Central neurocircuitry associated with emesis

Hornby, Pamela J.

doi:10.1016/s0002-9343(01)00849-x

Cited by 359 publications

(254 citation statements)

References 42 publications

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“…However, there is some evidence from drug‐induced AP syndrome 3. We emphasize the importance of a multimodal combinational therapy targeting the CTZ2: besides 5‐HT3‐receptor antagonists with major effects on peripheral vagal afferents, NK1R‐receptor antagonists are effective and well‐established antiemetic agents acting in the brainstem. Δ9‐tetrahydrocannabinol is likewise reported to target emetic brainstem centers.…”

Section: Discussionmentioning

confidence: 93%

“…Area postrema (AP) syndrome is characterized by intractable nausea, emesis, and singultus1 caused by various mechanisms involving the AP and nearby brainstem structures harboring the chemoreceptor trigger zone (CTZ) of the „vomiting center” that receives input from the abdominal vagus,2 vestibular region, higher cortical and thalamic centers, and chemoreceptors of the AP 3. Belonging to the sensory circumventricular organs,4 the AP fulfills an exclusive function in chemotactic sensing between the central nervous system (CNS) and the blood stream with the blood–brain barrier (BBB) being replaced by specialized capillaries 4, 5 permeable to certain substances 6.…”

Section: Introductionmentioning

confidence: 99%

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Area postrema syndrome as frequent feature of Bickerstaff brainstem encephalitis

Zeiner

Brandhofe

Müller–Eschner

et al. 2018

Ann Clin Transl Neurol

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ObjectiveArea postrema (AP) syndrome (defined as: nausea and/or emesis and/or singultus at onset of brainstem dysfunction) comprises complex pathophysiologic mechanisms triggered by different entities. The first objective was to assess the frequency of AP syndrome as a clinical feature in brainstem encephalitis (BE). Finding an especially high prevalence of AP syndrome in Bickerstaff brainstem encephalitis (BBE), we also analyzed the frequency of AP syndrome in other autoimmune diseases with anti‐ganglioside antibodies (Guillain–Barré syndrome (GBS) and its variants).MethodsWe systematically evaluated the prevalence of AP syndrome in BE in all patients treated at our university hospital during a 15‐year period. In a second step, BBE patients were compared to GBS and Miller Fisher syndrome (MFS) patients as clinical subtypes of a disease continuum without brainstem dysfunction.ResultsWe found AP syndrome in 8 of 21 BE patients, including 3 of 7 BBE and in 4 of 112 GBS/MFS patients. AP syndrome was as a frequent but under‐recognized feature of BE with a significant impact on patients’ well being.InterpretationManifestation of AP syndrome in BBE but also in GBS and its subtypes point toward a role of autoimmune antibodies that should be investigated in future studies. Considerable misdiagnosis or nonrecognition complicates diagnostic and therapeutic management. Therefore, AP syndrome should be considered in any episode of otherwise unexplained nausea, emesis, or singultus.

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Section: Discussionmentioning

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Area postrema syndrome as frequent feature of Bickerstaff brainstem encephalitis

Zeiner

Brandhofe

Müller–Eschner

et al. 2018

Ann Clin Transl Neurol

View full text Add to dashboard Cite

show abstract

“…More recent studies indicate that multiple brain stem sites mediate the act of vomiting (or emesis) and that no isolated centre exists. 10,11 The sites comprise groups of neurons that are spread throughout the medulla oblongata and the hindbrain. 10 The neurons are believed to be activated by a central pattern generator which coordinates the sequence of various autonomic neural changes that are associated with vomiting.…”

Section: Discussionmentioning

confidence: 99%

“…10,11 The sites comprise groups of neurons that are spread throughout the medulla oblongata and the hindbrain. 10 The neurons are believed to be activated by a central pattern generator which coordinates the sequence of various autonomic neural changes that are associated with vomiting. 10,11 Thus the hindbrain neurocircuitry of neurons controlling vomiting is closely linked to nuclei within the brain stem controlling vasomotor, respiratory, salivary, vestibular and cardiac activity.…”

Section: Discussionmentioning

confidence: 99%

“…10 The neurons are believed to be activated by a central pattern generator which coordinates the sequence of various autonomic neural changes that are associated with vomiting. 10,11 Thus the hindbrain neurocircuitry of neurons controlling vomiting is closely linked to nuclei within the brain stem controlling vasomotor, respiratory, salivary, vestibular and cardiac activity. The neurons receive impulses via the auricular (VIII), glossopharyngal (IX) and vagal (X) cranial nerves from the internal ear, the pharynx, the tongue, the palate, the oesophagus and the stomach.…”

Section: Discussionmentioning

confidence: 99%

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The use of acupuncture in controlling the gag reflex in patients requiring an upper alginate impression: an audit

Rosted

Bundgaard²,

Fiske

et al. 2006

Br Dent J

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The pathophysiology, incidence, impact, and treatment of opioid‐induced nausea and vomiting

Mallick-Searle

Fillman

2017

Journal of the American Association of Nurse Practitioners

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Purpose Opioid medications are integral in managing acute moderate‐to‐severe pain. Opioid analgesics bind to μ (mu), κ (kappa), or δ (delta) opioid receptors in the brain, spinal cord, and digestive tract. However, opioids cause adverse effects that may interfere with their therapeutic use. Some adverse effects wane over time, but patients using opioids for acute pain struggle with opioid‐induced nausea and vomiting (OINV) the entire time they take the opioid. This article discusses the underlying mechanisms, clinical implications, and treatment strategies of OINV. Data sources Systematic search and review of Medline, PubMed, and Google Scholar for articles relating to OINV. In addition, package inserts provided pharmacologic data and dose recommendations as needed. Conclusions Research suggests approximately 40% of patients may experience nausea and 15%–25% of patients may experience vomiting after opioid administration. Nausea often precedes vomiting, although they can occur separately. Many patients receiving opioids rate the nausea and vomiting as worse than their pain. Nausea and vomiting can lead to complications including electrolyte imbalances, malnutrition, and volume depletion, and can also negatively affect quality of life and postoperative recovery. Implications for practice There are several medications that can be used to treat OINV including serotonin receptor antagonists, dopamine receptor antagonists, and neurokinin‐1 receptor antagonists. Healthcare providers should be proactive about discussing OINV with patients, as this may improve patient outcomes and pain relief.

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Central neurocircuitry associated with emesis

Cited by 359 publications

References 42 publications

Area postrema syndrome as frequent feature of Bickerstaff brainstem encephalitis

Area postrema syndrome as frequent feature of Bickerstaff brainstem encephalitis

The use of acupuncture in controlling the gag reflex in patients requiring an upper alginate impression: an audit

The pathophysiology, incidence, impact, and treatment of opioid‐induced nausea and vomiting

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