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Maternal influenza and schizophrenia: A cohort study
3. Epidemiology
55
ophrenia, but not psychotic bipolar disorder, and this relationship is most emphatic for those with no family history of the illness. Our results suggest that environmental insults leading to compromised foetal development are linked to subsequent premorbid impairment in schizophrenia and especially in those less likely to carry susceptibility genes for the disorder.
MATERNAL INFLUENZA AND SCHIZOPHRENIA: A COHORT STUDY J. B. Watson,* S. A. Mednick, R. M a c h o n
Stanford University, San Francisco, CA, USA Previous studies have reported an increase in risk for schizophrenia among offspring whose mothers suffered from influenza during pregnancy. The purpose of our study was to investigate the interaction between family history of schizophrenia and second-trimester maternal influenza exposure. A search of the Finnish Hospital Psychiatric Register was conducted for schizophrenics exposed to the 1957 A2influenza epidemic (Influenza-Exposed) and for schizophrenics born two years prior to the influenza epidemic (Non-Exposed). Within the Influenza-Exposed, two groups were created: 1.) Influenza-Exposed schizophrenics with no first-degree relatives with schizophrenia were placed in the Exposed no relatives group or E-NR group, and 2.) Influenza-Exposed schizophrenics with one or more relatives with a schizophrenia diagnosis were placed in the Exposed One or More Relatives group or E-OR group. The same two groups were created within the Non-Exposed schizophrenics. The second-trimester effect was observed in the Exposed no relatives group of schizophrenics but not in the Exposed one or more relatives group of schizophrenics. A second-trimester effect was not observed in the Non-Exposed schizophrenics. In the absence of a genetic liability (i.e., schizophrenics with no relatives who have schizophrenia), the second trimester influenza effect was observed. However, the second trimester effect was not observed in the E-OR group, i.e., schizophrenics who had a genetic liability for schizophrenia. Thus, an interaction between genes and maternal influenza exposure was not observed.
HIGHER RATES OF CIGARETTE SMOKING IN MALE ADOLESCENTS BEFORE THE ONSET OF SCHIZOPHRENIA: A HISTORICALPROSPECTIVE COHORT STUDY M. Weiser,* A. R e i c h e n b e r g , I. Grotto, R. Yasvitzky, H. Y. Knobler, G. Lubin, D. N a h o n , M. D a v i d s o n
Psychiatry, Sheba Medical Center, Ramat-Gan, Israel The prevalence of smoking among patients with Schizophrenia is significantly higher than controls, perhaps reflecting self-medication of the symptoms and/or the side effects of treatment of the illness. Smoking may reflect, in addition, a nicotinic receptor dysfunction intrinsic to the disease present before the onset of psychosis and it's treatment. This hypothesis was examined by assessing the prevalence of cigarette smoking in futttre schizophrenia patients before the onset of their illness. A randomly selected five percent sample of the adolescents recruited to serve in the Israeli army complete a question-
naire regarding their smoking habits. These data were linked with the Israeli National Psychiatric Hospitalization Case Registry, which records all psychiatric hospitalizations in the country. Data on smoking habits were available for 16734 mate recruits, of whom 30.1% reported smoking one cigarette or more per day. Over a 1-18 year follow-up, the prevalence of schizophrenia was 0.3%. The risk for schizophrenia was increased in male adolescents who reported smoking at least one cigarette a day, RR=1.98, Wald Z2(1 )=6.28, 95%CI: 1.16-3.38. The risk for schizophrenia increased as a function of the number of cigarettes smoked: 0.2% of the non-smokers, 0.4% of the adolescents who smoked 1-9 cigarettes/day, and 0.6% of the adolescents who smoked more than 10 cigarettes/day were later hospitalized. This higher prevalence of smoking in future schizophrenia patients before the onset of their illness might reflect an intrinsic, disease related disorder of nicotinic transmission. This hypothesis is supported by other studies which reported abnormalities in nicotinic transmission in patients and their relatives. This enhanced rate of smoking present before tile onset of psychosis speaks to a biologically-related enhanced vulnerability to smoking in schizophrenia. The results of this study indicate the need for more intense research on the nicotinic system in schizophrenia.
