eMedicine Specialties > Physical Medicine and Rehabilitation > Stroke

Motor Recovery In Stroke: Treatment & Medication

Author: Auri Bruno-Petrina, MD, PhD, Clinical Trainee, Pemberton Marine Medical Clinic, N Vancouver
Contributor Information and Disclosures

Updated: Oct 6, 2009

Treatment

Rehabilitation Program

Physical Therapy

Rehabilitation should include therapy that is directed at specific training of skills and at functional training. Therapy should be given with sufficient intensity to promote skill acquisition. Major theories of rehabilitation training include the following:

  • Traditional therapy - Range of motion (ROM), strengthening, mobilization, and compensatory techniques
  • Bobath - Neurodevelopmental training
    • Muscle patterns, not isolated movements, used for motion.
    • Inability to direct nervous impulses to muscle in different combinations used by persons with intact central nervous system (CNS).
    • Abnormal muscle patterns suppressed before normal patterns are introduced.
    • Associated reactions - Mass synergies avoided because may strengthen weak, unresponsive muscles (reinforces abnormally increased tone reflexes and spasticity).
    • Reflex-inhibiting patterns used to inhibit abnormal postural reactions; facilitates automatic voluntary movements.
    • Abnormal patterns modified at proximal key points of control (eg, neck, spine, shoulder, pelvis).
  • Knott, Voss - Proprioceptive neuromuscular facilitation7
    • Stimulation of nerve/muscle/sensory receptors to evoke response through manual stimuli to increase ease of movement and promote function
    • Normal neuromuscular mechanism capable of wide range of motor activities within limits of anatomical structure, developmental level, and previously learned neuromuscular responses; integrated and efficient without awareness of individual muscle action, reflex activity, and other reactions
    • Deficient neuromuscular mechanism inadequate to meet demands of life because of weakness, incoordination, adaptive joint shortening/immobility, muscle spasm, or spasticity
    • Specific demands placed by physical and occupational therapists have facilitating effects of neuromuscular mechanism and reverse limitations of patient.
    • Mass-movement patterns are in keeping with Beevor axiom (ie, the brain knows nothing of individual muscle action but only movement).
  • Brunnstrom - Central facilitation using Twitchell's recovery; enhances specific synergies through the use of cutaneous/proprioceptive stimuli.

Results from a randomized, controlled, assessor-blinded study indicated that even long after a stroke, kinesthetic ability training, administered in combination with a conventional rehabilitation program, can improve balance in hemiparetic stroke patients.8

Occupational Therapy

Most patients with significant neurologic impairment who survive a stroke are dependent on others for performance of basic ADL (ie, bathing, dressing, feeding, toileting, grooming, transfers). The capacity of individuals to perform these activities usually is scored on disability rating scales, such as the Functional Independence Measure. Almost all patients show improved performance of ADL as recovery occurs.

Most improvement is noted in the first 6 months, although as many as 5% of patients show continued measurable improvement up to 12 months postonset. Other patients may show some functional improvement beyond 6 months, even though the disability scales usually fail to detect further improvement because of their limited sensitivity at the upper end of the functional range.

Reports of the levels of functional independence eventually reached by stroke patients after recovery vary from one author to another. This variability probably reflects differences between study populations, methods of treatment, follow-up, and data reporting. In most reports, 47-76% of patients achieve partial or total independence in performance of ADL. Most authors who have attempted to determine which factors predict ultimate ADL functional outcome have used multivariate analysis. Of the many independent variables tested, those listed below were reported to have the most influence on outcome. However, not all of these factors were shown to predict outcome status statistically in every study. Factors predicting poor ADL outcome include the following:

  • Advanced age
  • Comorbidities
  • Myocardial infarction
  • Diabetes mellitus
  • Severe stroke
  • Severe weakness
  • Poor sitting balance
  • Visuospatial deficits
  • Mental changes
  • Incontinence
  • Low initial ADL scores
  • Delay in initiating rehabilitation following onset

Speech Therapy

Approximately one third of patients with acute stroke have clinical features of aphasia. Language function in many of these patients improves, and, at 6 months or more after stroke, only 12-18% of patients have identifiable aphasia. Skilbeck and colleagues reported that patients with aphasia continue to show some late improvement in language function even more than 1 year after onset.

