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)

In an open study, 60 Parkinson patients with varying aetiology were submitted to a treatment with the long-acting antiparkinsonian drug dexetimide and L-Dopa. Rigor, tremor and akinesia were favourably influenced. An advantage over other antiparkinsonian agents is its long duration of action and the possibility of a simple dosage. Further investigations concerning its long-term effect and elucidation of its interactions with different drugs commonly administered in parkinsonian disorders seem desirable.
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PMID:Treatment of Parkinsonian syndrome with dexetimide. 55 48

Effects of ID-690 on motor systems were compared with those of clonazepam, diazepam and nitrazepam. ID-690 exerted muscle relaxant action in the rotarod method using rats and mice; this action was almost equal in potency to clonazepam and nitrazepam and more potent than diazepam. Pretreatment with ID-690, clonazepam and nitrazepam increased the sleeping time of mice under thiopental anesthesia to the same degree, whereas diazepam produced a lesser effect. ID-690 was almost equal in potency to diazepam and nitrazepam in protecting against oxotremorine-induced tremor in mice, and approximately 10 times as potent as clonazepam. The anticonvulsant action of ID-690 was similar to that of clonazepam. These benzodiazepines effectively augmented the dorsal root reflexes, while showing no effects on the ventral root reflexes. Rigidity in rats due to anemic decerebration was not affected after intraduodenal administration of these drugs, while phasic augmentation of the rigidity by mechanical stimulation of the hind limb was clearly depressed. These drugs had no effects on the neuromuscular junction. From these results, it is concluded that ID-690 has a wider pharmacological spectrum than clonazepam, is almost equal in potency to nitrazepam and is more potent than diazepam.
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PMID:[Pharmacological study on 5-(o-chlorophenyl)-1-methyl-7-nitro-1,3-dihydro-2H-1,4-benzodiazepin-2-one (ID-690), with special reference to the effects on motor systems]. 55 42

In two cases of chronic schizophrenia complicated by diabetes mellitus, the concomitant use of the neuroleptica and oral antidiabetics was attended by the appearance of symptoms simulative of syndrome malin, i.e. hyperpyrexia, tachycardia, blood pressure instability, disturbances of consciousness, muscle rigidity, tremor, dysphagia, salivation and urinary incontinence. In one of these cases, the patient, a 47-year-old man, died 10 days later. In the other case, a 62-year-old woman, almost all the symptoms subsided after 14 days, and oral dyskinesia persisted for only one additional month. In both cases, hypoglycemia due to oral antidiabetics was not seen. In Case 2, a combined regimen of oral antidiabetics and neuroleptica was later resumed. Again, a similar set of symptoms as seen initially were noted, along with an elevation of the serum CPK level. Parenterally administered biperiden proved to be highly effective in the control of the symptoms. The pathogenetic mechanism of these symptoms might possibly be explained as potentiation of the action of the neuroleptica by oral antidiabetics.
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PMID:"Syndrome malin"-like symptoms probably due to interaction between neuroleptica and oral antidiabetic agents. 65 48

Rigidity in Parkinson patients can be easily quantitated by determining net work required to passively flex and extend the forearm through an arc of 100 degrees. Rigidity thus measured can be subdivided into two very distinct types, resting and activated. Resting rigidity, measured while the patient is relaxed, responds to all effective therapeutic agents and correlates closely to degree of clinical improvement. Activated rigidity, measured during voluntary activity, is not relieved by any presently available medical treatment. It remains unchanged at pre-therapy levels even in patients who may temporarily appear to have dramatic improvement in clinical symptomatology. Longitudinal measurements made in hundreds of parkinson patients over intervals ranging from 5 to 15 years show continuing high levels of activated rigidity through the entire period of study. In marked contrast to our wide experience with parkinson patients is a single, well documented case of Wilson's disease who appears to have recovered completely both by clinical examination and by all of our machine measurements. This patient had high levels of extrapyramidal deficit, repeatedly measured over a period of four months when penicillamine therapy was being investigated. He then suddenly reverted to normal and returned to full time employment. High values of resting rigidity activated rigidity, akinesia and resting tremor all reverted to normal and have remained normal for the past 6 years. The implication of this study is that L-dopa and related treatments only mask the symptomatology of Parkinson's disease and are not retarding the underlying pathological process. Penicillamine, on the other hand, probably does relieve the destructive process in Wilson's disease and may in early cases, permanently relieve the extrapyramidal dysfunction.
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PMID:Failure of L-dopa to relieve activated rigidity in Parkinson's disease. 93 Jul 49

