Results suggest the consideration of impairment of QoL and functionality in addition to symptom intensity for treatment evaluation of chronic LBP. This can help to improve overall well-being of the patients and enhance efficacy in clinical pain trials and patient-centered treatment.

Completion of painDETECT was optional and therefore data was not available for all patients. Further studies for confirmation of these results are needed.

Patients with the same disease may suffer from completely different pain symptoms yet receive the same drug treatment. Several studies elucidate neuropathic pain and treatment response in human surrogate pain models. They show promising results toward a patient stratification according to the mechanisms underlying the pain, as reflected in their symptoms. Several promising new drugs produced negative study results in clinical phase III trials. However, retrospective analysis of treatment response based on baseline pain phenotyping could demonstrate positive results for certain subgroups of patients. Thus, a prospective classification of patients according to pain phenotype may play an increasingly important role in personalized treatment of neuropathic pain states. A recent prospective study using stratification based on pain-related sensory abnormalities confirmed the concept of personalized pharmacological treatment of neuropathic pain.

Cold hyperalgesia is a common side effect of oxaliplatin treatment; still, the pathophysiological and molecular mechanisms as well as the contribution of different primary afferent fiber systems are unclear. Therefore, patients with oxaliplatin-induced acute neuropathy with (n = 6) and without (n = 7) cold hyperalgesia were tested by applying a preferential blockade of peripheral myelinated A-fiber afferents in combination with quantitative sensory testing. Additionally, an interview-based questionnaire assessed the severity of symptoms and the impact on daily activities. Results indicate a deficit of cold perception in patients without cold hyperalgesia compared to patients with cold hyperalgesia prior to A-fiber blockade. In patients with cold hyperalgesia, a preferential blockade of A-fibers abolished cold hyperalgesia. This suggests that oxaliplatin-induced cold hyperalgesia is mediated by A-fibers and that a deficit in A-fiber function might prevent the development of cold hyperalgesia. The work supports findings in rodents and in human sural nerve biopsies indicating that oxaliplatin interferes with axonal ion conductance in intact A-fibers by sensitizing potassium and/or sodium channels. Drugs that act on these molecular targets might be of potential value to treat oxaliplatin-induced cold hyperalgesia.

To investigate sensory changes, physical function (pF), quality of life (QoL) and pain intensity of patients with osteoarthritis (OA) in the natural course of disease, and patients undergoing total joint replacement therapy (TJR) 31 (20 females, mean age 64.6 ± 10.4 years), patients with OA were investigated with questionnaires and quantitative sensory testing (QST) in the area of referred pain at the thigh at baseline and follow-up 22–49 weeks later; changes were analyzed separately for patients with (n = 13) and without TJR (n = 18). In patients without TJR pain intensity, pF, QoL did not improve, and increased pain sensitivity to cold and a stronger loss of detection were observed. In patients after TJR, however, a reduction in mechanical pain sensitivity and allodynia occurred in accordance with a reduction of pain intensity and improvement of functionality while QoL did not improve. Additionally, an increased sensitivity to heat pain and a more pronounced loss of mechanical detection could be observed in this group. TJR seems to stop peripheral pain input leading to a reduction of pain intensity and central sensitization, but surgery-induced sensory changes such as peripheral sensitization and loss of detection occur. Furthermore, TJR has favorable effects on pain intensity and functionality but not QoL.