NEUROLOGICAL SOFT SIGNS IN PSYCHOSIS AND THEIR EVOLUTION OVER THE FIRST FOUR YEARS OF ILLNESS R Whitty,* M. Clarke, O. M c T i g u e , S. B r o w n e , J. L. Waddington, C. Larkin, E. O ' C a l l a g h a n
Dept. of Adult Psychiatry, Stanley Research Centre, Dublin, Ireland Background: Neurological soft signs (NSS) are well described among patients with psychosis, however few studies have prospectively examined these signs over time. Method: We assessed 17 l cases (99 male, 72 female, mean age 29.1 years) presenting with a first episode of psychosis from a geographically defined catchment area using the Neurological Evaluation Scale (NES) and the Condensed Neurological Evaluaiton (CNE) at three time points; first presentation, 6 month and 4 year follow-up. All patients were diagnosed in accordance with DSM-IV criteria. Results: Neurological functioning improved in the majority (81%) of patients at 4 years. Total NES scores improved significantlyat 6 month (t=3.8, P<0.01) and 4 year follow-up (t = 2.2, P<0.04). Total CCNE scores also improved at both follow-up assessments, however only the improvement at 4 years was statistically significant (t=3.7, P<0.01). The factor structure of NSS changed over the course of the study. NSS scores were dependent on years in education, initial duration of untreated psychosis and psychopathology at presentation and primarily psychopathology at follow-up. Patients whose neurological functioning deteriorated had a longer initial duration of untreated psychosis compared to those who evidenced improvement. Conclusion: Neurological functioning in psychosis tends to improve over time. At presentation and 4 year follow-up NSS are closely related to psychopathology.
International Congress on Schizophrenia Research 2003
55
ophrenia, but not psychotic bipolar disorder, and this relationship is most emphatic for those with no family history of the illness. Our results suggest that environmental insults leading to compromised foetal development are linked to subsequent premorbid impairment in schizophrenia and especially in those less likely to carry susceptibility genes for the disorder.
MATERNAL INFLUENZA AND SCHIZOPHRENIA: A COHORT STUDY J. B. Watson,* S. A. Mednick, R. M a c h o n
Stanford University, San Francisco, CA, USA Previous studies have reported an increase in risk for schizophrenia among offspring whose mothers suffered from influenza during pregnancy. The purpose of our study was to investigate the interaction between family history of schizophrenia and second-trimester maternal influenza exposure. A search of the Finnish Hospital Psychiatric Register was conducted for schizophrenics exposed to the 1957 A2influenza epidemic (Influenza-Exposed) and for schizophrenics born two years prior to the influenza epidemic (Non-Exposed). Within the Influenza-Exposed, two groups were created: 1.) Influenza-Exposed schizophrenics with no first-degree relatives with schizophrenia were placed in the Exposed no relatives group or E-NR group, and 2.) Influenza-Exposed schizophrenics with one or more relatives with a schizophrenia diagnosis were placed in the Exposed One or More Relatives group or E-OR group. The same two groups were created within the Non-Exposed schizophrenics. The second-trimester effect was observed in the Exposed no relatives group of schizophrenics but not in the Exposed one or more relatives group of schizophrenics. A second-trimester effect was not observed in the Non-Exposed schizophrenics. In the absence of a genetic liability (i.e., schizophrenics with no relatives who have schizophrenia), the second trimester influenza effect was observed. However, the second trimester effect was not observed in the E-OR group, i.e., schizophrenics who had a genetic liability for schizophrenia. Thus, an interaction between genes and maternal influenza exposure was not observed.