Patients who are classified initially as having Broca aphasia have variable outcomes. In patients with large hemisphere lesions, Broca aphasia persists with little recovery. Patients with smaller lesions confined to the posterior frontal lobe often show early progressive improvement, but the impairment may evolve into a milder form of aphasia with anomia and difficulty finding words. Patients with global aphasia tend to progress slowly, with comprehension often improving more than expressive ability does. The communicative ability of patients who initially have global aphasia improves over a longer period of time, up to a year or more postonset. Patients with global aphasia associated with large lesions may show only minor recovery, but recovery may be quite good in patients with smaller lesions. The extent of language recovery associated with Wernicke aphasia is variable.

Medical Issues/Complications

  • Most patients with stroke who undergo rehabilitation have many other associated medical conditions that require professional attention. These problems might be preexisting medical illnesses that necessitate ongoing care (eg, hypertension, DM), secondary poststroke complications (eg, deep venous thrombosis, pneumonia), or acute poststroke exacerbations of preexisting chronic diseases (such as angina in a patient with ischemic heart disease). Management of these conditions can constitute major portions of the rehabilitation effort. Some patients may be more disabled by certain associated comorbid diseases than by the stroke itself.
  • The occurrence of these associated conditions has several implications for management of stroke cases during and after rehabilitation. First, these problems can detract from the benefits of rehabilitation. Some medical problems, such as heart disease, have been found to affect the course and outcome of rehabilitation adversely following a stroke. Intercurrent medical complications can limit the patient's ability to participate in therapeutic exercise programs, inhibit functional skill performance, and reduce the likelihood of achieving favorable outcomes from rehabilitation. The rehabilitation interventions also might affect the medical condition adversely, causing an exacerbation of the disease or necessitating an adjustment in the treatment program. Patients who are treated in a stroke unit have better outcomes at discharge than do patients who are not.9

Surgical Intervention

  • Tendon release - This can be performed in cases of severe spasticity or contractures.
  • Carotid endarterectomy - The surgery can be carried out for patients with stenosis of 70% or greater.
  • Carotid artery bypass to prevent a stroke or in patients who have had a TIA - There is no longer any clear indication for this; no benefit has been demonstrated from the surgery.
  • Surgical bypass or endarterectomy involving the posterior circulation - Although there are reports of successful cases, these procedures remain largely experimental.

Consultations

  • Psychologists
    • Psychosocial issues obviously are very important.
    • Numerous studies have reported on the influence of the psychological adjustment and coping mechanisms of the patient, as well as of his/her spouse and other family members, in determining the ultimate outcome.
  • Neurologists
  • Physiatrists

Other Treatment

  • Biofeedback attempts to modify autonomic functions, pain, and motor disturbances through acquired volitional control, using auditory, visual, and sensory clues.10
  • Functional electrical stimulation commonly is employed in UEs and LEs to improve strength, encourage and augment early active ROM, assist in the management of dependent peripheral edema through forceful isotonic muscle contraction, and establish early proprioceptive joint sense in the sensory-compromised patient.

Medication

Considerable effort has been invested in developing effective therapeutic agents that can arrest, delay, or reverse cerebral ischemia and neural injury. Current research has focused mainly on the following 4 pharmacologic treatments:

Heparin

 Intravenous heparin frequently is administered in the acute care setting to arrest stroke progression or to prevent its recurrence. Current available research has neither supported nor discredited the efficacy of heparin for acute stroke management, and clear guidelines for its use are lacking. The prevailing evidence supports the use of antiplatelet agents for the treatment of thrombotic stroke, but heparin may be appropriate for arresting an evolving stroke in some clinical situations. Because the risk of recurrent cardioembolic stroke is 12% within the first 3 weeks without anticoagulation therapy, the use of heparin and warfarin seem warranted if the risk of bleeding is otherwise low.

