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)

Eighty-two schizophrenic outpatients receiving maintenance antipsychotic medication were assessed for akathisia and tardive dyskinesia. Thirty-nine (48%) manifested patterns of nondyskinetic, restless movement characteristic of akathisia. On the basis of their clinical features, these patients were divided into three groups: "acute" akathisia (recent onset, related to an increase in antipsychotic drug dose); "pseudoakathisia" (motor signs but no subjective symptoms); and "chronic" akathisia (a mixed category including persistent acute akathisia and "tardive" akathisia with the pharmacologic characteristics of tardive dyskinesia). Coarse, jerky foot tremor was observed as an invariable accompaniment of acute akathisia. A significant association was found between choreoathetoid limb dyskinesias, orofacial dyskinesias, and the presence of chronic akathisia. Also, the findings suggested a possible relationship between pseudoakathisia, orofacial and limb dyskinesia, and the severity of negative schizophrenic symptoms.
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PMID:Akathisia variants and tardive dyskinesia. 286 31

A retrospective review of charts for the prevalence of tremor in patients with tardive dyskinesia revealed that 10% of 232 patients with a diagnosis of tardive dyskinesia also had parkinson-like tremor. No demographic or clinical risk factors for this tremor could be identified. The body areas affected by tremor are described, and it is suggested that tremor occurring in areas other than the wrist may pose a problem in differential diagnosis of patients with tardive dyskinesia. Changes in tremor and tardive dyskinesia after alterations in medication dose are reported, and recommendations for management are given.
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PMID:Tremor and tardive dyskinesia. 287 65

There are a number of different relationships among aging, psychosis and movement disorders, most of which have been proposed to involve the neurotransmitter dopamine. Dopamine content and dopamine receptors have been shown to decrease with age, which may relate to the time of onset of different motor and psychotic disorders, as well as to the appearance of these disorders. For example, some so-called senile movement disorders, such as senile tremor and senile chorea, may relate to alterations in dopaminergic transmission with age, as might the general findings of increased slowing of movements and mildly increased rigidity with age, although it is not clear how common some of these changes are in the medically healthy elderly. Decrease in dopamine with age may also be associated with the findings that choreiform and psychotic disorders (which have been proposed to be related to excess dopaminergic activity) tend to predominate at younger ages, whereas parkinsonism is more common at later ages. Certain findings support this notion, such as the appearance of both dyskinesia and psychosis in patients treated with L-dopa, the finding that psychosis may be less common in patients with later-onset Huntington's disease, and the fact that neuroleptic-induced parkinsonism is often more severe in the elderly. However, the situation is more complicated than this, because there are a number of phenomena that do not fit the pattern, including the observation of an increased incidence of tardive dyskinesia in the elderly. Age-related changes in other transmitters are undoubtedly important in both movements disorders and psychosis, and even dopamine has been proposed to have both trophic and toxic properties over the aging process. In general, care is warranted in the use of any psychotropic medications in the elderly, because there can be widespread and often unpredictable effects of these drugs on both motor and mental function.
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PMID:Association of psychosis and movement disorders in the elderly. 289 37

Initially, the reality of the existence of tardive dyskinesia raised some controversy, but rapidly this syndrome was recognized as a complication arising from usually long-term administration of neuroleptics. These extrapyramidal abnormal movements represent an important problem due to their prevalence, their potential irreversibility, their complex and still disputed physiopathologic mechanism, the absence of specific and generally effective treatment, and more recently the medico-legal problems entailed. At first, it was believed that these dyskinetic movements, of various intensity, were localized only at the oro-facial area (face, tongue, maxillary), or consisted of limited or generalized choreo-athetosic movements, or were a mixture of both types of movements. However, digestive and respiratory tardive dyskinesia also occur. Tardive dyskinesia can develop insidiously during neuroleptic treatment, or appear when this medication is decreased or ceased. It can coexist with parkinsonian signs. Age (over 50) and gender (female) appear to be risk factors. Other types of tardive syndromes associated with neuroleptic administration have been reported, such as tardive akathisia, tardive dystonia and a tardive Tourette-like syndrome. Involuntary movements resembling tardive dyskinesia can be observed in elderly individuals who never received neuroleptic medication. With respect to the rabbit syndrome, a rapid tremor of the perioral area, with a rhythmicity similar to the parkinsonian tremor, it is clearly different from tardive dyskinesia. It is essential to detect as precociously as possible tardive dyskinesia. The diagnosis is sometimes difficult and even if the clinical features seem pathognomonic of tardive dyskinesia, it is nevertheless important to establish a differential diagnosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical aspects of tardive dyskinesias induced by neuroleptics]. 290 48

Tardive dyskinesia (TD); abnormal involuntary movements appearing late in neuroleptic treatment) was described shortly after introduction of chlorpromazine and other antipsychotic agents in the 1950s. Consideration of this disorder as a common, progressive, and relentless problem of major public-health and medicolegal concern in the 1970s now appears to have been somewhat exaggerated. Several symptom patterns associated with neuroleptic treatment may or may not appropriately be lumped with the concept of TD (acute and withdrawal-emergent dyskinesias, dystonias, and akathisia, in particular); parkinsonism (with bradykinesia, rigidity, and tremor, including perioral tremor of the "rabbit syndrome") should be differentiated from TD, even though elements of both may occur together. Dyskinesias, more or less similar to TD, can occur in chronically ill neuropsychiatric patients not exposed to neuroleptics. Some may represent stereotyped behaviors of schizophrenia or undiagnosed neurological disorders, but a risk of spontaneous dyskinesias indistinguishable from TD averages about 5% (probably less in young patients). Mean prevalence rates for TD, corrected for spontaneous dyskinesias, average about 15-20% with higher risks at advancing ages. Incidence rates are less certain, but estimates average about 5% a year for at least several years in young patients, with higher rates within the first two years of treatment of elderly patients. Risk factors most clearly defined are advancing age, use of neuroleptic agents at relatively high daily doses for more than six months, and perhaps the diagnosis of a major affective disorder. Female gender and relatively high plasma levels of neuroleptic agents are less significant risk factors and other metabolic or neuroradiological indicators of risk remain unproved. The etiology of TD remains obscure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A summary of current knowledge of tardive dyskinesia. 290 54

