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)

Hexosaminidase deficiency diseases or GM2-gangliosidoses were originally described as infantile encephalopathies. Recently, hexosaminidase deficiencies have been found with different phenotypes, including juvenile and adult encephalopathies, cerebellar ataxias, and motor neuron diseases. Individual cases have resembled Ramsey-Hunt syndrome, olivopontocerebellar ataxia, Friedreich ataxia, amyotrophic lateral sclerosis, Kugelberg-Welander disease, Fazio-Londe disease, and Charcot-Marie-Tooth disease. Tremor, dystonia, spastic paresis, and psychosis have been seen. Since few diagnosable causes for these system atrophies are known, these patients should be tested for hexosaminidase deficiency. These recessive disorders fit a multiple loci/multiple alleles genetic scheme, and a clinical genetic classification is presented.
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PMID:The clinical spectrum of hexosaminidase deficiency diseases. 719 92

The records of 37 patients with systemic lupus erythematosus (SLE) followed at The Children's Hospital of Philadelphia between 1968 and 1978 were reviewed for evidence of central nervous system (CNS) involvement. Criteria for CNS involvement included evidence of organic brain syndrome, electroencephalographic abnormalities with symptoms referable to CNS, or objective neurologic signs. Sixteen of 37 children had CNS involvement (43%). Thirteen patients had CNS involvement at the onset of SLE. Three patients had late onset CNS manifestations 1 to 2 years after the diagnosis of SLE. The most frequently observed symptoms were headache, behavior disorder, lethargy, diplopia, blurred vision, memory alteration, dizziness, and alteration of consciousness. The most frequently observed neurologic signs were seizures, cranial nerve palsy, ataxia, papilledema, nystagmus, meningitis, tremor, rigidity, cortical blindness, and coma. Neuropsychiatric manifestations included organic brain syndrome, functional psychosis, and personality disorder. Laboratory tests showed elevated cerebrospinal fluid opening pressure and protein, negative cultures, and abnormal electroencephalograms and computerized axial tomography scans. Fourteen of 16 children with CNS manifestations are alive. Thirteen had a mean IQ of 89 by the Wechsler Intelligence Tests. Twelve are in educational programs. One required long-term psychiatric care. A residual neurologic abnormality, a seizure disorder, was present in 3. CNS involvement with SLE in children carries a favorable prognosis.
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PMID:Central nervous system involvement in childhood systemic lupus erythematosus. 731 16

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

The effects of the selective D2 DA receptor antagonist, (-)eticlopride, a drug belonging to the benzamide class, were investigated on the D2 DA agonist SND 919- and CQP 201-403-induced stereotyped behaviour and on CQP 201-403-induced shaking, in rats, and on isolation-induced aggression, in mice. (-)Eticlopride was also tested over a wide dose range (5-1200 micrograms kg-1, s.c.) for sedative and cataleptic activity, in rats. For comparison, some experiments were performed with (-)sulpiride (10 and 40 mg kg-1, s.c.) The data obtained show that (-)eticlopride differs from (-)sulpiride and potentially modifies animal behaviour, whether spontaneous or induced; moreover, they suggest a potential clinical use for this neuroleptic in the management of psychotic states.
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PMID:Behavioural assessment in rats of the antipsychotic potential of the potent dopamine D2 receptor antagonist, (-)eticlopride. 747 22

Parkinson's disease (PD) accounts for 58% of patients with Parkinsonism. The second most common cause is drug-induced Parkinsonism, diagnosed in 20% of patients. Levodopa remains as the mainstay of PD treatment. Although there is controversy regarding the timing for beginning levodopa, it should be used when the patient develops significant disability. Other drugs that may be used are anticholinergic agents, useful for tremor; amantadine, for rigidity and bradykinesia; dopamine agonists, for the management of levodopa complications; and selegiline which may be a neuroprotector agent. Problems in the management of PD include primary failure, secondary failure and levodopa complications. Antidopaminergic drugs, severe rest tremor and diagnosis error may lead to primary failure. Progression of PD is the most common explanation for secondary failure. The most important levodopa therapy complications are dyskinesias and fluctuations. Other common problems are dysautonomia, depression, psychosis and dementia. The author discusses the phenomenology and management of these complications. Future perspectives include brain repair surgeries.
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PMID:[Treatment of Parkinson disease]. 757 92

Concerns about the toxicities of psychomotor stimulants originate primarily from effects seen at high doses, when stimulants are abused. Low dose use in the apathetic medically ill patient has been generally associated with only minimal, short lived side effects, which are detailed herein. Confusion may be worsened in already delirious patients. Anxiety, psychosis, cardiovascular effects, insomnia, and tremor may occur but infrequently require discontinuation. Appetite is normally stimulated in the medically ill. In fact, stimulants are frequently utilized in the medically ill largely because of their minimal toxicity. The history of U.S. stimulant abuse in the twentieth century is briefly discussed. Abuse of prescribed stimulants appears to be infrequent. Over-zealous concern regarding abuse has previously led to unfortunate declines in appropriate utilization of stimulants, e.g., for attention deficit disorder. Guidelines for prescribing stimulants in light of abuse potential are included.
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PMID:Toxicity and abuse of prescribed stimulants. 764 19

