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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Before treatment 80 unselected patients suffering from delirium tremens were examined with regard to 13 psychopathological criteria. For the data a matrix of correlation was computed and it was factor analyzed according to the principal-component method. In consideration of the course of the value-curve two factors were interpreted. The result, however, is an undetailed classification. In addition to that, the data were cluster-analyzed according Ward. The results of the multivariate statistical analysis admit the assumption of two great, though heterogenous groups of symptoms (hallucination/vigilance). Factor I comprises the symptoms, disorder of orientation and consciousness, sweating, agitation and tremor on its positive pole, the duration of the delirant state on its negative pole. Factor II combines paranoid-hallucinatory symptoms, fearful affects and suggestibility on its positive pole, while on its negative, there are happy affect and grand-mal seizures. The bipolarity of this factor and additional diagnoses show that paranoid-hallucinatory symptoms without disorder of consciousness and grand-mal seizures mutually exclude each other. From this a differential therapy treating patients suffering from paranoid-hallucinatory symptoms with neuroleptics (e.g. Haloperidol) can be deduced, while the danger of grand-mal seizures has to be considered when disorders of consciousness appear.
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PMID:[Principle factors and symptom complexes in delirium tremens, factor and a group analytic study]. 717 1

Three cases are reported of patients who had episodic movement disorders triggered by foods or components of the diet. In the first patient, the movement consisted of shaking the head from side to side that was triggered by milk and a number of other foods. In the second patient, the movement consisted of a repeated shrugging of the shoulders that was triggered by egg and coffee. In the third, the movement consisted of rhythmic contractions of the arms and legs that were triggered by aspartame. The first patient agreed to participate in a study in which she drank 250 ml of skim milk, an amount sufficient to trigger head shaking, after pretreatment with drugs known to alter neurotransmission across beta-adrenergic, dopaminergic, GABAergic or purinergic synapses. At the doses used, propranolol and diazepam had no effect on the milk evoked movement disorder. Levodopa (plus carbidopa) blocked the reaction to milk. Haloperidol, salbutamol and theophylline by themselves triggered a reaction similar to that evoked by milk. These observations suggest that, in susceptible individuals, foods can trigger movement disorders through an action on dopamine and other neurotransmitter pathways in the brain. A videotape of the reactions of the first two patients is available.
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PMID:Neuropharmacological evaluation of movement disorders that are adverse reactions to specific foods. 796 Apr 70

This study aimed to differentiate chronically administered typical (haloperidol) and atypical (clozapine) neuroleptics in the dog using a complex temporal regulation schedule combining operant, voluntary, and involuntary motor parameters. Although clozapine and haloperidol showed some characteristics of neuroleptics, justifying their adherence to the same class of compounds, differences have also been highlighted and compared to the clinical observations. Haloperidol induced catalepsy, tremor, dystony, hyperkinesia, and stereotypy. Subjects produced anticipated responses before any stimulus. Incomplete and delayed responses were also produced. An interpretation in terms of akathisia and anhedonia has been suggested. Clozapine induced tremor, exploration, dystony, and hypersalivation. Subjects produced disinhibitory responses to the negative stimulus and incomplete responses but these latter were submitted to tolerance. The simultaneous presence of tranquilizing and disinhibitory effects has been reported on the clinical potential of clozapine both in cases of positive and negative schizophrenic symptomatologies.
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PMID:Differentiation of haloperidol and clozapine using a complex operant schedule in the dog. 843 Jan 21