1. This paper proposes that the neuropsychiatric symptoms of tardive dyskinesia, akathisia and pseudoparkinsonian tremor are modulated by a noradrenergic pathway that projects from the locus coeruleus to the limbic system. 2. The proposed pathway is found to the consistent with neuroanatomical and neurochemical data in the literature. 3. The proposed pathway is found to be clinically consistent with observations by ourselves and others on the efficacy of clonidine and beta-adrenoreceptor blockers like propranolol for treating akathisia and pseudoparkinsonian tremor. It is also consistent with reports by ourselves and others that some patients with tardive dyskinesia benefit from treatment with propranolol or clonidine. 4. Noradrenergic modulation of the limbic system by way of the locus coeruleus accounts for a number of clinical observations, such as the worsening of tardive dyskinesia by stress, the greater risk for tardive dyskinesia in patients with affective disorder, the time-of-onset of tardive dyskinesia, and the coexistence of tardive dyskinesia and pseudoparkinsonism. 5. The functional significance of beta-adrenoreceptors in the basal ganglia is considered from an evolutionary perspective. 6. The model proposed in this article appears to have considerable heuristic value because it may further our understanding of Gilles de la Tourette syndrome and attention deficit disorder (hyperkinesis).
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PMID:Noradrenergic effects in tardive dyskinesia, akathisia and pseudoparkinsonism via the limbic system and basal ganglia. 290 87

We describe the basic pharmacological principles underlying the activity of the alpha 2-adrenergic receptor agonist clonidine, including its interactions with the cholinergic, histaminergic, serotoninergic, endorphinergic and possibly dopaminergic systems. The use of clonidine for the therapy of various neuropsychiatric indications in which it appears to be beneficial is described. These conditions include migraine, Korsakoff's psychosis, Tourette's syndrome, withdrawal states, tardive dyskinesia, essential tremor, neuroleptic-induced akathisia, neurogenic bladder, idiopathic orthostatic hypotension, paroxysmal localised hyperhydrosis, diabetic neuropathy and stiff-man syndrome. The need for long term evaluation of this agent in some of these diseases is stressed.
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PMID:Clonidine in neuropsychiatric disorders: a review. 330 32

A case of severe life-threatening tardive dyskinesia resulting in esophageal and respiratory difficulties due to metoclopramide therapy is presented. A 66-year-old man with a primary diagnosis of clear cell carcinoma of the biliary duct was treated with metoclopramide for gastrointestinal symptoms related to his chemotherapy regimen. The patient initially presented with tremor and rigidity in the upper extremities. On antiparkinsonian therapy, symptoms progressed to hemiballism and involuntary movements of the face, mouth, and tongue, with respiratory and esophageal dyskinesia. Despite discontinuance of metoclopramide, severe tardive dyskinetic symptoms resulted in placement of a gastrostomy tube to maintain nutritional support. This case along with others in the literature should emphasize the need for continuous reevaluation of metoclopramide during long-term therapy, since serious side effects have been reported to occur.
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PMID:Life-threatening tardive dyskinesia caused by metoclopramide. 350 64

The ability of the selective GABA-receptor agonist, progabide, to suppress abnormal involuntary movements was evaluated in a preliminary open pilot study. 17 patients, 10 males and 7 females, aged 10-78 years, with hyperkinetic movement disorders were included in the study. Daily doses of progabide ranged from 900 to 3600 mg (median 2400 mg) corresponding to 14-45 mg/kg (median 45 mg/kg), while the duration of treatment varied from 2 to 52 weeks. Improvement, with a reduction of involuntary movements exceeding 25%, occurred in two of four patients with Gilles de la Tourette's syndrome, and in two of three patients with postanoxic intention myoclonus, while no consistent beneficial effects were registered in ten patients with Huntington's chorea, postanoxic choreoathetosis, torsion dystonia, tardive dyskinesia, action tremor, essential myoclonus, or oro-branchio-respiratory myoclonus.
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PMID:Progabide in the treatment of hyperkinetic extrapyramidal movement disorders. 386 33

Of 49 unselected patients with tardive dyskinesia (TD) 28 (57%) exhibited various parkinsonian signs. Isolated tremor was encountered in 11 patients, tremor with hypokinesia and rigidity in 13 patients, and hypokinesia and rigidity alone in 4. Tremor was detected among patients with scorable peripheral signs of TD. Hypokineto-rigidity, with or without tremor, was attributed to high doses of neuroleptics--notably fluphenazine. This study confirmed reports that isolated parkinsonian signs occurring concurrently with TD must be considered a regular phenomenon even when questionable cases (e.g. tremor in lithium-treated patients, action-tremor in the elderly) are disregarded. However, given the 'fragmentation' of the parkinsonian syndrome, often atypical tremor and signs of anosognosia in TD patients, the final diagnosis may necessitate pharmacological testing (discontinuation of neuroleptic medication, administration of anticholinergics).
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PMID:Parkinsonian symptoms in tardive dyskinesia. A prevalence study. 396 32


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