eMedicine Specialties > Physical Medicine and Rehabilitation > Stroke

Motor Recovery In Stroke

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

Updated: Oct 6, 2009

Introduction

Background

Stroke rehabilitation is a combined and coordinated use of medical, social, educational, and vocational measures for retraining a person to his/her maximal physical, psychological, social, and vocational potential, consistent with physiologic and environmental limitations. (See image below and Image 1.)

When the brain suffers an injury, such as a strok...

When the brain suffers an injury, such as a stroke, neurons release glutamate onto nearby neurons, which become excited and overloaded with calcium, after which they die (left). Normal neurotransmission (above) is altered during injury, causing excess calcium to activate enzymes, eventually leading to destruction of the cell. Since this process occurs via glutamate receptors, including N-Methyl-D-aspartate (NMDA) receptors, scientists believe that damage can be stopped through the use of agents that block these receptors.

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When the brain suffers an injury, such as a strok...

When the brain suffers an injury, such as a stroke, neurons release glutamate onto nearby neurons, which become excited and overloaded with calcium, after which they die (left). Normal neurotransmission (above) is altered during injury, causing excess calcium to activate enzymes, eventually leading to destruction of the cell. Since this process occurs via glutamate receptors, including N-Methyl-D-aspartate (NMDA) receptors, scientists believe that damage can be stopped through the use of agents that block these receptors.


Many studies show that stroke rehabilitation is effective and can improve functional ability, even in patients who are elderly or medically ill and who have severe neurologic and functional deficits. Experts in stroke rehabilitation abound, but none have proven anything about rehabilitation to the satisfaction of anyone else.

Evidence from clinical trials supports the premise that early initiation of therapy favorably influences the outcome. When the initiation of therapy is delayed, patients may in the interim develop avoidable secondary complications, such as contractures and deconditioning.

The course of motor recovery reaches a plateau after an early phase of progressive improvement. Most recovery takes place in the first 3 months, and only minor additional measurable improvement occurs after the 6 months following onset; however, recovery may continue over a longer period of time in some patients who have significant partial return of voluntary movement.

Pathophysiology

In the early phase following stroke, there is prompt initial improvement in function as the pathologic processes associated with the penumbra-ischemic metabolic injury, edema hemorrhage, and blood pressure (BP) resolve. The time frame for recovery of function in these reversibly injured neurons is relatively short, accounting for improvement in the first several weeks. The later ongoing improvement in neurologic function occurs by a different set of mechanisms that allow structural and functional reorganization within the brain. The processes involved in this reorganization represent neuroplasticity and may continue for many months. Restitution of partially damaged pathways and expansion of representational brain maps occur, implying recruitment of neurons that are not ordinarily involved in an activity.

A key aspect of neuroplasticity that has important implications for rehabilitation is the fact that the modifications in neuronal networks are use-dependent. Animal experimental studies and clinical trials in humans have shown that forced use and functional training contribute to improved function. On the other hand, techniques that promote nonuse may inhibit recovery.

In the past, the conventional wisdom was that benefits from rehabilitation are achieved primarily through training patients in new techniques that compensate for impairments (for example, using the uninvolved hand to achieve self-care independence). This approach avoided intense therapy on the weak upper limb. Currently, it is recognized that repeated participation by patients in active physical therapeutic programs probably provides direct influence on the process of functional reorganization in the brain and enhances neurologic recovery.

Theories of recovery

  • Collateral sprouting from intact cells to the denervated region after some or all input has been destroyed
  • Unmasking of neural pathways and synapses that are not normally used but that can be called upon when the dominant system fails (excitability to capture effects of remaining input)

Mechanisms of recovery of neurologic function

  • The first mechanism is resolution of harmful local factors, which generally accounts for early spontaneous improvement after stroke (usually within the first 3-6 mo). These processes include resolution of local edema, resorption of local toxins, improvement of local circulation, and recovery of partially damaged ischemic neurons.
  • The second recovery mechanism is neuroplasticity, which can take place early or late. Brain plasticity is the ability of the nervous system to modify its structural and functional organization. The 2 most plausible forms of plasticity are collateral sprouting of new synaptic connections and unmasking of previously latent functional pathways.
  • Other mechanisms of plasticity include assumption of function by undamaged redundant neural pathways, reversibility from diaschisis, denervation supersensitivity, and regenerative proximal sprouting of transected neuronal axons. Experimental evidence indicates that plasticity can be altered by several external factors, including pharmacologic agents, electrical stimulation, and environmental stimulation.

