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 development of neuroprotective agents for the prevention of neuronal loss in acute conditions such as stroke and epilepsy or chronic neurodegenerative disorders including Parkinson's disease, Alzheimer's disease, Huntington's chorea, and motor neuron disease is currently focusing on drugs that inhibit excitatory amino acid neurotransmission or exhibit antioxidant properties. Unfortunately, potent antagonists at the N-methyl-D-aspartate (NMDA) type glutamate receptor, which is thought to mediate excitotoxic neuronal injury, e.g., MK-801 or phencyclidine (PCP), share a high probability of inducing psychotomimetic side effects. Further, these drugs have been associated with acute neurotoxicity in vitro and in vivo, precluding their clinical use. In contrast, low affinity NMDA receptor antagonists like amantadine and its dimethyl derivative, memantine, have been administered clinically for the management of Parkinson's disease, dementia, neuroleptic drug-induced side effects, and spasticity. These agents have only rarely induced significant psychotomimetic side effects. Recent pharmacologic advances have helped to elucidate how high drug affinity for the PCP binding site of the NMDA receptor may enhance psychotogenicity. Low affinity and associated fast voltage-dependent channel unblocking kinetics are likely to be responsible for the better tolerance of amantadine and memantine compared with MK-801 and PCP. Further factors apparently modulating psychotogenicity of glutamate receptor antagonists include differential actions on neuronal populations in various brain regions and interactions with neurotransmitter receptors other than the NMDA type glutamate receptor.
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PMID:Psychotogenicity and N-methyl-D-aspartate receptor antagonism: implications for neuroprotective pharmacotherapy. 901 83

A 72-year-old man developed a sudden weakness in his left hand on October 5, 1991. He was admitted two weeks thereafter. Physical examination revealed minimal weakness, and clumsiness of the fingers on his left hand. Exaggerated tendon reflexes and spasticity were also noted only on his left upper limb. He had neither dementia nor psychiatric symptoms. Subsequently he developed weakness in his left leg on November 17. Within 12 days he developed left facial weakness, and myoclonic movements on the left side. By December 2, he developed spastic tetraparesis with bilateral facial palsy, and generalized myoclonic jerks. A few days after that he started to show decorticate posture. From December 16, his mental status deteriorated rapidly, and he became mute, and uncooperative within a week. His clinical course can be summarized as stepwise progression similar to a cerebrovascular accident. Electroencephalography was normal on admission, but periodic synchronous discharge developed in January 1992. Brain CT that showed only mild brain atrophy at first was considered to be compatible with his age, changed to have severe brain atrophy in March 1992. He died of pneumonia on May 24, 1992 after eight months of progressive clinical course. Autopsy was done. The brain weighed 930 grams. Macroscopically there was prominent cortical atrophy. Microscopic examination revealed severe spongy state throughout the cerebral cortex. Typical spongiform changes were confined to the hippocampus. The cerebral white matter appeared to be normal. In the cerebellar cortex, the granular cell layer disappeared and Purkinje's cells were reduced in number. Kuru plaques were not seen. The cerebellar white matter, dentate nucleus, and brainstem seemed to be normal. The spinal cord was not examined. There were no pathological changes to indicate cerebrovascular accident, except for a lacuna in the right basal ganglion and a small angionecrosis in the pons. Western blotting test using Anti-APC (amyloid plaque core) antibody was positive. Neuropathological changes of the present case were consistent with those of CJD. However, the sudden onset of monoparesis without dementia or ataxia is rare as the initial symptom of this disease. The subsequent clinical course with stepwise progression of hemiplegia, which was mimicking a progressive stroke, was also rare for CJD. In comparison to typical case of CJD, this case had a different clinical onset as acute monoparesis. We can find such cases of CJD presenting as stroke in 5.6% in the previous English literatures.
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PMID:[A case of Creutzfeldt-Jakob disease (CJD) started with monoparesis of the left arm]. 904 57

A new classification of motor disorders in patients after brain hemisphere's stroke as well as with its sequelae was proposed on the basis of clinical electromyographic studies. The classification validity was confirmed by mathematic statistic methods. The classification was composed of motor syndromes and is based on the following criteria: the severity of paresis, the correlation between gravity of paresis of the upper and lower limbs, muscular spasticity, alteration of integral estimation of active movements (the motor algorithm). The most informative signs of classification are the following: the paresis gravity, the degree of muscular spasticity, the alteration of motor algorithm, the parameters of stimulative electromyography. The described classification permits to carry out differentiated actions of neurorehabilitation directed to intensification of effectivity of treatment after hemisphere's stroke.
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PMID:[A new classification of the motor disorders in patients who have had a cerebral stroke]. 907 87

