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)

Based on Cooper's good results implantation of a bilateral cerebellar stimulator was performed in 2 children with cerebral palsy. The patients suffered from marked hypertonia of all limbs and involuntary movements. The follow-up study of 8 months revealed a decrease of spasticity and a progressive improvement of fine motor control. Our preliminary results justify the clinical application of cerebellar stimulation for functional treatment of sensory-motor disorders.
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PMID:[The influence of permanent cerebellar stimulation on senso-motor disorders in cerebral palsy (author's transl)]. 30 85

25 patients with multiple sclerosis (MS) and other spastic disorders, 33 MS patients and 10 control patients with MS were given clonazepam, baclofen or placebo over a period of 5 days to 20 weeks. Both clonazepam and baclofen were significantly more effective than placebo in the treatment of spasticity (p less than 0.005 or p less than 0.01). A clinical trial of clonazepam versus baclofen was carried out and this showed no significant difference between the two drugs. However, there was indication that clonazepam influenced with better improvement in patients with slight muscle hypertonia mainly of cerebral origin. Patients with more severe forms, mainly of spinal spasticity, benefited rather from baclofen treatment (Fisher's test, p = 0.003). There was suggestion that combination of the two drugs may be more effective in some patients than than clonazepam or baclofen alone.
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PMID:Clonazepam, baclofen and placebo in the treatment of spasticity. 35 38

Dantrolen sodium is a muscle relaxant, which is used in the treatment of spasticity. Although it is given chronically, little is known about its pharmacokinetic behaviour. The relationship between the effect of a single oral dose of dantrolene sodium and its plasma concentration in healthy volunteers was studied by measuring the effect on the twitch tension, and in spastic patients on the decrease in muscle hypertonia. On the twitch tension dantrolene gave a depression of 49.1 +/- 9.4% (+/- DS) within 1.15 and 3.45 h after ingestion of 100 mg. The mean maximal plasma concentration was 1.24 +/- 0.32 microgram/ml (+/- SD). The effect and the plasma concentration were correlated. No relationship between the plasma concentration of dantrolene sodium and its effect could be established in patients, although definite activity in 6 out of 7 patients was observed after a single oral dose of 100 mg, and plasma concentration of dantrolene sodium greater than 0.3 microgram/ml were consistenly associated with better results than placebo treatment in 6 out of 7 patients.
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PMID:Relationship between plasma concentration and effect of dantrolene sodium in man. 49 21

The authors present a modification of Foerster's Rhizotomy for the treatment of spasticity in cerebral palsy: functional posterior rhizotomy. The selection of the roots/rootlesses to be sectioned, is accomplished on functional data, based upon the analysis of the reflex responses to the intraoperative lumbar dorsal roots stimulation. With this method it is possible to selectively interfere with the pathological circuits responsible for hypertonia, saving proprioceptive afferences necessary for motor reeducation. The clinical results on hypertonia are the same as for total or partial rhizotomies, but sides effects (ataxia, hypotonia) are considerably reduced.
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PMID:[Functional posterior radiculotomy, in the treatment of cerebral spasticity. peroperative electric stimulation of posterior roots and its use in the choice of the roots to be sectioned]. 95 64

The triad of rigidity, fever, and elevation of serum creatine phosphokinase (CPK) levels, labeled 'neuroleptic malignant syndrome' (NMS), is a dangerous complication of neuroleptic drug treatment. Amantadine was introduced for the pharmacological management of NMS because of its beneficial effects in Parkinson's disease which were attributed to direct or indirect dopaminomimetic properties of amantadine. While the dopaminomimetic effects of amantadine are weak under experimental conditions, recent studies have confirmed that amantadine is an antagonist at the N-methyl-D-aspartate (NMDA) type of glutamate receptor. Two lines of evidence suggest that amantadine or other NMDA receptor antagonists could be effective drugs for the reversal of NMS symptoms. First, glutamate antagonists restore the balance between glutamatergic and dopaminergic systems when dopaminergic transmission has been antagonized by neuroleptic drugs. Second, by virtue of their effects against rigor and spasticity, NMDA antagonists may reduce increased muscle tone and prevent rhabdomyolysis. In conclusion, NMS may be considered an iatrogenic excitatory aminoacid syndrome which is amenable to NMDA receptor antagonist therapy.
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PMID:A rationale for NMDA receptor antagonist therapy of the neuroleptic malignant syndrome. 133 36

As part of our studies of the organization of the cat sacrocaudal spinal cord (S3-Ca7), the portion of the neuraxis that innervates the tail, we have begun to evaluate the behavioral effects of hemisection or complete transection at the level of Ca1. Clinical observations that the tail strongly deviated to the side of a hemisection indicated the presence of an ipsilateral hypertonia. After complete transection of the spinal cord, the tail became ventroflexed in a midline position and exhibited spasticity, i.e., hypertonia, hyperreflexia, and clonus. Bowel and bladder functions and hindlimb gait and reflexes remained intact following either lesion. Quantitative behavioral measures corroborated our clinical observations. With the tail tethered to a force transducer, tail muscle tone was measured after the tail was passively positioned. Following a transection, resistance to dorsiflexion of the tail was greater than resistance to ventroflexion. In addition, tonic deviation of the tail was documented with videotape analysis while cats walked on a plank. Normal cats walked with the tail sharply dorsiflexed and centered. In contrast, the tail deviated ipsilaterally in cats with a hemisection, and the tail was ventroflexed in cats with a transection. These observations indicate that the sacrocaudal spinal cord provides a model with special advantages for investigation of changes in segmental motor functions following spinal cord injury. The effects of lesions on the tail are quantifiable and can resemble that spasticity observed after spinal cord injury in humans. Importantly, minimal effects on locomotive and autonomic functions were observed following hemisection or transection of the sacrocaudal spinal cord.
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PMID:Lesions of cat sacrocaudal spinal cord: a minimally disruptive model of injury. 147 9

