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Risperidone vs. haloperidol on reaction time and fine motor speed
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h67 RISPERIDONE VS. HALOPERIDOL ON REACTION TIME AND FINE MOTOR SPEED Robert S. Kern, Michael F. Green, Barringer D. Marshall, Jr., William C. Wirshing, Donna Ames, Stephen R. Marder, Susan McGurk, Jim Mintz
Camarillo-UCLA Clinical Research Center. Box 6022. Camarillo, CA 93011, USA New antipsychotic medications such as risperidone have less neuromotor liability than conventional neuroleptics, and consequently, may yield better motor fun~tion!ng in patients. !he current study examined the effectsofnspendone vs. halopendol on reaction time and finemotor speed in a sample of treatmentresistant schizophrenia patients. Fifty-eight treatment-resistant schizophreniainpatients participated in a randomized, double-blind. co~parison of rispe~ done vs. haloperidol. Measures of reaction time from the Senal Reaction Time Test and fine motor speed from the Pin Test were administered at baseline, after four weeks of fixed dose medication, and after four weeks of flexible dose medication. Baseline performance served as a covariate for group comparisons at each medication phase. The results revealed that patients receiving risperidone showed faster reaction times at both phases than patients receiving haloperidol. Risperidone treatment also showed a trend for greater finemotor speedcompared with haloperidol. It is possible that risperidone's relatively reduced extrapyramidal side effect liability may extend to reaction time and fine motor speed.
c,06 THE NMDA RECEPTOR AND SCHIZOPHRENIA: FROM PHENOTYPE TO GENOTYPE
These data suggest that the genes that code for NMDA receptor subunits represent candidates for direct gene analysis in molecular genetic studies of schizophrenia. We are currently examining the gene coding for the RI subunit of the NMDA receptor for allelic variation in a Haplotype Relative Risk group of 75 schizophrenics and their parents. Using the polymerase chain reaction, single strand conformational polymorphism analysis (PCR·SSCP) and DNA sequencing, we have identified a rare allelic variant in the NMDARI gene and are investigating its functional significance and association with schizophrenia.
601 ADJUNCTIVE LOXAPINE IN A CLOZAPINE-RESISTANT COHORT OF SDHIZOPHRENIC PATIENTS Samuel Mowerman, Samuel G. Siris
75-59 263rdStreet, Glen Oaks. New York 11004. USA Objective: The purpose of this trial was to assess the potential utility of adjunctive treatment with a typical neuroleptic for patients with refractory psychosis insufficiently responsive to clozapine alone. Method: Seven chronic schizophrenic or schizoaffective patients who remained stabilized for at least 9 months on clozapine received open clinical trials with adjunctive loxapine lasting from 18 to 50 weeks. Their symptoms were documented with periodic Brief Psychiatric Rating Scale assessments. Results: All patients improved at least somewhat and two improved remarkably. In the 4 cases in which the assessment was made, the loxapine had no apparent effect on plasma clozapine levels. Conclusion: Adjunctive treatment with typical neuroleptics for patients with incomplete response to clozapine merits further investigation. Keywords: Clozapine, Loxapine, Schizophrenia, Treatment Resistant, Typical Neuroleptic
Anil K. Malhotra, Alan Breier, Robert Buchanan, David Goldman, David Pickar
Unitof Pharmacogenetics, Experimental Therapeutics Branch. NIMH, Bethesda, MD 20892, USA Several lines of evidence have implicated the glutamatergic N_methyl-d-aspartate (NMOA) recep~o~ in the pathophysi~ logy of schizophrenia. We have administered subanaesthetic doses (0.12 mg/kg bolus followed by 0.65 mg/kg/hr infusion) f the NMOA antagonist ketamine to probe human NMOA ;eceptor function. In healthy volunteers, ketamine produces thought disorder, perce~t~al abnormalities and co.gnitive impairment. Positron Emission Tomography (PET) With fluorodeoxyglucose (FOG) reveals that ketamine produces specific metabolic activation of prefrontal areas and that these metabolic effects correlate with ketamine-induced thought disorder. In a study of neuroleptic-free schizophrenic patients, ketamine exacerbated core psychotic and cognitive symptoms.