Magnetic transcranial stimulation was applied to 12 normal subjects and 30 patients (24 acute and 6 chronic) with hemiparesis contralateral to an ischaemic stroke. In the 24 acute patients, the recordings were made at the 7th day on the contralateral first dorsal interosseous (FDI) muscle. We studied the amplitudes of the motor evoked potential (MEP) responses and the post-MEP silent period durations (SPD) at different levels of stimulation intensity (SI) and voluntary isometric contraction (VIC). The evolution of these parameters was matched to the clinical status of the 24 acute patients evaluated 7, 30 and 90 days after the stroke (D7, D30 and D90). Our results may be summarised as follows: (1) in all cases, the MEP-amplitudes increased with facilitation and SI; (2) in the normal subjects and in patients who did recover, the SPD augmented with stronger SI but was found to be independent on the strength of voluntary contraction; (3) in the acute patients with poor recovery, as well as in the chronic patients with spasticity, the SPD decreased with stronger VIC. It may be concluded that MEP-amplitudes and SPD patterns point out excitatory and inhibitory mechanisms which may be differently affected in cerebral injuries. The association between shortening of the SPD with increasing VIC of the target muscle and poor recovery of the stroke after 3 months could be a useful clinical test to predict eventual recovery early after a stroke.
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PMID:Magnetic transcranial stimulation: dissociation of excitatory and inhibitory mechanisms in acute strokes. 911 36

Medical evaluation was performed on a group of paraplegics who were trained to walk with the Reciprocating Gait Orthosis powered with electrical muscle stimulation (RGO II). The evaluation included changes in spasticity, cholesterol level, bone metabolism, cardiac output and stroke volume, vital capacity, knee extensors torque, and heart rate at the end of a 30-meter walk. After an average of 14 weeks of training during which patients walked for 3 hours per week, significant reductions in spasticity, total cholesterol and low-density lipids, hydroxyproline/creatinine ratio, and increased knee extensor torque were evident. The data also showed that improvements occurred in the calcium/creatinine ratio, serum calcium and alkaline phosphatase levels, cardiac output and stroke volume, and vital capacity, yet these improvements were not statistically significant. The final heart rate at the end of a 30-meter walk showed that the RGO II required only a moderate level of exertion, which was found to be the lowest among the other mechanical or muscle stimulation orthoses available to paraplegics. It was concluded that the limited but reasonable level of functional regain provided by the RGO II is associated with a general improvement in the paraplegic's physiological condition if used for a minimum of 3 to 4 hours per week.
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PMID:Reciprocating gait orthosis powered with electrical muscle stimulation (RGO II). Part II: Medical evaluation of 70 paraplegic patients. 917 48

The aims of this study were to determine whether changes in the non-reflex component of spastic plantarflexors had developed 2 and 4 months after stroke and to study their relationship with the level of impairment. One group of adults with hemiparesis (HPs) was tested 2 and 4 months after the onset of stroke, and data were compared with a control group (CTLs) tested once. Twenty-two patients (14 males) admitted over a 4-month period in a rehabilitation centre (mean = 62 yrs +/- 14), and 11 (6 males) non-disabled (CTLs) subjects (mean = 57yrs +/- 12.8) agreed to participate in the study. The resistive torque (RT) recorded with a myometer during slow (8-10 degrees/s) passive dorsiflexions imposed manually served as the primary outcome, whereas, the Ashworth score (spasticity), ankle ROM and Fugl-Meyer motor subscore were used as secondary measures to determine the level of impairment. The mean RT values measured at 0 degrees dorsiflexion on the affected and unaffected sides were compared with those in CTLs. As expected, the RT values 2 and 4 months post-stroke on the unaffected side did not differ from corresponding values in CTLs. Significantly higher RT values on the affected side when compared to the unaffected side were found both at 2 months (39%; p < 0.05) and at 4 months (43%; p < 0.01). No significant difference existed on the affected side between the 2nd and 4th months. A high (r = 0.80) and significant (p < 0.0001) correlation coefficient was calculated between the changes in RT values recorded at 2 and 4 months. Low and not significant correlations were computed between these RT changes and factors such as the ROM (r = -0.24), the Ashworth score (r = 0.23) and the Fugl-Meyer lower extremity motor subscore (r = -0.26). Present results indicate that: (1) changes in the non-reflex component are already present 2 months after stroke but do not increase significantly between the 2nd and 4th months; (2) these changes are not related to the level of impairment; and (3) myometry testing at 2 months could be used as a preventive measure to detect patients more at risk of developing severe passive muscle stiffness.
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PMID:Non-reflex mediated changes in plantarflexor muscles early after stroke. 927 Nov 48

