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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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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.
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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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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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Certain drugs can affect how neurotransmitters called catecholamines, are released or taken back up in the adrenergic neuron. They can have different effects on the body's sympathetic transmission. Reserpine, a natural compound found in the Rauwolfia shrub, blocks a transporter called vesicular monoamine transporter (VMAT), which leads to a buildup of catecholamines in the cell and reduces sympathetic transmission. Another drug called guanethidine works in multiple ways, including blocking...
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Antipsychotic Drugs: Therapeutic Uses and Side Effects01:21

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Antipsychotic drugs primarily block dopamine and serotonin receptors and cholinergic, adrenergic, and histaminergic receptors, thereby reducing hallucinations and delusions in conditions like schizophrenia. However, they can trigger unwanted extrapyramidal effects such as dystonias, Parkinson-like symptoms, and tardive dyskinesia.
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Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity
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[Anticancer Drugs and the Nervous System].

Toshio Fukutake1

  • 1Department of Neurology Kameda Medical Center.

Brain and Nerve = Shinkei Kenkyu No Shinpo
|December 28, 2020
PubMed
Summary

Anticancer drugs can cause disabling neurotoxicity affecting both central and peripheral nervous systems. Early recognition and management of this treatment-related neurotoxicity are crucial to prevent permanent patient injury.

Area of Science:

  • Neuroscience
  • Oncology
  • Pharmacology

Background:

  • Anticancer therapies, including chemotherapy, biologics, and targeted agents, are increasingly associated with neurotoxic side effects.
  • The rising incidence of neurotoxicity is linked to longer patient survival and complex, extended treatment regimens.
  • Understanding treatment-related neurotoxicity is vital for managing cancer patients.

Purpose of the Study:

  • To review the clinical features of neurotoxicity in the peripheral and central nervous systems caused by various anticancer drugs.
  • To highlight the importance of recognizing and managing treatment-related neurotoxicity in clinical practice.

Main Methods:

  • Literature review of clinical features of neurotoxicity from conventional cytotoxic chemotherapy, biologics, and targeted therapies.

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  • Exclusion of newer immunotherapies such as immune checkpoint inhibitors and chimeric antigen receptor T cells.

    • Main Results:

    • Anticancer drugs can lead to significant and disabling peripheral and central nervous system toxicities.
    • Neurologic complications are increasingly frequent due to improved cancer survival and combination therapies.
    • Prompt intervention, such as drug discontinuation or dose adjustment, can mitigate or prevent permanent neurologic damage.

    Conclusions:

    • Clinicians, particularly neurologists, must be aware of the spectrum of neurotoxicity associated with anticancer treatments.
    • Early identification and appropriate management of treatment-related neurotoxicity are essential for preserving neurological function in cancer patients.