Neurogenesis is part of the wider processes encompassed by the term neuroplasticity. Neuroplasticity is an intimate part of continued development which, like neurogenesis, remains regulated by activity and many other factors, e.g., stress, experience, etc. I, along with some other schizophrenia researchers, have made a case for the schizophrenias, only at the level of CNS (to avoid the errors of neuroreductionism), to be disorders of neuroplasticity, particularly, involving social and affective processes (the emerging fields of affective and social neuroscience). I have clearly demonstrated the significant overlap between the neuroscience of severe mental illness and the neuroscience of profound acute and chronic anxiety/stress/fear (see research reported in my volume in progress: The Schizophrenias: Brain, Mind and Culture).

This neuroplasticty perspective is an effective antidote to the therapeutic nihilism which is too often communicated to our patients (by caregivers, mental health clinicians as well as by their own feelings of hopelessness and helplessness). The crucial aspect is that it is congruent with current research in a multiplicity of domains, including epidemiology, developmental neurobiology and psychobiology, epigenetics, neurophenomenology, stress research, attachment research, as well as course and outcome data. A comprehensive model of schizophrenia must address the following factors in a coherent manner: neurogenesis, symptom formation, etiology, onset, and heterogeneity ( Heinrichs, R. W. 2001 In Search of Madness: Schizophrenia and Neuroscience. Oxford, UK: Oxford University Press). To this list I would add variable courses and outcomes. I believe that my theory is both scientifically coherent and clinically helpful.

Brian Koehler PhD
Postdoctoral Faculty of New York University
80 East 11th Street #339
New York NY 10003
212.533.5687
brian_koehler@psychoanalysis.net