There is little information on the silent period during facilitation of the target muscle at the acute stage of stroke and the ultimate clinical status. We studied 69 subjects with transcranial magnetic stimulation: 20 matched controls and 49 hemiparetic patients investigated 7 and 90 days after the stroke (D7, D90). We measured the silent period duration (SPD) in the first dorsal interosseous muscle at 10 and 100% of maximal voluntary isometric contraction (VIC). The SPD index (the ratio of SPD at VIC 100% by SPD at VIC 10%) at D7 was matched with the clinical outcome at D90. Two patterns of responses could be determined at D7. In the normal subjects and in 27 out of 32 patients who eventually recovered satisfactory function at D90, the SPDs were stable during facilitation (SPD index 100%). On the contrary, in 10 out of the 17 patients with a poor functional outcome, the mean SPD decreased when VIC was increased (SPD index 80%); besides, their muscle tone was significantly increased at D90. Similar patterns were still present in the patients at D90: the mean SPD indexes were not significantly different from D7. We conclude that in the early stage of stroke, a low SPD index appears to be correlated with the eventual occurrence of spasticity.
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PMID:Magnetic transcranial stimulation: clinical interest of the silent period in acute and chronic stages of stroke. 928 36

To establish whether botulinum A toxin (BTX-A) acts on modifying reciprocal inhibition between forearm muscles in spasticity, 20 patients with post-stroke upper limb spasticity lasting for more than 1 year were studied. Clinical examination, physiotherapeutic evaluation, standardized video-tape assessment and electrophysiological testing (flexor carpi radialis muscle M and H responses with study of reciprocal inhibition) were performed at baseline and 2 weeks, 1, 2, 3, 4 months after BTX-A treatment. BTX-A induced a significant decrease of tone and an improvement of motility and functional status, with a significant decrease of the M wave and the H reflex. The reduction in both inhibitory phases of reciprocal inhibition did not change after BTX-A treatment differently from that reported in upper limb dystonia. These findings indicate that the efficacy of BTX-A in upper limb spasticity is mainly due to peripheral effects.
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PMID:Botulinum toxin in upper limb spasticity: study of reciprocal inhibition between forearm muscles. 933 11

The object of this study is to determine if the functional motor capacity of the paretic extremity can be improved by stimulation with low intensity low frequency (1.7 Hz) transcutaneous electric nerve stimulation (Low-TENS), started 6-12 months after a stroke. Forty-four patients who had a paretic arm as a consequence of their first stroke were included and randomly assigned to either a treatment group (n = 26) or a control group (n = 18). Patients in both groups received physiotherapy at a day-care center, usually twice a week. The treatment group received, in addition, Low-TENS for 60 min, five days a week for three months. Results showed that motor function increased significantly in the treatment group, compared to controls. The Low-TENS did not decrease either pain or spasticity. It is concluded that stimulation by means of Low-TENS could be a valuable complement to the usual training of arm and hand function in the rehabilitation of stroke patients.
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PMID:Stimulation with low frequency (1.7 Hz) transcutaneous electric nerve stimulation (low-tens) increases motor function of the post-stroke paretic arm. 960 71

Motor evoked potentials (MEPs) elicited over hand muscles by transcranial magnetic stimulation (TMS) were studied in healthy individuals and, bilaterally, in patients with cerebral infarction. Conduction time of the central motor pathways (CMCT), threshold intensity, and amplitude of the MEPs were correlated with recovery motor hand function after stroke. Following MEPs by TMS during tonic muscle contraction, there is a transient suppression of muscle action. This inhibitory period (IP) was significantly shorter in the upper paretic limb of stroke patients with spasticity than in normal limb of the patients and healthy individuals. Shortening of the IP duration was correlated to degree of upper limb spasticity (Ashworth scale) and may be due to supraspinal level reduction of the inhibitory function. The IP study contributes to a better quantification of the hand function in stroke patients.
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PMID:The muscle inhibitory period by transcranial magnetic stimulation. Study in stroke patients. 963 46


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