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Tardive dyskinesia and deficit schizophrenia
Author(s) -
Telfer S.,
Shivashankar S.,
Krishnadas R.,
McCreadie R. G.,
Kirkpatrick B.
Publication year - 2011
Publication title -
acta psychiatrica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.849
H-Index - 146
eISSN - 1600-0447
pISSN - 0001-690X
DOI - 10.1111/j.1600-0447.2011.01751.x
Subject(s) - tardive dyskinesia , schizophrenia (object oriented programming) , antipsychotic , akathisia , dyskinesia , psychiatry , extrapyramidal symptoms , cognitive deficit , psychology , odds ratio , medicine , cognition , parkinson's disease , disease , cognitive impairment
Telfer S, Shivashankar S, Krishnadas R, McCreadie RG, Kirkpatrick B. Tardive dyskinesia and deficit schizophrenia. Objective:  Despite comparable antipsychotic exposure, some patients experience involuntary movements yet others do not. Negative symptoms have been associated with tardive dyskinesia (TD), but it is not certain whether this is an association with primary negative symptoms or the effects of medications. The aim of the present study was to determine whether patients with deficit schizophrenia (who have primary negative symptoms) are more likely to experience TD than those with non‐deficit schizophrenia. Method:  In 2006, all the people with a clinical diagnosis of schizophrenia in Nithsdale, Southwest Scotland, were identified using the ‘key informant’ method. These patients were categorized into those with and without the deficit syndrome and assessed for the presence of TD. Patients were also assessed for akathisia and extrapyramidal side effects. Results:  Of the 131 people assessed, 31 were categorized as having deficit schizophrenia (23.7%) and 100 people (76.3%) as non‐deficit. There was no difference between the two groups with regard to age, antipsychotic exposure, and duration of illness. There was a significant association between deficit features and TD with an odds ratio = 2.97 [95% CI 1.128–6.88, P  = 0.009]. Conclusion:  Our findings support the proposal that the pathological process underlying deficit schizophrenia can predispose to the development of TD.

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