T. Vasse

Saccadic and smooth-pursuit eye movements in deficit and non-deficit schizophrenia

We have analyzed eye movement performances in schizophrenics showing primary negative or deficit symptoms (n=16) and non-deficit schizophrenics (n=55), and compared them with those of controls (n=34) in order to study the relationships between negative symptoms and eye movement abnormalities. Patients were subtyped into deficit and non-deficit subgroups using the Schedule for the Deficit Syndrome. Three oculomotor paradigms were used: smooth pursuit, a reflexive saccade paradigm and an antisaccadic task. The smooth pursuit gain was significantly decreased (and the rate of catch-up saccades increased) in schizophrenics as compared with controls, but no difference was observed between patient groups. In the reflexive saccade paradigm, no difference was found between controls and patients, except for latency in deficit patients. In the antisaccade paradigm, the number of errors and the latency of successful antisaccades were significantly increased in schizophrenics as compared with controls. The latency of successful antisaccades in both directions was significantly increased in deficit patients as compared with non-deficit patients. The latency of rightward successful antisaccades was significantly increased as compared with the latency of leftward antisaccades in deficit patients only. However, when patients were classified into negative and non-negative groups using the PANSS, no difference was found in the antisaccade paradigm. Smooth pursuit impairment does not seem to depend on the primary enduring negative symptoms.In deficit schizophrenics, the abnormalities observed in the antisaccadic task are consistent with prefrontal dysfunction, and may suggest parietal lobe dysfunction as well.

Association study between dopamine D1, D2, D3, and D4 receptor genes and schizophrenia defined by several diagnostic systems

Whether an alteration of dopaminergic function exists in schizophrenia or not, it is tempting to speculate that a genetic abnormality of dopamine (DA) receptors--e i ther structural or affecting gene expression--might play a causative role in the pathogenesis of schizophrenia. Recently, five subtypes of DA receptors were characterized and the human genes corresponding to these different subtypes were cloned and assigned to chromosomes 5q35.1(Dl), l lq22.23(D2), 3q13.3(D3), l lp15.5(D4), and 4p16.1 (D5), respectively (Grandy et al 1989, 1990, 1992; LeConiat et al 1991; Gelernter et al 1992; see Campion et al, 1994). Each of these genes can be regarded as a candidate for a genetic defect in schizophrenia; however, except for a mutation described for the DA D4 receptor in delusional disorder (Catalano et al 1993), no linkage or association between schizophrenia and any of these genes has so far been found (Moises et al 1991; Campion et al 1994; Sabat6 et al 1994; Macciardi et al 1994; Ravindranathan et al 1994). This could be due to the use of incorrect genetic parameters in linkage analyses, or to the etiologic heterogeneity of schizophrenia, but also to misdiagno-

Association study between schizophrenia and monoamine oxidase A and B DNA polymorphisms.

Monoamine oxidases (MAO) A and B, which are encoded by two distinct genes located on the human X chromosome, are both involved in the oxidative metabolism of dopamine. Decreased levels of platelet MAO-B activity has been reported in patients with schizophrenia and genetic variation in MAO activity had been proposed as a significant factor in the etiology of this disease. We carried out an association study using two intragenic polymorphisms within the MAO-A and MAO-B genes in 110 schizophrenic patients and 87 control subjects. For each polymorphic marker, no significant difference in allelic frequencies was observed between patients and controls. Nevertheless, a trend toward an association between allele 1 of the MAO-B gene and paranoid schizophrenia was found. Our results do not support the hypothesis that inherited variants of MAO genes might play a major role in a genetic predisposition to schizophrenia. Since several previous reports found a low MAO-B platelet activity in patients with paranoid schizophrenia, the identification of polymorphisms related to enzyme activity would be useful.