Does schizophrenia exist?

Abstract

The question sounds rather strange, one hundred years after Kraeplin teased out dementia praecox (renamed Schizophrenia by Eugene Bleuler) and manic depressive insanity. Yet the title, borrowed from a recent Maudsley Discussion Paper [1], is more than mere rhetoric. As Kraeplin himself soon realised, the differentiation was a nosological artefact rather than a naturalistic entity, but it was hoped that once the specific neuropathological constellation underlying the disorder was found, the concept would become more concrete. More than a hundred years on, this has unfortunately not happened. The International Pilot Study of Schizophrenia (IPSS), demonstrated the cross-cultural comparability of epidemiological data [2], as well as a remarkably stable clinical picture [3] and lifetime prevalence rates of around 1% of schizophrenia across national boundaries [4, 5]. These data, however, are an index of reliability, rather than validity. Irreverent critics [6] have compared this to McDonald's hamburgers, which taste the same regardless of where you buy them. The same holds good for the Burger King product which is as reliable. This leaves the crucial issue of validity open and the consumer has only the vendors’ word that the product contains meat. Does it, really? Substitute McDonald with DSM and Burger King with ICD and the picture becomes clearer. The diagnosis of schizophrenia in both systems identifies individuals who are seriously unwell but who have little else in common. There is no evidence of a specific underlying brain disease [7]. Many patients have significant mood as well as psychotic symptoms [8], with the former often posing higher risk and requiring greater therapeutic effort [9]. Clinical features show a high degree of variability between individuals and within the same patient at different points of time [7]. The course and outcome of the disorder varies widely, and the consistently observed better prognosis, on five out of six course and outcome dimensions regardless of the acuity of onset, in developing countries [3] has not been satisfactorily explained, though several contextual, primarily psychosocial factors have been proposed [10]. There is accumulating evidence for shared genetic/environmental risk factors and neurobiological abnormalities between schizophrenia and bipolar disorder [11]. Imaging studies have failed to reveal any consistent patterns of brain pathology and while a recent computational morphometry study flagged some grey matter changes specific to schizophrenia, this finding was undermined by white matter abnormalities common to both schizophrenia and bipolar disorder [12].