Abstract
In the first part of the twentieth century, after his first highly successful work on experimental catatonia in collaboration with the Dutchman De Jong, Henri Baruk (1897–1999) developed his research on catatonigenic substances and the etiopathogenesis of schizophrenia. For him, one of the candidate substances is a neurotropic toxin extracted from an Escherichia coli. In addition to his laboratory research, Baruk reports clinical observations that allow him to confirm the hypothesis of catatonic syndromes by hepatic (biliary) poisoning. Continuing in this direction, he also describes cases of schizophrenia which he attributes the symptoms to an infection with E. coli and which seems to have been cured by an appropriate antibiotic treatment. These facts prompted Baruk challenged the uniqueness of the concept of schizophrenia. Throughout his career, he defended the interest of looking behind the psychotic manifestations, the possible biological causes, especially toxic and infectious. This approach was very controversial, even totally despised at the time, before progressing gradually to the rank of (pseudo) scientific curiosity disconnected from the daily clinical reality. But recent discoveries on the influence of the immune system, inflammation, digestive system, and especially the microbiota, on the nervous system, brain and mental state, necessarily question this observation, perhaps not so wacky…
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