" 11 DOSE-DEPENDENT INSULIN-INDUCED INCREASES IN MEMORY PERFORMANCE IN HEALTHY HUMANS John W. Newcomer, Joy Coleman, Neil Bhargava, Gregg Selke, Angela Kelly, Desiree White
Dept. ofPsychiatry, Washington Univ. Sch. of Med; St. Louis 63110, USA The principal energy substrate for the brain is glucose. Increases in memory performance have been reported during increases in circulating glucose levels in rodents, healthy humans and individuals with Alzheimer's and schizophrenia. This study aims to define the dose-response relationship of
h67 RISPERIDONE VS. HALOPERIDOL ON REACTION TIME AND FINE MOTOR SPEED Robert S. Kern, Michael F. Green, Barringer D. Marshall, Jr., William C. Wirshing, Donna Ames, Stephen R. Marder, Susan McGurk, Jim Mintz
Camarillo-UCLA Clinical Research Center. Box 6022. Camarillo, CA 93011, USA New antipsychotic medications such as risperidone have less neuromotor liability than conventional neuroleptics, and consequently, may yield better motor fun~tion!ng in patients. !he current study examined the effectsofnspendone vs. halopendol on reaction time and finemotor speed in a sample of treatmentresistant schizophrenia patients. Fifty-eight treatment-resistant schizophreniainpatients participated in a randomized, double-blind. co~parison of rispe~ done vs. haloperidol. Measures of reaction time from the Senal Reaction Time Test and fine motor speed from the Pin Test were administered at baseline, after four weeks of fixed dose medication, and after four weeks of flexible dose medication. Baseline performance served as a covariate for group comparisons at each medication phase. The results revealed that patients receiving risperidone showed faster reaction times at both phases than patients receiving haloperidol. Risperidone treatment also showed a trend for greater finemotor speedcompared with haloperidol. It is possible that risperidone's relatively reduced extrapyramidal side effect liability may extend to reaction time and fine motor speed.
c,06 THE NMDA RECEPTOR AND SCHIZOPHRENIA: FROM PHENOTYPE TO GENOTYPE
These data suggest that the genes that code for NMDA receptor subunits represent candidates for direct gene analysis in molecular genetic studies of schizophrenia. We are currently examining the gene coding for the RI subunit of the NMDA receptor for allelic variation in a Haplotype Relative Risk group of 75 schizophrenics and their parents. Using the polymerase chain reaction, single strand conformational polymorphism analysis (PCR·SSCP) and DNA sequencing, we have identified a rare allelic variant in the NMDARI gene and are investigating its functional significance and association with schizophrenia.
601 ADJUNCTIVE LOXAPINE IN A CLOZAPINE-RESISTANT COHORT OF SDHIZOPHRENIC PATIENTS Samuel Mowerman, Samuel G. Siris
75-59 263rdStreet, Glen Oaks. New York 11004. USA Objective: The purpose of this trial was to assess the potential utility of adjunctive treatment with a typical neuroleptic for patients with refractory psychosis insufficiently responsive to clozapine alone. Method: Seven chronic schizophrenic or schizoaffective patients who remained stabilized for at least 9 months on clozapine received open clinical trials with adjunctive loxapine lasting from 18 to 50 weeks. Their symptoms were documented with periodic Brief Psychiatric Rating Scale assessments. Results: All patients improved at least somewhat and two improved remarkably. In the 4 cases in which the assessment was made, the loxapine had no apparent effect on plasma clozapine levels. Conclusion: Adjunctive treatment with typical neuroleptics for patients with incomplete response to clozapine merits further investigation. Keywords: Clozapine, Loxapine, Schizophrenia, Treatment Resistant, Typical Neuroleptic
Anil K. Malhotra, Alan Breier, Robert Buchanan, David Goldman, David Pickar
Unitof Pharmacogenetics, Experimental Therapeutics Branch. NIMH, Bethesda, MD 20892, USA Several lines of evidence have implicated the glutamatergic N_methyl-d-aspartate (NMOA) recep~o~ in the pathophysi~ logy of schizophrenia. We have administered subanaesthetic doses (0.12 mg/kg bolus followed by 0.65 mg/kg/hr infusion) f the NMOA antagonist ketamine to probe human NMOA ;eceptor function. In healthy volunteers, ketamine produces thought disorder, perce~t~al abnormalities and co.gnitive impairment. Positron Emission Tomography (PET) With fluorodeoxyglucose (FOG) reveals that ketamine produces specific metabolic activation of prefrontal areas and that these metabolic effects correlate with ketamine-induced thought disorder. In a study of neuroleptic-free schizophrenic patients, ketamine exacerbated core psychotic and cognitive symptoms.
" 11 DOSE-DEPENDENT INSULIN-INDUCED INCREASES IN MEMORY PERFORMANCE IN HEALTHY HUMANS John W. Newcomer, Joy Coleman, Neil Bhargava, Gregg Selke, Angela Kelly, Desiree White
Dept. ofPsychiatry, Washington Univ. Sch. of Med; St. Louis 63110, USA The principal energy substrate for the brain is glucose. Increases in memory performance have been reported during increases in circulating glucose levels in rodents, healthy humans and individuals with Alzheimer's and schizophrenia. This study aims to define the dose-response relationship of