Nausea and vomiting historical perspective

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Overview

Historical perspective

Discovery

  • In 1830, Marshall Hall was the first to discover the reflex theory and the association between nervous mechanisms and the development of nausea and vomiting
  • In 1865, Gianuzzi speculated on the possible existence of a regulating center of the emetic reflex in the brain .
  • In 1881, Thumas, pointed to an area on the floor of the fourth ventricle in animals which, if damaged, made apomorphine’s emetic action impossible
  • In 1889, Clarke described a case of an 8-year-old boy with uncontrollable hiccups and vomiting. The outcome of the case was the death of the patient, and a tumorin the middle of the fourth ventricle was found at the postmortem examination, leaving the author curious about the absence of manifestations other thanvomiting.
  • Retzius produced the most important work on the macroscopic anatomy of the encephalon and he described a structure on thefloor of the fourth ventricle, adjacent to the nucleus of the solitary tract, named it as the area postrema (AP), in Latin meaning, the hindmost area. [1]
  • In 1906, Wilson in a descriptive work on the human bulb, mentioned the AP as being richly vascularized, as well as detailing histological aspects and pointing out the high density of neurons in area postrema.
  • In 1924, Wislocki and Putnam speculated about the postrema region as an area of diffusion between blood andcerebrospinal fluid, after observing dye granules deposited in the perivascular space, especially amongependymal cells.
  • In 1942, Dow and Berglund, in an article on the vascular patterns ofmultiple sclerosis lesions, also described the case of a 38-year-old woman with some of the symptoms involving incessantvomiting, and showing postmortem plaques on the pons andmedulla oblongata.
  • In 1951, Borison and Brizzee while studying the medulla oblongata of cats, identified the AP as a chemoreceptor zone sensitive to the vomiting reflex, integrating the hypothesis of the researchers of late 19 th century, and in 1974, Borison published a review article condensing the advances made by countless other researchers since the early 1950s, concluding that the AP acted primarily as a chemoreceptor trigger zone to the emetic response.
  • In 1979, McFarling and Susac13, reported on patients with multiple sclerosis with intractablehiccups, a symptom not reported within their clinical manifestations, relating to probable disinhibition of the hiccup reflex by the multiple sclerosisplaques.
  • In 1986, Leslie published a meticulous comparative study between several animal species and humans, detailing the microscopic ultrastructure of the AP, and demonstrating that it was an area of permeability of the blood-brain barrier serving as a zone of fine control of autonomic and neurochemical information.
  • In the 2000s, a profusion of papers correlated area postrema syndrome cases to neuromyelitis optica spectrum disorders, with AP in a central role as the target of anti-aquaporin 4 antibodies.[2]

References

  1. DE SOUZA, Thiago Ferreira Simões (2020). "A concise historical perspective of the area postrema structure and function". Arquivos de Neuro-Psiquiatria. 78 (2): 121–123. doi:10.1590/0004-282x20190118. ISSN 1678-4227.
  2. Sarikcioglu, Levent; Yildirim, Fatos Belgin (2008). "Area Postrema: One of the Terms Described by Magnus Gustaf Retzius". Journal of the History of the Neurosciences. 17 (1): 109–110. doi:10.1080/09647040701236578. ISSN 0964-704X.

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