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

Associations between a physically active leisure, physical fitness, impairment and disability have been tested in 123 volunteers (73 with paraplegia and 50 with quadriplegia). Active physical leisure was assessed by the questionnaire of Godin and Shephard (Canadian Journal of Sports Sciences 10, 141-6 1985). Fitness measures included body mass index, peak oxygen intake on a wheelchair ergometer, and tests of muscle strength and endurance (peak isokinetic torque, average muscle power and total muscle work for shoulder flexion, shoulder adduction and elbow flexion at movement speeds of 60 degrees and 180 degrees s-1). Primary impairment was assessed by the ISMGF scale, and secondary impairment was judged from reported pressure scores, spasticity, and urinary infections over the previous 12 months. Scores for self-care and mobility were obtained using a modified Barthel Index. Physically active leisure and fitness were unrelated to secondary impairment. However, functional ability for a given primary impairment was significantly correlated with peak oxygen intake and the three indices of muscle strength, particularly in individuals with high level lesions. Associations between physical activity and functional ability were weaker, but tended in the same direction. Although longitudinal studies are needed to prove the causality of these relationships, the findings point towards a significant influence of fitness status upon functional ability. Rehabilitation teams should thus give a stronger emphasis to systematic exercise conditioning programmes when planning overall treatment following SCI.
Int J Rehabil Res 1993 Dec
PMID:Relationship of impairment and functional ability to habitual activity and fitness following spinal cord injury. 817 29

Baclofen is a central nervous system agent that is commonly used for the treatment of muscle spasticity in spinal cord injury patients. Acute withdrawal of this medication can induce the development of neurological symptoms, including seizure disorder, psychosis, hallucinations and visual disturbances. We report 3 cases of acute central nervous system symptoms that developed in spinal cord injury patients. Each patient had been chronically maintained on a baclofen regimen to control muscle spasticity. Symptoms developed shortly after baclofen therapy was interrupted following genitourinary surgery. It is important that urologists become familiar with the symptomatology of baclofen withdrawal, the methods of its prevention and the appropriate therapy should the syndrome develop.
J Urol 1993 Dec
PMID:Neurological manifestations of baclofen withdrawal. 823 May 32

Recurrent inhibition via Renshaw cells provides a mechanism by which spinal and supraspinal centers exert control over movement. The conditioned H-reflex technique of Pierrot-Deseilligny and Bussel permits noninvasive assessment of recurrent inhibitory pathways. We employed this technique to investigate changes in Renshaw cell activity due to nicotine (a potent CNS cholinergic agonist that excites Renshaw cells in animals) contained in inhaled tobacco smoke. In 10 normal subjects, cigarette smoking caused a large, rapid drop in the conditioned H-response amplitude, implying increased activation of Renshaw cells. The time course of the change in conditioned H-response amplitude closely approximated the known pharmacokinetics of inhaled nicotine. Nicotine administered via chewing gum had a much slower and less dramatic effect, probably due to the slower rise in blood levels with this mode of administration. Increased activity in Renshaw cells may contribute to spasticity in spinal cord-injured patients, raising the possibility that cigarette smoking could cause further increases in tone in such patients.
Neurology 1993 Dec
PMID:The effect of nicotine on recurrent inhibition in the spinal cord. 825 71

Potential advantages of intramuscular botulinum toxin for the treatment of spasticity include the lack of sensory effects, ability to target specific muscle groups, ability to weaken muscles in a graded fashion and absence of caustic chemicals such as phenol. We describe the use of botulinum toxin for the treatment of severe lower extremity spasticity in two subjects with multiple sclerosis. Both subjects showed an improvement in spasticity, as measured by the modified Ashworth scale, and in functional status. Both subjects exhibited reductions in muscle tone not only in injected muscles, but also in noninjected muscles in the region. These more distant clinical effects have not been emphasized in previous studies after therapeutic injections of botulinum toxin. Further research is needed to clarify the cause and prevalence of these regional motor effects, as well as to further examine the safety and efficacy of botulinum toxin for spasticity treatment.
Am J Phys Med Rehabil 1993 Dec
PMID:Botulinum toxin for the treatment of spasticity in multiple sclerosis. New observations. 826 Jan 29

This study was conducted to determine the feasibility of quantifying spasticity by measuring the resistance to passive movement using an isokinetic dynamometer. A quantifiable method was developed by determining the summation of the four consecutive resisting torque amplitudes during flexion and extension of the knee at specified speeds and range of motion. A more rigorous assessment was made by finding the slope of the linear regression curve of torque-velocity data. Although the values of maximum torque were higher in the spastic group than in the normal group, the difference was statistically significant only when the sum of the torque amplitudes was considered (P < 0.0028). Values of the maximum torque as well as the sum of the torque amplitudes increased in a linear fashion (r > 0.75) with increasing velocity. The slopes of the torque-velocity curves were greater in spastic subjects than in normal subjects. The sensitivity to the rate of stretch was statistically greater (P < 0.0004) for the spastic group than normals only when the sum of torque amplitudes was considered. The corresponding data obtained during the flexion and extension of the knee were not statistically different (P > 0.05). Serial summation of torque amplitudes and measurement of slope in the torque-velocity curve are sensitive and repeatable methodologies for the measurement of spasticity assessment.
Am J Phys Med Rehabil 1993 Dec
PMID:Isokinetic dynamometric technique for spasticity assessment. 826 Jan 32

