of body weight over a treadmill or other
surface, while a therapist can observe and correct any unwanted gait pattern. BWS gait training has been
shown to improve ambulation in hemiparetic stroke patients producing a more symmetric, efficient
hemiparetic gait pattern. However, superiority of BWS therapy over conventional post-stroke gait training
therapies has not been established.

Robotics: Robotic assisted gait devices have generally not been shown to be superior to traditional physical
therapy of the same intensity.23Lightweight, motorized exoskeletons have become available very recently, but
they are very expensive and slow. Studies are needed to show if they can be used as an augment to standard

Brain-computer interface25: The brain computer interface is one of the most promising research avenues,
which involves developing neuroprosthetic devices and brain-computer interface (BCI) technologies to bypass
brain damage via adaptive neuroplasticity of uninvolved distal brain areas. Parts of the nervous system not
involved in specific tasks can be harnessed to reconstruct the neural substrate that interacts with a
neuroprosthesis or BCI-driven devices. A brain-machine interface uses brain signals to drive external devices
without the use of peripheral physiologic activities. Patients with locked-in syndrome from brainstem stroke
benefit the most from these devices. There are issues with cost and reliability.

Noninvasive Brain Stimulation (NIBS) – Transcranial magnetic and direct current stimulation:7,14This
therapy involves applying mild magnetic or electric stimulation to the scalp. The benefit is achieved through
neuromodulation of plasticity and cortical excitability. A growing number of studies support its therapeutic
potential and safety in stroke rehabilitation, however a meta-analysis showed the effects to be inconsistent for
motor recovery. NIBS has been shown to improve motor function, gait, language (aphasia) and cognitive
(neglect) deficits, and mood.

Mental Practice(MP)/Motor Imagery7: This refers to mental rehearsal of a movement. Imaging studies have
shown that this motor imagery stimulates overlapping cortical areas as the actual movements. Most studies
have shown a positive effect on upper extremity function. A recent Cochrane Review found MP in
combination with routine rehabilitation is more effective in restoring arm function compared to rehabilitation
Mirror Therapy7,15: Initially applied to amputation patients, this therapy involves placing a mirror in the mid-
sagittal plane, allowing the patient to visualize the reflection of the non-paretic limb as if it were the paretic
limb. Studies have generally shown statistically significant gains in motor function. The underlying theory is
that the visual illusions of the limb induce beneficial brain plasticity and counteract maladaptive neuroplastic

Virtual reality (VR): Virtual environments and objects provide the user with visual feedback and repetitive
skills practice. The interface may be through a head-mounted device, projection systems, or involving
sensations of hearing, touch, movement, balance, or smell. The user interacts with the environment by devices,
such as a mouse or joystick, or more complex systems using cameras, sensors, or haptic feedback devices. A
2015 Cochrane review17 found evidence that VR and interactive video gaming may be beneficial in improving
upper limb function and ADL function as an adjunctive therapy or when compared with the same amount of
standard therapy. There was insufficient evidence to make conclusions about the effect on grip strength, gait
speed or global motor function. Other 2015 review studies have shown efficacy of VR in improving neglect18,
balance and mobility19.


Current 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
 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
 Neuropsychology: Psychological support and cognitive assessment and interventions
 Nursing: Assistance with bed mobility and positioning, bowel and bladder management, skin care,
 Recreational therapy: community integration, functional cognitive tasks (games, music, social interaction,
 Social work/Case management: Discharge planning, resource and benefits counseling, and
 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
 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
 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
 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
 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).
 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.
 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.
 Cognitive assessment should address arousal, attention, visual neglect, learning, memory, executive
function, and problem solving.
 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.
 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
 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.
 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
 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

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
 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
 The following treatment or preventative techniques may be employed:
 Counseling, psychotherapy, local stroke support groups, and antidepressant medications may be utilized
for depression.
 Range of motion exercises and physical therapies can help prevent limb contractures and shoulder pain.
 Good nutrition and frequent pressure relief, including turning while in bed, will help prevent pressure
 Swallowing exercises and precautions, deep breathing exercises, and respiratory therapy can minimize
risk of pneumonia.
 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.


