Nausea and vomiting historical perspective

Jump to navigation Jump to search

Nausea and vomiting Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Nausea and Vomiting from other Conditions

Epidemiology and Demographics

Risk Factors

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X Ray

CT

MRI

Echocardiography or Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Nausea and vomiting historical perspective On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Nausea and vomiting historical perspective

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Nausea and vomiting historical perspective

CDC on Nausea and vomiting historical perspective

Nausea and vomiting historical perspective in the news

Blogs on Nausea and vomiting historical perspective

Directions to Hospitals Treating Nausea and vomiting

Risk calculators and risk factors for Nausea and vomiting historical perspective

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 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.
  • 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 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 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 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

Template:WH Template:WS