Spasticity is a motor dysfunction affecting persons with an UMN injury in varying ways. Nurses can identify spasticity in their patients by the presence of hyperactive DTRs and hypertonicity (increased muscle tone). Other characteristics often present with spasticity are clonus and spasms. Spasticity interfering with recreation, work, or basic activities of daily living may be decreased through the use of a variety of nursing interventions. Some of these interventions are more advantageous for spasticity caused by brain injury, whereas others are more helpful for spasticity caused by the spinal cord injury. Interventions research has begun; however, more research needs to be done to identify the most effective nursing measures to decrease spasticity.
Nurs Clin North Am 1993 Dec
PMID:Spasticity. Mechanisms and nursing care. 826 21

The 1-aminoadamantanes memantine (1-amino-3,5-dimethyl-adamantane) and amantadine (1-amino-adamantane) are clinically used as anti-parkinsonian, anti-spasticity, anti-dementia and antiviral drugs. In the present investigation we have tested a series of 1-aminoadamantane derivatives including memantine and amantadine for their ability to compete with [3H](+)-pentazocine in homogenates of post-mortem human frontal cortex. The Ki values ranged from 0.237 +/- 0.019 microM for 1-N-dimethyl-amino-3,5-dimethyl-adamantane to 20.25 +/- 16.48 microM for amantadine. The Ki value of memantine was 19.98 +/- 3.08 microM and was thus very similar to that of amantadine. Memantine, at therapeutic concentrations, probably does not interact with the sigma binding site. Amantadine, at therapeutic concentrations, probably binds both to the sigma site and to the phencyclidine (PCP) binding site of the N-methyl-D-aspartate (NMDA) receptor.
Neurosci Lett 1993 Dec 12
PMID:Affinity of 1-aminoadamantanes for the sigma binding site in post-mortem human frontal cortex. 830 17

Flexor and extensor spasms associated with severe spasticity frequently cause pain and suffering in neurologically impaired patients, and greatly interfere with comfort and activities. When high doses of oral medications are necessary to keep the symptoms under control and are poorly tolerated, the long-term spinal-selective intrathecal infusion of baclofen by means of implanted drug pump and catheter is a safe, efficient and reversible alternative to destructive surgical procedures. Between September 1991 and March 1995, intrathecal baclofen was infused in 18 selected patients out of a series of 42 severely disabled spastic cases. We report here our preliminary experience with the criteria of selection, the initial intrathecal bolus test and the long-term benefit of the selected patients. Our results confirm the dramatic immediate and long-term benefit reported in other series. After a period of treatment of 1 to 42 months, 13 patients had a complete disappearance of their spastic symptoms without any oral treatment, one patient kept unchanged clonus despite the use of low-dose oral treatment and another one a severe, not improved dysuria although in both of them hypertonia and spasms were abolished. Finally, 2 patients had important joint stiffness slightly impairing the benefit from the treatment. None of the 18 patients had central side-effects related to baclofen. With time, a slight increase in daily dose (inferior to 10%) was necessary in most patients.
Acta Neurol Belg 1995 Dec
PMID:Chronic intrathecal baclofen in severely disabling spasticity: selection, clinical assessment and long-term benefit. 900 75

Autosomal dominant cerebellar ataxia type I was diagnosed in three unrelated families from Martinique (French West Indies), and linkage to the locus for spinocerebellar ataxia 2 (SCA2) was established. Neuropathological findings in two patients were those of olivopontocerebellar atrophy without oligodendroglial cytoplasmic inclusions. Cerebellar ataxia was associated with hyporeflexia in 68% of 31 examined patients, with slowed and/or limited eye movements in 65% and with dementia in 29%. No patients had optic atrophy, pigmentary retinal degeneration, spasticity or parkinsonism. Mean age at onset was 33 +/- 16 years, and onset before the age of 20 years was correlated with a more rapid and severe course of the disease. Movement disorders, oculomotor disturbances, sphincter disturbances and cognitive impairment were significantly more frequent in early than in late onset patients. This explains why the phenotype was strikingly different in one family, in which mean age at onset was much earlier. Comparison with previously described SCA2 families indicated similarities, such as reduced saccade velocity, supranuclear ophthalmoplegia and decreased reflexes, although phenotypic heterogeneity remains the outstanding feature of this disorder.
Brain 1995 Dec
PMID:Autosomal dominant cerebellar ataxia type I in Martinique (French West Indies). Clinical and neuropathological analysis of 53 patients from three unrelated SCA2 families. 859 86

Fucosidosis, a progressive neurodegenerative disease, evident in early childhood, is associated with progressive loss of mental and motor function and increasing spasticity and hyperreflexia. We report a Canadian male, with clinical features similar to previously reported fucosidosis patients, however, since age 5 he has exhibited progressive dystonic posturing, initially unilateral, but recently involving both lower limbs. Extensive study of his cultured lymphoblasts demonstrated that alpha-fucosidase activity and immunoreactive alpha-fucosidase protein were absent. He is homozygous for the Q422X mutation, a C to T transition within exon 8 of the alpha-fucosidase gene which results in loss of an EcoR1 restriction enzyme cut site. Even among the 4 other reported fucosidosis families having one or more individuals homozygous for this same (Q422X) mutation there was no previous report of dystonia.
Neuropediatrics 1995 Dec
PMID:Fucosidosis with dystonia. 871 50


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>