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)

During a 6-year period, 23 Navajo adolescents were hospitalized 47 times for presumed lead intoxication secondary to gasoline sniffing. Most patients were male (87%) and sniffed gasoline as a social activity, more frequently in spring and summer. Sixty-five percent of the patients first presented with toxic encephalopathy. Of total episodes, 31% involved asymptomatic lead overload; 31% involved tremor, ataxia, and other neurologic signs; and 38% involved encephalopathy with disorientation and hallucinations. Free erythrocyte protoporphyrin levels were not consistently high, although blood lead levels were all elevated. One death occurred. Approximately 11% of 537 Navajo adolescents said they inhaled gasoline for enjoyment at least occasionally. Among 147 junior high school students, blood lead levels averaged 18 +/- 6 micrograms/dL with no values greater than 40 micrograms/dL. Three of these students had elevated zinc protoporphyrin levels and all three were anemic. No correlation was found between levels of blood lead or zinc protoporphyrin and whether or not the youth reported sniffing gasoline. However, sniffing gasoline was associated with poor school performance and delinquent behavior. Although apparently many Navajo adolescents experiment with gasoline inhalation, only a few engage in this activity frequently enough to develop either asymptomatic or symptomatic lead overload.
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PMID:Gasoline sniffing and lead toxicity in Navajo adolescents. 684 58

A 15 year old boy was evaluated in the psychiatric emergency room for the acute onset of "confusion,"insomnia, headache, and shaking of one week's duration. Two days later hallucinations, formication and a movement disorder emerged characterized by action tremor, myoclonus, chorea and ataxia. Further history revealed inhalation of gasoline for its euphoric effects. Plasma lead levels were in the toxic range. Chelation therapy reversed the clinical symptoms. Behavioral changes and a movement disorder in the context of gasoline inhalation are highly suggestive of organic lead encephalopathy. Recognition of this syndrome is important as chelation therapy is effective.
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PMID:Organic lead encephalopathy: behavioral change and movement disorder following gasoline inhalation. 705 7

The pattern and severity of alcohol withdrawal in 49 alcohol dependent subjects admitted to the Manchester Detoxification Centre are described. Assessment over 10 days involved the use of the Selected Severity Assessment Scale (SSA) and allocation of patients to subgroups of the alcohol withdrawal syndrome. There were associations between tremor, clouding of sensorium, hallucinations and convulsions (items of the SSA) and the four pre-delirious clinical sub-groups identified. We concluded that clinical assessment of the pre-delirious stage took into account these four variables and that there was little value in the routine use of the SSA on a unit such as ours.
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PMID:Measurement of alcohol withdrawal in detoxification centre patients. 710 37

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

Lisuride is a soluble ergolene derivative with endocrine effects similar to but more potent than those of bromocriptine. In nine subjects with idiopathic, postencephalitic, or drug-induced parkinsonism, lisuride at a dosage of 0.05 to 0.15 mg intravenously caused an immediate improvement in tremor, rigidity, akinesia, and postural deformity, but also caused chorea and orofacial dyskinesia. Improvement lasted 2 to 3 hours. Lisuride had little or no effect in a single patient with progressively supranuclear palsy. Oral lisuride therapy, 0.8 to 4.8 mg daily, had similar effects but occasionally caused reduced awareness and hallucinations.
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PMID:Lisuride in parkinsonism. 721 65

Phenylpropanolamine hydrochloride is an amphetamine-like substance that is found in 64 different over-the-counter preparations for colds and appetite suppression. It is also found in numerous prescription drugs. Recently, it has been reported to cause symptoms of sympathomimetic-like effects, such as severe hypertension, hypertensive crisis, and possible renal failure. Also, several cases of psychotic episodes while taking phenylpropanolamine have been reported. This is the report of seven patients who have experienced acute CNS effects. These effects range from stimulation of the medullary respiratory center to tremor, restlessness, increased motor activity, agitation, and hallucinations.
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PMID:Amphetamine-like reactions to phenylpropanolamine. 745 88

We present an autopsied case of striatonigral degeneration (SND) combined with olivopontocerebellar atrophy (OPCA) with subcortical dementia and hallucinatory state. A Japanese woman without a remarkable family history showed hand tremor at the age of 35 years, followed by bradykinesia, muscle rigidity, orthostatic hypotension, neurogenic bladder and pyramidal signs. No obvious cerebellar symptoms were found. Various antiparkinsonian drugs were administered, but were not markedly effective for the parkinsonism. She developed a mild dementia characterized by mild memory disturbance with preservation of orientation, slowing of thought processes, emotional lability toward sadness, impaired ability to manipulate acquired knowledge and poor calculating, and by the absence of aphasia, apraxia and agnosia. The features in this patient were consistent with those seen in subcortical dementia. She also had auditory hallucinations. MRI revealed hypointense T2 signals in the putamina and substantia nigra. T1-weighted MRI demonstrated atrophy of both the pons and cerebellum in addition to atrophy of the putamina and substantia nigra. EEG showed slowing of background activity. She died of cardiac failure at the age of 47. Autopsy disclosed brain stem tegmental atrophy, SND, OPCA and many glial cytoplasmic inclusions in the central nervous system, but well-preserved cerebrum. We discuss the relationship between the psychiatric symptoms and pathologic findings of brain stem tegmentum.
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PMID:Striatonigral degeneration combined with olivopontocerebellar atrophy with subcortical dementia and hallucinatory state. 755 Jun 4

