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

Following acceptance of clozapine as a superior antipsychotic agent with low risk of adverse extrapyramidal syndromes (EPS), such as dystonia, parkinsonism, akathisia or tardive dyskinesia, several novel antipsychotic drugs have been developed with properties modelled on those of clozapine. Though generally considered 'atypical' in their relatively low risk of inducing EPS, these agents vary considerably in their pharmacology and impact on neurological functioning. Although few comparative data are available, the atypical antipsychotics can be tentatively ranked by EPS risk (excluding akathisia and neuroleptic malignant syndrome) in the following order: clozapine < quetiapine < olanzapine = ziprasidone. At higher doses, risperidone is ranked with a higher EPS risk than olanzapine and ziprasidone, but its risk of EPS is lower with lower doses. In general, this ranking is inversely related to antidopaminergic (D2 receptor) potency. The high antiserotonergic (5-HT2A receptor) potency of risperidone, clozapine, ziprasidone and olanzapine, but not quetiapine, as well as the antimuscarinic activity of olanzapine and clozapine may also limit EPS. For the treatment of psychotic reactions to dopamine agonist therapy in Parkinson's disease, clozapine is both effective and relatively well tolerated; quetiapine may be tolerated, olanzapine is not well tolerated, risperidone is poorly tolerated, and amisulpride and ziprasidone have not been well evaluated. Clozapine, perhaps because of its anticholinergic activity, can reduce parkinsonian tremor. It is useful for ongoing psychosis with tardive dyskinesia, especially for dystonic features. No atypical antipsychotic is clearly effective for motor abnormalities in Huntington's disease or Tourette's syndrome, and the effect of these drugs on other neurological disorders have been well evaluated in only small numbers of patients. In summary, with the exception of clozapine, and perhaps quetiapine, atypical antipsychotics have brought only relative avoidance of EPS, strongly encouraging continued searches for novel antipsychotic agents.
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PMID:Effects of newer antipsychotics on extrapyramidal function. 1177 17

Of 49 state hospital patients referred for movement disorder consultation for tardive dyskinesia (TD), 11 (23.9%) of 46 meeting inclusion criteria had movement disorders other than TD. These other disorders led to a false diagnosis of TD in 6 subjects (12.2%). Between-day dyskinesia variability affected TD ascertainment in only 3.2 percent of subjects. Prevalences of other neurological conditions in the 30 patients identified with definite TD were parkinsonism (90%), dystonia (25%), akathisia (16%), cerebellar signs (40%), dysmetria (23%), cerebellar tremor (17%), tardive dystonia (3.3%), and tardive akathisia (3.3%). Concurrence rates of parkinsonism with TD varied significantly according to which clinical signs were used to define parkinsonism. Using a rating score threshold of at least mild, rigidity occurred in 79.3 percent, bradykinesia in 55.2 percent, and resting tremor in 41.4 percent of subjects with TD; more significant rigidity occurred in 41.4 percent, bradykinesia in 31.0 percent, and resting tremor in 20.7 percent. Concurrence rates of neurological conditions with TD subsyndromes were distributed rather evenly according to condition prevalences, except for an association of cervicotruncal TD with bradykinesia (perhaps because of ventromedial striatal presynaptic and postsynaptic D2 blockade, respectively). These findings, as well as the occurrence of equal gender ratio and relative under-representation of bipolar and alcohol disorders in subjects with definite TD, are discussed.
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PMID:Tardive dyskinesia--diagnostic issues, subsyndromes, and concurrent movement disorders: a study of state hospital inpatients referred to a movement disorder consultation service. 1182 87

