Basil Alevizos

Risperidone-induced obsessive-compulsive symptoms: a series of six cases.

Risperidone is a novel and atypical agent with a dual antagonistic effect on 5-HT2 and D2 receptors. Open-label reports and one controlled study suggest that risperidone addition is effective in patients with obsessive-compulsive disorder refractory to treatment with serotonin reuptake inhibitors. However, risperidone has also been implicated in the production or exacerbation of obsessive-compulsive symptoms. We report six cases (schizophrenia, five cases; psychotic depression, one case) in which risperidone was effective in the treatment of the psychotic symptoms but produced de novo obsessive-compulsive symptoms (four cases) or caused exacerbation of previous obsessive-compulsive symptoms (two cases). In all but one case, obsessive-compulsive symptoms emerged shortly after initiation of risperidone treatment with a dose above 3 mg/day. The mechanisms and risk factors for risperidone and other atypical antipsychotics to induce or exacerbate obsessive-compulsive symptoms are as yet not clear. Risperidone-induced obsessive-compulsive symptoms appear to be dose-dependent and are probably produced by serotoninergic-dopaminergic imbalance. Close monitoring of the patients receiving risperidone, especially those vulnerable to the development of obsessive-compulsive symptoms, may be of value. Gradual escalation and low final dose may be helpful.

Obsessive–compulsive symptoms with olanzapine

The emergence or exacerbation of obsessive-compulsive (OC) symptoms during treatment with atypical antipsychotics, mostly clozapine, has been documented by numerous case reports (reviewed by Lykouras et al., 2003). In six recent reports involving nine cases, (Jonkers and de Haan, 2002; Lykouras et al., 2003) olanzapine was found either to cause de novo emergence or to exacerbate OC symptoms. In six of these cases olanzapine caused exacerbation and in three cases caused de novo emergence of OC symptoms.

Psychophysiological differences in schizophrenics with and without delusional misidentification syndromes: a P300 study.

There is a debate on whether delusional misidentification syndromes (DMSs) and schizophrenia are distinct disorders. Information-processing deficits have been found in both. Since the P300 component of event-related potentials (ERPs) reflects attention and working memory (WM) mechanisms, the P300 elicited during a WM test was studied in schizophrenic patients with DMS in comparison to schizophrenic patients without DMS and controls. Nine schizophrenic patients with DMS, 11 without DMS and 11 healthy controls were tested with a computerized version of the digit span test of the Wechsler batteries. Auditory ERPs were measured during the anticipatory period of the test. P300 amplitude in prefrontal areas was found to be significantly reduced in schizophrenics without DMS and markedly less in DMS patients compared to controls. P300 latency in the central midline brain region was significantly prolonged in DMS patients compared to the other groups. Memory performance was significantly reduced in both patient groups as compared to healthy controls. The results may indicate abnormalities in both allocation of attentional resources and automatic orienting in schizophrenic patients with DSM. In contrast, even though schizophrenic patients without DMS exhibit partial similarities with patients suffering from DMS, they show excessive reduction of P300 amplitude located at the left frontal area. Future studies might clarify these issues.

γ-Glutamyl transpeptidase

Abstract γ-Glutamyl transpeptidase, a membrane-bound enzyme playing an important role in the active amino acid transport across cellular membranes, is shown to be elevated in the serum of patients with myotonic muscular dystrophy. No increase of AP, LAP, GOT and GPT activities in the sera of some of the patients studied is observed. Possible interpretations in relation to the pathogenesis of myotonic dystrophy are discussed.

Analysis of polymorphisms in the α-subunit of the olfactory G-protein Golf in lithium-treated bipolar patients

Objective This study examines the &agr;‐subunit of the olfactory G‐protein (Golf) as a possible candidate gene for bipolar disorder. The &agr;‐subunit of the Golf gene maps to a region on chromosome 18p that has been implicated in several linkage studies as a potential site of a bipolar disorder susceptibility loci. Methods We investigated whether two polymorphisms in the &agr;‐subunit of the Golf gene (A→G in intron 3 and T→G in intron 10) are associated with bipolar disorder in a sample of 149 bipolar patients under lithium treatment compared with 139 healthy controls using haplotype analysis. Results There was no evidence for an association between the investigated polymorphisms in the Golf gene and bipolar disorders, as well as to response to lithium treatment or common side effects, like hand tremor, weight gain and cognitive dysfunction. Conclusion The results of the present study do not support the hypothesis that the Golf gene is a major susceptibility factor for bipolar disorders.

Psychophysiological correlates of patients with delusional misidentification syndromes and psychotic major depression

BACKGROUND Psychotic major depression (PMD) and delusional misidentification syndromes (DMS) exhibit cognitive deficits. Since the P300 component of event-related potentials (ERPs) provides valuable information concerning cognition, we studied this component of ERPs in DMS and PMD patients. METHODS Nine patients with DMS, 15 patients with PMD, and 11 healthy controls, matched for age, sex and educational level, were tested using the auditory P300 component of ERPs. RESULTS Both patient groups showed significant reductions in P300 amplitude at the right frontal region, while DMS group showed significant attenuation of the P300 amplitude at the right parietal area. P300 latency was significantly prolonged in the central midline brain region in the DMS group. LIMITATIONS The smallness of the sample size and the hypothetical post-hoc assignation of psychological function to regional activation. CONCLUSION PMD and DMS patients may share similar psychophysiological alterations connected to the right frontal region, mediating automatic processes, while DMS are associated with dysfunction of effortful mechanisms and allocation of attentional resources involving the interhemispheric and right parietal circuitry.

Clinical, endocrine and neurochemical effects of moclobemide in depressed patients

The clinical efficacy of the monoamine oxidase A inhibitor moclobemide and its effect on the dexamethasone suppression test (DST) and plasma and urine methoxyhydroxyphenylglycol (MHPG) were investigated in 26 depressed patients during a 4‐week clinical trial. Fourteen patients (54%) responded favourably to the treatment (50% or more reduction of the Hamilton Rating Scale for Depression score). All (8) patients with an abnormal DST responded to treatment; 11 of 16 patients with a normal DST did not respond. Patients with low pretreatment MHPG excretion, according to the median value, were more frequently treatment responders. Plasma and urine MHPG were significantly decreased by treatment. The results indicate that low excretion of MHPG and cortisol nonsuppression may be considered as predictors of favourable clinical response to moclobemide treatment.