From Research to Treatment in Clinical Neuroscience

Vol 2 n° 3 - From Research to Treatment in Clinical Neuroscience

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One of the most important trends in the treatment of schizophrenia involves its early diagnosis and inter- vention. The ultimate goal of research is the preven- tion of the disorder. A major impediment to the devel- opment of prevention strategies, however, is that we do not yet know what the liability for schizophrenia is before the onset of psychosis. Consequently, early treatment attempts are focused on the “prodrome,” which involves the early symptoms of psychosis. In a companion paper, we recently suggested that preven- tion work should focus not only on the prodrome, but also on “schizotaxia,” which is a clinically meaningful condition that may reflect the vulnerability to schizo- phrenia in the absence of psychosis. Because schizo- taxia can be assessed prior to the prodrome, studies of schizotaxia might lead to more effective prevention programs. We continue the characterization of schizo- taxia in this paper by focusing on the etiological roots of schizotaxia, plus its likely neurodevelopmental course, clinical expression, and treatment. Finally, the importance of including neurobiological variables in the conceptualization and eventual diagnosis of schizotaxia is reviewed. An understanding of how schizophrenia devel- ops is essential for developing treatment strategies aimed at preventing the disorder. Before such strategies can be formulated, it will be necessary to identify the liability for schizophrenia. That is, what is the vulnerability to schiz- ophrenia before the onset of psychosis? Recently, we addressed this issue in a companion paper to this one by describing “schizotaxia,” a clinically meaningful condi- tion that may reflect liability for schizophrenia.¹ In this paper, we describe the model of schizotaxia further by focusing on its etiology and development, and on its clin- ical, neuropsychological, and biological bases. We begin with a brief review of the concept, followed by a consid- eration of its genetic and environmental etiologies, and its likely neurodevelopmental course. Associated clini- cal and neuropsychological components of schizotaxia are then reviewed, followed by an update on our attempts to use these symptoms to develop treatment protocols. Finally, prospects for future research center on the need to incorporate biological function into the conceptualization and treatment of the syndrome. Schizotaxia Paul Meehl introduced the term “schizotaxia” in 1962 to describe the genetic predisposition to schizophrenia,² which he believed resulted in a subtle, neural integrative defect. He proposed that schizotaxic individuals would eventually develop either schizotypy or schizophrenia, depending on environmental circumstances. Although schizotypy (in the form of schizotypal personality disor- der) eventually entered the psychiatric nomenclature, schizotaxia did not. Instead, it became associated with Schizophrenia: vulnerability versus disease Ming T. Tsuang, MD, PhD, DSc, FRCPsych; Keywords: schizophrenia; schizotaxia; schizotypal disorder; genetic influence; environment; prevention.

Address for correspondence: Ming T. Tsuang, MD, PhD, Stanley Cobb Professor of Psychiatry, and Head, Harvard Medical School Department of Psychiatry at the Massachusetts Mental Health Center, 74 Fenwood Rd, Boston, MA 02115, USA
(e-mail: ming_tsuang@hms.harvard.edu) 2 5 7 C l i n i c a l r e s e a r c h Author affiliations: Harvard Medical School Department of Psychiatry at the Massachusetts Mental Health Center; Brockton West Roxbury Veterans Affairs Medical Center; Harvard Institute of Psychiatric Epidemiology and Genetics, Boston, Mass, USA (Ming T. Tsuang, William S. Stone, Stephen V. Faraone); Department of Epidemiology, Harvard School of Public Health, Boston, Mass, USA (Ming T. Tsuang); Pediatric Psychopharmacology Unit, Psychiatry Service, Massachusetts General Hospital, Boston, Mass, USA (Stephen V. Faraone)