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Readiness potential in catatonic syndromes
Abstracts / PsychiatryResearch: Neuroimaging68 (1997) 155-184 lumbar vertebra and over Cz during the akathisic phase and after complete remission. Lumbar spinal SEP amplitudes were measured base to peak, and cortical amplitudes were determined peak to peak. In a two-tailed Wilcoxon-test for paired groups lumbar and cortical SEP reveal an increase of the mean amplitudes in the remission phase. After right tibial nerve stimulation the mean lumbar amplitude was 48% higher without akathisia, the increase of the mean cortical SEP amplitudes reveals the following values: 66% P60-N75 ( P < 0.05). After left tibial nerve stimulation the mean lumbar SEP amplitude was 75% higher in the remission phase; the 'increase' of the mean cortical amplitudes was: 14% for N33-P40 ( P < 0.05), 34% for P40-N50, 51% for N50-P60 and 35% for P60-N75. Our SEP results show an amplitude attenuation during akathisia. Modification of central sensory processes during motor activity is referred to as 'gating' and is a wellknown phenomena for SEP. In the somatosensory system "gating' is observed even before movement onset during the pre-concentration period. Sensory gating phenomena are caused by the action of central efferent systems. Since our registrations were done without movements of the patients, the results cannot be contributed to a movement-related SEP alteration. Our data suggest that during akathisia the somatosensory system is functionally altered on a spinal and a cortical level by disease-related motor tract inputs and that for interpretation of SEP amplitudes the usual normative data are not valuable. Readiness potential in catatonic syndromes
J. Eckert a, T. Dierks a, G. Northoff b, B. Weber a, K. Maurer a
aKlinik j~r Psychiatrie and Psychotherap&L University Hospital Frankfitrt/Main, Germany. bKlinik fiir Psychiatrie und Psychotherapie 11, University Hospital, Frankfurt~Main, Germany Earlier studies documented alterations of pre-motor preparation in schizophrenia on the basis of the 'readiness potential'. Although catatonic patients reveal striking motor disturbances, the 'readiness potential' has never to our knowledge been investigated in catatonic patients. We examined five medicated akinetic catatonic patients (diagnosed according to the criteria of Rosebush (1990) and Lohr (1987) in a post-acute state and compared them with four healthy controls using a flexion task of the right index finger. Compared to controls, time onset of the beginning negative deflection of the 'readiness potential' measured at Cz was significantly later in patients ( - 7 3 0 +_ 206 ms in controls; - 4 7 9 + 75 ms in patients; P < 0.02). Computing the mean area under the curve from the individual beginning of the 'readiness potential' until EMGonset, patients showed at pre-central and central scalp sites the tendency to have a larger negative DC-shift compared to controls, whereas at parietal electrodes the mean negative area was higher in volunteers ( P < 0.02 at Pz). Our data give evidence that the preparation of self-initiated movements at the cortical level is functionally altered in catatonic patients. The cortical preparation period is shorter and there seems to be an imbalance of the involved frontocentral cortical regions in relation to the parietal areas during the pre-movement
161
phase, although the anatomical interpretation of referencedependent topograhical data has to be cautious. SPECT findings and psychiatric scores in 24 never treated schizophrenics
R. Erkwoh a, O. Sabri b, E.M. Steinmeyer a, U. Biillb, H. Sag a
aclinics of Psychiatry, RWTH Aachen, Germany. bClinics of Nuclear Medicine, RWTH Aachen, Germany Twenty-four neuroleptic-naive schizophrenics (16 males and eight females, mean age 31.9) were examined during active phases (DSM-III-R) by PANSS and rCBF was measured by 99 mTc-HMPAO- SPECT (740 MBq i.v.) with a Siemens double head ROTA camera, 13 slices, 6.25 ram. Twenty-two were reexamined in a pre/post-treatment design. Data were compared to 20 age-adjusted controls. Of untreated positive symptoms, formal thought disorders and ideas of grandeur had strongest positive correlations to frontal inferior regions, where distrust and persecutory ideas were inversely correlated. Delusions correlated negatively to anterior cingulate. After therapy none but negative symptoms correlated inversely to ROIs. In a three-Factor-Solution, Factor one is essentially defined by formal thought disorders, weakly defined by hallucinations and mannerism and includes all ROIs. Highest value for ROI is found in frontal superior left. Factor two is essentially defined by delusions and lack of judgment and insight and shows highly negative correlations to temporal inferior right, temporomesial right and cingulate. Factor three represents the schizophrenic negative syndrome with negative correlations to all ROIs except frontal superior. Chronic lithium does not alter human myo-inositol or phosphomonoester concentrations as measured by 1H and 32P MRS.