Predictors for the development of tardive dyskinesia (TD) have been studied extensively over the years, yet there are few studies of predictors of the course of TD after it has developed. Moreover, few studies have examined predictors of the course of other extrapyramidal side effects (EPS) in patients maintained on neuroleptics. The purpose of this study was to determine which modifiable variables are important in the prediction of EPS in patients with persistent TD over a period of as long as 2 years. One hundred fifty-eight patients enrolled in the Veterans Affairs Cooperative Study 394 were included in this study. A linear mixed-effects (LME) analysis to estimate the Abnormal Involuntary Movement Scale score (for TD severity), Simpson-Angus Scale (for parkinsonism severity), and Barnes Akathisia Scale at any given time after intake assessment was performed. The severity of each of the TD and EPS outcomes at any given visit was predicted by their respective baseline severity scores. Additional predictors of a favorable course of TD included lower doses of antipsychotic medications and use of anticholinergic medications. Other predictors of a favorable course of EPS included younger age and the use of atypical antipsychotic medication (for rigidity) and the use of anticholinergic medication (for tremor). These findings indicate that clinician-modifiable factors related to medication usage can influence the outcome of TD and EPS in patients with persistent TD.
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PMID:Treatment predictors of extrapyramidal side effects in patients with tardive dyskinesia: results from Veterans Affairs Cooperative Study 394. 1191 Feb 66

The effects of dizocilpine (MK-801), a noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist, were studied on dopamine-related behaviors induced by reserpine treatments. This study focuses on behavioral syndromes that may used as models for Parkinson's disease, or tardive dyskinesia, and its response after glutamatergic blockage. Reserpine (1 mg/kg), administered once every other day for 4 days, produced increases in orofacial dyskinesia, tongue protrusion and vacuous chewing in mice, which are signs indicative of tardive dyskinesia. Reserpine also produced tremor and catalepsy, which are signs suggestive of Parkinson's disease. MK-801 (0.1 mg/kg), administered 30 min before the observation test, prevented the vacuous chewing movements, tongue protrusions and catalepsy induced by reserpine. However, MK-801 injection produced a significant increase of tremor in reserpine-treated mice. Reserpine (1 mg/kg), administered 90 min before the test and followed by apomophine injection (0.1 mg/kg) 5 min before the test, did not produce oral dyskinesia in mice. On the other hand, reserpine induced increases in tremor and catalepsy compared to control mice. MK-801 (0.1 mg/kg) administration attenuated the catalepsy and tremor induced by reserpine. Pretreatment with reserpine (1 mg/kg) 24 h before the observation test produced increases in vacuous chewing movements and tongue protrusion, as well as increases in tremor and catalepsy, whereas MK-801 (0.1 mg/kg) injection 90 min before the test reversed the effects of reserpine. These results show that reserpine produces different and abnormal movements, which are related to dose and schedule employed and can be considered as parkinsonian-like and tardive dsykinesia signs. The glutamatergic blockage produced by NMDA can restore these signs, such as vacuous chewing movements, tongue protrusions, catalepsy and tremor according to the employed model.
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PMID:Behavioral effects of MK-801 on reserpine-treated mice. 1199 99

Tardive tremor is a very uncommon neuroleptic-induced tardive syndrome which was initially described in five patients by Stacy and Jankovic (Stacy and Jankovic, Mov Disord 1992;7:53-57). Since then, there have been only three additional case reports attesting to the apparent rarity of this condition, although it is unknown whether other unreported cases have been observed. We describe a patient with persistent tardive tremor that was associated with tardive dyskinesia, who closely resembles previously reported cases.
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PMID:Tardive tremor due to metoclopramide. 1211 24

The movement disorder syndrome of tardive dyskinesia arises as a consequence of prolonged regimens of neuroleptic medication, and is characterized, although not exclusively, by jerky and sometimes rhythmical stereotypical motions in a wide range of muscle systems. It is well established that the degree and variability of tremor in tardive dyskinesia is greater than that in normal age-matched subjects. The findings from the current experiment show that the dimension of the tardive dyskinetic finger tremor time series is systematically lower than that evident in normal finger tremor. Furthermore, the variability of finger motion in both groups is inversely related to the dimension of the respective attractor dynamic. The neuroleptic medication appears to constrain the degrees of freedom regulated in organization of the motor system. (c) 1995 American Institute of Physics.
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PMID:The dynamical structure of tremor in tardive dyskinesia. 1278 Jan 53

