DSM-IV characterizes psychotic disorders as those that feature delusions or prominent hallucinations, possibly without individual insight into their pathological nature, possibly accompanied by other positive symptoms (e.g. disorganized speech, grossly disorganized or catatonic behavior). DSM-IV emphasizes it groups psychotic disorders together “for convenience” even though they may not share a common etiology. I previously have advocated a hybrid bio-psychological model to explain personality disorders (such as BPD) and (to a lesser extent) addiction disorders (such as substance abuse). However with psychotic disorders it seems clear a biological model has considerably more diagnostic utility and clinical efficacy. The reason why is because psychotic disorders involve substantial alterations to brain chemistry.
More than many other mental disorders schizophrenia has been subject to cultural interpretation. As DSM-IV admits ideas that may appear to be delusional in one culture (e.g. sorcery and witchcraft) may be commonly held in another. In some cultures visual or auditory hallucinations with a religious content may be part of normal religious experience. These wide discrepancies and variations of interpretation of symptoms suggest any explanation based on purely cognitive-psychological or socio-psychological causes is likely to be invalid.
Heritability. The DSM-IV section on schizophrenia is unusually detailed. Unlike other DSM-IV discussions it summarizes considerable work that has been done on schizophrenia’s etiology. First-degree biological relatives of individuals with schizophrenia are 10x more at risk than the general population and concordance rates are higher in monozygotic twins than in dizygotic ones. Adoptive relatives have no increased risk whereas biological relatives do. Heritability and genetic inter-relationships of neurocognitive traits are factors supporting their diagnostic use (Husted et al., 2009).
Neurochemistry. Although it has undergone substantial modification over the years the most prevalent view is that dopamine and dopaminergic mechanisms are central to schizophrenia (there are over 6,700 peer-reviewed articles since 1991 on this topic) (Howes & Kapur, 2009). The most effective treatment for schizophrenia is with DA D2 receptor blockers suggesting a hyperdopamine basis. Glutamate agonists also are effective to treat schizophrenia suggesting it also may be based on hypoglutamate states (Seeman, 2009).
Brain defects or injury. From the standpoint of structural neuroimaging the primary findings are enlargement of the lateral ventricles and decreased brain tissue such as widened cortical sulci and decreased volumes of gray and white matter, primarily in the temporal lobe. Others include decreased thalamic volume; increased basal ganglia size; and large cavum septum pellucidi. From the standpoint of in vivo functional brain imaging the primary finding is hypofrontality, which is directly correlated with low CSF dopamine metabolite levels (Batts, 2009). Schizophrenic patients show significant dysregulation between the excitatory (amygdala) and inhibitory (prefrontal) limbic regions (Radulescu & Mujica, 2008).
Infections, prenatal damage, nutrition, toxins. Epidemiological evidence indicates that prenatal nutritional deprivation increases the risk of schizophrenia. A recent study evaluated animal models and concluded prenatal protein deficiencies not only enhance risk for schizophrenia in humans but also may have implications for developmental processes leading to differential sensitivity to substance abuse (Palmer et al., 2008).
Batts, S. (2009). “Brain Lesions and their Implications in Criminal Responsibility.” Behavioral Sciences & the Law, 27(2), 261 – 272.
Howes, O. & Kapur, S. (2009). “The Dopamine Hypothesis of Schizophrenia: Version III – The Final Common Pathway.” Schizophrenia Bulletin (Advance access published 26 Mar. 2009).
Husted, J., Lim, S., Chow, E., Greenwood, C. & Bassett, A. (2009). “Heritability of neurocognitive traits in familial schizophrenia.” American J. of Medical Genetics – Neuropsychiatric Genetics (29 Jan. 2009).
Palmer, A., Brown, A., Keegan, D., Siska, L., Susser, E., Rotrosen, J. & Butler, P. (2008). “Prenatal protein deprivation alters dopamine-mediated behaviors and dopaminergic and glutamatergic receptor binding.” Brain Research, 1237, 62 – 74.
Radulescu, A. & Mujica-Parodi, L. (2008). “A Systems Approach to Prefrontal-Limbic Dysregulation in Schizophrenia.” Neuropsychobiology, 57(4), 206 – 216.
Seeman, P. (2009). “Glutamate and dopamine components in schizophrenia.” J. Psychiatry Neurosci., 34(2), 143 – 149.