Schizophrenia and Bipolar Disorder: Differences and Overlaps

Wolfgang Maier; Astrid Zobel; Michael Wagner


Curr Opin Psychiatry. 2006;19(2):165-170. 

In This Article

Abstract and Introduction


Purpose of Review: Following the recent progress mainly in the fields of genetics and neurobiology, the validity of the diagnostic distinction between schizophrenia and bipolar disorder is increasingly challenged.
Recent Findings: Evidence for basic neurobiological processes common for both disorders is expanding with regard to (a) susceptibility genes, (b) neurodevelopment (for example myelination), and (c) brain functions (for example sensory gating, visuospatial achievement). Recent epidemiological studies also stress communalities.
Summary: The diagnostic split between schizophrenia and bipolar disorder is unable to define distinct etiological and/or pathophysiological entities.


The nature of severe mental illness has been under debate for more than a century. On the one hand, a continuum of severity but only one disease process is claimed; on the other hand, two or more disease processes are postulated that can be identified by cross-sectional symptom patterns and features of long-term course. The most influential position of the last kind was introduced by Kraepelin who distinguished between schizophrenia and manic-depressive illness (Kraepelin's dichotomy). Kraepelin was impressed by the differential symptomatic long-term course and outcome with a predominantly enduring symptomatic impairment in schizophrenia compared with episodic course in bipolar disorder ('Diagnose-Verlaufs-Einheiten'). A vast majority of clinicians and all diagnostic manuals accepted and reformulated this position.

Both disorders, schizophrenia and bipolar disorder - diagnosed according to the prevailing manuals International Classification of Diseases, Tenth Revision (ICD-10) and Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) - reveal striking similarities: (a) lifetime prevalence of about 1% in males and females (independent of culture); (b) early age at onset (between late adolescence and early adulthood); (c) familial aggregation due to genetic influences with very similar recurrence risks of the same disorder among relatives (~10-fold increase in children); and (d) comparable concordance rates for monozygotic and dizygotic twins with heritability estimates of 60-80%. The fact that both disorders are genetically complex with multiple genes operating in concert with nongenetic environmental factors has now gained consensus.

During recent decades, arguments in favor of a basic dichotomy were discussed along the subsequent criteria:

  1. differential clinical phenomenology and long-term course,

  2. differential etiology (particularly family history),

  3. differential biological correlates, and

  4. differential treatment response (not discussed here).

Evidence was compiled over decades so that the diagnostic split is supported by criteria (1)-(4). A vast majority of phenomenological long-term follow-ups and family and twin studies were interpreted in favor of Kraepelin's dichotomy. New methodological approaches, however, opened new perspectives on this classical issue challenging a strict dichotomy.[1] In line with this tendency, treatment for both disorders became more similar (but will not be discussed here).


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