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Chemotherapy-Induced Neurotoxicity

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Methods of Cancer Diagnosis, Therapy, and Prognosis

Part of the book series: Methods of Cancer Diagnosis, Therapy and Prognosis ((HAYAT,volume 7))

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Abstract

Chemotherapy-induced neurotoxicity is a common and dose-limiting side effect of many cancer treatments. While other dose-limiting toxicities such as myelosupression and hypersensitivity reactions are largely amenable to treatment, chemotherapy-induced neurotoxicity remains a significant problem, with limited treatment options and no standardized diagnostic or management criteria. Receiving a full course of chemotherapy on schedule is a critical factor that determines patient survival. Neurotoxicity may necessitate changes to dosage level, scheduling or intensity, and thereby interfere with the ability to complete a full treatment regimen, even if therapy is proving effective.

With the majority of chemotherapies, the pathophysiological mechanisms of neurotoxicity remain unknown (Hausheer et al. 2006). Neurotoxicity may occur as a consequence of treatment with platinum agents (cisplatin, carboplatin, oxaliplatin), taxanes (paclitaxel, docetaxel) and vinca alkaloids (vincristine). Other therapies such as suramin, thalidomide, and bortezomib can also produce significant neurotoxicity (Quasthoff and Hartung 2002; Hausheer et al. 2006). Previous or coincident administration of neurotoxic chemotherapy or preexisting neuropathy may serve to accelerate the severity of symptoms (Chaudhry et al. 2003). While neuropathy may be regarded as an acceptable outcome if disease progression has been arrested, neurotoxicity becomes more problematic in the setting of adjuvant therapy.

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Abbreviations

CIPN:

chemotherapy-induced peripheral neuropathy

CMAP:

compound muscle action potential

CNS:

central nervous system

DRG:

dorsal root ganglia

ECOG:

Eastern Cooperative Onco­logy Group

EMG:

electromyography

EORTC:

European Organization for Research and Treatment of Cancer

FACT/GOG:

Functional Assessment of Cancer/Gynecologic Oncol­ogy Group

GST:

glutathione s-transferase genes

Ih :

hyperpolarization activated cation conductance

K +f :

fast potassium channels

K +s :

slow potassium channels

Na +p :

persistent sodium channels

Na +t :

transient sodium channels

NCI-CTC:

National Cancer Institute - Common Toxicity Criteria

NCI-CTCAE:

National Cancer Institute - Common Terminology Criteria for Adverse Events

NCS:

nerve conduction studies

OSNS:

Oxaliplatin Specific Neuro­toxicity Scale

PNS:

peripheral nervous system

QST:

quantitative sensory testing

RRP:

relative refractory period

SNAP:

sensory nerve action potential

VPT:

vibration perception threshold

WHO:

World Health Organization

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Acknowledgements.

The support of the National Health and Medical Research Council of Australia (Project grant 400938) and the Sydney Foundation for Medical Research are gratefully acknowledged.

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Correspondence to Susanna B. Park .

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Park, S.B., Kiernan, M.C. (2010). Chemotherapy-Induced Neurotoxicity. In: Hayat, M. (eds) Methods of Cancer Diagnosis, Therapy, and Prognosis. Methods of Cancer Diagnosis, Therapy and Prognosis, vol 7. Springer, Dordrecht. https://doi.org/10.1007/978-90-481-3186-0_8

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  • DOI: https://doi.org/10.1007/978-90-481-3186-0_8

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