Calcium channel blockers
Calcium channel blocking agents, such as nimodipine, are effective in the prevention of death from vasospastic complications of subarachnoid hemorrhage (SAH) and are recommended for routine use during the first 21 days after hemorrhage. Several trials testing nimodipine for acute ischemic stroke treatment have had disappointing results. The vasodilating effect of calcium channel blockers can hamper stroke recovery by increasing intracranial pressure.

Thrombolytic agents

In studies that have enrolled subjects within the first 2-6 hours after onset of infarction, thrombolytic agents have achieved recanalization of occluded cranial arteries in acute stroke. Although the employment of agents such as tissue plasminogen activator (tPA) seems promising, acute hemorrhagic complications have limited their use.11,12 Medications such as ancrod, an agent that binds to and inactivates fibrinogen, have subsequently come under study in an effort to find a safer thrombolytic treatment for acute stroke. (See image below and Image 3.)

The bar graphs show the percentages of patients w...

The bar graphs show the percentages of patients with stroke who demonstrated different outcomes on the modified Rankin Scale of global disability. These results were recorded 3 months following treatment of patients with tissue plasminogen activator (tPA) or placebo, in the National Institutes of Neurological Disorders and Stroke tPA trials 1 and 2. Rankin 0 = no symptoms; 1 = no significant disability, despite symptoms (able to perform all usual duties and activities); 2 = slight disability (unable to perform all previous activities but able to look after own affairs without assistance); 3 = moderate disability (requires some help, but able to walk without assistance); 4 = moderately severe disability (unable to walk without assistance and unable to attend to own bodily needs without assistance); 5 = severe disability (bedridden, incontinent, and requires constant nursing care and attention); 6 = dead. Image courtesy of UCLA Stroke Center.

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The bar graphs show the percentages of patients w...

The bar graphs show the percentages of patients with stroke who demonstrated different outcomes on the modified Rankin Scale of global disability. These results were recorded 3 months following treatment of patients with tissue plasminogen activator (tPA) or placebo, in the National Institutes of Neurological Disorders and Stroke tPA trials 1 and 2. Rankin 0 = no symptoms; 1 = no significant disability, despite symptoms (able to perform all usual duties and activities); 2 = slight disability (unable to perform all previous activities but able to look after own affairs without assistance); 3 = moderate disability (requires some help, but able to walk without assistance); 4 = moderately severe disability (unable to walk without assistance and unable to attend to own bodily needs without assistance); 5 = severe disability (bedridden, incontinent, and requires constant nursing care and attention); 6 = dead. Image courtesy of UCLA Stroke Center.


Several new oral anticoagulant medications are in the final stages of clinical trials for use in the prophylaxis of ischemic thromboembolic stroke. Once approved for use, the potential of such drugs in the arena of stroke treatment is significant.

Management of spasticity requires careful evaluation, goal setting, and selection of appropriate therapies. Dantrolene has been used for many years for pharmacologic treatment of hemiplegic spasticity caused by stroke, but early use of dantrolene did not improve function in a double-blind study.

A small number of patients are bothered by spontaneous spasms, occurring mostly in bed at night. These spasms usually can be adequately controlled with small doses of diazepam before bedtime. For localized spasticity, such as in the forearm flexors or calf muscles, intramuscular neurolysis with phenol or chemodenervation with intramuscular botulinum toxin injections can be very effective.

Neuroprotective medications
Another class of medications for the treatment of acute stroke is the neuroprotective agents. In particular, the N -methyl-D-aspartate (NMDA) receptor antagonists have shown the potential ability to delay neuronal injury. During ischemic injury, excitatory neurotransmitters, such as glutamate and aspartate, are released extracellularly. In high concentrations, these amino acids act on NMDA membrane receptors, causing an influx of cations that results in rapid neuronal death. Controlled studies testing the ability of NMDA antagonists to prevent cytotoxic injury during acute stroke are underway.

