S-69 Tardive Dyskinesia in Schizophrenia: Illness-Related Factor the DSM-IV mood disorders field trial (Hirschfeld & Holzer, 1994) 58% of current dysthymics and 45% of major depressives were found to elicit depressive personality disorders. Koenigsberg et al, (1985) reported a 34% rate of AXIS-II diagnoses in a patient sample. Sanderson et al, (1992) reported an equal rate of personality disorders in a comparison of major depressive with dysthymic patients (50% vs. 52%). In a sample of students of psychology, 78% of dysthymics were found to suffer from a depressive personality and 45% from a mood disorder (Klein & Miller, 1993). In the longitudinal Zurich cohort study of a community sample, 36 dysthymics were identified, 28 of which were assessed over five interviews from ages 22-35. Dysthymics have striking personality features, the seeds of which are recognizable as early as childhoodJadolesence; the majority describe themselves as anxious and report low quality oflife during childhoodJadolesence. Moreover, they elicit behavioural symptoms and sociopathy in adolesence, and often develop cyclothymic personality disorders later. In contrast to major depressives and controls, dysthymics are characterized by the following personality features: high neuroticism and introversion, high SCL-90 scores, as well as high scores on the dysthymia and hypomania scales of the GEl (Depue et aI., 1981), low coping capacities, i.e. low self-esteem and mastery, and finally elevated avoidance, denial and rumination scores.
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S-69 Tardive Dyskinesia in Schizophrenia: Illness-Related Factor 1
I8-69-1 IThe Concept of Tardive Dyskinesia: A Review of Its Validity and Limitations D.G.C. Owens. University of Edinburgh, Scotland Tardive dyskinesia (TD) is an epidemiological concept founded on a statistical association. Since it was first described the boundaries of the concept have varied in terms of constituent features, 'causative' agents and necessary duration of exposure. Nonetheless there is considerable information on prevalence (pooled data method and point prevalence) as well as on incidence and long-term risk, but a lack of clarity still exists with regard to demographic correlates and predisposition. Studies on the non-psychiatric elderly confirm a baseline prevalence of involuntary movements, phenomenologically similar to those comprising TD. The prevalence depends on the setting but higher frequencies in the physically ill suggests that neuromedical disturbance may underlie such disorders. In considering predisposition to TD it may also be worth including biological aspects relating to the illness for which drugs are prescribed. A small but still active literature has reported movement disorders in antipsychotic naive schizophrenics. Where quantitative and qualitative comparison has been possible, striking similarities to the disorders of drug-treated patients have been found. This raises the question as to whether antipsychotic drugs may sometimes act as agents provoking a tendency inherent to certain forms of schizophrenia. TD has validity, but understanding the association needs awareness of the limitations of a purely epidemiological concept.
I8-69-21 Spontaneous Dyskinesia and Psychopathology in the Pre-Neuroleptic Era
W.S. Fenton, R.I. Wyatt, CR. Blyler, T.H. McGlashan. Chestnut Lodge Research Institute, Rockville, MD, USA The authors describe the prevalence, clinical correlates, and prognostic significance of spontaneous dyskinesias among patients with schizophrenia treated at Chestnut Lodge Hospital who had never received neuroleptic treatment up to and including baseline assessment. Extensive case records were screened and descriptions of abnormal movements recorded verbatim for blind ratings. Neuroleptic naive patients with and without abnormal oral-facial movements were compared across diagnostic categories, signs and symptoms, diagnostic and illness natural history variables. The records of 15% of patients with schizophrenia documented oral-facial dyskinesias with significant detail so that their presence was
223 considered nearly certain. Compared to patients with schizophrenia without oral-facial movements, those with spontaneous dyskinesias were more likely to demonstrate a lower IQ score, had more negative symptoms at index admission, and were more symptomatic at follow-up (an average of 23 years later). The prevalence of spontaneous dyskinesia was 9.5% for patients with schizotypal personality, 3% among patients with schizoaffective disorder and 0% for schizophreniform disorder. The data suggest that in many cases oral-facial dyskinesias in patients with intellectual impairment and negative symptoms may represent spontaneous movement disorders and that these are relatively specific to schizophrenia.
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8-69-31 Choreoathetoid Movements OccurSpontaneously in Never-Medicated Patients with Schizophrenia
W. Hoffman, N. Kadri, D. Fenn, A. Tilane, C Green, M. Lakloumi, F. Bousaid, B. Bentounssi, D. Moussaoui, D. Casey. Department of Psychiatry, Portland VA Medical Center, Portland, OR; Universitaire Centre Psychiatrique Ibn Rochd, Casablanca, Morocco Tardive dyskinesia (TD) purportedly results from chronic neuroleptic treatment. However, evidence is accumulating that choreoathetoid movements resembling TD occur in patients who have never been treated with neuroleptics [I]. We studied [04 Moroccan patients who met DSM-IV criteria for schizophrenia; 62 had been ill for at least one year and were neuroleptic-naive, while 42 had been chronically treated with neuroleptics for at least one year. Twenty-one control patients, free of psychiatric illness, were studied for comparison. Choreoathetosis was scored on the AIMS scale and cases of probable TD were identified according to the criteria of Schooler and Kane [21. Somewhat more neuroleptic-naive patients (26%) than controls ( 19%) met criteria for TD (McNemar Xl = 6.48, p = 0.01); none of the controls met TD criteria. Mean total AIMS scores did not differ (F = 0.843, P = 0.4) between never-medicated (3.9 ± 2.9) and chronically medicated patients (3.3 ± 3.4). Both patient groups differed significantly from controls (mean AIMS = 0.67 ± 0.86). There were no significant differences between the patient groups on any of the AIMS items. These findings provide evidence that choreoathetoid movements are part of the clinical course of schizophrenia and neuroleptic treatment may only exacerbate a predisposition to hyperkinesia. [I] Fenn D, Moussaoui D, Hoffman W, Kadri N, Bentounssi B, THane A, Khomeis M, Casey D, Psvchopharmacologv In Press. 12] Schooler N, Kane J, Arch Gen Psychiatry 39 (1982) 486-487.
I8-69-41 Prospective Study of Cognitive Impairment in
Relation to the Emergence of Tardive Dyskinesia in Schizophrenia
1.1. Waddington, H.A. Youssef, E. 0' Callaghan, C Larkin. Royal College of Surgeons in Ireland, Dublin, Ireland Given the evidence that in schizophrenia the contribution of spontaneous, disease-related involuntary movements to tardive dyskinesia appears to have been underestimated, we have been seeking correlates of sueh movement disorder among features of the illness. In younger outpatients, we found those with orofacial dyskinesia to evidence an increased ratio of minor physical anomalies of the head to those of the periphery, indicating an association with a predominance of early craniofacial dysgenesis, and greater neuropsychological impairment on frontal lobe testing, In older inpatients followed prospectively over 10 years, those with persistent orofacial dyskinesia showed poorer function in more basic cognitive domains than did those consistently without such movement disorder, though in neither group did that function change over the decade; the only patients to show significant deterioration in these cognitive domains were those evidencing the de novo emergence of orofacial dyskinesia, and this deterioration was restricted to the time frame in which their dyskinesia developed. Orofacial dyskinesia emerging during long-term neuroleptic treatment in schizophrenia appears intimately related to features of the illness for which that treatment was prescribed. Supported by the Health Research Board.