Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study reports results from experiments designed to test common, clinically useful anti-convulsants for their effectiveness, if any, against the high pressure nervous syndrome (HPNS) in rats. Phenytoin, carbamazepine, phenobarbitone, or diazepam were administered orally to rats before compression. Endpoints used to assess the progression of the HPNS were T1, T3, and T5 (onset of, continuous, and severe tremor), myoclonus, and seizures. Of the four drugs tested, only phenobarbitone increased the onset pressure for tremor and seizures by: T1 33%; T3 11%; T5 14%; seizures 10%. Neither phenytoin, carbamazepine, nor diazepam had any significant effect on any of the endpoints studied. High dose chronic pretreatment with phenytoin also had no effect on the HPNS. These data suggest that conventional anticonvulsant treatment would be of limited value for HPNS in man, and the lack of effect also suggests that HPNS seizures are of an unusual type.
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PMID:Effects of four common anticonvulsants on the high pressure nervous syndrome in the rat. 153 60

An autopsy case of ataxic form of Creutzfeldt-Jakob disease (Brownell and Oppenheimer, 1965) was reported. The patient, a 71-year-old male, noticed ataxic gait at the beginning of June in 1988, and was admitted to the Hiroshima City Hospital for the neurological examination at the end of June. He showed ataxia of the left arm and legs and diplopia. Gradually he became delirious at night. On July 16, tremor-like involuntary movement of the left hand was noticed. On July 20, he became somnolent and doubly incontinent. Myoclonus and paratonic rigidity were also observed. The EEG showed periodic synchronous discharge on July 25. The brain CT and MRI were normal. He became apallic gradually and died on October 28. The duration of illness was 5 months. At autopsy, brain weighed 1000gr. Cerebral atrophy and slight enlargement of the ventricles were observed. The cerebellum was also slightly atrophic. Histologically, the destruction of the cerebral cortical layer, slight sieve-like spongy state of the neuropil, slight neuronal loss of the thalamus and sieve-like spongy state of the striatum were observed. The cerebellar lesion was the most severe, where granular cell loss and gliosis of the cortex were observed.
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PMID:[An autopsy case of ataxic form of Creutzfeldt-Jakob disease]. 156 39

The administration of veratramine produced generalized tremor, myoclonus, hindlimb abduction, backward gait and Straub tail, similar to the "5-hydroxytryptamine (5-HT) syndrome", in mice. Pretreatment with metergoline, methysergide, mainserin or cyproheptadine ameliorated veratramine-induced myoclonus and tremor. For suppression of other symptoms, mianserin and cyproheptadine were effective. Metergoline improved hindlimb abduction and Straub tail, but did not inhibit backward gait. Methysergide was ineffective for the remaining symptoms. 5-Methoxy-N,N-dimethyltryptamine (5-MeODMT) enhanced all these symptoms except for Straub tail. 8-Hydroxy-2-[di-n-propylamino] tetralin hydrobromide (8-OH-DPAT) augmented tremor, hindlimb abduction and backward gait, but did not influence myoclonus and Straub tail. 5-Methoxy-3[1,2,3,6-tetrahydropyridin-4-yl] 1H-indole (RU 24969) did not modify the symptoms. Destruction of 5-HT neurons using 5,6-dihydroxytryptamine (5,6-DHT) resulted in suppression of the syndrome. The denervation supersensitivity caused by 5,6-DHT did not increase the response to veratramine. These findings indicate that part of the site of action of veratramine may be the presynaptic 5-HT neurons.
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PMID:Veratramine-induced behavior associated with serotonergic hyperfunction in mice. 171 Feb 97

The forearm electromyogram (EMG), pharyngeal EMG, and wrist tremor were recorded simultaneously from a 74-year-old woman with the syndrome of palatal myoclonus and progressive ataxia. Her wrist tremor had the characteristics of enhanced physiologic tremor. The enhancement of her tremor was attributable to 50- to 80-ms silent periods in the forearm EMG that followed the 1.9-Hz bursts of palatal myoclonus by 50 to 60 ms. This observation and those of previous authors support the notion that rhythmic olivocerebellar discharges can cause tremorogenic excitation and inhibition of postural EMG activity in the upper extremities.
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PMID:Inhibition of forearm EMG by palatal myoclonus. 175 50

Drug-induced and tardive movement disorders represent a large number of extrapyramidal disorders seen in neurologic practice. Iatrogenically induced, most commonly by neuroleptics, these disorders can be characterized by any abnormal body movement including tremor, chorea, athetosis, dyskinesias, dystonia, myoclonus, tics, ballismus or akathisia. Parkinsonism, dyskinesias and dystonia tend to be the most common. Management of patients with drug-induced or tardive syndromes is complex. Prognosis is frequently poor as patients usually need the offending agent to manage their underlying psychiatric or medical problem. Neuroleptics and other drugs known commonly to cause movement disorders should be used cautiously and significant consideration of all risks and benefits measured before initiating therapy.
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PMID:Drug-induced and tardive movement disorders. 183 84