Other agents have been used to treat stroke, including antioxidants, barbiturates, beta-adrenergic blockers, corticosteroids, dextran, hyperventilation drugs, naloxone, and vasodilators. Various opinions exist concerning the usefulness of these agents, but their effectiveness has not been demonstrated.

Antiplatelet agents

These agents inhibit platelet function by blocking cyclooxygenase and subsequent platelet aggregation. Antiplatelet therapy has been shown to reduce mortality by reducing the risk of fatal strokes, fatal myocardial infarctions, and vascular death in patients with a history of TIAs.


Ticlopidine (Ticlid)

Provides time- and dose-dependent inhibition of platelet aggregation and release of granules, which impedes ADP-induced platelet-fibrinogen binding. Maximum effect occurs by 8-11 d of use. Indicated to reduce risk of thrombotic stroke in patients who have stroke precursors, have already had a stroke, are intolerant of or allergic to aspirin, or have failed aspirin therapy.

Adult

250 mg PO bid for 3 mo

Pediatric

Not established

Phenytoin and propranolol levels might be increased; avoid use with salicylic acid because of adverse effects (higher doses)

Documented hypersensitivity, neutropenia, thrombocytopenia, hemostatic disorder, and severe liver impairment

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Rash and diarrhea are relatively common side effects; need 2-wk discontinuation for return of normal platelet function; reversible neutropenia, thus, monitor CBC count biweekly for 3 mo (including platelet count), from just before treatment is initiated to the end of the third month of therapy; potential early symptoms of thrombotic thrombocytopenic purpura (TTP) include fever, weakness, aphasia, convulsions, jaundice, hematuria or dark urine, pallor, and petechiae

Calcium channel blockers

The vasodilating effect of this medication can hamper stroke recovery by increasing intracranial pressure.


Nimodipine (Nimotop)

Has a greater effect on cerebral arteries than on arteries elsewhere in the body (probably because of its highly lipophilic properties). Mechanism to reduce neurologic deficits following subarachnoid hemorrhage not known. Peak plasma levels occur at 1 h. Half-life is 1-2 h. Significantly bound (over 95%) to plasma protein. Undergoes first-pass metabolism in the liver; metabolites excreted through the urine. Effective in the prevention of death from vasospastic complications of SAH and are recommended for routine use during the first 21 days after hemorrhage.

Adult

Capsules with 60 mg PO q4h beginning within 96 h after SAH and continuing for 21 consecutive d; reduce dose to 30 mg q4h in patients with hepatic impairment; can be taken with or without food

Pediatric

Not established; while no specific information on the use of this medication in younger patients exists, no special problems are expected

Although advantageous in some patients, coadministration with beta blockers may result in increased adverse effects because of depressant effects on myocardial contractility or on AV conduction; administered with fentanyl, severe hypotension or increased fluid volume requirements may occur in patients receiving calcium channel blockers; cimetidine may increase nimodipine blood levels

Documented hypersensitivity; <90 mm Hg systolic, sick sinus syndrome, or second- or third-degree AV block except when using a pacemaker

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Indicated only for reduction of cerebral vasospasm following SAH; must start within 96 h of the bleed; caution in impaired hepatic function and reduced hepatic blood flow; half-life may be increased in geriatric patients; side effects include hypotension, peripheral edema, CHF, ECG abnormalities, tachycardia, bradycardia, palpitations, rebound vasospasm, hypertension, hematoma, DIC, DVT, nausea, dyspepsia, diarrhea, abdominal discomfort, cramps, GI hemorrhage vomiting, headache, depression, lightheadedness, dizziness, abnormal LFT, hepatitis, jaundice, thrombocytopenia, anemia, purpura, ecchymosis, rash, dermatitis, pruritus, urticaria, dyspnea, muscle pain or cramps, acne, itching, flushing, diaphoresis, wheezing, and hyponatremia

Thrombolytic agents

The use of thrombolytic agents in acute stroke has been successful in achieving recanalization of occluded cranial arteries within the first 2-6 hours after onset of infarction. Treatment should be initiated only after exclusion of intercranial hemorrhage by a CT scan or other diagnostic imaging method sensitive for the presence of hemorrhage.

