ReviewBrain sciences2024
Centralizing the Knowledge and Interpretation of Pain in Chemotherapy-Induced Peripheral Neuropathy: A Paradigm Shift towards Brain-Centric Approaches.
Review in Brain sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed.
- Electroacupuncture Ameliorates Hyperalgesia and Anxiety-Like Behaviors in Chemotherapy-Induced Peripheral Neuropathy Mice Through Inhibition of Astrocyte-Mediated Neuronal Activation in the Anterior Cingulate Cortex.Journal of pain research · 2026Article
- Inhibition of Soluble Epoxide Hydrolase Prevents Docetaxel-Induced Painful Peripheral Neuropathy.International journal of molecular sciences · 2025Article
- The Power of Movement: How Exercise Influences Chemotherapy-Induced Peripheral Neuropathy.Biomedicines · 2025Review
- Transcranial magnetic stimulation measures of corticospinal excitability in Black and Hispanic/Latino people with painful peripheral neuropathy.Frontiers in human neuroscience · 2025Article
- Feasibility of trancutaneous auricular vagus nerve stimulation in Black and Hispanic/Latino people with peripheral neuropathy.Frontiers in pain research (Lausanne, Switzerland) · 2024Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chemotherapy-induced peripheral neuropathy (CIPN) is a side effect of cancer treatment, often linked with pain complaints. Patients report mechanical and thermal hypersensitivity that may emerge during chemotherapy treatment and may persist after cancer remission. Whereas the latter situation disturbs the quality of life, life itself may be endangered by the appearance of CIPN during cancer treatment. The causes of CIPN have almost entirely been ascribed to the neurotoxicity of chemotherapeutic drugs in the peripheral nervous system. However, the central consequences of peripheral neuropathy are starting to be unraveled, namely in the supraspinal pain modulatory system. Based on our interests and experience in the field, we undertook a review of the brain-centered alterations that may underpin pain in CIPN. The changes in the descending pain modulation in CIPN models along with the functional and connectivity abnormalities in the brain of CIPN patients are analyzed. A translational analysis of preclinical findings about descending pain regulation during CIPN is reviewed considering the main neurochemical systems (serotoninergic and noradrenergic) targeted in CIPN management in patients, namely by antidepressants. In conclusion, this review highlights the importance of studying supraspinal areas involved in descending pain modulation to understand the pathophysiology of CIPN, which will probably allow a more personalized and effective CIPN treatment in the future.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.