Natural spontaneous neurologic recovery

  • Patients recover after stroke in 2 different, but related, ways.
    • A reduction in the extent of neurologic impairment can result from spontaneous natural neurologic recovery (via the effects of treatments that limit the extent of the stroke) or from other interventions that enhance neurologic functioning. A patient demonstrating this form of recovery presents with improvements in motor control, language ability, or other primary neurologic functions.
    • The second type of recovery demonstrated by stroke patients is the improved ability to perform daily functions within the limitations of their physical impairments. A patient who has sensorimotor, cognitive, or behavioral deficits resulting from stroke may regain the capacity to carry out activities of daily living (ADL), such as feeding himself/herself, dressing, bathing, and toileting, even if some degree of residual physical impairment remains. The ability to perform these tasks can improve through adaptation and training in the presence or absence of natural neurologic recovery, which is thought to be the element of recovery on which rehabilitation exerts the greatest effect.

Frequency

United States

Stroke is the most common serious neurologic disorder in the United States, comprising 50% of all patients admitted to a hospital for a neurologic disease. In the 1960s, 500,000 new cases of stroke were reported per year. A decline in the overall incidence was noted late in the 1970s, but this decline flattened out in the 1980s. Since then, a small rise in incidence may be noted.

International

In most European countries, stroke is of great importance because of the tremendous expenditures arising from cost-intensive treatment and the large demand for continued nursing care. In Japan and other Asian countries, stroke is the second most frequent cause of death in patients aged 65 years or more. For Chinese stroke patients, disability at admission is the most important predictor of disability at discharge because of a lack of subacute care and rehabilitation facilities.1,2

Mortality/Morbidity

Stroke is the third leading cause of death, exceeded only by cardiovascular disease and cancer. The mortality rate for stroke has nonetheless decreased, mainly because of advances in emergency and preventive medicine.

  • Mortality rates in the general stroke survivor population are difficult to predict.
    • At 3 weeks to 1 month - 22-37%
    • At 1 year - 25-50%
    • At 5 years - 68-72%
    • At 6 years - 55%
    • At 10 years - 65%
  • Individuals who survive the initial insult have good life expectancy.
    • Fifty percent remain alive after 5 years, and those surviving for longer than 18 months lived for periods comparable to those for general age-matched and sex-matched populations.
    • The average life expectancy is 7 years following rehabilitation; 30% survive for 11 years.
  • Intracerebral hemorrhage carries the highest mortality rate of all types of strokes. (See image below and Image 2.)
    • A reduction in mortality of 28% has been noted after 4 and 12 months if patients are treated for stroke on a stroke unit.3
    • The mortality rate is 24.6% on a stroke unit and 32.7% on a medical unit.
Large intracerebral hemorrhage with midline shift.

Large intracerebral hemorrhage with midline shift.

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Large intracerebral hemorrhage with midline shift.

Large intracerebral hemorrhage with midline shift.


Race

Many common risk factors for stroke are found in higher frequency among African Americans, including hypertension, diabetes mellitus (DM), heart disease, smoking, excessive alcohol use, and sickle cell disease. The incidence of stroke mortality among black men and women is double that seen in whites. Moreover, stroke mortality is 3- to 4-fold higher among blacks younger than 65 years than it is among whites.

Sex

The incidence of stroke is 19% higher among men than women of all races.

Age

Stroke is primarily a disease of older individuals, although 28% of strokes occur in persons younger than 65 years. Incidence is age-related. Stroke is uncommon in persons younger than 50 years, but incidence doubles each decade after age 55 years. After age 80 years, the incidence may be as high as 2.5 cases per 1000 population.

The effect of age on outcome may be related in part to more frequent co-impairments. If elderly patients have lost function before sustaining a stroke, less favorable outcomes following a stroke would be expected. Furthermore, elderly patients often do not receive as intensive a therapy as that provided to younger patients, perhaps because of a greater intolerance to activity. Older patients may be discharged sooner from a rehabilitation program.

Clinical

History

Hemiparesis and motor recovery have been the most studied of all stroke impairments. As many as 88% of patients with acute stroke have hemiparesis. In a classic report, Twitchell described in detail the pattern of motor recovery following stroke.4 At onset, the upper extremity (UE) is more involved than the lower extremity (LE), and eventual motor recovery in the UE is less than in the LE. The severity of UE weakness at onset and the timing of the return of movement in the hand are both important predictors of eventual motor recovery in the UE. The prognosis for return of useful hand function is unfavorable when UE paralysis is complete at onset or grasp strength is not measurable by 4 weeks. However, as many as 9% of patients with severe UE weakness at onset may gain good recovery of hand function. As many as 70% of patients showing some motor recovery in the hand by 4 weeks make a full or good recovery. Full recovery, when it occurs, usually is complete within 3 months of onset.