It has been considered imperative that tPA be administered within 3 hours of symptom onset. (In patients who wake up with symptoms or in those who cannot accurately describe the time of their symptom onset, the window is timed according to when they were last known to be well.) In 2009, however, the American Heart Association/American Stroke Association (AHA/ASA) published a science advisory recommending that the time window for tPA administration be increased to 4.5 hours after a stroke, although this change has not been approved by the US Food and Drug Administration (FDA).13

Although research indicates that tPA is effective in patients even when administered within the 3- to 4.5-hour window,14,15,16 the AHA/ASA stated in its advisory that, despite its recommendation, the effectiveness of tPA administration in comparison with other treatments for thrombosis, within that time period, is not yet known.

The eligibility criteria for treatment between 3 and 4.5 hours are similar to those employed for treatment prior to 3 hours, as established in the AHA/ASA's 2007 guidelines,17  but with the exclusion criteria expanded to include any of the following patient characteristics:

  • Age greater than 80 years
  • Use of oral anticoagulants
  • Baseline National Institutes of Health (NIH) Stroke Scale score >25
  • A history of both stroke and diabetes


Tissue plasminogen activator or alteplase (Activase)

A tissue plasminogen activator produced by recombinant DNA technology. This drug is a sterile purified glycoprotein of 527 amino acids; it is synthesized using the complementary DNA (cDNA) for natural human tissue plasminogen activator obtained from a human melanoma cell line. The manufacturing process involves secretion of the enzyme alteplase into a culture medium by an established mammalian cell line (Chinese hamster ovary cells), into which the cDNA for alteplase has been genetically inserted. Fermentation is carried out in a nutrient medium containing the antibiotic gentamicin, 100 mg/L; however, the presence of the antibiotic is not detectable in the final product.

Adult

50 mg vials or 100 mg administered using either a polyvinyl chloride bag or glass vial and infusion set; recommended total dose is 0.9 mg/kg (maximum of 90 mg) infused (IV) over 60 min with 10% of total dose administered as intravenous bolus over 1 min - during first 6 h from onset; not to exceed 90 mg
Recommended dose is 90 mg administered as 60 mg in first h (of which 6-10 mg is administered as bolus), 20 mg over second h, and 10 mg over third h; for smaller patients (<65 kg), a dose of 0.7 mg/kg administered over 3 h, as described above, may be used

Pediatric

Not established

As with all thrombolytic agents, alteplase therapy increases the risk of bleeding complications; concomitant use of heparin anticoagulation may contribute to bleeding; some of the hemorrhage episodes occurred 1 or more days after effects of alteplase had dissipated but while heparin therapy was continuing; interaction of alteplase with other cardioactive or cerebroactive drugs has not been studied; in addition to bleeding associated with heparin and vitamin K antagonists, drugs that alter platelet function (eg, aspirin, dipyridamole, abciximab) may increase the risk of bleeding if administered prior to, during, or after alteplase therapy

Evidence of intracranial hemorrhage on pretreatment evaluation; suspicion of SAH; recent intracranial surgery, serious head trauma, or recent previous stroke; history of intracranial hemorrhage; uncontrolled hypertension at time of treatment (eg, >185 mm Hg systolic or >110 mm Hg diastolic); seizure at the onset of stroke; active internal bleeding; intracranial neoplasm, arteriovenous malformation, or aneurysm; known bleeding diathesis, including, but not limited to, current use of oral anticoagulants (eg, warfarin sodium) with PT >15 seconds, administration of heparin within 48 hours preceding onset of stroke and elevated aPTT at presentation, and platelet count <100,000/µL