L-Dopa pioneered the symptomatic therapy of Parkinson's disease. While this treatment proved effective in the treatment of parkinsonian akinesia, rigidity and tremor, prolonged L-dopa treatment was often noted to result in dyskinesia, psychosis and 'on-off' phenomena. This increasing disability of L-Dopa-treated parkinsonian patients, however, is not correlated with the duration of L-dopa treatment. Mortality due to Parkinson's disease has decreased significantly after the introduction of L-dopa treatment. The development of D1-selective dopamine agonists and the introduction of neuroprotective rather than symptomatic therapy are required for treating Parkinson's disease.
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PMID:Dilemma in the treatment of Parkinson's disease with L-dopa. 782 30

Physiological dependence on benzodiazepines is accompanied by a withdrawal syndrome which is typically characterized by sleep disturbance, irritability, increased tension and anxiety, panic attacks, hand tremor, sweating, difficulty in concentration, dry wretching and nausea, some weight loss, palpitations, headache, muscular pain and stiffness and a host of perceptual changes. Instances are also reported within the high-dosage category of more serious developments such as seizures and psychotic reactions. Withdrawal from normal dosage benzodiazepine treatment can result in a number of symptomatic patterns. The most common is a short-lived "rebound" anxiety and insomnia, coming on within 1-4 days of discontinuation, depending on the half-life of the particular drug. The second pattern is the full-blown withdrawal syndrome, usually lasting 10-14 days; finally, a third pattern may represent the return of anxiety symptoms which then persist until some form of treatment is instituted. Physiological dependence on benzodiazepines can occur following prolonged treatment with therapeutic doses, but it is not clear what proportion of patients are likely to experience a withdrawal syndrome. It is also unknown to what extent the risk of physiological dependence is dependent upon a minimum duration of exposure or dosage of these drugs. Withdrawal phenomena appear to be more severe following withdrawal from high doses or short-acting benzodiazepines. Dependence on alcohol or other sedatives may increase the risk of benzodiazepine dependence, but it has proved difficult to demonstrate unequivocally differences in the relative abuse potential of individual benzodiazepines.
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PMID:The benzodiazepine withdrawal syndrome. 784 56

Recent research on the role of clozapine in the treatment of Parkinson's disease and other movement disorders is discussed. Most clinical trials have shown resolution of or improvement in psychotic symptoms accompanying Parkinson's disease without worsening of parkinsonian symptoms. Adverse effects appear to be mild at dosages of < 100 mg/day; sedation is the most frequent problem. Most of these studies have serious limitations, however; until better studies have been completed, the decision to use clozapine for Parkinson's disease-related psychosis should be made on a case-by-case basis, with thorough evaluation of risks, benefits, and other therapeutic options. Some patients with Parkinson's disease have shown improvement in tremor and other abnormal movements when given clozapine. Clozapine cannot be recommended for treating tardive dyskinesia on the basis of the research done so far; some trials show dramatic resolution of symptoms, others no benefit. Anticholinergics or dopamine-reuptake inhibitors should be considered before clozapine is given to patients with tardive dyskinesia because of clozapine's potential for serious adverse effects. A few patients with Huntington's disease have responded to clozapine, but again no conclusions can be drawn. Clozapine appears to offer no real advantage over haloperidol for treating choreiform movements in Huntington's disease. The frequency of tics in Tourette's syndrome does not seem to be reduced by clozapine. Clozapine has shown some efficacy as a treatment for psychosis and abnormal movements in Parkinson's disease. Results have been less promising for other movement disorders. Further study in larger populations is needed before any definitive conclusions about clozapine's place in movement disorder therapy can be made.
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PMID:Clozapine therapy for Parkinson's disease and other movement disorders. 853 51

Studies of extrapyramidal motor function in patients with schizophrenia have contributed to our understanding of the phenomenology and therapeutic outcome associated with neuroleptics. An increasing body of literature suggests that extrapyramidal motor abnormalities associated with schizophrenia may be linked to the pathophysiological mechanisms responsible for schizophrenia. Similarly, it has been documented that the extrapyramidal system may be involved in motor abnormalities in patients with Alzheimer's disease (AD). The present study was undertaken to examine motor function in schizophrenia and AD patients with psychosis. Quantitative instrumental procedures were used to examine rigidity, tremor, and bradykinesia in 13 neuroleptic-naive patients with schizophrenia, 13 AD patients with psychosis, and 26 age-comparable controls. Both schizophrenia and AD patients had significantly higher tremor and rigidity scores than did normal subjects. This comparative study of schizophrenia and AD patients with psychosis suggests that the effect of dementia in patients with psychosis is to prolong movement time, whereas abnormal parkinsonian postural tremor tends to be associated with psychosis in the absence of dementia.
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PMID:Extrapyramidal motor abnormalities associated with late-life psychosis. 790 62


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