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Objective: The authors' goal was to improve the diagnosis of schizophrenia by using virtual reality technology to build a complex, multimodal environment in which cognitive functions can be studied (and measured)in parallel. Method: The authors studied sensory integration within working memory by means of computer navigation through a virtual maze. The simulated journey consisted of a series of rooms, each of which included three doors. Each door was characterized by three features (color, shape, and sound), and a single combination of features--the door-opening rule--was correct. Subjects had to learn the rule and use it. The participants were 39 schizophrenic patients and 21 healthy comparison subjects. Results: Upon completion, each subject was assigned a performance profile, including various error scores, response time, navigation ability, and strategy. A classification procedure based on the subjects' performance profile correctly predicted 85% of the schizophrenic patients (and all of the comparison subjects). Several performance variables showed significant correlations with scores on a standard diagnostic measure (Positive and Negative Syndrome Scale), suggesting potential use of these measurements for the diagnosis of schizophrenia. On the other hand, the patients did not show unusual repetition of response despite stimulus cessation (called 'perseveration' in classical studies of schizophrenia), which is a common symptom of the disease. This deficit appeared only when the subjects did not receive proper explanation of the task. Conclusions: The ability to study multimodal performance simultaneously by using virtual reality technology opens new possibilities for the diagnosis of schizophrenia with objective procedures.

Olanzapine is a substrate of the cytochrome P450 enzyme (CYP) 1A2. In this study, pharmacokinetic interactions and clinical effects of adding the CYP1A2 inhibitor fluvoxamine to steady-state olanzapine was examined in patients suffering from schizophrenia. Eight patients had been treated for at least 3 months with 10 to 20 mg/day olanzapine. Fluvoxamine (100 mg/day) was added (week 0) to the olanzapine treatment and continued for 8 weeks. Concentrations of olanzapine and its metab-olite N-desmethylolanzapine and of fluvoxamine were analyzed at weeks 0, 1, 4, and 8. Addition of fluvoxamine resulted in a 12 to 112 (p< 0.01) increase of olanzapine from 31 ± SD 15 ng/mL (week 0) to 56 ± 31 ng/mL (week 8) in all patients. N-desmethylolanzapine concentrations were not significantly changed (p> 0.05). Fluvoxamine concentrations were 48 ± 26 ng/mL on week 1 and 83 ± 47 ng/mL on week 8. It is concluded that fluvoxamine affects olanzapine degradation and thus increases olanzapine concentrations. Although the combination was well tolerated in this sample and the negative symptom response appeared to be favorable in at least five patients, the combination therapy of olanzapine and fluvoxamine should be used cautiously and should be controlled by therapeutic drug monitoring to avoid olanzapine-induced side effects or intoxications.

A neural network model with dynamic thresholds, asymmetric connections, and clustered memories simulates spread activation that is hypothesized for semantic networks in the brain. By altering the parameters of the dynamic threshold a large range of disturbances can be generated in the model. These disturbances show metaphorical resemblance to certain general clinical descriptions of mental disturbances found in psychiatric patients engaged in various cognitive tasks. Even though the model is highly theoretical and metaphoric, it may help to gain certain insights into the relation between alterations of certain neural parameters, for example, thresholds and connectivity, and clinical symptoms in patients. (JINS, 2000, 6, 608–619.)