Bard and Hirshberg claim that if no initial motion is noticed during the first 3 weeks or if motion in one segment is not followed within a week by the appearance of motion in a second segment, the prognosis for recovery of full motion is not favorable.

Movement typically returns 43-60 days (but no later than 3 months) poststroke. Almost all spontaneous recovery occurs within 6 months, but gains continue to occur 6-12 months following the stroke. Recovery occurs for months or years. Indeed, cessation of recovery after 6 months may be a self-fulfilling prophecy.

Physical

The initial clinical examination of a patient with an acute stroke includes a thorough, detailed neurologic examination. The neurologic findings are used by the rehabilitation team for prognostication, development of the specific details of the rehabilitation plan, and selection of the appropriate setting for rehabilitation. Reassessment of the patient's condition during rehabilitation provides a means of monitoring progress and subsequently evaluating outcome. The initial rehabilitation assessment should begin immediately following onset, within 2-7 days, and then subsequently at repeated intervals.

After stroke occurs, total loss of voluntary movement may be noted in involved extremities, with loss or decrease in muscle stretch reflexes (MSRs). Within 48 hours, MSRs and finger jerks are more active on the involved side, although they may require 3-29 days to develop. Within a short period, tone appears in the wrist and finger flexors, as well as in the ankle plantar flexors. As a result, the UE is prone to demonstrate the adductor/flexor pattern and the LE, the adductor/extensor pattern.

In 1-30 days, spasticity appears, resulting in resting posture, as follows:

  • Upper extremity
    • Shoulder is in adduction and internal rotation.
    • Elbow is in flexion.
    • Forearm is in pronation/supination.
    • Wrist and fingers are in flexion.
  • Lower extremity
    • Hip is in adduction and extension.
    • Knee is in extension
    • Ankle is in plantar flexion
    • Foot is in inversion
    • Within 1-38 days after stroke, clonus appears in ankle plantar flexors.
    • Onset of clasp-knife phenomenon occurs within 3-31 days.
    • Spasticity decreases with increased volitional movement, but MSRs always remain increased, despite total recovery.
  • Recovery of movement
    • UE flexor synergy
      • Shoulder flexion (6-33 days) ® elbow flexion (1-6 days later) ® finger and wrist flexion (1-13 days later) ® shoulder adduction/internal rotation
      • Clinically, flexor synergy can also present as scapula retraction/elevation, shoulder abduction (90°)/external rotation, elbow flexion (acute angle), and forearm supination (full range).
    • UE extensor synergy
      • Shoulder ® elbow ® wrist/finger extension
      • Clinically, extensor synergy presents as scapula protraction, humerus flexion/internal rotation, elbow extension, and forearm pronation.
    • LE flexor synergy - Hip flexion/adduction (1-31 days) ® knee flexion (1-2 days later) ® ankle/toe dorsiflexion (25-90 days)
    • LE extensor synergy - Hip/knee extension ® ankle plantar flexion

Causes

  • Causes of stroke in children and young adults include the following:
    • Cerebral embolism
    • Trauma to extracranial arteries
    • Subarachnoid hemorrhage
    • Sickle cell anemia
    • Vasculopathy
    • Coagulopathy
    • Cardiogenic emboli
    • Homocystinuria
    • Oral contraceptives
    • Childbirth
    • Drug use (cocaine)
    • HIV-associated disease
  • Risk factors for stroke in asymptomatic patients include the following:
    • Hypertension
    • Heart disease (atrial fibrillation)
    • Smoking
    • Diabetes mellitus
    • Elevated fibrinogen
    • Erythrocytosis
    • Hyperlipidemia
  • Risk factors for stroke in symptomatic patients include transient ischemic attacks (TIAs).
  • Risk factors for recurrent stroke5 include the following:
    • Previous stroke
    • Hypertension
    • Heart disease
    • Heavy alcohol consumption
    • Diabetes mellitus
  • Early death following a stroke usually is related to the underlying pathology and to the severity of the lesion. The 30-day survival rate for patients with cerebral infarction is 85%, but for patients with intracerebral hemorrhage, survival is reported to be only 20-52%.
  • Better management of cardiac and respiratory disorders has reduced early mortality. However, hypertension, heart disease, and DM remain risk factors for recurrence of stroke.
  • Coma following stroke onset indicates an unfavorable prognosis, presumably because coma occurs frequently in cerebral hemorrhage. When coma occurs in association with cerebral infarction, it reflects a large lesion with cerebral edema.

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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