Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026838 (spasticity)
 6,471 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors of this prospective, single-case study evaluated the potential for functional recovery from chronic spinal cord injury (SCI). The patient was motor complete with minimal and transient sensory perception in the left hemibody. His condition was classified as C-2 American Spinal Injury Association (ASIA) Grade A and he had experienced no substantial recovery in the first 5 years after traumatic SCI. Clinical experience and evidence from the scientific literature suggest that further recovery would not take place. When the study began in 1999, the patient was tetraplegic and unable to breathe without assisted ventilation; his condition classification persisted as C-2 ASIA Grade A. Magnetic resonance imaging revealed severe injury at the C-2 level that had left a central fluid-filled cyst surrounded by a narrow donutlike rim of white matter. Five years after the injury a program known as "activity-based recovery" was instituted. The hypothesis was that patterned neural activity might stimulate the central nervous system to become more functional, as it does during development. Over a 3-year period (5-8 years after injury), the patient's condition improved from ASIA Grade A to ASIA Grade C, an improvement of two ASIA grades. Motor scores improved from 0/100 to 20/100, and sensory scores rose from 5-7/112 to 58-77/112. Using electromyography, the authors documented voluntary control over important muscle groups, including the right hemidiaphragm (C3-5), extensor carpi radialis (C-6), and vastus medialis (L2-4). Reversal of osteoporosis and an increase in muscle mass was associated with this recovery. Moreover, spasticity decreased, the incidence of medical complications fell dramatically, and the incidence of infections and use of antibiotic medications was reduced by over 90%. These improvements occurred despite the fact that less than 25 mm2 of tissue (approximately 25%) of the outer cord (presumably white matter) had survived at the injury level. The primary novelty of this report is the demonstration that substantial recovery of function (two ASIA grades) is possible in a patient with severe C-2 ASIA Grade A injury, long after the initial SCI. Less severely injured (lower injury level, clinically incomplete lesions) individuals might achieve even more meaningful recovery. The role of patterned neural activity in regeneration and recovery of function after SCI therefore appears a fruitful area for future investigation.
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PMID:Late recovery following spinal cord injury. Case report and review of the literature. 1507 Jan 54

Spasticity is an abnormal increase in muscle contraction often caused by damage to central motor pathways that control voluntary movement. During clinical examination, spasticity manifests as an increase in stretch reflexes, producing tendon jerks and resistance appearing as muscle tone. There are many causes of spasticity, including demyelination from multiple sclerosis, congenital damage from diseases such as cerebral palsy, trauma to the brain or spinal cord, hemorrhage or infarction, and other pathologic conditions that interrupt neural pathways. Effects of spasticity range from mild muscle stiffness to severe, painful muscle contractures and repetitive spasms that reduce mobility and substantially impede normal activities of daily living. Botulinum toxin therapy reduces spasticity and pain associated with several disorders. Local treatment with botulinum toxins can be used as adjunctive therapy, along with oral antispasticity medications, or alone to provide localized decrease in symptoms of spasticity and pain. Botulinum toxin therapy may be particularly useful for patients with spasticity due to stroke, whose treatment can be tailored based on recovery of function over time. In addition, botulinum toxin therapy is safe for pediatric patients, including children with cerebral palsy, who may not be able to tolerate the cognitive side effects of oral medications. Results of studies evaluating botulinum toxin for the treatment of spasticity due to various causes are presented here.
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PMID:Treatment of spasticity with botulinum toxin. 1256 67

Harmful spasticity after cerebral or spinal damage disturbs functional recovery in neurorehabilitation, but neurosurgical interventions for relief of spasticity are not widely performed, at least in Asian countries including Japan. We have been performing various types of neurosurgical treatment for spasticity such as selective peripheral neurotomy, selective dorsal rhizotomy, microsurgical DREZotomy, and intrathecal baclofen administration. We deal with both children and adults. From our experience of tibial neurotomy, in particular, we describe functional microsurgical anatomy of the tibial nerve in the popliteal fossa. This is the first report on this regional functional anatomy.
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PMID:The role of neurosurgical interventions for control of spasticity in neurorehabilitation: new findings on functional microanatomy of the tibial nerve. 1451 34

Shoulder pain is a common complication in poststroke hemiplegia that reduces functional recovery. Many types of shoulder pathology have been suggested as causes of shoulder pain in hemiplegia,including shoulder subluxation, capsulitis, tendinitis, rotator cuff injury, bursitis, impingement syndrome, spasticity, complex regional pain syndrome, brachial plexus injury, and proximal mononeuropathies. More than one type of pathology may exist in a given patient. Shoulder pain improves in many cases with prompt diagnosis and appropriate management. Although the relationship between subluxation and pain is controversial, upper limb support to reduce subluxation is the standard of care and may prevent the development of pain and secondary complications. Further work is needed to elucidate the natural history of shoulder pain in hemiplegia, including the identification of physiologic common denominators that can lead to improved strategies to treat and prevent shoulder pain.
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PMID:Shoulder pain in hemiplegia. 1521 95

