The neuropathology of schizophrenia is substantial in scope and complexity. In patients, structural abnormalities in about 20 brain regions span wide swaths of cortical and subcortical tissue, reflecting processes presumably well advanced at birth. Roughly half as many regions are abnormal in unaffected relatives (cf. Swerdlow, 2011). Within any region, laminar synaptic and cellular arrangements may be perturbed, replacing ‘intended’ spatial and chemical connections with dysfunctional alternatives. The likelihood that medications will functionally untangle these chaotic and dispersed connections in schizophrenia seems increasingly far-fetched.

Cognitive therapies, broadly including cognitive-behavioral and neurorehabilitative therapies and cognitive training, may reduce symptoms and restore function in schizophrenia (McGurk et al, 2007; and Wykes et al, 2008) by engaging healthy neural systems to learn adaptive cognitive and behavioral strategies. The biology underlying learning-based neuroplasticity has been elaborated at levels extending from molecules to systems, and studies are now identifying neural changes accompanying clinical benefits of these specialized ‘learning therapies.’ Conceivably, these neural changes and their corresponding therapeutic impact might be augmented via medications.

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