Perospirone is a novel serotonin-2 and dopamine-2 receptor antagonist (SDA) developed in Japan. Premarketing trials suggested that this agent was effective in reducing positive and negative symptoms of schizophrenia and had a favorable side-effect profile. However, these trials included only a few elderly patients, so the usefulness of perospirone in this population remains unknown. In this report we describe the treatment of 2 elderly patients with schizophrenia for whom perospirone therapy was efficacious. Case 1 was a patient with acute exacerbation of schizophrenic symptoms after discontinuance of medication. He was treated with 12 mg of perospirone daily and his symptoms reduced markedly from the 4th day of perospirone therapy. Efficacy was assessed by the positive and negative symptom scale (PANSS); all subscales of PANSS (positive symptom, negative symptom, and general psychopathology) reduced and the total score reduced from 78 to 38 by the end of the 6th week of treatment. No side effects such as extrapyramidal symptoms were noted. Thus, perospirone may be a useful antipsychotic for elderly patients with acute schizophrenia. Case 2 was a patient who had severe negative symptoms and extrapyramidal symptoms such as tardive dyskinesia, tardive dystonia, and sialorrhea. She had been hospitalized for more than 7 years. In this patient 12 mg of perospirone was administered daily after 3 mg of risperidone had been tapered off. The negative symptom subscale and general psychopathology subscale in PANSS were gradually reduced after perospirone therapy was started. Extrapyramidal symptoms were assessed by the drug-induced extrapyramidal symptoms scale (DIEPSS), which consists of eight individual parameters and one global assessment, and each parameter is graded on a 5-point (0 = none to 4 = severe) scale. Sialorrhea, muscle rigidity, tremor, dystonia and overall sererity were improved more than 2 points by the end of the 6th week. The clinical course of this patient suggests that the clinical characteristics of perospirone and risperidone may be different, even though these agents are categorized into the same class of antipsychotics, SDA. Because this is a case report, evaluations are limited the clinical properties of perospirone. Further examination is necessary to evaluate the efficacy and safety of perospirone for elderly patients with schizophrenia, who are more vulnerable to the side effect of antipsychotics than the younger population.
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PMID:[Perospirone therapy in elderly patients with schizophrenia]. 1467 81

Orthostatic tremor (OT) is a rare condition characterized by unsteadiness when standing still that is relieved when sitting or walking and is thought to arise from a central generator in the cerebellum or brainstem. OT is considered to be a distinct, discrete condition, and little is known about its demographic characteristics, natural history, associated features, and treatment response. We have reviewed these aspects in 41 OT patients fulfilling current diagnostic criteria, seen at our institution between 1986 and 2001. We classified 31 (75%) as having idiopathic "primary OT" either with (n = 24) or without an associated postural arm tremor. We found that 10 of 41 (25%) cases had additional neurological features, and we defined this group as having "OT plus" syndrome. Of these 10, 6 had parkinsonism; 4 of these had typical Parkinson's disease (PD), 1 had vascular and 1 had drug-induced parkinsonism. Among the remaining 4 patients, 2 had restless legs syndrome (RLS), 1 had tardive dyskinesia, and 1 orofacial dyskinesias of uncertain etiology. One patient with PD and the patient with vascular parkinsonism also had RLS. Age at onset was significantly earlier in the "primary OT" (mean +/- SD, 50.4 +/- 15.1) than in the "OT plus" (61.8 +/- 6.4; z = 2.7; P =.006) group. In 7 of the 10 "OT plus" patients, OT leg symptoms preceded the onset of additional neurological features. OT appeared to be underdiagnosed, and on average, it took 5.7 years from the initial complaints until a diagnosis was made. In general, treatment response to a variety of drugs such as clonazepam, primidone, and levodopa was poor. In most cases, OT symptoms remain relatively unchanged over the years, but in 6 of 41 cases (15%), the condition gradually worsened over the years, and in some of these cases, symptoms spread proximally to involve the trunk and arms. OT may not be a discrete disorder as commonly believed and associated features like parkinsonism present in nearly 25% of cases. Dopaminergic dysfunction may have a role in the pathophysiology of this disorder.
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PMID:Natural history and syndromic associations of orthostatic tremor: a review of 41 patients. 1525 36

