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

Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists

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 these...
Chemotherapy-Induced Nausea and Vomiting: Dopamine Receptor Antagonists01:29

Chemotherapy-Induced Nausea and Vomiting: Dopamine Receptor Antagonists

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 Antagonists

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: Cannabinoids

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.
Two synthetic agonists of THC,...
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Diabetic Neuropathy

DefinitionDiabetic neuropathy is nerve damage caused by long-standing diabetes mellitus. It results directly from prolonged high blood sugar levels.PathophysiologyThe pathophysiology of diabetic neuropathy involves both metabolic and vascular disturbances triggered by chronic hyperglycemia.Metabolic injury: Elevated glucose levels activate the polyol pathway within nerve cells, leading to the accumulation of sorbitol and fructose. This increases oxidative stress, disrupts normal nerve...
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Drug Toxicity: Dose-Dependent Reactions

Drug toxicities can be stratified into pharmacological, pathological, or genotoxic based on their mechanisms. The incidence and severity of these toxicities generally increase with the drug's concentration in the body and exposure time.Pharmacological toxicity is evident when the therapeutic effects of drugs overshoot into adverse reactions in a predictable, dose-dependent manner. Central nervous system (CNS) depression from barbiturates is a classic example, with effects escalating from...

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Updated: Jul 6, 2026

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity
07:42

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity

Published on: April 26, 2012

Chemotherapy-induced neuropathy.

Anthony J Windebank1, Wolfgang Grisold

  • 1Division of Neuroscience, Department of Neurology, Mayo Clinic College of Medicine, Rochester, MN 55905, USA. windebank.anthony@mayo.edu

Journal of the Peripheral Nervous System : JPNS
|March 19, 2008
PubMed
Summary
This summary is machine-generated.

Cancer therapy can cause toxic neuropathies, which are difficult to treat. Early diagnosis and management are crucial for improving patient quality of life, as preventative strategies are limited.

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Last Updated: Jul 6, 2026

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity
07:42

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity

Published on: April 26, 2012

Area of Science:

  • Neuroscience
  • Oncology
  • Pharmacology

Background:

  • Neurotoxic side effects are common in cancer therapy, second only to hematological toxicity.
  • Unlike hematological side effects, toxic neuropathies currently lack effective treatments or preventative strategies.
  • Diagnosis relies on clinical history, electrophysiological findings, and knowledge of specific neurotoxic agents.

Purpose of the Study:

  • To review the diagnosis, management, and prevention of chemotherapy-induced peripheral neuropathies (CIPN).
  • To highlight the challenges in managing neurotoxicity and the need for better supportive care strategies.

Main Methods:

  • Review of literature on chemotherapy-induced neurotoxicity.
  • Analysis of diagnostic approaches for toxic neuropathies.
  • Discussion of management strategies including pain control and physical therapy.

Main Results:

  • Toxic neuropathies are typically length-dependent, sensory, or sensorimotor, often presenting with pain.
  • Platinum compounds are unique in causing sensory ganglionopathy with potential "coasting" progression after treatment cessation.
  • Synergistic neurotoxicity from combination therapies and pre-existing neuropathies are significant concerns.

Conclusions:

  • Early identification and intervention are critical for managing toxic neuropathies in cancer patients.
  • Focus on symptomatic management, pain control, and physical therapy is essential for maintaining quality of life.
  • Further research into preventative measures and synergistic neurotoxicity is warranted.