P.H. Silverstone, J. Fabian, C. Hanstock, R. Staab, P.S. Allen
Departments of Psychiatry and Applied Sciences in Medicine, University of Alberta, Edmonton, Canada Lithium may act by decreasing intracellular concentrations of myo-inositol. The present study measured the effects of chronic lithium on myo-inositol concentrations in volunteers as measured by magnetic resonance spectroscopy (MRS). Eleven subjects received either lithium (n = 7) or placebo (n = 4) for 7 days. Myo-inositol concentrations at baseline and day 8 were measured in vivo using 1H MRS. The results showed that lithium did not alter brain myo-inositol concentrations compared to placebo. In five other subjects we used lH MRS and 31P MRS to measure changes in both myo-inositol and phosphomonoester concentrations. This second study showed that lithium did not alter myo-inositol or phosphomonoester concentrations. Thus, the present studies do not support the hypothesis that lithium significantly affects the brain concentrations of myo-inositol or phosphomonoesters. However, it is possible these findings represent an inability to detect the changes in concentrations that may have occurred following lithium administration.
J. Eckert a, T. Dierks a, G. Northoff b, B. Weber a, K. Maurer a
aKlinik j~r Psychiatrie and Psychotherap&L University Hospital Frankfitrt/Main, Germany. bKlinik fiir Psychiatrie und Psychotherapie 11, University Hospital, Frankfurt~Main, Germany Earlier studies documented alterations of pre-motor preparation in schizophrenia on the basis of the 'readiness potential'. Although catatonic patients reveal striking motor disturbances, the 'readiness potential' has never to our knowledge been investigated in catatonic patients. We examined five medicated akinetic catatonic patients (diagnosed according to the criteria of Rosebush (1990) and Lohr (1987) in a post-acute state and compared them with four healthy controls using a flexion task of the right index finger. Compared to controls, time onset of the beginning negative deflection of the 'readiness potential' measured at Cz was significantly later in patients ( - 7 3 0 +_ 206 ms in controls; - 4 7 9 + 75 ms in patients; P < 0.02). Computing the mean area under the curve from the individual beginning of the 'readiness potential' until EMGonset, patients showed at pre-central and central scalp sites the tendency to have a larger negative DC-shift compared to controls, whereas at parietal electrodes the mean negative area was higher in volunteers ( P < 0.02 at Pz). Our data give evidence that the preparation of self-initiated movements at the cortical level is functionally altered in catatonic patients. The cortical preparation period is shorter and there seems to be an imbalance of the involved frontocentral cortical regions in relation to the parietal areas during the pre-movement
161
phase, although the anatomical interpretation of referencedependent topograhical data has to be cautious. SPECT findings and psychiatric scores in 24 never treated schizophrenics
R. Erkwoh a, O. Sabri b, E.M. Steinmeyer a, U. Biillb, H. Sag a
aclinics of Psychiatry, RWTH Aachen, Germany. bClinics of Nuclear Medicine, RWTH Aachen, Germany Twenty-four neuroleptic-naive schizophrenics (16 males and eight females, mean age 31.9) were examined during active phases (DSM-III-R) by PANSS and rCBF was measured by 99 mTc-HMPAO- SPECT (740 MBq i.v.) with a Siemens double head ROTA camera, 13 slices, 6.25 ram. Twenty-two were reexamined in a pre/post-treatment design. Data were compared to 20 age-adjusted controls. Of untreated positive symptoms, formal thought disorders and ideas of grandeur had strongest positive correlations to frontal inferior regions, where distrust and persecutory ideas were inversely correlated. Delusions correlated negatively to anterior cingulate. After therapy none but negative symptoms correlated inversely to ROIs. In a three-Factor-Solution, Factor one is essentially defined by formal thought disorders, weakly defined by hallucinations and mannerism and includes all ROIs. Highest value for ROI is found in frontal superior left. Factor two is essentially defined by delusions and lack of judgment and insight and shows highly negative correlations to temporal inferior right, temporomesial right and cingulate. Factor three represents the schizophrenic negative syndrome with negative correlations to all ROIs except frontal superior. Chronic lithium does not alter human myo-inositol or phosphomonoester concentrations as measured by 1H and 32P MRS.
P.H. Silverstone, J. Fabian, C. Hanstock, R. Staab, P.S. Allen
Departments of Psychiatry and Applied Sciences in Medicine, University of Alberta, Edmonton, Canada Lithium may act by decreasing intracellular concentrations of myo-inositol. The present study measured the effects of chronic lithium on myo-inositol concentrations in volunteers as measured by magnetic resonance spectroscopy (MRS). Eleven subjects received either lithium (n = 7) or placebo (n = 4) for 7 days. Myo-inositol concentrations at baseline and day 8 were measured in vivo using 1H MRS. The results showed that lithium did not alter brain myo-inositol concentrations compared to placebo. In five other subjects we used lH MRS and 31P MRS to measure changes in both myo-inositol and phosphomonoester concentrations. This second study showed that lithium did not alter myo-inositol or phosphomonoester concentrations. Thus, the present studies do not support the hypothesis that lithium significantly affects the brain concentrations of myo-inositol or phosphomonoesters. However, it is possible these findings represent an inability to detect the changes in concentrations that may have occurred following lithium administration.