Neuropathy In Cancer Research Articles

Incidence and relative risk of peripheral neuropathy in cancer patients treated with eribulin: a meta-analysis.

BackgroundEribulin is a microtubule inhibitor, which is approved for the treatment of breast cancer. Peripheral neuropathy has been reported in the studies of eribulin, but the incidence and relative risk (RR) of eribulin-associated peripheral neuropathy varied greatly in cancer patients. The purpose of this meta-analysis was to determine the overall incidence and RR of eribulin-associated peripheral neuropathy in cancer patients.Materials and MethodsPubmed database and Embase and abstracts presented at the American Society of Clinical Oncology (ASCO) meetings were systematically reviewed for primary studies. Eligible studies included prospective clinical trials and expanded access programs of cancer patients treated with eribulin. Statistical analyses were performed to calculate the incidences, RRs, and 95% confidence intervals (CIs).ResultsAltogether, 4,849 patients from 19 clinical trials were selected for this meta-analysis. The incidences of all-grade and high-grade peripheral neuropathy were 27.5% (95% CI: 23.3–32.4%) and 4.7% (95% CI: 3.6–6.2%), respectively. The relative risks of peripheral neuropathy of eribulin compared to control were increased for all-grade (RR = 1.89, 95% CI: 1.10–3.25) but not statistically significant for high-grade (RR = 2.98, 95% CI: 0.71–12.42).ConclusionsThe use of eribulin is associated with an increased incidence of peripheral neuropathy. The RR is increased for all-grade peripheral neuropathy.

Neurophysiological and clinical outcomes in chemotherapy-induced neuropathy in cancer.

Chemotherapy induced peripheral neuropathy (CIPN) is a significant toxicity of cancer treatment, with the potential to affect long-term function and quality of life in cancer survivors. There remains a lack of consensus around optimal assessment techniques. While current approaches to CIPN assessment are focused on clinical grading scales, it is becoming increasingly evident that a more comprehensive multimodal assessment package is necessary to accurately characterise the impact of CIPN as well as gauge the utility of neuroprotective mechanisms. Neurophysiological techniques provide objective biomarkers and may enable early detection of toxicity while patient reported outcomes are necessary to determine the significance of symptoms to individual patients. In addition to providing an objective assessment, clinical neurophysiological techniques provide important insights into the contributory pathophysiological mechanisms of CIPN with different chemotherapy agents. There is a paucity of implementation of these techniques in the clinical trial setting. The present Review aims to facilitate the use of neurophysiological studies as part of comprehensive assessment packages for the monitoring of CIPN by summarising current understanding of neurophysiological changes that underlie the development of neuropathy, clinical presentations and patient reported outcomes as well as advantages and limitations of current techniques for the neurophysiological assessment of CIPN.

(112) Exploratory and confirmatory factor analysis of PROMIS pain quality version-2 dichotomous items

Pain quality descriptive measures are important outcome measures and may have a role in pain diagnosis and phenotyping. The objective of this study was to examine the factor structure of the revised PROMIS pain quality dichotomous item bank. Pain quality item bank data were collected on samples of patients with rheumatoid arthritis (n=314), osteoarthritis (n=106), fibromyalgia (n=228), cancer neuropathy (n=134), and diabetic neuropathy (n=181). The revised pain quality item bank contains 26 dichotomous items (yes/no). The total sample was randomly split into two subsamples. Exploratory factor analysis (EFA) was performed on one mixed diagnosis subsample (N=483), followed by confirmatory factor analysis (CFA) on the remaining mixed diagnosis subsample (N=480). The EFA resulted in 4 extracted factors [eigen-values: 16.236, 1.870, 1.574, 1.236; comparative fit index (CFI)=0.995; root mean square error of approximation (RMSEA)=0.033]. The factors were interpreted as intolerable/unbearable (7 items), worrying/horrible (9 items), annoying/uncomfortable (7 items), and nauseating (3 items). The CFA confirmed these 4 pain quality factors (CFI=0.973; RMSEA=0.07). We found evidence supporting meaningful pain quality descriptors based on the revised PROMIS pain quality item bank. Future research needs to evaluate whether the derived factor scores differentiate across chronic diseases and are useful for diagnosis or outcome evaluation.

Hypoxia-Inducible Factor 1 Regulates Heat and Cold Pain Sensitivity and Persistence

The present study assessed the functions of the transcription factor hypoxia-inducible factor (HIF) in sensory neurons in models of acute, inflammatory, ischemic, and neuropathic pain. The alpha subunit, HIF1α, was specifically deleted in neurons of the dorsal root ganglia by mating HIF1α(fl/fl) mice with SNScre mice. SNS-HIF1α(-/-) mice were more sensitive to noxious heat and cold pain stimulation than were HIF1α(fl/fl) control mice. They also showed heightened first-phase nociceptive responses in the formalin and capsaicin tests with increased numbers of cFos-positive neurons in the dorsal horn, and intensified hyperalgesia in early phases after paw inflammation and hind limb ischemia/reperfusion. The behavioral cold and heat pain hypersensitivity was explained by increased calcium fluxes after transient receptor potential channel activation in primary sensory neurons of SNS-HIF1α(-/-) mice and lowered electrical activation thresholds of sensory fibers. SNS-HIF1α(-/-) mice however, developed less neuropathic pain after sciatic nerve injury, which was associated with an abrogation of HIF1-mediated gene up-regulation. The results suggest that HIF1α is protective in terms of acute heat and cold pain but in case of ongoing activation in injured neurons, it may promote the development of neuropathic pain. The duality of HIF1 in pain regulation may have an impact on the side effects of drugs targeting HIF1, which are being developed, for example, as anticancer agents. Specifically, in patients with cancer neuropathy, however, temporary HIF1 inhibition might provide a welcome combination of growth and pain reduction.

NCCN Task Force Report: Management of Neuropathy in Cancer

Neuropathy is a common, often debilitating complication of cancer and its treatment. Effective management of this disorder depends on early diagnosis and an understanding of its underlying causes in the individual patient. In January 2009, NCCN gathered a multidisciplinary group to review the literature and discuss intervention strategies currently available to patients as well as areas that require research efforts. The task force, which comprised experts in anesthesiology, medical oncology, neurology, neuro-oncology, neurophysiology, nursing, pain management, and rehabilitation, was charged with the goal of outlining recommendations for the possible prevention, diagnosis, and management of neuropathy. This report documents the proceedings of this meeting with a general background on neuropathy and neuropathy in oncology, followed by discussions on challenges and research issues, evaluation criteria, and management of different symptoms associated with this disorder.