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Tardive dyskinesia longitudinal follow-up study
130A
BIOL PSYCHIATRY 1990;27:41A-179A
Neuroleptic-lnduced Syndromes
treatment; t :rance to the antipsychotic effect of neuroleptics; new or worsened psychotic symptoms after abrupt decr ase in dose. Patients received antiepileptic drugs on an open-label basis. Over half of our patients improved significantly. Of these, 2 were rated as extremely improved, 4 very much improved, 12 much improved, 7 minimallyimproved, 6 showed no change, and I became minimallyworse. The response of patients with SSP to antiepileptic drugs supports the notion that SSP may be caused by a neurolepticinduced kindling phenomenon in the limbic system.
199 INDEPENDENCE BETWEEN NEUROLEPTIC-1NDUCED
PARKINSONISM AND TARDIVE DYSKINESIA Stephen R. Paige, W. Steven Metzer, J.E.O. Newton, D.E. McMillan University of Arkansas for Medical Services and Veterans Affairs Medical Center, North Little Rock, AR 72114. Previous investigations have suggested that the presence of neuroleptic-induced Parkinsonism (NIP) is commonly associated with the development of tardive dyskinesia (TD) and may be a risk factor for the development of TD. We examined 69 American schizophrenic patients chronically treated with neuroleptics for the presence of NIP and TD. Of the 69 subjects, 56 were found to have a movement disorder: 12 with both NIP and TD and 44 with NIP or TD alone. This finding of a greater than expected number of chronically treated schizophrenics with only one of these movement disorders is statistically significant and cannot be attributed to such factors as psychiatric diagnosis, gender, age, duration of neuroleptic exposure, neuroleptic dose, or anticholinergic exposure. The clinical differential susceptibility to develop different drug-induced movement disorders is discussed in terms of a theory of interin~ividual variation in striatal inhomogeneity.
200 TARDIVE DYSKINESIA LONGITUDINAL FOLLOW-UP STUDY
Shawn L. Cassady, Gunvant K. Thaker, Marianne J. Moran, James A. Nguyen, Carol A. Tamminga Maryland Psychiatric Research Center, University of Maryland, Baltimore, MD 21228. We will report clinical outcome data that has been collected over five years from the MPRC/Motor Disorder Clinic. The clinic was established as a state-wide, tertiary outpatient facility for the diagnosis and treatment of tardive dyskinesia. In addition, the clinic provides consultation and education to psychiatrists in state institutions, community mental health clinics, and private practice. We have seen 677 patients and have followed up 423 on a longitudinal basis. The MPRC Involuntary Movement Scale quantifying specific type and distribution of hyperkinetic involuntary movements was used to rate patients over time. Demographics of our patient population will be presented, including age, diagnosis, gender, race, and neuroi.ptic duration. Neuroleptic dose and change over time and TD score and change over time will be reported. The distribution of abnormal movements and the course of TD are analyzed with respect to these variables. A preliminary multiple regression analysis of 134 patients showed that the significant predictors of TD improvement are initial dyskinesia score (partial r = 0.65, p < 0.0001) and amount of neuroleptic dose decrease (partial r = 0.19, p < 0.02). The length of follow-up was negatively correlated with the amount of decrease in dyskinesia.
BIOL PSYCHIATRY 1990;27:41A-179A
Neuroleptic-lnduced Syndromes
treatment; t :rance to the antipsychotic effect of neuroleptics; new or worsened psychotic symptoms after abrupt decr ase in dose. Patients received antiepileptic drugs on an open-label basis. Over half of our patients improved significantly. Of these, 2 were rated as extremely improved, 4 very much improved, 12 much improved, 7 minimallyimproved, 6 showed no change, and I became minimallyworse. The response of patients with SSP to antiepileptic drugs supports the notion that SSP may be caused by a neurolepticinduced kindling phenomenon in the limbic system.
199 INDEPENDENCE BETWEEN NEUROLEPTIC-1NDUCED
PARKINSONISM AND TARDIVE DYSKINESIA Stephen R. Paige, W. Steven Metzer, J.E.O. Newton, D.E. McMillan University of Arkansas for Medical Services and Veterans Affairs Medical Center, North Little Rock, AR 72114. Previous investigations have suggested that the presence of neuroleptic-induced Parkinsonism (NIP) is commonly associated with the development of tardive dyskinesia (TD) and may be a risk factor for the development of TD. We examined 69 American schizophrenic patients chronically treated with neuroleptics for the presence of NIP and TD. Of the 69 subjects, 56 were found to have a movement disorder: 12 with both NIP and TD and 44 with NIP or TD alone. This finding of a greater than expected number of chronically treated schizophrenics with only one of these movement disorders is statistically significant and cannot be attributed to such factors as psychiatric diagnosis, gender, age, duration of neuroleptic exposure, neuroleptic dose, or anticholinergic exposure. The clinical differential susceptibility to develop different drug-induced movement disorders is discussed in terms of a theory of interin~ividual variation in striatal inhomogeneity.
200 TARDIVE DYSKINESIA LONGITUDINAL FOLLOW-UP STUDY
Shawn L. Cassady, Gunvant K. Thaker, Marianne J. Moran, James A. Nguyen, Carol A. Tamminga Maryland Psychiatric Research Center, University of Maryland, Baltimore, MD 21228. We will report clinical outcome data that has been collected over five years from the MPRC/Motor Disorder Clinic. The clinic was established as a state-wide, tertiary outpatient facility for the diagnosis and treatment of tardive dyskinesia. In addition, the clinic provides consultation and education to psychiatrists in state institutions, community mental health clinics, and private practice. We have seen 677 patients and have followed up 423 on a longitudinal basis. The MPRC Involuntary Movement Scale quantifying specific type and distribution of hyperkinetic involuntary movements was used to rate patients over time. Demographics of our patient population will be presented, including age, diagnosis, gender, race, and neuroi.ptic duration. Neuroleptic dose and change over time and TD score and change over time will be reported. The distribution of abnormal movements and the course of TD are analyzed with respect to these variables. A preliminary multiple regression analysis of 134 patients showed that the significant predictors of TD improvement are initial dyskinesia score (partial r = 0.65, p < 0.0001) and amount of neuroleptic dose decrease (partial r = 0.19, p < 0.02). The length of follow-up was negatively correlated with the amount of decrease in dyskinesia.