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The present study aimed to test the hypothesis that dopamine agonists may enhance cognitive function. The effect of amantadine on neuropsychological function in medicated schizophrenia patients was investigated. The study comprised an add-on, double-blind, placebo-controlled, cross-over 6-week trial. Participants comprised 29 inpatients at Sha'ar Menashe Mental Health Center who were diagnosed with chronic schizophrenia or schizoaffective disorder. Amantadine 200 mg/day or identical placebo was added to ongoing antipsychotic treatment for 3 weeks. Study medications were then switched for an additional 3 weeks. Assessments were performed at baseline, and weeks 3 and 6, including cognitive and visuomotor assessments. Clinical ratings included positive, negative and depressive symptoms and extrapyramidal side-effects. Blood prolactin levels were assayed. A mixed model was used to examine differences in the data at the three assessment points. Amantadine was associated with improved visuomotor coordination compared to placebo. No significant changes in cognitive functions were noted. Clinical symptoms, extrapyramidal side-effects and blood prolactin levels were not altered. Amantadine improved visuomotor coordination independently of extrapyramidal side-effects but not cognitive function. Because prolactin concentrations were unchanged, the mechanism is more likely to involve glutaminergic NMDA than dopaminergic mechanisms. Further studies of amantadine with different doses and treatment duration, as well as more glutamate selective agents such as memantine, are indicated.

We studied the relationship between abstraction and other, more basic, cognitive functions in 78 schizophrenia patients and 57 healthy controls. Patients' performance was impaired compared to that of healthy individuals. Regression analysis showed significant contributions of task latency, spatial working memory, and verbal working memory to abstraction performance. The model explained 56.9% of the variance. The latency contribution included linear and quadratic components indicating optimal strategies for normal abstraction performance. Abnormal (suboptimal) processing strategies and working-memory dysfunctions predict impaired abstraction in schizophrenia. The model presented may enable differentiation between impaired and compensating components in schizophrenia patients with an abstraction deficit.