In order to compare and contrast the behavioral effects of the typical neuroleptic haloperidol with the atypical neuroleptic clozapine, ten daily doses of these drugs were administered to separate groups of rats trained to extend the forelimb through a rectangular hole and to exert downward pressure on a force transducer to gain access to water. Doses were individually titrated daily for each rat in an attempt to achieve a 50% reduction in time on task (analogous to response rate) during 8-min daily sessions. Clozapine-treated rats exhibited dramatic tolerance to the drug's suppressive effect on time on task. In contrast, haloperidol rats displayed little tolerance on this measure. Despite the tolerance reflected by time on task, no tolerance was seen in clozapine's marked slowing of the dominant frequency of oscillations in forelimb force as measured by Fourier analysis of the force-time recordings. Haloperidol did not slow the dominant frequency. No tolerance was seen for clozapine's effects on forelimb force or tremor measures. Haloperidol did not significantly affect forelimb force. Both haloperidol and clozapine produced increases in the duration of long-duration forelimb responses, and no tolerance was seen for either drug on this measure of behavior. For clozapine, the dissociation between the tendency to respond (time on task) and the observed slowing of the dominant frequency may reflect effects peculiar to atypical neuroleptics, while the lengthening of long-duration responses by both drugs may reflect a more general behavioral effect that is characteristic of both typical and atypical antipsychotic drugs.
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PMID:Subchronic effects of clozapine and haloperidol on rats' forelimb force and duration during a press-while-licking task. 915 59

Neuroleptic-induced orofacial movements in rats have been widely utilized as an animal model of tardive dyskinesia (TD). The present study investigated the role of the oral motor cortex in these movements by applying direct cortical stimulation in rats exposed to chronic haloperidol. Rats received depot i.m. injections of haloperidol decanoate or sesame oil vehicle every 3 weeks (10 rats per group). After 24 weeks of injections and a 3-week withdrawal period, bilateral guide cannulae were implanted into the primary oral motor cortex. After a 1-week recovery, bilateral microinfusions of saline vehicle followed by 1, 3, and 10 mM N-methyl-D-aspartate (NMDA) were given and observations of oral activity, locomotion, rearing, and grooming were recorded. Haloperidol-treated rats displayed a significant emergence of NMDA stimulated oral activity (nondirected oral movements, oral tremor, audible teeth grinding, and directed oral movements). In addition, rearing and locomotion were significantly elevated in these animals. In contrast to haloperidol-treated rats, sesame oil-treated rats showed no significant emergence of any motor activity. These results suggest that chronic haloperidol administration alters primary motor cortex efferents, and that this effect may be a factor in the manifestation of chronic neuroleptic induced motor side effects, such as TD.
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PMID:Emergence of oral and locomotor activity in chronic haloperidol-treated rats following cortical N-methyl-D-aspartate stimulation. 961 Sep 39

The neuroleptic malignant syndrome (NMS) consists in an idiosyncratic reaction to neuroleptic drugs, probably related to a blockage of dopamine receptors in basal ganglia. Research criteria for diagnosing NMS from DSM-IV require severe rigidity and fever accompanied by 2 of 10 minor features including diaphoresis, dysphagia, tremor, incontinence, altered mentation, mutism, tachycardia, elevated or labile blood pressure, leukocytosis and elevation of creatine phosphokinase. From a clinical point of view, the NMS may range a large spectrum of presentations. Haloperidol is the most frequent drug associated with this syndrome. We report the case of a 30 year-old man who developed NMS at two different occasions, the first related to haloperidol and chlorpromazine and the second related to olanzapine, to our knowledge without previous mention in the indexed literature.
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PMID:[Neuroleptic malignant syndrome: case report with recurrence associated with the use of olanzapine]. 1002 91

