Commentary on the Modified Rogers Scale and the ‘Conflict of Paradigms' Hypothesis

1991 ◽  
Vol 158 (3) ◽  
pp. 337-339 ◽  
Author(s):  
Peter F. Liddle

The variety and complexity of schizophrenic movement disorders renders them difficult to assess. In particular, the complex disorders of motility that appear to reflect disturbance of the will demand an evaluation of the purpose of the movement. The difficulties of assessment are compounded by the fact that the antipsychotic drugs used to treat the illness can produce motor disorders that resemble the disorders intrinsic to the illness. In advancing his ‘conflict of paradigms' hypothesis, Rogers (1985) implied that emphasis on the distinction between intrinsic and drug-induced movement disorders might be misplaced because of overlap not only in the observable characteristics of these disorders, but also in the underlying neuropathology.

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.


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):  
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.


Author(s):  
Amy Lustig ◽  
Cesar Ruiz

The purpose of this article is to present a general overview of the features of drug-induced movement disorders (DIMDs) comprised by Parkinsonism and extrapyramidal symptoms. Speech-language pathologists (SLPs) who work with patients presenting with these issues must have a broad understanding of the underlying disease process. This article will provide a brief introduction to the neuropathophysiology of DIMDs, a discussion of the associated symptomatology, the pharmacology implicated in causing DIMDs, and the medical management approaches currently in use.


2009 ◽  
Vol 15 ◽  
pp. S11
Author(s):  
D. Tarsy ◽  
S. Bohlega

Author(s):  
Anton J. M. Loonen ◽  
Cees H. Doorschot ◽  
Dianne A. van Hemert ◽  
Marc C. J. M. Oostelbos ◽  
Arnold E. S. Sijben ◽  
...  

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