The 27 February didactic session covered the inflammation hypothesis of schizophrenia.
Excessive or misdirected inflammatory responses can cause symptoms of psychosis. There are numerous examples of autoimmune illnesses causing symptoms that closely resemble schizophrenia. It’s also clear that chronic inflammation is not only a risk factor for developing schizophrenia, but also can negatively impact the clinical course of people with schizophrenia.
An unresolved dilemma is whether inflammation is a contributing factor to schizophrenia – or whether “inflammatory psychosis” is a distinctly different illness that produces symptoms more or less identical to classically-defined schizophrenia.
Another unsettled question is the extent to which inflammation-reducing drugs are likely to help people with schizophrenia. If so, is this a benefit that can be expected by anyone with schizophrenia? Or would the benefit only apply to those with blood tests that show an inflamed state. These are important questions in light of numerous case reports of psychosis being caused by over-the-counter anti-inflammatory medications such as aspirin, indomethacin, ibuprofen, etc.