Experiments with animals have shown that D2 dopamine (DA) receptors are involved in prepulse inhibition of the acoustic startle reflex (suppression of the reflex response evoked by a loud sound by prior presentation of a low-intensity stimulus). The present experiment attempted to extend this observation to man. Twelve healthy males (18-30 years), screened for normal hearing thresholds, participated in four sessions in which they received oral doses of placebo, bromocriptine 1.25 mg (a D2 receptor agonist), haloperidol 3 mg (a D2 receptor antagonist) and combined treatment with bromocriptine 1.25 mg+haloperidol 3 mg, according to a balanced double-blind protocol. Thirty-minute electromyographic recordings from the orbicularis oculi muscle of the right eye were carried out 120 min after ingestion of haloperidol and/or 90 min after ingestion of bromocriptine. Subjects received 36 40-msec sound pulses (115 dB), separated by variable intervals (mean 25 sec); in 24 of the trials the pulse was preceded by a 40-msec prepulse (75 dB in 12 trials and 85 dB in 12 trials; prepulse-pulse interval, 120 msec). The amplitude of the startle response was not significantly altered by any of the active treatments. Under the placebo condition, both 75- and 85-dB prepulses inhibited the startle response. Bromocriptine significantly attenuated this prepulse inhibition; haloperidol also produced a small but statistically significant attenuation of prepulse inhibition. Haloperidol significantly antagonized the attenuation of prepulse inhibition produced by bromocriptine. Neither drug altered self-rated alertness, physiological finger tremor, systolic or diastolic blood pressure or salivation. Bromocriptine significantly suppressed and haloperidol significantly elevated serum prolactin levels, these changes being absent when the two drugs were given in combination. The results provide evidence for the involvement of D2 DA receptors in prepulse inhibition of the startle reflex in man.
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PMID:Effects of bromocriptine and haloperidol on prepulse inhibition of the acoustic startle response in man. 1140 22

We have demonstrated involvement of the serotonergic system in orexin-induced behavioral responses in rats. Orexin-A and -B (hypocretin-1 and -2) significantly increased total locomotor activity when administered centrally. They also induced behavioral alterations; increasing grooming, face washing and wet dog shaking in rats. Haloperidol inhibited orexin-induced hyperlocomotion and these behavioral alterations. Serotonin antagonists, ritanserin and metergoline, did not attenuate orexin-induced hyperlocomotion but partly inhibited orexin-induced behavioral alterations. These results suggest that the dopaminergic system might be involved in orexin-induced hyperlocomotion, while both the serotonergic system as well as the dopaminergic system might be involved in orexin-induced behavioral responses.
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PMID:Involvement of the serotonergic system in orexin-induced behavioral alterations in rats. 1183 Feb 86

Parkinson's disease (PD) exhibits symptoms of motor dysfunction such as tremor, akinesia and rigidity. Agents that selectively disrupt or destroy catecholaminergic systems, such as reserpine, methamphetamine, 6-hydroxydopamine and 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine, have been used to develop PD models and to study the animal behavior like catalepsy, akinesia, swim-test, etc. The major apprehension while working with these chemicals is their irreversible neuro-toxic effect. Haloperidol is a classical antipsychotic drug, which produces extra-pyrimidal Parkinson's symptoms (EPS). Measuring catalepsy and akinesia in the treated mice monitored the haloperidol-induced EPS. Alternatively, swimming disability was tested as a new parameter to monitor haloperidol-induced EPS. The results showed that the restoration of swimming disability in haloperidol-induced L-dopa and caffeine pre-treated mice could be used as pre-clinical model to study PD.
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PMID:Antagonism of haloperidol-induced swim impairment in L-dopa and caffeine treated mice: a pre-clinical model to study Parkinson's disease. 1914 80

Haloperidol decanoate is a typical antipsychotic drug used as maintenance therapy for schizophrenia and mood disorders formulated as an ester for intramuscular injection. Cases of oral haloperidol decanoate intoxications have not been described in literature. In this report, we present for the first time a case of an oral ingestion of haloperidol decanoate of a young woman who presented to the emergency department following an intentional oral ingestion of 1 ampoule of haloperidol decanoate 100mg. At presentation, she had a bilateral rest tremor of both hands and mild hypothermia. No other obvious signs of an intoxication were observed. She was treated with a single dose of activated charcoal and laxative and was admitted to the intensive care for rhythm monitoring and observation. During the night the QTc interval increased to 453ms, but stayed within the normal range. Haloperidol plasma levels increased as well, but also stayed within therapeutic ranges. These findings indicate that treatment with oral activated charcoal was sufficient to prevent any serious events.
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PMID:An acute oral intoxication with haloperidol decanoate. 2870 42


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