After 9 years of treatment for Parkinson's disease, a 68-year-old woman developed the complications of neuroleptic malignant syndrome (NMS) and disseminated intravascular coagulation (DIC) while she was still receiving levodopa, bromocriptine and amantadine hydrochloride. The patient displayed a high fever (40 degrees C), impaired consciousness, marked systemic muscle rigidity, tremor and bloody stools. The diagnosis of NMS and DIC was made on the basis of the symptoms and the results of blood serological tests. The antiparkinsonian drugs that had been administered until her admission to our hospital were continued unchanged, while the NMS was treated with dantrolene sodium and the DIC, with nafamostat mesilate. Both of the above-mentioned therapies were effective. The present case is rare in that the patient developed NMS and DIC during treatment and not after the discontinuation of the antiparkinsonian drugs.
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PMID:Successful treatment of levodopa-induced neuroleptic malignant syndrome (NMS) and disseminated intravascular coagulation (DIC) in a patient with Parkinson's disease. 129 27

The purpose of the present study was to investigate physical dependence upon diazepam systematically in two inbred strains of rats, Lewis (LEW) and Fischer 344 (F344). Rats were chronically fed food containing diazepam on an escalating drug dosage schedule, from 1 and 2 to 12 mg/g of food, over a period of 30 days. During treatment, the growth curve in LEW and F344 rats was suppressed compared with the respective controls. Motor incoordination was evaluated by a rotarod performance test. The ranking of the motor incoordination during the final concentration of diazepam was as follows: F344 greater than LEW. After substitution of normal food for the diazepam-admixed food, various signs of diazepam withdrawal occurred 16-120 h later. These signs included vocalization, irritability, muscle rigidity, ear-twitching, Straub's tail, piloerection, fascicular twitch, tremor, convulsion, and death. The incidences of vocalization, ear-twitching, piloerection, and tremor in F344 were significantly higher than those in LEW rats. Furthermore, two of six F344 rats showed spontaneous convulsions and one rat died of convulsions. Overall withdrawal scores were significantly greater in F344 (16.0) than in LEW (6.3) rats. These results suggest that diazepam withdrawal severity is strongly influenced by genetic factors, and F344 rats are highly susceptible to dependence upon benzodiazepines.
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PMID:Genetic differences in the development of physical dependence upon diazepam in Lewis and Fischer 344 inbred rat strains. 143 78

Ethanol (EtOH) withdrawal is characterized by a hyperexcitable state that includes anxiety, tremor, muscle rigidity and seizures. The present three experiments examined the effects of EtOH dependence and withdrawal on the acoustic startle response, an easily quantifiable measure of behavioral reactivity to exteroceptive stimuli. Two intensities of startle stimuli, 105 and 120 dB pulses, were presented to rats during chronic EtOH exposure and during EtOH withdrawal. Prepulse inhibition, which is a sensitive measure of sensorimotor gating processes associated with filtering sensory stimulation, was also assessed during chronic EtOH exposure and withdrawal. Prepulse inhibition was induced by the presentation of a weak 80 dB acoustic stimulus 100 ms prior to a 120 dB stimulus pulse. After 14 days of EtOH liquid diet administration the magnitude of responses elicited by 105 and 120 dB startle stimuli was less in ethanol-treated subjects during continued EtOH access than in animals fed a control liquid diet. When EtOH liquid diet treatment was continued for an additional 3-day period and animals were tested 8 h after withdrawal from EtOH, withdrawn animals were more reactive to startle stimuli at both intensities than were animals maintained on the EtOH liquid diet. A time-course experiment with repeated startle testing at 4, 8, and 12 h post-EtOH exposure revealed significant increases in responding to the 105 dB startle intensity at 8 h post-EtOH exposure. The ability of animals to respond to a prepulse stimulus was not affected during chronic EtOH treatment, but was reduced during withdrawal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Responding to acoustic startle during chronic ethanol intoxication and withdrawal. 157 Mar 82

