Nausea and vomiting historical perspective: Difference between revisions
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* 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 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 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 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 tumor in the middle of the fourth ventricle was found at the postmortem examination, leaving the author curious about the absence of manifestations other than vomiting. | * 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 [[tumor]]in the middle of the [[fourth ventricle ]]was found at the postmortem examination, leaving the author curious about the absence of manifestations other than[[ vomiting]]. | ||
* Retzius produced the most important work on the macroscopic anatomy of the encephalon and he described a structure on the floor 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. | * Retzius produced the most important work on the macroscopic anatomy of the encephalon and he described a structure on the[[ floor 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. | ||
* 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 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 and cerebrospinal fluid, after observing dye granules deposited in the perivascular space, especially among ependymal cells | * In 1924, Wislocki and Putnam speculated about the [[postrema ]]region as an area of diffusion between blood and[[ cerebrospinal fluid]], after observing dye granules deposited in the perivascular space, especially among[[ ependymal cells]]. | ||
* In 1942, Dow and Berglund, in an article on the vascular patterns of multiple sclerosis lesions, also described the case of a 38-year-old woman with some of the symptoms involving incessant vomiting, and showing postmortem plaques on the pons and medulla oblongata. | * In 1942, Dow and Berglund, in an article on the vascular patterns of[[ multiple sclerosis ]]lesions, also described the case of a 38-year-old woman with some of the symptoms involving incessant[[ vomiting]], and showing postmortem plaques on the [[pons]] and[[ medulla 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 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 intractable hiccups, a symptom not reported within their clinical manifestations, relating to probable disinhibition of the hiccup reflex by the multiple sclerosis plaques. | * In 1979, McFarling and Susac13, reported on patients with [[multiple sclerosis]] with intractable[[ hiccups]], a symptom not reported within their clinical manifestations, relating to probable disinhibition of the hiccup reflex by the [[multiple sclerosis]]plaques. | ||
* 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 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. | * 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. | ||
==References== | ==References== | ||
Revision as of 01:52, 20 January 2021
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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.
- 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.