HIGHER RATES OF CIGARETTE SMOKING IN MALE ADOLESCENTS BEFORE THE ONSET OF SCHIZOPHRENIA: A HISTORICALPROSPECTIVE COHORT STUDY M. Weiser,* A. R e i c h e n b e r g , I. Grotto, R. Yasvitzky, H. Y. Knobler, G. Lubin, D. N a h o n , M. D a v i d s o n
Psychiatry, Sheba Medical Center, Ramat-Gan, Israel The prevalence of smoking among patients with Schizophrenia is significantly higher than controls, perhaps reflecting self-medication of the symptoms and/or the side effects of treatment of the illness. Smoking may reflect, in addition, a nicotinic receptor dysfunction intrinsic to the disease present before the onset of psychosis and it's treatment. This hypothesis was examined by assessing the prevalence of cigarette smoking in futttre schizophrenia patients before the onset of their illness. A randomly selected five percent sample of the adolescents recruited to serve in the Israeli army complete a question-
naire regarding their smoking habits. These data were linked with the Israeli National Psychiatric Hospitalization Case Registry, which records all psychiatric hospitalizations in the country. Data on smoking habits were available for 16734 mate recruits, of whom 30.1% reported smoking one cigarette or more per day. Over a 1-18 year follow-up, the prevalence of schizophrenia was 0.3%. The risk for schizophrenia was increased in male adolescents who reported smoking at least one cigarette a day, RR=1.98, Wald Z2(1 )=6.28, 95%CI: 1.16-3.38. The risk for schizophrenia increased as a function of the number of cigarettes smoked: 0.2% of the non-smokers, 0.4% of the adolescents who smoked 1-9 cigarettes/day, and 0.6% of the adolescents who smoked more than 10 cigarettes/day were later hospitalized. This higher prevalence of smoking in future schizophrenia patients before the onset of their illness might reflect an intrinsic, disease related disorder of nicotinic transmission. This hypothesis is supported by other studies which reported abnormalities in nicotinic transmission in patients and their relatives. This enhanced rate of smoking present before tile onset of psychosis speaks to a biologically-related enhanced vulnerability to smoking in schizophrenia. The results of this study indicate the need for more intense research on the nicotinic system in schizophrenia.
NEUROLOGICAL SOFT SIGNS IN PSYCHOSIS AND THEIR EVOLUTION OVER THE FIRST FOUR YEARS OF ILLNESS R Whitty,* M. Clarke, O. M c T i g u e , S. B r o w n e , J. L. Waddington, C. Larkin, E. O ' C a l l a g h a n
Dept. of Adult Psychiatry, Stanley Research Centre, Dublin, Ireland Background: Neurological soft signs (NSS) are well described among patients with psychosis, however few studies have prospectively examined these signs over time. Method: We assessed 17 l cases (99 male, 72 female, mean age 29.1 years) presenting with a first episode of psychosis from a geographically defined catchment area using the Neurological Evaluation Scale (NES) and the Condensed Neurological Evaluaiton (CNE) at three time points; first presentation, 6 month and 4 year follow-up. All patients were diagnosed in accordance with DSM-IV criteria. Results: Neurological functioning improved in the majority (81%) of patients at 4 years. Total NES scores improved significantlyat 6 month (t=3.8, P<0.01) and 4 year follow-up (t = 2.2, P<0.04). Total CCNE scores also improved at both follow-up assessments, however only the improvement at 4 years was statistically significant (t=3.7, P<0.01). The factor structure of NSS changed over the course of the study. NSS scores were dependent on years in education, initial duration of untreated psychosis and psychopathology at presentation and primarily psychopathology at follow-up. Patients whose neurological functioning deteriorated had a longer initial duration of untreated psychosis compared to those who evidenced improvement. Conclusion: Neurological functioning in psychosis tends to improve over time. At presentation and 4 year follow-up NSS are closely related to psychopathology.
International Congress on Schizophrenia Research 2003