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Olfactory fuction in monozygotic twins discordant for schizophrenia
1945
Poster session m
BIOL. PSYCHIATRY 1997;42:15-2975
psychopathology (PANSS) at baseline, severity of positive symptoms after 6 weeks of treatment, and the extend of clinical Improvement after neuroleptic therapy. As the clinical value of T2 measurements is not clear as yet, and taking Into consideration that RIs rarely.
vs. RIS 5.3 ± 6.6, P .. 0.09). Changes In all neurological scaJes were smaI during the trial and did not show dlfferances between the two groups. Weighl Increase was mora frequently reported wRh AIS compared with AMI (5.3% vs.2.6%).
165-170 1 Amlsulprlde versus rlsperldone In the treatment
165-171
of acute schizophrenIa
I Olfactory functIon In monozygotic twIns discordant for schIzophrenIa
O. Fleurot 2 , P. Bach 1, S. Tu~anski 2 for the Amisulpride Study Group. 1 General Hospital, Hil/erad. Denmark, 2 Synthelabo. Le Plessis Robinson. France Amlsulpride (AMI), a selective dopamine 03 and 02 antagonist, was compared to risperidone (RIS), a 02 and 5HT2 antagonist, In a multicentre double blind randomlsed trial including acutely III schizophrenic patients (OSM IV). After a washout period of 3 to 6 days patients were treated for 6 weeks with either AMI 800 mgld or RIS 8 mgld. Efficacy criteria were the BPRS, the PANSS Positive and Negative subscales and the CGI, safety was assessed via open reporting and neurological symptoms specifically with the Simpson-Angus scale, the Bames akathlsla scale and the AIMS for dyskinesia. A total of 228 patients (AMI 115, AIS 113, mean age 36.5 ± 11.2 yrs., mean duration of Illness 9.0 ± 9.5 yrs) were randomlsed. Patients were comparable for baseline characteristics and Initial rating scale scores. A total of 78 AMI patients (68%) and 81 AIS patients (72%) completed the study. The discontinuation rates for lack of efficacy (AMI 8, RIS 10) and edverse events (AMI 15. RIS 14) were similar In both groups. Patients In both groups had equivalent improvement of their BPRS total scores (AMI 17.7 ± 14.9 vs. RIS 15.2 ± 13.9). The response rate (OGI 2 very much and much Improved) was higher in the AMI group (AMI 67% vs. RIS 58%) but this difference did not reach significance (p 0.17). Improvement In PANSS Positive scores was similar In both groups (AMI 9.6 ± 6.5
=
L. Kopala, K.P. Good, E. Torrey-Fuller, W.G. Honer. Department 01 Psychiatry. Dalhousie University. Halifax. Nova Scotia Olfactory Identification dellcits In schizophrenia provide further evidence for cerebral dysfunction, aRhough the etiology of this abnormality remains unknown. To assess potential genetic contributions to olfactory dysfunction In schizophrenia, we studied monozygotic twins who were discordant lor schizophrenia and a matched normal control group. The University 01 Pennsylvania Smell Identification Test (UPSIT) was completed by 12 twin pairs and twelve normal controls. All subjects were classified according to olfactory status (normosmlc vs. microsmic). Using a Chi square analysis, the percentage of Individuals who would be classified as mia'osmic was compared among the diagnostic categories. A significant result was observect (x~ • 22.9; p < 0.0005). Fifty percent of the affected twins, 25% 01 Itle unaffected twins and none of the normal control subjects were microstric.. Both affected and unaffected twins had lower mean UPSIT scores ~ to the control group (T33 .. 5.2; p < 0.05). When the unaftectecl were compared to the affected twins, no difference was observed (T33 • 2.0; p • ns). A final analysis revealed that the twin pairs who had a positive family history of serious mental Illness scored signillcantly lower on the UPSIT than those twins with a negative family history (33.4 VS 36.3) (~ • 1_9; p < 0.05). These findings suggest that there Is a genetic contribution to the c:et'8brM dysfunction associated with olfactory deficits In schiZophrenia.
