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CEREBROVASCULAR DISORDERS PART 1 Author(s): Nneka L. Ifejika-Jones, MD MPH Originally published:7/30/2012 Last updated:4/19/2016

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 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.

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.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.

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 apparentdiffusion 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 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 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 See Cerebrovascular Disorders Part 2.

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.

REFERENCES

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; 372:11-20. 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; 80:12232. 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.

CEREBROVASCULAR DISORDERS PART 2: Author(s): Rani Haley Lindberg, MD, Mustafa Khan, MD Originally published:10/3/2012 Last updated:05/05/2016

1. DISEASE/DISORDER: Definition See Cerebrovascular Disorders Part 1.

2. ESSENTIALS OF ASSESSMENT See Cerebrovascular Disorders Part 1.

3. CUTTING EDGE/EMERGING AND UNIQUE CONCEPTS AND PRACTICE 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 therapy. 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 alone.16

Mirror Therapy7,15: Initially applied to amputation patients, this therapy involves placing a mirror in the midsagittal 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 changes. 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.

4. REHABILITATION MANAGEMENT AND TREATMENTS 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 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). 

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 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: 

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 ulcers.



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 17, 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.

5. GAPS IN THE EVIDENCE-BASED KNOWLEDGE 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, mindbody 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

REFERENCES 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: www.healthquality.va.gov/guidelines/Rehab/stroke. 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-2DTGXQKH 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. doi:10.3969/j.issn.1673-5374.2012.32.010 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. 2010;41(10):2402–2448 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. doi:10.1155/2012/159391. 12. Saver JL. Blood Pressure Management in Early Ischemic Stroke. JAMA. 2014;311(5):469-470. doi:10.1001/jama.2013.282544. 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. doi:10.1589/jpts.27.1681. 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: 10.1002/14651858.CD008349.pub3. 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. doi:10.3389/fnbeh.2015.00226 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):93105. 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):27989. 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 EvidenceBased Review. Evidence-based Complementary and Alternative Medicine : eCAM. 2013;2013:672097. doi:10.1155/2013/672097.

Source: https://now.aapmr.org/cerebrovascular-disorders-part-1-diseasedisorder-principles-ofassessment/ https://now.aapmr.org/cerebrovascular-disorders-part-2-diseasedisorder-principles-of-assessment/

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