The present meta-analysis investigated the characteristics of sleep in patients with schizophrenia without neuroleptic treatment at the time of sleep recording. The 20 selected studies included 652 participants (321 patients with schizophrenia and 331 healthy subjects). Effect sizes were evaluated using d values for the following sleep variables: sleep latency (SL), total sleep time (TST), sleep efficiency index (SEI), total awake time (TAT), stage 2 percentage (S2%), stage 4 percentage, slow-wave-sleep percentage, rapid-eye-movement (REM) percentage, and REM latency. The initial meta-analysis revealed that patients with schizophrenia have the following sleep disorders: increased SL, decreased TST, and decreased SEI. A moderator analysis revealed that these sleep disorders were worse for the neuroleptic-withdrawal group relative to the never-treated group. However, only never-treated patients showed significantly increased TAT and diminished S2%. These results confirm that patients with schizophrenia have sleep disorders that are not necessarily a consequence of neuroleptic treatments, suggesting that sleep disorders are an intrinsic feature of schizophrenia. However, it must be noted that some sleep disorders may be amplified by residual effects of neuroleptic withdrawal, while others appear to be dampened by neuroleptic treatment.

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Rivastigmine treatment did not appear to enhance cognition in SZ patients with important cognitive impairments. This finding needs to be interpreted with care and requires substantiation with larger sample size studies with patients treated with cognitive enhancer for longer periods.

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Summary. Persistent polyclonal B-cell lymphocytosis (PPBL)is an intriguing disorder diagnosed predominantly in women, usually cigarette smokers, characterized by an increase in the number of polyclonal B lymphocytes. Abnormality of the B-cell population is also evidenced by the presence of multiple bcl-2/Ig gene rearrangements and the finding of an additional long arm chromosome 3q1 (i3)(q10) within a significant proportion of B cells. The physiopathology of PPBL is unknown but its association with the HLA DR7 phenotype suggests a possible genetic disorder. To further determine whether PPBL has a genetic predisposition, we have undertaken an extensive study in a large family of a patient diagnosed with PPBL. Three individuals among the first-degree relatives presented all the criteria for a diagnosis of PPBL. A slight increase in serum IgM without evidence of B-cell proliferation was shown in two additional siblings. Multiple bcl-2/Ig gene rearrangements, a typical feature of PPBL, were identified in 8/10 individuals among first-degree relatives. A statistically significant association was found between the presence of these rearrangements and of a paternal HLA haplotype. We conclude that PPBL has a familial occurrence suggesting an underlying genetic defect. The development of the complete syndrome probably relies on unidentified additional cofactors.

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