Poster session m
BIOL. PSYCHIATRY 1997;42:15-2975
psychopathology (PANSS) at baseline, severity of positive symptoms after 6 weeks of treatment, and the extend of clinical Improvement after neuroleptic therapy. As the clinical value of T2 measurements is not clear as yet, and taking Into consideration that RIs rarely.
vs. RIS 5.3 ± 6.6, P .. 0.09). Changes In all neurological scaJes were smaI during the trial and did not show dlfferances between the two groups. Weighl Increase was mora frequently reported wRh AIS compared with AMI (5.3% vs.2.6%).
165-170 1 Amlsulprlde versus rlsperldone In the treatment
165-171
of acute schizophrenIa
I Olfactory functIon In monozygotic twIns discordant for schIzophrenIa
O. Fleurot 2 , P. Bach 1, S. Tu~anski 2 for the Amisulpride Study Group. 1 General Hospital, Hil/erad. Denmark, 2 Synthelabo. Le Plessis Robinson. France Amlsulpride (AMI), a selective dopamine 03 and 02 antagonist, was compared to risperidone (RIS), a 02 and 5HT2 antagonist, In a multicentre double blind randomlsed trial including acutely III schizophrenic patients (OSM IV). After a washout period of 3 to 6 days patients were treated for 6 weeks with either AMI 800 mgld or RIS 8 mgld. Efficacy criteria were the BPRS, the PANSS Positive and Negative subscales and the CGI, safety was assessed via open reporting and neurological symptoms specifically with the Simpson-Angus scale, the Bames akathlsla scale and the AIMS for dyskinesia. A total of 228 patients (AMI 115, AIS 113, mean age 36.5 ± 11.2 yrs., mean duration of Illness 9.0 ± 9.5 yrs) were randomlsed. Patients were comparable for baseline characteristics and Initial rating scale scores. A total of 78 AMI patients (68%) and 81 AIS patients (72%) completed the study. The discontinuation rates for lack of efficacy (AMI 8, RIS 10) and edverse events (AMI 15. RIS 14) were similar In both groups. Patients In both groups had equivalent improvement of their BPRS total scores (AMI 17.7 ± 14.9 vs. RIS 15.2 ± 13.9). The response rate (OGI 2 very much and much Improved) was higher in the AMI group (AMI 67% vs. RIS 58%) but this difference did not reach significance (p 0.17). Improvement In PANSS Positive scores was similar In both groups (AMI 9.6 ± 6.5
=
L. Kopala, K.P. Good, E. Torrey-Fuller, W.G. Honer. Department 01 Psychiatry. Dalhousie University. Halifax. Nova Scotia Olfactory Identification dellcits In schizophrenia provide further evidence for cerebral dysfunction, aRhough the etiology of this abnormality remains unknown. To assess potential genetic contributions to olfactory dysfunction In schizophrenia, we studied monozygotic twins who were discordant lor schizophrenia and a matched normal control group. The University 01 Pennsylvania Smell Identification Test (UPSIT) was completed by 12 twin pairs and twelve normal controls. All subjects were classified according to olfactory status (normosmlc vs. microsmic). Using a Chi square analysis, the percentage of Individuals who would be classified as mia'osmic was compared among the diagnostic categories. A significant result was observect (x~ • 22.9; p < 0.0005). Fifty percent of the affected twins, 25% 01 Itle unaffected twins and none of the normal control subjects were microstric.. Both affected and unaffected twins had lower mean UPSIT scores ~ to the control group (T33 .. 5.2; p < 0.05). When the unaftectecl were compared to the affected twins, no difference was observed (T33 • 2.0; p • ns). A final analysis revealed that the twin pairs who had a positive family history of serious mental Illness scored signillcantly lower on the UPSIT than those twins with a negative family history (33.4 VS 36.3) (~ • 1_9; p < 0.05). These findings suggest that there Is a genetic contribution to the c:et'8brM dysfunction associated with olfactory deficits In schiZophrenia.