Enhance Motor Recovery Research Articles

Percutaneous intramuscular neuromuscular electric stimulation for the treatment of shoulder subluxation and pain in patients with chronic hemiplegia: A pilot study

Yu DT, Chae J, Walker ME, Fang Z-P. Percutaneous intramuscular neuromuscular electric stimulation for the treatment of shoulder subluxation and pain in patients with chronic hemiplegia: a pilot study. Arch Phys Med Rehabil 2001;82:20-5. Objective: To investigate the feasibility of percutaneous intramuscular neuromuscular electric stimulation (perc-NMES) for treating shoulder subluxation and pain in patients with chronic hemiplegia. Design: Before-after trial. Setting: University-affiliated tertiary care hospital. Participants: A convenience sample of 8 neurologically stable subjects with chronic hemiplegia and shoulder subluxation. Intervention: Six weeks of perc-NMES to the subluxated shoulder. Main Outcome Measures: Shoulder subluxation (radiograph), shoulder pain (Brief Pain Inventory), motor impairment (Fugl-Meyer score), shoulder pain-free external rotation (handheld goniometer), and disability (FIM™ instrument) were assessed before treatment (T1), after 6 weeks of neuromuscular stimulation (T2), and at 3-month follow-up (T3). A 1-way, repeated-measures analysis of variance using the generalized estimating equation approach was used to evaluate differences from T1 to T2 and from T1 to T3 for all outcome measures. Results: Subluxation (p =.0117), pain (p =.0115), shoulder pain-free external rotation (p <.0001), and disability (p =.0044) improved significantly from T1 to T2. Subluxation (p =.0066), pain (p =.0136), motor impairment (p <.0001), shoulder pain-free external rotation (p =.0234), and disability (p =.0152) improved significantly from T1 to T3. Conclusions: Perc-NMES is feasible for treating shoulder dysfunction in hemiplegia and may reduce shoulder subluxation, reduce pain, improve range of motion, enhance motor recovery, and reduce disability in patients with chronic hemiplegia and shoulder subluxation. Further investigation is warranted. © 2001 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation

Locomotor Capacity Attributable to Step Training Versus Spontaneous Recovery After Spinalization in Adult Cats

Locomotor performance, hindlimb muscle activity and gait patterns during stepping were studied in step-trained and non-trained female, adult spinal cats. Changes in locomotor characteristics relative to prespinalization bipedal and quadrupedal stepping patterns were used to evaluate the effects of step training on the capacity to execute full weight-bearing stepping after spinalization. Step training consisted of full weight-bearing stepping of the hindlimbs at the greatest range of treadmill speeds possible at any given stage of locomotor recovery. In the initial stages of training the limbs were assisted as needed to execute successful steps. On the basis of two behavioral criteria, the maximum speed of treadmill stepping and the number of successful steps per unit time, the ability to step was at least 3 times greater in animals trained to step versus those allowed to recover spontaneously, i.e., the non-trained. The greater success in stepping was reflected in several physiological and kinematic properties. For example, the amplitude of electromyograph (EMG) bursts in the tibialis anterior (an ankle dorsiflexor), the amount of extension at the end of both the stance (E3) and swing (E1) phases of the step cycle, and the amount of lift of the hindlimb during swing were greater in step-trained than in non-trained spinal cats. The changes that occurred in response to training reflected functional adaptations at specific phases of the step cycle, e.g., enhanced flexor and extensor function. The improved stepping capacity attributable to step training is interpreted as a change in the probability of the appropriate neurons being activated in a temporally appropriate manner. This interpretation, in turn, suggests that step training facilitated or reinforced the function of extant sensorimotor pathways rather than promoting the generation of additional pathways. These results show that the capacity of the adult lumbar spinal cord to generate full weight-bearing stepping over a range of speeds is defined, in large part, by the functional experience of the spinal cord after supraspinal connectivity has been eliminated. These results have obvious implications with regards to 1) the possibility of motor learning occurring in the spinal cord; 2) the importance of considering "motor experience" in assessing the effect of any postspinalization intervention; and 3) the utilization of use-dependent interventions in facilitating and enhancing motor recovery.

Synthesis of Intervention Trials To Improve Motor Recovery following Stroke

Therapists have used multiple interventions to improve motor recovery following stroke. However, the clinical research studies to support efficacy of the interventions are few. The purpose of this article is to synthesize the results of the clinical trials that have assessed therapeutic interventions to enhance motor recovery. The results of the current research provide some evidence that physical interventions may improve intrinsic motor recovery. The interventions that have been shown to be effective require active participation of the patient and repetitive training. The improvements in motor control have been limited to select patients with volitional motor control.