The objectives of this study were to describe the demographic characteristics and the nature of the functional recovery in a group of Turkish survivors of traumatic brain injury (TBI) who were referred for inpatient rehabilitation and identify variables correlated with discharge functional status as measured by the Functional Independence Measure (FIM). There were 40 patients in the study, 32 (69.6%) male and eight (17.4%) female, mean age 28+/-9.8 years. Motor vehicle accidents accounted for 62.5% of injuries, 22.5% of injuries occurred from violence and 15% resulted from falls. The mean durations of acute hospital stay, coma, and rehabilitation stay was 68, 26.7, and 78.4 days, respectively. Extracranial injuries including bone fractures were the most common associated injuries and medical complications such as spasticity and contractures were present in more than half of the patients.TBI survivors in this study made statistically significant functional improvements. Discharge FIM were significantly correlated with the admission FIM, durations of acute hospital stay and coma, and time since TBI. Multiple regression analysis of the data disclosed that FIM score obtained at the time of discharge from rehabilitation service was best predicted by two variables, time since brain injury and the FIM score at admission (multiple R=0.78, R=0.60, P<0.001). This sample of Turkish TBI survivors showed significant functional improvements after rehabilitation and admission functional status and the time since TBI had the most impact on discharge functional outcome.
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PMID:Functional outcome following traumatic brain injury: the Turkish experience. 1557 87

Prior studies have shown that neurons within the spinal cord are sensitive to response-outcome relations, a form of instrumental learning. Spinally transected rats that receive shock to one hind leg learn to maintain the leg in a flexed position that minimizes net shock exposure (controllable shock). Prior exposure to uncontrollable stimulation (intermittent shock) inhibits this spinally mediated learning. Here it is shown that uncontrollable stimulation undermines the recovery of function after a spinal contusion injury. Rats received a moderate injury (12.5 mm drop) and recovery was monitored for 6 weeks. In Experiment 1, rats received varying amounts of intermittent tailshock 1-2 days after injury. Just 6 min of intermittent shock impaired locomotor recovery. In Experiment 2, rats were shocked 1, 4, or 14 days after injury. Delaying the application of shock exposure reduced its negative effect on recovery. In Experiment 3, rats received controllable or uncontrollable shock 24 and 48 h after injury. Only uncontrollable shock disrupted recovery of locomotor function. Uncontrollably shocked rats also exhibited higher vocalization thresholds to aversive stimuli (heat and shock) applied below the injury. Across the three experiments, exposure to uncontrollable shock, (1) delayed the recovery of bladder function; (2) led to greater mortality and spasticity; and (3) increased tissue loss (white and gray matter) in the region of the injury. The results indicate that uncontrollable stimulation impairs recovery after spinal cord injury and suggest that reducing sources of uncontrolled afferent input (e.g., from peripheral tissue injury) could benefit patient recovery.
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PMID:Uncontrollable stimulation undermines recovery after spinal cord injury. 1568 70

Following stroke, persons experience deficits in motor control, reduced muscle strength, disuse atrophy, reduced cardiovascular fitness and elevated energy expenditure during locomotion. Recent exercise studies with few subjects, report beneficial outcomes after strength and low intensity aerobic exercise training. Progressive strength and aerobic exercise programmes from 3 to 6 months produced gains in functional recovery and health-related functional status such as motor function, peak isokinetic torque, balance, endurance, peak aerobic capacity and overall fitness without exacerbating spasticity. Increased access to community-based physical activity programmes is recommended to prevent deconditioning and to improve health related quality of life in persons after stroke. Well-functioning rehabilitation from acute care, through special rehabilitation units to community-based physical activity programmes is important.
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PMID:[Adapted exercise important after stroke. Acute and long-term effects of different training programs]. 1575 82

