Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0026837 (muscle rigidity)
 1,077 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In addition to anamnestic and clinical data electrophysiological and pharmacokinetic investigations may be necessary for the diagnosis of stiff man syndrome. Continuous activity of motor units with superimposed bursts during muscular spasms was found by electromyography in the two patients reported. Rigidity and continuous activity disappears during sleep, after i.v. application of Tubocurarine and Diazepam, during Thiopenal anesthesia and after neural block with Procaine. Dipropylacetate and Baclofen improved the condition but did not lead to complete relaxation. Biperidenlactat and Magnesiumlaevulinat have only a temporary effect on rigidity. Neostigmine, Phenytoine, Glycine, Dopa and 5-Hydroxy-Tryptophan had no effect. Passive shortening or stretching of the m. biceps brachii as well as touching the skin increased motor activity which spread to other segments and to the contralateral side. The H/M ratio was increased but the silent period was normal. A combination of Diazepam and Dipropylacetate or Clonazepam was therapeutically effective in the cases reported. A central genesis, of the pathogenetic mechanisms discussed, is the most probable in our cases.
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PMID:Electrophysiological studies on the "stiff-man" syndrome. 7 57

Tetanus is caused by the organism Clostridium tetani, which produces tetanospasmin, a neurotoxin responsible for the clinical manifestations of muscle rigidity and reflex spasms. The majority of cases follow an anaerobic wound infection associated with trauma. Incubation period is usually 3 days to 3 weeks. 75% of patients present with trismus. Reflex spasms are seen in 70% of patients and characterize the severity of the disease. Treatment involves removal of the offending organism, neutralization of free neurotoxin, controlling rigidity and reflex spasm, and minimizing complications. Diazepam may be used alone in mild cases. Severe cases require the addition of nondepolarizing neuromuscular blocking agents and mechanical ventilation. Respiratory complications occur early and require aggressive airway management. A serious, late complication is the syndrome of sympathetic nervous system overactivity that is treated with alpha and beta blockade. High mortality rates seen in the United States may be due to delays in diagnosis and lack of familiarity with treatment. The disease is preventable with adequate immunization.
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PMID:Tetanus: a review. 44 55

Our electromyographical findings show no evidence for a spinal or neurogenic origin of muscle stiffness in stiff-man syndrome. It is assumed that the tonic muscle rigidity is induced by abnormal impulses from the brainstem. The measured latencies of electrically induced muscle spasm in the legs are in accordance with this hypothetic site of origin. Muscle stiffness and spasm are decreased by the GABA derivative Baclofen as well as by Clonacepam, which is preferable to Diazepam because of less intense sedation. Spasms are increased by Chlorimipramine which may by used as a provocative test in uncertain cases. These pharmacological influences suggest an imbalance between a gabaminergic inhibitory and a noradrenergic and/or serotoninergic excitatory neuronal system.
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PMID:[The stiff-man syndrome. A case report with regard to clinical, electromyographical and pharmacological signs (author's transl)]. 84 10

We studied three groups of 30 patients each, undergoing minor orthopaedic surgery, anaesthetized with alfentanil (30 micrograms/kg bolus followed by an infusion of 0.3 micrograms/kg/min), thiopental 3 mg/kg and 70% N2O via facial mask. Patients in group I were treated, three minutes before induction, with vecuronium 0.02 mg/kg i.v., while those in group II were premedicated with diazepam 0.15 mg/kg i.m. 30-45 minutes before induction. Group III served as control. Muscular rigidity was evaluated clinically with a subjective score based on a scale of 0 (no rigidity) to 3 (severe rigidity). Diazepam did not give significant protection from muscular rigidity. Vecuronium administration did not significantly reduced the number of patients who became rigid, but significantly decreased the incidence of severe rigidity (p less than 0.005), the mean rigidity score (p less than 0.05) and the incidence of rigidity at the induction of anaesthesia (p less than 0.0005). We also observed a progressively increasing incidence of rigidity with increasing age (not significantly) and body weight (p less than 0.05 total rigidity, p less than 0.01 severe rigidity).
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PMID:[Muscular rigidity caused by alfentanil: prevention]. 257 21

Abecarnil (isopropyl-6-benzyloxy-4-methoxymethyl-beta-carboline-3-carboxylate) is a metabolically stable anxiolytic and anticonvulsant beta-carboline derivative with few sedative and muscle relaxant effects in rodents. Abecamil binds with high affinity to benzodiazepine receptors. Because long-term treatment with benzodiazepines leads to development of dependence, we evaluated in mice whether abecarnil also possesses a potential for producing dependence, using electroencephalographic and electromyographic monitoring, and behavioral assessment of anxiety to detect withdrawal responses after chronic treatment. Diazepam was used as a reference. Mice withdrawn from chronic treatment with diazepam (15 mg/kg/day for 12 days) showed a time-related evolution of anxiety, muscle rigidity and seizures between days 4 and 21 after discontinuation of the treatment. A period between withdrawal days 1 and 3 was symptom free. Mice withdrawn from chronic administration of abecarnil (6 mg/kg/day for 12 days) showed no anxiety and no changes in seizure susceptibility and muscle tone. The doses of diazepam and abecarnil used for chronic treatment were equivalent in terms of kinetics and binding to benzodiazepine receptors. These data indicate that long-term treatment with abecarnil does not induce benzodiazepine-like dependence in mice. Thus, it may be predicted that chronic treatment with abecarnil in humans may offer an important alternative to benzodiazepines in the treatment of anxiety.
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PMID:Long-term treatment with abecarnil does not induce diazepam-like dependence in mice. 809 51