We report of 51-year-old man with early onset parkinsonism. The patient was well until 38 years of age, when he noted a difficulty in the use of his right leg; this difficulty improved after he received a medicine from his physician. He did not take medicine regularly, and he noted difficulty in standing up from a chair and in rolling over at age 40. Tremor was not a feature, but he noted slowness in his movements at age 42; at age 49, he noted diurnal fluctuation in his symptoms and at times he experienced hallucination. He was admitted to our hospital in September of 1992 for the first time when he was 50-year-old. At that time, neurologic examination revealed an alert and somewhat bradyphrenic man; Hasegawa dementia rating scale was 20/30. Cranial nerves were intact except for masked face and small voice. He showed stooped posture and small step gait cogwheel rigidity was noted in the four limbs more on the left; tremor was absent. Deep reflexes were within normal range and the sensation was intact. As he showed diurnal fluctuation in his symptoms, his medication was switched to levodopa 3,000 mg/day without a peripheral decarboxylase inhibitor. He was discharged for out patient follow up. But he did not take drugs regularly, and his neurologic condition deteriorated; he was admitted to another hospital. Neurologic examination at that time was essentially similar to that of his first admission to our hospital, except that he showed more severe rigidity and akinesia; again tremor was not detected. His cranial CT scan showed a mild ventricular dilatation without cortical or brain stem atrophy. During his hospital stay, he developed episodes of oculogyric crisis during peak dose of levodopa, and orthostatic hypotension. He developed pneumonia and expired on October 28, 1993. He was discussed in a neurological CPC, and the chief discussion arrived at the conclusion that the patient had early onset Parkinson's disease of Lewy body type. As differential diagnoses, early onset parkinsonism without Lewy body, pure form of diffuse Lewy body disease, pallidoluysian atrophy, and other conditions were considered; however, all of those possibilities were excluded. Early onset parkinsonism without Lewy body would have much earlier onset than this patient, and diffuse Lewy body disease would show more profound dementia 13 years after the onset. Pallidoluysian atrophy would be complicated with some dystonic features. Post-mortem examination showed marked discoloration and degeneration of the substantia nigra. The degeneration was most prominent in the ventrolateral tier of the substantia nigra.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 51-year-old man with early onset parkinsonism]. 760 92

The aim of the present work was to study the behavioral effects elicited in adult cats by the selective D1 agonist, SKF 38393, and the D2 agonist, LY 171555, comparing their effects with those evoked by apomorphine. In 10 adult cats, 0.5, 1.0, 4.0, and 8.0 mg/kg IP of SKF 38393 were administered at random. A dose-response effect was observed related to alertness, indifference, and locomotion. The overall effect of SKF 38393 was inhibitory. To the same 10 animals, LY 171555 in doses of 0.25, 0.5, and 1.0 mg/kg were injected IP. This drug had an excitatory and more complex effect than what was observed with the D1 agonist. Increases in locomotion, in alertness, indifference, fear, olfaction, pupillary dilation, hallucination, limb flicking, and head shaking were recorded. Apomorphine given to the same cats, in a dose equimolar to 1.0 mg/kg of LY 171555, elicited behaviors that resembled those elicited by the latter drug, but of a lesser intensity and duration. The interval between the different treatments was approximately 2 months. These results show clearly that the D2 receptor is the main dopaminergic receptor involved in the mechanism of production of most of the behavioral effects produced by some of the dopaminergic agonist drugs like apomorphine.
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PMID:Behavioral effects evoked by SKF 38393 and LY 171555 in adult cats. 761 Jan 53

The diagnosis, evaluation and assessment, supportive care, and pharmacologic treatment of acute alcohol withdrawal are reviewed. Patients in alcohol withdrawal have decreased or stopped their heavy, prolonged ingestion of alcohol and have subsequently begun to have at least two of the following symptoms: autonomic hyperactivity, tremor, nausea or vomiting, hallucinations, psychomotor agitation, anxiety, and grand mal seizures. Evaluation of the patient at risk for alcohol withdrawal should include a complete history and physical examination; laboratory tests are often indicated. The patient's progress should be assessed before, during, and after therapy, preferably with a validated instrument. After the initial evaluation and assessment but before the administration of dextrose-containing solutions, a 100-mg dose of thiamine hydrochloride should be given by i.m. or i.v. injection. Routine supplementation with calcium, magnesium, and phosphate is questionable. The need for fluid and electrolyte administration varies depending on losses. Most patients in alcohol withdrawal can be managed with supportive care alone, but for more severe or complicated withdrawal, pharmacologic therapy may be necessary. Benzodiazepines, especially diazepam and chlordiazepoxide, are the drugs of choice. Barbiturates, beta-blockers, and antipsychotics are generally not recommended as first-line therapy. Several drugs in other classes, including carbamazepine and clonidine, have been shown to be about as effective as benzodiazepines in a few studies, but the studies were small, the patients were usually in mild withdrawal, and validated instruments for assessing withdrawal were often not used. Some agents, such as beta-blockers, may play a role as adjuncts to, not replacements for, benzodiazepine therapy. For patients in alcohol withdrawal who do not respond to supportive care, benzodiazepines are the treatment of choice.
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PMID:Management of alcohol withdrawal. 762 38


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