Gaps in the evidence-based knowledge

 Although several different forms of rehabilitation techniques have been proven effective, these studies often
involve small and highly selective populations and are not generalizable to the stroke population.
 Further studies are needed to develop optimal treatment protocols for many of the cutting edge therapies,
including constraint-induced movement therapy, indirect brain stimulation, and mirror therapy. There are
questions on timing, intensity, ideal patient populations, and combinations with other therapies, etc.
 Blood pressure management during early stroke management continues to be an area of conflict. Larger
trials with well-defined criteria are needed and appear to be forthcoming. Current guidelines should be
followed until such time.1,12,13
 The most recent AHA guidelines suggest further study is needed in specific areas of early acute ischemic
stroke management, including in intravenous fibrinolysis, endovascular interventions, anticoagulants,
antiplatelet agents, and induced hypertension. 1
 The use of complementary and alternative medicine (CAM) in cardiovascular disease and stroke patients
has gained in popularity over recent years and appears common. These include biological therapies such as
dietary supplements, herbal medicine, and aromatherapy; mind-body therapies such as deep breathing,
meditation, yoga, tai chi, and praying; manipulative and body-based therapies such acupressure,
chiropractic manipulation, massage, osteopathic manipulation, and reflexology; whole medical systems
which include acupuncture, Ayurveda, homeopathy, and naturopathy; and finally energy medicine which
includes healing touch, light therapy, magnetic therapy, Reiki, and sound energy therapy. Biologic, mind-
body therapies, and acupuncture (especially among stroke patients) are the most commonly used. Potential
interactions and adverse effects may exist for biological CAM therapies. CAM is poorly studied and there
are conflicting results. Further sound and rigorous studies are needed, especially in regard to effects of
CAM therapies on clinical outcomes and safety. Further studies are also needed in regard to CAM as it
applies specifically to stroke patients.28,29


