Chronic Pain and Neuropathy Following Adjuvant Chemotherapy.

Objective: To determine symptoms and characteristics of chronic sensory neuropathy in patients treated with oxaliplatin and docetaxel, including patterns of somatosensory abnormalities, pain descriptors, and psychological functioning. Design: A retrospective cross-sectional study. Setting: A chronic pain research center. Subjects: Thirty-eight patients with chronic peripheral pain and/or dysesthesia following chemotherapy. Methods: Sensory profiles, psychological functioning, and quality of life were assessed using standardized questionnaires. In addition, standardized quantitative sensory testing and nerve conduction studies were carried out. Results: The sensory profiles and clinical symptoms were very similar in the two groups. Pricking, numbness, and burning were common descriptors in both groups, and the predominant finding was sensory loss to A beta-mediated sensory modalities with decreased mechanical and vibration detection thresholds. A high frequency of abnormalities in thermal sensory limen and the presence of paradoxical heat sensation seem to be sensitive markers of small fiber loss. Both groups had mainly sensory, axonal large fiber or mixed fiber polyneuropathy, which tended to be most severe in the oxaliplatin group. Conclusions: Both oxaliplatin-induced and docetaxel-induced polyneuropathies represent a significant problem that affects the daily life of the patients. Our results, defining the somatosensory phenotype, can improve the understanding of the pathophysiological mechanisms useful for future studies in the tailored treatment of prevention of chemotherapy-induced peripheral neuropathy and pain.

Differential effects of a 5% lidocaine medicated patch in peripheral nerve injury.

INTRODUCTION: We examined the effect of topical lidocaine on the function of small and large fibers in patients with peripheral neuropathic pain due to traumatic or postoperative nerve injury. METHODS: In an open-label study, 24 patients were treated with a 5% lidocaine patch for up to 12 weeks. We recorded contact heat evoked potentials (CHEPs) and performed quantitative sensory testing (QST) before and after treatment with the contralateral side as control. RESULTS: Twenty-one patients (mean age 47.6 ± 13.5 years) completed the study. Lidocaine increased cold pain threshold (P = 0.04) and reduced CHEP amplitude (P = 0.007) with no effect on other QST parameters. Patients responding to treatment had less cold detection deficit on the affected side and had a larger increase in cold pain detection threshold following treatment than nonresponders. CONCLUSIONS: Controlled trials are warranted to further understand the mechanisms mediating the effects of topical lidocaine.

Cutaneous noradrenaline measured by microdialysis in complex regional pain syndrome during whole-body cooling and heating.

Complex regional pain syndrome (CRPS) is characterised by autonomic, sensory, and motor disturbances. The underlying mechanisms of the autonomic changes in CPRS are unknown. However, it has been postulated that sympathetic inhibition in the acute phase with locally reduced levels of noradrenaline is followed by an up-regulation of alpha-adrenoceptors in chronic CRPS leading to denervation supersensitivity to catecholamines. This exploratory study examined the effect of cutaneous sympathetic activation and inhibition on cutaneous noradrenaline release, vascular reactivity, and pain in CRPS patients and in healthy volunteers. Seven patients and nine controls completed whole-body cooling (sympathetic activation) and heating (sympathetic inhibition) induced by a whole-body thermal suit with simultaneous measurement of the skin temperature, skin blood flow, and release of dermal noradrenaline. CRPS pain and the perceived skin temperature were measured every 5 min during thermal exposure, while noradrenaline was determined from cutaneous microdialysate collected every 20 min throughout the study period. Cooling induced peripheral sympathetic activation in patients and controls with significant increases in dermal noradrenaline, vasoconstriction, and reduction in skin temperature. The main findings were that the noradrenaline response did not differ between patients and controls or between the CRPS hand and the contralateral unaffected hand, suggesting that the evoked noradrenaline release from the cutaneous sympathetic postganglionic fibres is preserved in chronic CRPS patients.

Pharmacology and treatment of neuropathic pains.

PURPOSE OF REVIEW: This review briefly discusses the definition and clinical presentation of neuropathic pain and highlights recent advances in the treatment of neuropathic pain. RECENT FINDINGS: Recent publications have confirmed the efficacy of tricyclic antidepressants, gabapentin, pregabalin, opioids, and tramadol for various neuropathic pain conditions. Selective serotonin noradrenaline reuptake inhibitors have been found to reduce pain in painful neuropathy. The new anticonvulsant lacosamide may have some effect in painful polyneuropathy, whereas levetiracetam has failed to relieve postmastectomy and spinal cord injury pain. The role of the old anticonvulsant phenytoin is still unsettled. A recent trial has found an effect of cannabinoids also in peripheral neuropathic pain. Various topical treatments such as topical lidocaine, topically applied capsaicin in high concentrations (8%), and botulinum toxin have recently been shown to have a pain-relieving effect in various peripheral neuropathic pain conditions. Spinal cord and transcranial magnetic stimulation are stimulation therapies with some evidence for efficacy. SUMMARY: Treating neuropathic pain remains a great challenge, and the treatment has to be individualized to the single patient, taking into account side effects, pain type, comorbidities, and drug interactions.