. Author manuscript; available in PMC: 2020 Jun 1.

Published in final edited form as: Semin Oncol Nurs. 2019 Apr 30;35(3):253–260. doi: 10.1016/j.soncn.2019.04.006

Table 1.

Agents that cause chronic painful CIPN.

Drug Class	Specific Agents	Prominent Manifestations	Pain Incidence	Sensitization Mechanism
Proteasome inhibitors	Bortezomib	^*Neuropathic pain and allodynia^32,33 Hypoesthesia Loss of fine motor function Cramps^2,3	Up to 47%^3,34	TRPV, TRPA1, and NMDA receptor up-regulation Inflammation (cytokine release and macrophage infiltration) Altered enzyme activity (reductions in phosphoglycerate dehydrogenase and L-serine; protein kinase C → NMDA receptor upregulation and increased glutamate release)
Platinums	Oxaliplatin, cisplatin, carboplatin	Acute cold hyperalgesia (oxaliplatin alone) ^*Sensory Loss of vibration sensation and sensory ataxia	5%−50%^14,33,36	TRPV, TRPA1, and NMDA receptor upregulation Ion channel (sodium, calcium, and potassium) dysfunction
Taxanes	Paclitaxel, docetaxel	^* Sensory¹⁴ Muscle weakness	Up to 30%¹⁴	TRPV, TRPA1, and NMDA receptor upregulation Ion channel (sodium, calcium, and potassium) dysfunction Inflammation (cytokine release and macrophage infiltration)
Vinca alkaloids	Vincristine, vinblastine, vinorelbine, vindesine	^* Sensory and motor^29,37,38 Autonomic	11%−44%^29,39–41	Serotonin increase and channel upregulation
Thalidomides	Thalidomide, lenalidomide	^Autonomic⁴² ^Hypoesthesia^43,44	Uncommon⁴⁴	Inflammation (cytokine release, and macrophage infiltration)

Indicates the most prominent manifestations. Sensory refers primarily to numbness and tingling.

Abbreviations: NMDA, N-methyl-D-aspartate; TRP, transient receptor potential.