Tardive dyskinesia is a movement disorder that develops after exposure to dopamine receptor blocking agents. Less well-appreciated are other, more recently described tardive syndromes that are phenomenologically distinct from tardive dyskinesia and respond to different treatments. Patients may simultaneously have more than one tardive syndrome. Major subtypes of tardive syndromes include tardive dyskinesia, characterized by orobuccolingual, truncal, or appendicular, choreiform movements; tardive dystonia, characterized by sustained, stereotyped muscle spasms of a twisting or turning character; and tardive akathisia, characterized by an inner sense of restlessness or unease. The sensation often is unpleasant and may be accompanied by repetitive, purposeless movements (stereotypies), such as pacing. Less common tardive syndromes include tardive myoclonus, tardive tourettism, and tardive tremor. Tardive syndromes often are a source of great distress and disability to patients and may be permanent, despite discontinuing the responsible medication. Prevention, early detection, and prompt management are the major clinical focus. When a patient develops a tardive syndrome appropriate actions include 1) review of the primary diagnosis that prompted starting a dopamine receptor blocking agent; 2) characterization of the movement disorder(s); 3) where possible, discontinuation of dopamine blocking agent or replacement with a less potent alternative agent; 4) gradual withdrawl of the offending drug because some patients have an exacerbation of a tardive syndrome after abrupt withdrawal; and 5) assessment of the severity of symptoms and development of a treatment plan based on the phenomenology, with the goal of maximizing patient comfort and function. Although tardive dyskinesia typically develops after chronic exposure to dopamine receptor blocking agents, it, and other variants (such as tardive dystonia) can develop very rapidly after treatment. There seems to be no minimal safe duration of exposure for the development of a tardive syndrome. It is important to recognize that anti-emetics, which are dopamine receptor blockers, such as prochlorperazine, promethazine and metoclopramide, can cause tardive syndromes. Clinicians should become familiar with antipsychotic agents that have a lower risk of causing tardive syndromes, such as clozapine, quetiapine, and olanzapine. We review treatment options for tardive dystonia.
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PMID:Tardive Dystonia. 1581 76

Movement disorders (ataxia, dystonic disorders, gait disorders, Huntington disease, myoclonus, parkinsonism, spasticity, tardive dyskinesia, tics and tremor) are clinically, pathologically and genetically heterogeneous and are characterized by impairment of the planning, control or execution of movement. Current classifications of these disorders have inherent shortcomings due to the complex nature of movement disorders and the lack of diagnostic tests for the majority. Undiscriminating terminology, as well as the clinical, pathological and genetic heterogeneity, further complicate the development of comprehensive categorizations. Modern classification schemes tend to focus on clinical, pathological or genetic/molecular criteria, but more recent attempts have been made to integrate across these levels. From a historical perspective, two 'golden ages' have shaped the current and evolving classification schemes: (1) the definition of clinical pathological entities in the early twentieth century and (2) the application of molecular neurogenetics in the past 10-15 years. However, the classification of movement disorders on clinical grounds (according to age at onset, distribution of symptoms, disease course, provoking factors and therapeutic response) remains one of the most useful modes of categorization. Postmortem criteria have been employed to distinguish between degenerative and nondegenerative disorders, and specific hallmarks may be required to establish or confirm a diagnosis. Genetic features used for classification purposes include mode of inheritance and molecular genetic data, such as linkage to a known gene locus or identification of a specific genetic defect. A final classification scheme is based on alterations in molecular mechanisms (e.g. trinucleotide expansions) or protein function (e.g. channelopathies). Despite recent advances, it may not be possible to develop the 'ultimate' classification of movement disorders, and different patterns of lumping and splitting may be useful for the clinician, the pathologist or the geneticist/molecular biologist. Furthermore, certain individual cases with unique features may not fit into any particular category. Continued research by both clinicians and basic scientists is necessary in order to refine and redefine classification schemes of movement disorders.
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PMID:Movement disorders: classifications. 1586 75


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