Dyskinesias Associated with Tricyclic Antidepressants

1976 ◽  
Vol 128 (5) ◽  
pp. 490-493 ◽  
Author(s):  
William E. Fann ◽  
John L. Sullivan ◽  
Bruce W. Richman

SummaryHyperkinetic movement disorders may occur as side effects of antipsychotic drugs; and a hyperdopaminergic state induced by the neuroleptic compounds is thought to be a cause of extrapyramidal disorders such as tardive dyskinesia. We have observed two cases of the dyskinetic syndrome in patients receiving tricyclic antidepressants (TCA). Because the TCA are known to have little effect on striatal dopamine but do share with the neuroleptics potent anticholinergic activity, these cases appear to support the hypothesis that the drug-induced hyperkinetic disorders are related to a diminution of CNS acetylcholine activity as well as to an increase in dopamine activity.

Author(s):  
Susan H. Fox

Tardive syndromes are drug-induced hyperkinetic movement disorders that occur as a consequence of dopamine D2 receptor antagonism/blockade. There are several types, including classical tardive dyskinesia, tardive dystonia, tardive tics, tardive myoclonus, and tardive tremor, and it is important to the management of these disorders that the type of movement disorder induced is identified. Tardive syndromes can occur with all antipsychotic drugs, including so-called atypical drugs. Patients taking these drugs should be evaluated frequently for side effects. Evaluating the nature of the movement (i.e., chorea or dystonia) is important because treatment options can differ according to the type of dyskinesia present.


PEDIATRICS ◽  
1986 ◽  
Vol 77 (4) ◽  
pp. 553-556
Author(s):  
HARVEY S. SINGER

Antipsychotic drugs, such as the phenothiazines (chlorpromazine, fluphenazine, thioridazine), butyrophenones (haloperiodol), and diphenylbutylpiperidines (pimozide) are used in children and adolescents to treat a variety of clinical entities including psychoses, tics, behavior disorders, and movement problems. Because virtually all of these drugs have a potential to affect body movements and posture, they have also been termed neuroleptics.1 Most physicians are aware of the more common acute extrapyramidal side effects of these drugs, such as oculogyria, pseudoparkinsonism, dystonia, and restlessness (akathisia). Despite the widespread use of neuroleptics, however, little is known about the long-term neurologic consequences of such treatment. Of particular concern, based originally on data in adults, is the risk of severe and persistent tardive dyskinesia developing in persons receiving neuroleptic therapy.


2012 ◽  
Vol 1 (7) ◽  
pp. 159-163 ◽  
Author(s):  
John E. Kalachnik

While the rate of tardive dyskinesia (TD) and other extrapyramidal side effects (EPSE) is lower with second generation antipsychotic medications compared to first generation antipsychotic medications, these side effects remain of clinical concern. This paper reviews the basis for the continued concern and the importance of secondary prevention, or early detection, within the primary-secondary-tertiary prevention model. The importance of standardized assessment instruments, education, and training is reviewed. Given the widespread use of antipsychotic drugs, the fact that antipsychotic drugs are the standard of care for several psychiatric conditions (with little indication that the magic bullet is on the immediate horizon to replace current antipsychotic drugs) applied monitoring and the early detection of TD and EPSE takes on added importance.


2009 ◽  
Vol 24 (S1) ◽  
pp. 1-1
Author(s):  
B. Luft ◽  
E. Berent

Introduction:Long-acting depot antipsychotic medication is associated with extrapyramidal side effects (EPS). This may reduce adherence to medication, and precipitate relapse (1). Clearly, EPS is a major drawback and early detection is essential. However, in an earlier review of patients’ medical notes, we identified only one patient with an examination that recorded the presence of EPS. Despite the fact that a number of rating scales are available. We proposed that the application of these rating scales, would allow us to improve the assessment of EPS.Method:All patients prescribed a depot antipsychotic or long-acting risperidone injection, were identified. the Barnes Akathisia Scale (2) was chosen to rate akathisia, a modified Simpson-Angus scale (3) was chosen to rate parkinsonism and the Abnormal Involuntary Movement Scale (4) was chosen to rate tardive dyskinesia.Results:A total of 43 patients were evaluated. 23 (53%) patients showed drug induced EPS. the total number of positive cases of akathisia was 12 (28%), and 10 (23%) patients were found to have tardive dyskinesia. 13 (30%) patients were found to have drug induced parkinsonism.Conclusions:Our screening programme has identified high rates of previously undiscovered drug induced EPS.