Treatment Strategies for Enhancing Motor Recovery in Stroke Rehabilitation

Motor dysfunction, the most common clinical accompaniment of stroke, is associated with functional disability, and is a major concern of patients and family. Although current strategies to treat mo...

Sialyl cholesterol enhances the development of grafted neurons and motor recovery

Trophic actions of α-sialyl cholesterol (SC) and its sialidase-tolerant derivative, α-(3β-hydroxysialyl) cholesterol (SCt), were carried out on the development of midbrain neurons both in vitro and in vivo transplantation studies. Low to moderate concentrations of SC (0.01 to 0.05 μg/ml) facilitated neurite extension but had no effects on cell survival of primary cultured midbrain neurons. However, high concentration of SC (0.1 Mg/ml) disturbed both neunte genesis and cell survival. SCt had a similar effect on midbrain neurons. At higher concentrations, SC and SCt induced concentration-dependent morphological changes in astrocytes from flat to fibrous. The effect on astrocytes was stronger in SCt than SC. At highest concentration tested (20 μg/ml), the proliferation of astrocytes was completely blocked, cells became detached and finally died. This effect of SC and SCt was partially blocked by simultaneous application of aFGF. Following dopaminergic cell grafting in vivo, SC and SCt had biphasic effects: a low dose (0.2 mg/kg, SC) enhanced motor recovery at 4 and 6 weeks after transplantation, while the highest dose (20 mg/kg, SC) disturbed motor recovery at all periods tested. These effects on motor recovery were paralleled by an effect on neurite genesis as studied by tyrosine hydroxylase immunostaining. Thus, at low concentrations, SC and SCt are neurotrophic agents that stimulate the development and differentiation of dopaminergic neurons.

Siagoside selectively attenuates morphological and functional striatal impairments induced by transient forebrain ischemia in rats.

Transient forebrain ischemia induced in rats by the four-vessel occlusion method is known to produce severe neural damage in the hippocampus and striatum and a behavioral syndrome the major symptom of which is a working memory deficit. Recent evidence suggests that monosialogangliosides can ameliorate postischemic symptoms. Our purpose was to study the effect of siagoside, the inner ester of GM1 ganglioside, on some behavioral and morphological impairments induced by four-vessel occlusion in rats. Rats were injected daily with 5 mg/kg i.p. siagoside starting 4 hours after the cerebral ischemia. After 14 days the rats were tested for working memory in a water T maze or scored for apomorphine-induced stereotypy. The rats were killed 21 days after the cerebral ischemia. Histological and computer-assisted morphometric analyses were performed on cresyl violet-stained brain sections, which were graded according to a neuropathologic score, and on sections stained with a monoclonal antiserum against dopamine and cyclic adenosine-3',5'-monophosphate-regulated phosphoprotein, a marker for striatal dopaminoceptive neurons. Siagoside treatment reduced the stereotypy score induced by low doses of apomorphine and the extent of striatal lesions but did not affect the working memory deficit or the extent of hippocampal lesions. Daily siagoside treatment after acute cerebral ischemia attenuates some morphological and functional deficits related to striatal damage. These effects can be interpreted as a selective protective action on striatal neural populations or as a modulatory action on neural systems involved in striatal control. These data are consistent with preliminary clinical reports showing that monosialogangliosides enhance motor recovery after acute ischemic stroke.

Spinal cord injury models: neurophysiology.

Spinal cord injury models: neurophysiology.

Opiate antagonists and thyrotropin-releasing hormone. II. Potential role in the treatment of central nervous system injury.

PARALYSIS resulting from CNS injury has been recognized for more than 2,000 years. Although much has been learned about the pathophysiology of spinal cord injury, head injury, and stroke, therapeutic management of such patients, particularly with regard to pharmacologic interventions, has progressed relatively little. This lack of progress has generated a sense of futility among physicians who treat these conditions. Yet a number of novel therapeutic measures have been suggested over the past few years, based on the successful alteration of neurological outcome following experimental CNS injury. Of particular interest have been the observations that opiate antagonists may improve neurological recovery in experimental stroke, head injury, and spinal cord injury and that thyrotropin-releasing hormone (TRH) may significantly enhance motor recovery after traumatic spinal cord injury. CNS Injury—Pathophysiological Considerations During the past decade it has become increasingly clear that traumatic or ischemic insults to the CNS may cause neurological deficits through