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Not effective if given later, and risk of inducing cerebral hemorrhage exists; thus, prescribe only if <3 h from onset and no evidence of hemorrhage on CT scan; patient selection and follow-up procedures include: (1) obtaining baseline CT scan to exclude intercranial hemorrhage, (2) treating eligible patients within 3 h of acute ischemic stroke symptom onset, (3) maintaining blood pressure at <185 mm Hg systolic and <110 mm Hg diastolic, (4) monitoring vital signs and neurologic status, and (5) providing no anticoagulant or antiplatelet therapy for 24 h

More on Motor Recovery In Stroke

Overview: Motor Recovery In Stroke
Differential Diagnoses & Workup: Motor Recovery In Stroke
Treatment & Medication: Motor Recovery In Stroke
Follow-up: Motor Recovery In Stroke
Multimedia: Motor Recovery In Stroke
References
Further Reading
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Keywords

stroke, strokes, stroke rehabilitation, stroke patients, hemiplegia, hemiplegic, brain stroke, after stroke, after a stroke, stroke motor, stroke recovery, stroke therapy, Brunnstrom, stroke rehab, post stroke, stroke exercises, stroke exercise, rehabilitation for stroke, treatment for stroke, treatment of stroke, stroke occupational therapy, neuroplasticity, recovery after cerebrovascular accident, recovery of neurologic function, stroke impairments

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Contributor Information and Disclosures

Author

Auri Bruno-Petrina, MD, PhD, Clinical Trainee, Pemberton Marine Medical Clinic, N Vancouver
Auri Bruno-Petrina, MD, PhD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, Canadian Association of Physical Medicine and Rehabilitation, College of Physicians and Surgeons of British Columbia, and International Society of Physical and Rehabilitation Medicine
Disclosure: Nothing to disclose.

Medical Editor

Milton J Klein, DO, MBA, Consulting Physiatrist, Heritage Valley Health System-Sewickley Hospital, Allegheny General Hospital, and Ohio Valley General Hospital.
Milton J Klein, DO, MBA is a member of the following medical societies: American Academy of Disability Evaluating Physicians, American Academy of Medical Acupuncture, American Academy of Osteopathy, American Academy of Physical Medicine and Rehabilitation, American Medical Association, American Osteopathic Association, American Osteopathic College of Physical Medicine and Rehabilitation, American Pain Society, and Pennsylvania Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Richard Salcido, MD, Chairman, Erdman Professor of Rehabilitation, Department of Physical Medicine and Rehabilitation, University of Pennsylvania School of Medicine
Richard Salcido, MD is a member of the following medical societies: American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American College of Physician Executives, American Medical Association, and American Paraplegia Society
Disclosure: Nothing to disclose.

CME Editor

Kelly L Allen, MD, Regional Medical Director, IMX-Medical Management Services
Disclosure: Nothing to disclose.

Chief Editor

Denise I Campagnolo, MD, MS, Director of Multiple Sclerosis Clinical Research and Staff Physiatrist, Barrow Neurology Clinics, St Joseph's Hospital and Medical Center; Investigator for Barrow Neurology Clinics; Director, NARCOMS Project for Consortium of MS Centers
Denise I Campagnolo, MD, MS is a member of the following medical societies: Alpha Omega Alpha, American Association of Neuromuscular and Electrodiagnostic Medicine, American Paraplegia Society, Association of Academic Physiatrists, and Consortium of Multiple Sclerosis Centers
Disclosure: Teva Neuroscience Honoraria Speaking and teaching; Serono-Pfizer Honoraria Speaking and teaching; Genzyme Corporation Grant/research funds investigator; Biogen Idec Grant/research funds investigator; Genentech, Inc Grant/research funds investigator; Eli Lilly & Company Grant/research funds Novaritis; Novaritis  Novaritis; MSDx LLC Grant/research funds investigator; BioMS Technology Corp Grant/research funds investigator; Avanir Pharmaceuticals Grant/research funds investigator

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