Botulinum toxin A (BoNT-A) is a potent biological toxin widely used for the management of skeletal muscle spasticity or dynamic joint contracture. Intramuscular injection of BoNT-A causes muscle denervation, paresis, and atrophy. This clinical effect of botulinum toxin A lasts 3 to 6 months, and injected muscle eventually regains muscle mass and recovers muscle function. The goal of the present study was to characterize the molecular and cellular mechanisms leading to neuromuscular junction (NMJ) regeneration and skeletal muscle functional recovery after BoNT-A injection. Fifty-six 1-month-old Sprague-Dawley rats were used. Botulinum toxin A was injected into the left gastrocnemius muscle at a dosage of 6 units/kg body weight. An equivalent volume of saline was injected into the right gastrocnemius muscle to serve as control. The gastrocnemius muscle samples were harvested from both hind limbs at 3 days, 7 days, 15 days, 30 days, 60 days, 90 days, 180 days, and 360 days after administration of toxin. In addition, the gastrocnemius muscles from 1-month-old rats with no injections were harvested to serve as uninjected control group. Muscle samples were processed and mRNA was extracted. Real-time polymerase chain reaction (PCR) and gene microarray technology were used to identify key molecules involved in NMJ stabilization and muscle functional recovery. More than 28,000 rat genes were analyzed and approximately 9000 genes are expressed in the rat gastrocnemius muscle. Seven days following BoNT-A injection, 105 genes were upregulated and 59 genes were downregulated. Key molecules involved in neuromuscular junction (NMJ) stabilization and muscle functional recovery were identified and their time course of gene expression following BoNT-A injection were characterized. This animal study demonstrates that following intramuscular injection of BoNT-A, there is a sequence of cellular events that eventually leads to NMJ stabilization, remodeling, and myogenesis and muscle functional recovery. This recovery process is divided into two stages (aneural and neural) and that the IGF-1 signaling pathway play a central role in the process.
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PMID:How muscles recover from paresis and atrophy after intramuscular injection of botulinum toxin A: Study in juvenile rats. 1660 9

The presence of alterations in the muscular tone and in the normal motorial synergies at an articular level causes interferences in the functional recovery of patients with stroke consequences. In the rehabilitative field there are some aids that are useful to replace the compromised functions and to make the patient as autonomous as possible in the common movements of the everyday life. The orthoses are used mainly in two cases: to prevent and/or to contain myofascial retractions (spasticity passive component) and to improve the neuromuscolar control of movement through integration of a partially or totally insufficient function. Hemiparesis patients mainly show synergy alteration of the heel muscles and especially of the peroneus, with the consequent tendency of equinism-supination deviation. Analysis of literature shows a scientific validation especially in the use of dynamic orthoses of legs, the most known being the ankle-foot-orthoses.
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PMID:Aids and orthoses in patients with stroke consequences. 1683 50

Transient spinal cord ischemia in humans can lead to the development of permanent paraplegia with prominent spasticity and rigidity. Histopathological analyses of spinal cords in animals with ischemic spastic paraplegia show a selective loss of small inhibitory interneurons in previously ischemic segments but with a continuing presence of ventral alpha-motoneurons and descending cortico-spinal and rubro-spinal projections. The aim of the present study was to examine the effect of human spinal stem cells (hSSCs) implanted spinally in rats with fully developed ischemic paraplegia on the recovery of motor function and corresponding changes in motor evoked potentials. In addition the optimal time frame for cell grafting after ischemia and the optimal dosing of grafted cells were also studied. Spinal cord ischemia was induced for 10 min using aortic occlusion and systemic hypotension. In the functional recovery study, hSSCs (10,000-30,000 cells/0.5 mul/injection) were grafted into spinal central gray matter of L2-L5 segments at 21 days after ischemia. Animals were immunosuppressed with Prograf (1 mg/kg or 3 mg/kg) for the duration of the study. After cell grafting the recovery of motor function was assessed periodically using the Basso, Beattie and Bresnahan (BBB) scoring system and correlated with the recovery of motor evoked potentials. At predetermined times after grafting (2-12 weeks), animals were perfusion-fixed and the survival, and maturation of implanted cells were analyzed using antibodies recognizing human-specific antigens: nuclear protein (hNUMA), neural cell adhesion molecule (hMOC), neuron-specific enolase (hNSE) and synapthophysin (hSYN) as well as the non-human specific antibodies TUJ1, GFAP, GABA, GAD65 and GLYT2. After cell grafting a time-dependent improvement in motor function and suppression of spasticity and rigidity was seen and this improvement correlated with the recovery of motor evoked potentials. Immunohistochemical analysis of grafted lumbar segments at 8 and 12 weeks after grafting revealed intense hNSE immunoreactivity, an extensive axo-dendritic outgrowth as well as rostrocaudal and dorsoventral migration of implanted hNUMA-positive cells. An intense hSYN immunoreactivity was identified within the grafts and in the vicinity of persisting alpha-motoneurons. On average, 64% of hSYN terminals were GAD65 immunoreactive which corresponded to GABA immunoreactivity identified in 40-45% of hNUMA-positive grafted cells. The most robust survival of grafted cells was seen when cells were grafted 21 days after ischemia. As defined by cell survival and laminar distribution, the optimal dose of injected cells was 10,000-30,000 cells per injection. These data indicate that spinal grafting of hSSCs can represent an effective therapy for patients with spinal ischemic paraplegia.
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PMID:Functional recovery in rats with ischemic paraplegia after spinal grafting of human spinal stem cells. 1752 65


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