We report a case of a 52-year-old man with posttraumatic parkinsonism. He was admitted to our department because of right-sided hand tremor and gait disturbance. He had suffered from a severe head injury incurred in a traffic accident with brief unconsciousness 6 months before admission. Three weeks after his injury, tremor and rigidity in the right upper limb developed, and he walked dragging his right leg. Five months after his injury, he received 1-dopa therapy, exhibiting a moderate improvement in parkinsonian symptoms. On admission, he was demented to a mild degree with masked face and monotonous speech. He presented with resting-postural-kinetic tremor and muscle rigidity on the right side. Cranial CT and MRI showed no abnormality. Inter-peak latencies of waves III to V of BAEP were significantly longer in this patient than in normal subjects. This BAEP findings suggested an upper brainstem lesion. 123I-IMP SPECT disclosed decreased cerebral blood flow in the left thalamus, bilateral frontal and parietal cortices. We diagnosed this case as having posttraumatic parkinsonism. Parkinsonism in the present case may be due to the involvement of multiple neuronal circuits of the extrapyramidal system at the level of the midbrain to the thalamus.
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PMID:[A case of posttraumatic parkinsonism]. 176 60

This report describes a case of cerebrotendinous xanthomatosis (CTX) accompanied by clinical manifestations of parkinsonism, including oily and masked face, marked akinesia, muscle rigidity and resting hand tremor. Magnetic resonance imaging (MRI) of the brain showed high intensity areas on T2 weighted imaging, and slightly low intensity areas on T1 weighted imaging in the right globus pallidus and the left putamen. Cerebral cortical atrophy with slight ventricular dilatation and cerebellar atrophy were present as well. This is a case report of CTX which manifested parkinsonism. Parkinsonism may not be a coincidental manifestation in CTX, but rather represent a symptom of the same underlying diathesis.
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PMID:Parkinsonism in cerebrotendinous xanthomatosis. 186 93

1. Neuroleptic drugs (antipsychotics) produce numerous side effects which include serious extrapyramidal symptoms consisting of akathisia, dystonia, neuroleptic malignant syndrome, parkinsonian reactions such as postural abnormality, tremor, akinesia or bradykinesia, rigidity, and tardive dyskinesia. 2. Among the complications of neuroleptic chemotherapy, the most serious and potentially fatal complication is malignant syndrome, which is characterized by extreme hyperthermia, "lead pipe" skeletal muscle rigidity causing dyspnea, dysphagia, and rhabdomyolysis, autonomic instability, fluctuating consciousness, leukocytosis, and elevated creatine phosphokinase. 3. Neuroleptic malignant syndrome should be differentiated from malignant hyperthermia, lethal catatonia, and other pathological states producing some of these same symptoms. 4. In addition to neuroleptics, malignant syndrome has been caused by thymoleptics (antidepressants), metoclopramide (antiemetic), metoclopramide combined with cimetidine, tetrabenazine, overdosage of benzodiazepine, phenelzine, dothiepin and alcohol, and amphetamine. 5. Factors leading to and/or facilitating the emergence of neuroleptic malignant syndromes are reportedly organic brain syndrome, dehydration, exhaustion, external heat load, excessive sympathetic discharge, use of long acting neuroleptics, high doses of neuroleptics, rapid dose titration with neuroleptics, abrupt discontinuation of antiparkinsonism agents, and concurrent lithium therapy. 6. Although, the pathogenesis of neuroleptic malignant syndrome is not understood completely, a blockade of dopaminergic receptors in the hypothalamus, spinal cord and striatum, an alteration of dopaminergic-serotonergic transmission in the body, an enhanced synthesis and action of prostaglandin E1 and E2, and a modification of calcium-mediated signal transduction in the body have been suggested. 7. The treatment of malignant syndrome includes immediate withdrawal of neuroleptic drugs, i.v. infusion of dantrolene, and oral administration of bromocriptine; or alternatively i.v. infusion of dantrolene and the combination of levodopa-carbidopa. 8. Other measures to enhance the therapeutic effectiveness of the aforementioned regimens are to include the use of anticholinergic drugs such as benztropine to enhance the effectiveness of bromocriptine, of lorazepam if catatonic symptoms persist, or of electroconvulsive therapy (ECT) if psychotic symptoms persist. 9. These treatments, however, must be "active" rather than "passive", in order to avert fatalities and/or unfortunate sequelae from this iatrogenic and incompletely understood disease.
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PMID:Pathogenesis and treatment of neuroleptic malignant syndrome. 197 19


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