You’ve come a long way, baby. But maybe not long enough, according to Dr Rajiv Tandon, Professor of Psychiatry at the University of Florida College of Medicine and Chief of Psychiatric Services for North Florida/South Georgia Veterans Health System. Dr Tandon shared the evolution of schizophrenia diagnosis and highlighted the current status for attendees at the US Psychiatric and Mental Health Congress in Las Vegas.
Although the disease has been “recognized” for more than 100 years, we have only made a series of baby steps in understanding the etiology, pathology, and treatment of the disease, he said. Psychiatry has moved from very broad definitions, as was found in the DSM II, to extremely narrow definitions, as psychiatry created DSM III in reaction to DSM II. In the 1950s, the idea that “bad mothering” may cause schizophrenia became popular in response to Freud’s influences. With each new revision of the DSM, psychiatry committed to a bit more details in its etiology and pathology.
Starting in the 1980s, for instance, science recognized that genetics played an important role in schizophrenia, but nothing was known about the mode of transmission. In the 1990s, we learned genetics coupled with environment played a role in its etiology. Now, Tandon explained, we know that genetic factors are 60% to 80% liable for the disease. However, science still cannot point to a single or group of major genes responsible for such. On the other hand, he noted, research also demonstrated that some genes may have protective effects for developing schizophrenia. So while understanding of the genetic component has increased, there are still many unanswered questions.
Our understanding of the environmental factors associated with schizophrenia has also increased, Tandon said.1 The mother role comes up again, but instead of associating schizophrenia with mothers’ over adulation, now we know the concern is with second trimester insults and obstetric complications. Urbanization, migration (especially to a place where the person is very different from the new population), cannabis use (especially in youth), advanced paternal age, childhood abuse/trauma, and social marginalization also have been linked to increased schizophrenia risk.
Nonetheless, the exact neurobiological pathway to pathogenesis and how the various genetic and environmental factors interact still eludes psychiatry, Tandon said.
We’ve also seen advances in the understanding of pathophysiology. In the 1980s, it was understood that there was too much dopamine somewhere in the brain, Tandon explained. Those advances were a result of CT scans showing smaller brains and larger ventricular regions in patients with schizophrenia. By the 1990s, it became evident that too much dopamine in the mesolimbic circuit causes positive symptoms and too little dopamine in mesocortical circuit combined with ventricular enlargement caused the negative symptoms.
1. Tandon R, Keshavan MS, Nasrallah HA. Schizophrenia, “just the facts” what we know in 2008. Epidemiology and etiology. Schizophr Res. 2008;102(1-3).