2021 ◽  
Vol 13 (6) ◽  
pp. 91-97
Author(s):  
T. M. Ostroumova ◽  
O. D. Ostroumova ◽  
A. S. Soloveva

Drug-induced parkinsonism (DIP) is the most common drug-induced movement disorder and is most commonly associated with antipsychotic drugs, monoamine reuptake inhibitors, and calcium channel blockers. DIP manifests as a typical movement disorder, which makes it practically indistinguishable from idiopathic Parkinson's disease (PD) and requires differential diagnosis. DIP symptoms develop fairly quickly (hours to weeks) after the antipsychotic is started or after the dose is increased. Therefore, DIP is predominantly a clinical diagnosis that must be kept in mind when a patient develops typical symptoms during treatment onset or increasing the dose of drugs that most often lead to such an adverse reaction (ADR). DIP evaluation includes using the Naranjo algorithm, which helps assess a causal relationship between drug intake and the development of parkinsonism symptoms. The primary DIP treatment is the reduction of the dose of the inducer drug, or its cancellation, or replacement with another drug. In patients with schizophrenia and antipsychotic-induced DIP, dose reduction, replacement with another medication, or prescription of a drug with anticholinergic activity may be possible. The awareness of the doctor and the patient about the possibility of developing this ADR is crucial in the prevention of DIP. Therefore, choosing a drug with the lowest risk of developing DIP is necessary for pharmacotherapy.


2020 ◽  
pp. 137-154
Author(s):  
Hiroshi Shibasaki ◽  
Mark Hallett ◽  
Kailash P. Bhatia ◽  
Stephen G. Reich ◽  
Bettina Balint

Dyskinesia is characterized by complex, irregular involuntary movements involving lips, tongue, extremities, and/or trunk. The term “dyskinesia” is often used to encompass complex involuntary movements that do not fit into another category of involuntary movements. Focal dyskinesia is commonly seen in the lips and tongue (orolingual dyskinesia or oral dyskinesia). Drug side effects are the most common cause of generalized dyskinesia, usually those that influence dopamine such as L-dopa and neuroleptics (drug-induced dyskinesia, tardive dyskinesia). Motor stereotypies are repetitive occurrences of the same movements; movements commonly encountered in this condition range from simple movements like shaking arms and nodding to complex movements. Motor stereotypies are commonly observed in children with Asperger syndrome, Rett syndrome and other automatisms, and mental retardation. In adults, stereotyped movements are seen in cases of severe infectious encephalitis, autoimmune encephalitis (e.g., limbic encephalitis), cerebrovascular diseases involving the frontal lobe, and neurodegenerative diseases like frontotemporal lobar degeneration. Tics are irregular, typically brisk movements ranging from shock-like simple movements resembling myoclonus (simple tic) to complex movements (complex tic). Patients with tics tend to repeat certain movements like blinking or grimacing, but in the patients with Gilles de la Tourette syndrome, tics appear as a variety of movements including vocalization (vocal tic). These patients can stop the movements for several seconds, but it is often followed by rebound; they often feel an urge to move before a bout of tics and feel release after the bout.


Author(s):  
Pierre J. Blanchet

Very early in the process of diagnosing abnormal involuntary movement (AIM) disorders, one can be rewarded by keeping a high index of suspicion for possible drug-induced causes, not only through a complete list of current medications, but also identification of the drugs the patient used to take and other possible offending medications that might be available from family members and other sources. Among drug-induced movement disorders, antipsychotic drugs and other dopamine receptor blocking agents occupy a central place. Their various acute and tardive motor complications provide the template of this short review. Movement disorders caused by antidepressants, lithium, antiemetics, antiparkinsonian agents, anticonvulsants, calcium channel blockers, sympathomimetics and others are only briefly covered in table form.


CNS Spectrums ◽  
2020 ◽  
pp. 1-10
Author(s):  
Robert A. Hauser ◽  
Jonathan M. Meyer ◽  
Stewart A. Factor ◽  
Cynthia L. Comella ◽  
Caroline M. Tanner ◽  
...  

Abstract Accurate diagnosis and appropriate treatment of tardive dyskinesia (TD) are imperative, as its symptoms can be highly disruptive to both patients and their caregivers. Misdiagnosis can lead to incorrect interventions with suboptimal or even deleterious results. To aid in the identification and differentiation of TD in the psychiatric practice setting, we review its clinical features and movement phenomenology, as well as those of other antipsychotic-induced movement disorders, with accompanying links to illustrative videos. Exposure to dopamine receptor blocking agents (DRBAs) such as antipsychotics or antiemetics is associated with a spectrum of movement disorders including TD. The differential diagnosis of TD is based on history of DRBA exposure, recent discontinuation or dose reduction of a DRBA, and movement phenomenology. Common diagnostic challenges are the abnormal behaviors and dyskinesias associated with advanced age or chronic mental illness, and other movement disorders associated with DRBA therapy, such as akathisia, parkinsonian tremor, and tremor related to use of mood stabilizing agents (eg, lithium, divalproex). Duration of exposure may help rule out acute drug-induced syndromes such as acute dystonia or acute/subacute akathisia. Another important consideration is the potential for TD to present together with other drug-induced movement disorders (eg, parkinsonism, parkinsonian tremor, and postural tremor from mood stabilizers) in the same patient, which can complicate both diagnosis and management. After documentation of the phenomenology, severity, and distribution of TD movements, treatment options should be reviewed with the patient and caregivers.


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