1. Jauch EC, Saver JL, Adams HP Jr, et al.; American Heart Association Stroke Council; Council on
Cardiovascular Nursing; Council on Peripheral Vascular Disease; Council on Clinical Cardiology.
Guidelines for the early management of patients with acute ischemic stroke: a guideline for healthcare
professionals from the American Heart Association/American Stroke Association. Stroke2013
Mar;44(3):870-947. doi: 10.1161/STR.0b013e318284056a. Epub 2013 Jan 31.
2. Hemphill JC, Greenberg SM, Anderson CS, et al. Guidelines for the Management of Spontaneous
Intracerebral Hemorrhage: A Guideline for Healthcare Professionals From the American Heart
Association/American Stroke Association. Stroke. 2015 Jul;46(7):2032-60. doi:
10.1161/STR.0000000000000069. Epub 2015 May 28.
3. Department of Veterans Affairs, Department of Defense, and The American Heart Association/American
Stroke Association. VA/DoD Clinical Practice Guideline for the Management of Stroke Rehabilitation.
2010. Available at:
4. Kernan WN, Ovbiagele B, Black HR, et al; American Heart Association Stroke Council, Council on
Cardiovascular and Stroke Nursing, Council on Clinical Cardiology, and Council on Peripheral Vascular
Disease. Guidelines for the prevention of stroke in patients with stroke and transient ischemic attack: a
guideline for healthcare professionals from the American Heart Association/American Stroke
Association. Stroke. 2014;45:2160–2236. DOI: 10.1161/STR.0000000000000024.
5. Wells, George A., et al. “Ottawa Panel Evidence-Based Clinical Practice Guidelines for Post-Stroke
Rehabilitation.” Topics in Stroke Rehabilitation 2006; 13(2), 1-269. DOI: 10.1310/3TKX-7XEC-2DTG-
6. Powers WJ, Derdeyn CP, Biller J, et al; on behalf of the American Heart Association Stroke Council. 2015
AHA/ASA focused update of the 2013 guidelines for the early management of patients with acute ischemic
stroke regarding endovascular treatment: a guideline for healthcare professionals from the American Heart
Association/American Stroke Association. 2015;46 000-000. DOI: 10.1161/STR.0000000000000074
7. Claflin ES, Krishnan C, Khot SP. Emerging Treatments for Motor Rehabilitation After Stroke. The
Neurohospitalist. 2015;5(2):77-88. doi:10.1177/1941874414561023.
8. Blanton S, Wilsey H, Wolf SL. Constraint-induced movement therapy in stroke rehabilitation: perspectives
on future clinical applications. 2008;23:15-28
9. Wang W, Wang A, Yu L, et al. Constraint-induced movement therapy promotes brain functional
reorganization in stroke patients with hemiplegia. Neural Regeneration Research. 2012;7(32):2548-2553.
10. Miller EL, Murray L, Richards L, et al. Comprehensive overview of nursing and interdisciplinary
rehabilitation care of the stroke patient: a scientific statement from the American heart association. Stroke.
11. Reiss AP, Wolf SL, Hammel EA, McLeod EL, Williams EA. Constraint-Induced Movement Therapy
(CIMT): Current Perspectives and Future Directions. Stroke Research and Treatment. 2012;2012:159391.
12. Saver JL. Blood Pressure Management in Early Ischemic Stroke. JAMA. 2014;311(5):469-470.
13. Carcel, Cheryl, and Craig S. Anderson. “Timing of Blood Pressure Lowering in Acute Ischemic
Stroke.” Current atherosclerosis reports8 (2015): 1-8.
14. Ifejika-Jones NL, Barrett AM. Rehabilitation—Emerging Technologies, Innovative Therapies, and Future
Objectives. Neurotherapeutics. 2011;8(3):452-462. doi:10.1007/s13311-011-0057-x.
15. Park J-Y, Chang M, Kim K-M, Kim H-J. The effect of mirror therapy on upper-extremity function and
activities of daily living in stroke patients. Journal of Physical Therapy Science. 2015;27(6):1681-1683.
16. Barclay-Goddard RE, Stevenson TJ, Poluha W, Thalman L. Mental practice for treating upper extremity
deficits in individuals with hemiparesis after stroke. Cochrane Database Syst Rev. 2011;(5):Cd005950.
17. Laver KE, George S, Thomas S, Deutsch JE, Crotty M. Virtual reality for stroke rehabilitation. Cochrane
Database of Systematic Reviews 2015, Issue 2. Art. No.: CD008349. DOI:
18. Pedroli E, Serino S, Cipresso P, Pallavicini F, Riva G. Assessment and rehabilitation of neglect using virtual
reality: a systematic review. Frontiers in Behavioral Neuroscience. 2015;9:226.
19. Darekar A, McFadyen BJ, Lamontagne A, Fung J. Efficacy of virtual reality-based intervention on balance
and mobility disorders post-stroke: a scoping review. Journal of NeuroEngineering and Rehabilitation.
2015;12:46. doi:10.1186/s12984-015-0035-3
20. Laver KE, et al. Virtual reality for stroke rehabilitation. Cochrane Database Syst Rev. 2011;9 CD008349.
21. Sheffler LR, Chae J. Technological Advances in Interventions to Enhance Post-Stroke Gait. Physical
medicine and rehabilitation clinics of North America. 2013;24(2):305-323. doi:10.1016/j.pmr.2012.11.005.
22. Kwakkel G, Kollen BJ, Van der Grond J, Prevo AJ. Probability of regaining dexterity in the flaccid upper
limb: impact of severity of paresis and time since onset in acute stroke. 2003;34:2181-2186
23. Mehrholz J, Pohl M. Electromechanical-assisted gait training after stroke: a systematic review comparing
end-effector and exoskeleton devices. J Rehabil Med. 2012 Mar;44(3):193–199
24. Maulden S.A. et al. Timing of Initiation of Rehabilitation After Stroke. Arch Phys Med Rehabil. 2005. 86
(Suppl 2): S34-40.
25. Venkatakrishnan A, Francisco GE, Contreras-Vidal JL. Applications of Brain–Machine Interface Systems
in Stroke Recovery and Rehabilitation. Current physical medicine and rehabilitation reports. 2014;2(2):93-
105. doi:10.1007/s40141-014-0051-4.
26. Hollender, KD. Screening, diagnosis, and treatment of post-stroke depression. J Neurosci Nurs. 2014 June;
46(3): 135–141. doi: 10.1097/JNN.0000000000000047
27. Nabavi SF, et al. Post-stroke depression therapy: where are we now? Curr Neurovasc Res. 2014;11(3):279-
28. Shah SH, Engelhardt R, Ovbiagele B. Patterns of complementary and alternative medicine use among
United States stroke survivors. J Neurol Sci. 2008;271:180–5. doi: 10.1016/j.jns.2008.04.014
29. Rabito MJ, Kaye AD. Complementary and Alternative Medicine and Cardiovascular Disease: An Evidence-
Based Review. Evidence-based Complementary and Alternative Medicine : eCAM. 2013;2013:672097.