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Related Concept Videos

Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists01:28

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Neurokinin 1 (NK1) receptors are distributed across the GI tract, vagal afferents, and key CNS regions including the central vomiting center and chemoreceptor trigger zone (CTZ) Chemotherapy agents stimulate enterochromaffin cells in the gastrointestinal (GI) tract to release large amounts of substance P (SP). SP is a neuropeptide released by specific sensory nerves in response to many different stressors, including those in the GI mucosa affected by chemotherapy.  SP binds and activates...
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Chemotherapy-Induced Nausea and Vomiting: Dopamine Receptor Antagonists01:29

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Dopamine receptor antagonists, also known as antipsychotic agents, are critical in managing chemotherapy-induced vomiting. These antiemetic agents block dopamine receptors in the chemoreceptor trigger zone (CTZ), inhibiting signal transmission to the vomiting center. Antipsychotic agents encompass phenothiazines (PTZ), butyrophenones, benzamides, and thienobenzodiazepines (Zyprexa), which are utilized for their antiemetic and sedative properties.
Phenothiazines, such as prochlorperazine...
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Chemotherapy-Induced Nausea and Vomiting: 5-HT3 Receptor Antagonists01:27

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5-HT3 receptor antagonists, such as dolasetron, granisetron (Kytril), ondansetron (Zofran), and palonosetron (Axoli), are crucial in managing chemotherapy-induced nausea and vomiting (CINV) and postoperative nausea. These drugs selectively block 5-HT3 receptors in the visceral vagal and spinal afferent nerves, chemoreceptor trigger zone, and the vomiting center. They have a rapid onset of action and can be given as a single dose before chemotherapy. Ondansetron and granisetron, in particular,...
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Chemotherapy-Induced Nausea and Vomiting: Cannabinoids01:21

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Tetrahydrocannabinol (THC) is a phytocannabinoid that primarily interacts with the CB1 receptor, a type of G protein-coupled receptor (GPCR) predominantly in and around the chemoreceptor trigger zone (CTZ) and emetic center. THC also blocks the serotonin receptor activity in the dorsal vagal complex (DVC) by inhibiting serotonin release. THC exerts its anti-emetic effects through these interactions, which are beneficial for patients undergoing chemotherapy.
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Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
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Cancer therapies are various modes of treatment, such as surgery, radiation therapy, and chemotherapy that are administered to cancer patients.
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Updated: Oct 22, 2025

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity
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Chemotherapy and peripheral neuropathy.

Tiffany Li1, David Mizrahi2,3, David Goldstein2

  • 1Faculty of Medicine and Health, School of Medical Sciences, Brain and Mind Centre, The University of Sydney, CamperdownSydney, NSW, 2050, Australia.

Neurological Sciences : Official Journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
|August 26, 2021
PubMed
Summary
This summary is machine-generated.

Chemotherapy-induced peripheral neurotoxicity (CIPN) significantly impacts cancer survivors. This review details CIPN

Keywords:
Chemotherapy-induced peripheral neuropathyFeaturesMechanismsPreventionRisk factorsTreatment

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Area of Science:

  • Oncology
  • Neuroscience
  • Pharmacology

Background:

  • Chemotherapy-induced peripheral neurotoxicity (CIPN) is a significant dose-limiting side effect of numerous anti-cancer drugs.
  • CIPN symptoms can persist long after treatment, diminishing survivors' quality of life and functional capacity.
  • Current management often relies on dose reduction, posing a challenge in balancing treatment efficacy with neurotoxicity.

Purpose of the Study:

  • To review the clinical presentations, signs, symptoms, and long-term outcomes of CIPN across various neurotoxic anti-cancer drug classes.
  • To update knowledge on proposed mechanisms of nerve damage and identify clinical and genetic risk factors for CIPN.
  • To examine current research, clinical trials, and consensus recommendations for CIPN prevention and management.

Main Methods:

  • Literature review of clinical presentations, mechanisms, risk factors, and treatment strategies for CIPN.
  • Analysis of data from current clinical trials and consensus guidelines on CIPN management.

Main Results:

  • Detailed examination of CIPN clinical manifestations associated with taxanes, platinums, and other neurotoxic agents.
  • Updated insights into the underlying mechanisms of neurotoxicity and identified clinical/genetic predispositions.
  • Overview of emerging research and established recommendations for managing and preventing CIPN.

Conclusions:

  • Effective management of CIPN requires a comprehensive understanding of its varied presentations and risk factors.
  • Ongoing research and clinical trials are crucial for developing better strategies to prevent and treat CIPN.
  • Balancing anti-cancer treatment intensity with the risk of long-term neurotoxicity remains a critical clinical challenge.