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Relationship between tardive dyskinesia and neuroleptic-induced parkinsonism
ExtrapyramidalSyndromes
BIOL PSYCHIATRY 1989:25:69A-l4A
71A
specific membrane effects of neuroleptics, or a phenomenon associated with the disease process that is independent of neuroleptic effects. Additional data will be presented and the possible significance of the findings discussed.
145 LIPID PEROXIDATION IN CSF: RELATIONSHIP TO CATECHOLAMINES AND TARDIVE DYSKINESIA James B. Lohr, Sandra Underhill, Melinda Moir, Dilip V. Jeste San Diego, CA We have been studying the possibility that tardive dyskinesia (TD) is related to free radical formation. Neuroleptics, by increasing catecholamine turnover and metabolism, may cause increased production of free radicals, highly reactive chemical species with an unpaired electron. We measured concentrations of catecholamine metabolites and indicators of lipid peroxidation in the cerebrospinal fluid (CSF) of psychiatric patients with and without TD. Subjects were patients with schizophrenia and mood disorders, on and off neuroleptics and with and without TD. CSF was collected and analyzed for metabolites of dopamine (DOPAC and HVA), and norepinephrine (MHPG), as well as thiobarbituric acid (TBA)-reactive products and diene conjugates, both of which have been considered indicators of lipid peroxidation, and hence, indirect measures of free radical activity. Preliminary analysis of the data reveals an association of increased DOPAC and HVA with increased TBA-reactive products in the CSF. We also found an association of diene conjugates with AIMS score. Our results are consistent with the idea that increased dopamine metabolism may be associated with increased lipid peroxidation in the CSF, and increased lipid peroxidation may be associated with TD.
146 RELATIONSHIP BETWEEN TARDIVE DYSKINESIA NEUROLEPTIC-INDUCED PARKINSONISM Michael P. Caligiuri, Dilip V. Jeste, James B. Lohr
AND
San Diego, CA Neuroleptic-induced Parkinsonism (NIP) is considered by many as an early risk factor for the development of tardive dyskinesia (TD). Yet, traditional ratings of parkinsonism are insensitive to subclinical bradykinesia, rigidity and postural tremor. The purpose of the present study was to compare the sensitivity of a clinical rating scale with that of quantitative instrumental techniques in identifying NIP in TD and non-TD patients. Forty schizophrenic patients (subgrouped into TD and non-TD cohorts based on AIMS ratings) were administered the Simpson-Angus Scale (SAS) for parkinsonism and evaluated instrumentally for the presence of muscle rigidity, postural tremor (6-8 Hz) and bradykinesia in the upper extremities. All patients had been on stable doses of neuroleptics for at least one month prior to study. Among the TD patients, both the SAS and instrumental measures were equally sensitive in identifying 71% of the patients with at least mild NIP. However, among non-TD patients, the SAS identified 42% with at least mild NIP, while instrumental measures identified as many as 74%. These findings support the use of instrumental measures in identifying subclinical NIP among patients who have not developed TD. Validity of an instrumental approach in identifying NIP as a risk factor associated with TD awaits longitudinal studies.
BIOL PSYCHIATRY 1989:25:69A-l4A
71A
specific membrane effects of neuroleptics, or a phenomenon associated with the disease process that is independent of neuroleptic effects. Additional data will be presented and the possible significance of the findings discussed.
145 LIPID PEROXIDATION IN CSF: RELATIONSHIP TO CATECHOLAMINES AND TARDIVE DYSKINESIA James B. Lohr, Sandra Underhill, Melinda Moir, Dilip V. Jeste San Diego, CA We have been studying the possibility that tardive dyskinesia (TD) is related to free radical formation. Neuroleptics, by increasing catecholamine turnover and metabolism, may cause increased production of free radicals, highly reactive chemical species with an unpaired electron. We measured concentrations of catecholamine metabolites and indicators of lipid peroxidation in the cerebrospinal fluid (CSF) of psychiatric patients with and without TD. Subjects were patients with schizophrenia and mood disorders, on and off neuroleptics and with and without TD. CSF was collected and analyzed for metabolites of dopamine (DOPAC and HVA), and norepinephrine (MHPG), as well as thiobarbituric acid (TBA)-reactive products and diene conjugates, both of which have been considered indicators of lipid peroxidation, and hence, indirect measures of free radical activity. Preliminary analysis of the data reveals an association of increased DOPAC and HVA with increased TBA-reactive products in the CSF. We also found an association of diene conjugates with AIMS score. Our results are consistent with the idea that increased dopamine metabolism may be associated with increased lipid peroxidation in the CSF, and increased lipid peroxidation may be associated with TD.
146 RELATIONSHIP BETWEEN TARDIVE DYSKINESIA NEUROLEPTIC-INDUCED PARKINSONISM Michael P. Caligiuri, Dilip V. Jeste, James B. Lohr
AND
San Diego, CA Neuroleptic-induced Parkinsonism (NIP) is considered by many as an early risk factor for the development of tardive dyskinesia (TD). Yet, traditional ratings of parkinsonism are insensitive to subclinical bradykinesia, rigidity and postural tremor. The purpose of the present study was to compare the sensitivity of a clinical rating scale with that of quantitative instrumental techniques in identifying NIP in TD and non-TD patients. Forty schizophrenic patients (subgrouped into TD and non-TD cohorts based on AIMS ratings) were administered the Simpson-Angus Scale (SAS) for parkinsonism and evaluated instrumentally for the presence of muscle rigidity, postural tremor (6-8 Hz) and bradykinesia in the upper extremities. All patients had been on stable doses of neuroleptics for at least one month prior to study. Among the TD patients, both the SAS and instrumental measures were equally sensitive in identifying 71% of the patients with at least mild NIP. However, among non-TD patients, the SAS identified 42% with at least mild NIP, while instrumental measures identified as many as 74%. These findings support the use of instrumental measures in identifying subclinical NIP among patients who have not developed TD. Validity of an instrumental approach in identifying NIP as a risk factor associated with TD awaits longitudinal studies.