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Clozapine is the only antipsychotic agent with proven efficacy in treatment-resistant schizophrenia¹; however, a substantial minority of patients fail to respond or have only a partial response to clozapine, leading clinicians to search for potential augmentation strategies to improve outcomes. To date, these augmentation strategies with clozapine have generally been disappointing.

Glutamate is an excitatory neurotransmitter, and clozapine acts as a glutamate antagonist. Lamotrigine, an anticonvulsant and mood stabilizer, inhibits excessive release of glutamate.² Both drugs block the psychotomimetic effects of phencyclidine (PCP). These schizophrenia-like symptoms are attributed to PCP's activity at the NMDA (glutamate) receptor. The biochemical significance of these glutamate interactions in schizophrenia remains unclear and is hotly debated. There is evidence to suggest that there is abnormal glutamatergic binding in the areas of the brain associated with psychotic symptoms in patients with schizophrenia.³

We are reporting on a small, open-label, nonrandomized case series of 6 outpatients . . . [Full Text of this Article]

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