**1. Introduction**

Treating cancer requires an understanding of cellular kinetics [1]. DNA mutations that occur during DNA replication can aide in the development of cancer cells. Activation for DNA repair in a normal cell cycle uses checkpoints to facilitate the repair; however, checkpoint integrity is lost in tumor cells and DNA repair is bypassed [2]. The resulting mutations impact the regulatory mechanisms the restrict cell proliferation in a normal cell [3].

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The use of chemotherapeutic agents works by disrupting the cell cycle to prevent cell proliferation before it begins [4]. The negative of systemic chemotherapeutic agents is that normal cells, as well as malignant cells, are disrupted. This leads to untoward effects and longterm morbidities [4] that negatively impact functional ability and quality of life. Chemother‐ apy-induced peripheral neuropathy (CIPN) is the most common neurological side effect of chemotherapy [5]. This condition is characterized by damage to the nervous system that is a direct result of the medications associated with chemotherapy. Often, this damage to the central nervous system pain pathways results in neuropathic pain [6], frequently described as burning, paroxysmal, stabbing, or elective shock-like [7], accompanied by pins-and-needles sensations and itching. The presence and severity of neuropathic pain is often shown to be associated with impairments in walking, general activities, sleep, work, mood, enjoyment of life, and relationships with others [2, 8].

Little is known about the mechanisms responsible for the development of CIPN [4]. The peripheral toxicity involved with CIPN is specific to each chemotherapy drug class and appears to be dose and duration dependent. However, it can evolve even after a single-drug application [9]. The type and cause of neuropathy are dependent on the chemotherapy agent administered, with vincristine, paclitaxel, and cisplatin being the most neurotoxic [10].

Currently, prophylactic and symptomatic treatments have been ineffective because the neurobiology underpinning CIPN is not fully understood [11]. Thus, the purpose of this chapter was to outline the differences in treatment options available to patients with CIPN and analyze the benefits of exercise in the management of symptoms related to this disorder.