Intrathecal baclofen has not been previously evaluated for the treatment of the disabling hypertonia associated with hereditary spastic paraparesis. Muscle tone and deep-tendon reflexes were evaluated in three patients with hereditary spastic paraparesis after a double-blind, cross-over bolus injection of intrathecal baclofen. Patients underwent placement of a subcutaneous pump for continuous infusion of intrathecal baclofen. Three months after implantation the muscle tone decreased 2.04 points (p less than .0001) and the reflex score decreased 2.25 points (p less than .001). Patients initially reported subjective weakness, but muscle testing revealed either an increase or no change in voluntary motor function. Baclofen doses of 60 to 264 micrograms per day were required for effective control of muscle tone and spasticity. Much of the disability in familial spastic paraparesis may be related to the loss of suprasegmental inhibition of spinal reflexes overwhelming the residual voluntary motor function.
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PMID:Intrathecal baclofen in hereditary spastic paraparesis. 151 85

To develop a reliable and objective technique for quantifying spastic hypertonia, ten chronically hemiplegic patients with varying degrees of spasticity were studied on three occasions during several weeks. The modified Ashworth scale, a clinical assessment of extremity tone, was performed before and after each of the following objective tests: (1) torque and EMG measurements during ramp and hold angular displacement about the elbow, (2) pendulum test of the lower extremity, and (3) H/M ratio studies of upper and lower extremities. Subject motor function was also quantified using the Fugl-Meyer motor assessment scale. A regression analysis was performed to determine how successfully each of the objective measures correlated with the clinical yardstick, the modified Ashworth scale. A similar correlation between the objective measures and the Fugl-Meyer motor assessment scale was performed. Temporal reproducibility of a test for a given subject was evaluated by performing an ANOVA of repeated measures for each test over the three study sessions in a given subject. We conclude that (1) both the ramp and hold threshold measurements and pendulum test offer acceptable objective measures of spastic hypertonia since they correlate closely with clinical perception, (2) the Fugl-Meyer motor assessment scale also correlates closely with the severity of spastic tone, and (3) objective measures of spastic hypertonia are often surprisingly reproducible when repeatedly applied to a selected group of chronic hemiplegic patients with long-standing spasticity.
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PMID:Objective quantification of spastic hypertonia: correlation with clinical findings. 155 7

This investigation estimated the mechanisms of baclofen action on spasticity using a battery of electromyographic methods. Thirty patients with old post-stroke spastic hemiparesis took part in the investigation. They were treated with baclofen-mean daily dose 54.3 alpha 11.6 mg for a mean of 26.3 alpha 4.9 days. A questionnaire for assessment of subjective improvement after treatment used a 5-point scale. For standardization of the neurological examination 5-point scales were used to assess muscle tone, muscle force and tendon reflexes. A battery of electromyographic methods was used to analyse different mechanisms of spasticity: for alpha motoneurone activity--the F wave parameters; for gamma motoneurone activity--the T/H reflex amplitude ratio; for presynaptic inhibition--the ratio of H reflex amplitudes before and after vibration on the achilles tendon (Hvibr./Hmax); for common interneurone activity--the flexor reflex parameters. Our results revealed that baclofen reduces spastically increased muscle tone and Babinski sign. It has no influence on muscle force, tendon reflexes and ankle clonus. Baclofen acts by normalizing the altered interneurone activity and decreasing of alpha motoneurone activity. When spasticity has altered interneurone activity and increased motoneurone activity, it is better to treat with baclofen.
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PMID:Mechanisms of baclofen action on spasticity. 162 92

Repeated monthly intracisternal inoculations of N-butyl benzenesulfonamide induced a chronic, slowly progressive myelopathy in young adult New Zealand white rabbits that was manifested by hyperreflexia, spasticity, hypertonia, gait impairment and altered tonic immobility responses. The neuropathological features consisted of scattered neuroaxonal spheroids, fusiform distention of the intramedullary portions of the spinal cord ventral roots and, as defined by microtubule-associated protein-2 (MAP 2) immunoreactivity, an initial distention and subsequent loss of dendritic processes in neurons of the nucleus motoris lateralis with the perikaryon of these cells remaining intact. A similar chronic progressive myelopathy was induced by repeated low dose intracisternal inoculations of aluminum chloride in New Zealand white rabbits. However, the neuropathological changes were more extensive and consisted of dendritic, axonal and perikaryal inclusions of phosphorylated and nonphosphorylated neurofilament localized to spinal motor neurons in the nucleus motoris medialis, substantia grisea intermedia and select brainstem nuclei with only minimal involvement of the nucleus motoris lateralis. The co-administration of these two neurotoxins over the course of 8 months induced striking behavioral changes as well as a fulminant myelopathy. This was accompanied by a loss of neuronal perikarya in the nucleus motoris accompanied by a loss of neuronal perikarya in the nucleus motoris lateralis and topographically extensive neocortical neurofilamentous degeneration. These features suggest that potentiation occurs when the two toxins are co-administered, a view supported by an estimation of the co-neurotoxicity coefficient (CNC greater than 1). Our results have implications for understanding human neurodegenerative disorders in which potentiation of insults may occur, producing a clinical and neuropathological disease state not expected from either agent alone.
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PMID:Potentiation in the neurotoxic induction of experimental chronic neurodegenerative disorders: N-butyl benzenesulfonamide and aluminum chloride. 174 33


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