Neurophysiological interactions between the competitive N-methyl-D-aspartate (NMDA) preferring receptor antagonist, CPP (3-((+-)-2-carboxypiperazine-4-yl)-propyl-1-phosphonate) and the high pressure neurological syndrome (HPNS) have been investigated in the non-human primate Papio anubis. Eight animals were exposed on two occasions to environmental pressures of 81 atmospheres absolute (ATA) in a hyperbaric chamber, using helium and oxygen. One exposure followed pretreatment with CPP (either 5 or 10 mg/kg i.v. plus 5 mg/kg/hr infusion), the other a saline control. Pretreatment with CPP delayed moderate signs of face tremor and myoclonus and abolished severe signs of whole body tremor and seizure activity. By 81 ATA, scores representing severity of HPNS were significantly reduced by CPP to a mean score, reflecting a level of just mild to moderate limb tremoring (P less than 0.001). Changes in the EEG were observed in channels associated with the frontal, parietal and occipital regions of the left cortex. Amplitude and frequency spectra were calculated and changes with pressure in the 4 conventional wavebands were analysed. The most striking change was the complete prevention by CPP of the 100% increase in the amplitude of alpha waves at 81 ATA in the frontal region (P less than 0.001). It is concluded that NMDA transmission has a major role in the expression of HPNS.
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PMID:The effects of the competitive NMDA receptor antagonist CPP on the high pressure neurological syndrome in a primate model. 183 61

Substance P-like and somatostatin-like immunoreactivities (SPLI and SLI) were determined in ventricular fluid of patients with chronic pain syndromes and in a comparison group with multiple sclerosis, essential tremor, epilepsy and postanoxic myoclonus. Concentrations of SPLI and SLI were non-significantly decreased by 40% and 33% in chronic pain patients as compared with control patients without pain. There were no differences apparent between subgroups of pain patients (deafferentation pain, neoplasia-induced pain, thalamic pain). High pressure liquid chromatography combined with radioimmunoassay showed marked heterogeneity of SPLI and SLI.
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PMID:Substance P-like immunoreactivity and somatostatin-like immunoreactivity in the ventricular fluid of patients with chronic pain syndromes. 183 80

To study the purported relation of 5-HT1A and 5-HT2 receptors, we chronically injected rats with a low dose of selective 5-HT agonists to induce behavioral tolerance and then tested for cross-tolerance. Acutely, in naive rats, both the putative 5-HT2 agonist DOI and 5-HT1A agonist 8-OH-DPAT induced some behaviors of the "serotonin syndrome" but the two drugs could be differentiated. Only DOI evoked shaking behavior, "skin jerks" (spinal myoclonus), and hyperthermia. Only 8-OH-DPAT induced flat body posture, head weaving, hypothermia, and occasional hindlimb hyperextension (dystonic posture). Both drugs, especially 8-OH-DPAT, evoked forepaw tapping. Chronic (21 day) treatment with DOI prevented DOI-evoked behaviors but not behaviors evoked by 8-OH-DPAT. Behaviors evoked by 8-OH-DPAT and not DOI decreased significantly after chronic 8-OH-DPAT treatment. Development of selective tolerance suggests that putative selective 5-HT2 and 5-HT1A agonists exert both shared and distinctive behavioral effects through separate sites whose relation is behavior-specific. For some behaviors (forepaw myoclonus, shaking behavior, thermoregulation), there is a functional interaction between 5-HT1A and 5-HT2 sites, while for other behaviors (skin jerks, flat body posture, head weaving), there is no interaction.
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PMID:The relation of central 5-HT1A and 5-HT2 receptors: low dose agonist-induced selective tolerance in the rat. 183 98

The clinical and electromyographic characteristics of tremor were studied in 45 patients presenting with various forms of idiopathic dystonia. Dystonic tremor was shown to be postural, localized, and irregular in amplitude and periodicity, absent during muscle relaxation, exacerbated by smooth muscle contraction, and associated frequently with myoclonus. Although it resembles essential tremor, dystonic tremor seems to be a distinct entity: it is more irregular with a broader range of frequencies; it is asymmetric and remains localized; myoclonus is sometimes associated. This type of tremor is most often seen in the presence of dystonia, but may be observed without evident dystonic symptoms.
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PMID:Tremor and idiopathic dystonia. 192 28

Actual phenomena of various types of involuntary movements listed below were demonstrated by moving pictures, which were followed by comments on symptomatology, in particular the fundamental characteristics of an individual involuntary movement. These characteristics are the essence of each involuntary movement, and it is necessary to recognize both its phenomenon itself and its accumulated knowledge in order to realize and interpret the involuntary movement. The following involuntary movements are treated: (1) typical tremor-at-rest in paralysis agitans, (2) atypical parkinsonian tremor, (3) essential tremor, (4) chorea, (5) ballism, (6) athetosis, (7) choreoathetosis, (8) dystonia, (9) spontaneous myoclonus at rest, (10) intention or action myoclonus, (11) intention tremor and (12) hyperkinesis.
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PMID:[Symptomatology of the involuntary movement]. 201 97


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