The belief that infectious organisms might be the cause of many mental diseases is not new. In the early decades of the twentieth century, between a quarter and a third of patients admitted to mental hospitals in industrialised countries were suffering from general paresis, a condition produced in the tertiary stage of syphilis.[26]
The discovery of penicillin, and its success in treating syphilis, has implanted a belief amongst some psychiatric researchers that an infectious cause and medical remedy can also be found for schizophrenia. Viral theories of aetiology are particularly attractive to some researchers because they can tie up a number of loose ends such as the perceived seasonality of schizophrenic births,[27] the difficulties some schizophrenic women are said to have in childbirth, the frequency of auditory hallucinations and an assumed genetic component of the disease.[28]
The viral theories are essentially of two types: those which postulate an active but undetected virus that directly affects the brain and gives rise to unusual psychological phenomena; and theories which postulate a past infection that, although no longer active, caused abnormalities in brain development. Retroviruses have been suggested as the likely culprit for the first type of possibility, but researchers have been unable to find any positive link between schizophrenia and this type of virus.[29] Borna disease was recently discounted as a virus that might be active in schizophrenics.[30]
One explanation for the second type of possibility is that schizophrenics might be part of a sub-population with special resistance to disease. Although the resistance itself may not be a factor in the development of schizophrenia, it might result in fetal vulnerability to hormonal disturbances during prenatal viral infection. This vulnerability might in turn lead to neurodevelopmental damage. It is further argued that if this were so then schizophrenia could be seen as a price that a population has to pay for surviving epidemics.[31]
Enthusiasm for the viral epidemic theory has recently focussed on polio. There are a number of attractive features to the polio theory—a claimed decrease in numbers of schizophrenics coinciding with the advent of polio vaccine, a higher number of winter births confirming the possibility of second trimester infection in summer months, when polio is most active, and a higher incidence of schizophrenia amongst immigrants to the United Kingdom whose countries of origin also have a higher incidence of polio. Once again it is postulated that prenatal infection with polio might cause developmental problems in the brain that do not emerge until sexual maturity.[32] But no significant evidence has been found yet to provide confirmation for the polio hypothesis.
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[26] Thomas Szasz, Schizophrenia: The Sacred Symbol of Psychiatry, p. 7.
[27] R. L. O’Reilly, ‘Viruses and Schizophrenia’, pp. 222–8.
[28] E. F. Torrey, ‘Viral-Anatomical Explanation of Schizophrenia’, pp. 15–18.
[29] M. A. Coggiano et al., ‘The Continued Search for Evidence of Retroviral Infection in Schizophrenic Patients’, pp. 243–7.
[30] J. A. Richt et al., ‘Failure to detect Borna disease virus infection in peripheral blood leukocytes from humans with psychiatric disorders’, pp. 174–8.
[31] G. Rubinstein, ‘Schizophrenia, Infection and Temperature. An Animal Model For Investigating Their Interrelationships’, pp. 95–102.
[32] R. F. Squires, ‘How a poliovirus might cause schizophrenia: a commentary on Eagles’ hypothesis’, pp. 647–56.