**2. Etiology of CIPN**

In healthy individuals, peripheral and central nervous system pain pathways function in a protective and adaptive manner [12]. The transduction, conduction, and transmission of nociceptor activity involve these pathways when carrying out activity within the cell. Whether induced by cancer or its treatments, damage to these pathways can result in neuropathic pain [13]. Discontinuation of treatment can result in the development of acute and chronic neurotoxic effects, and these effects can be seen immediately or within weeks or months after discontinuation. Symptoms seen immediately following the first course of treatment can often be contributed to vincristine and oxaliplatin-based regimens. Though both regimens typical‐ ly produce symptoms immediately following treatment, these symptoms vary between treatments. Vincristine use typically involves the cranial nerve and can lead to symptoms such as seizures, quadriparesis, and numbness. In contrast, oxaliplatin use often produces acute sensory symptoms seen in the mouth or throat that can be intensified by exposure to cold [14]. Regimens that do not present symptoms for up to several weeks after the final treatment may induce a length-dependent neuropathy on small fibers [15].

Incidence of CIPN is estimated to range anywhere from 10 to 100%, depending on the antineoplastic agent, dose, and other factors as presented by the patient [16]. Patients previ‐ ously affected by diabetes, alcoholism, or inherited neuropathies may be at an increased risk for CIPN [1, 16]. Clinical diagnosis of CIPN is complex, as there is often more than one contributing mechanism [17]. Therefore, testing is multi-faceted and includes neurological examination, quantitative sensory testing, nerve conduction studies, and toxicity grading. Positive symptoms include hypersensitivity to innoculous and noxious stimuli, such as gentle and/or blunt pressure and pinprick [18, 19].
