As typically only 30% of patients respond to even the gold standard FDA approved treatments (Finnerup et al., 2010), identification of the pattern of mechanisms

present in an individual should be a useful approach for identifying patients more likely to respond to a particular treatment and establishing individualized pain treatment. The pattern of expression of pain-related sensory abnormalities, the individual sensory phenotype, should reveal clues of the underlying pathophysiological dysfunction. Since one specific symptom (e.g., burning pain) may be generated by several different underlying pathophysiological mechanisms (e.g., peripheral sensitization, gain of function EPZ-6438 order mutations in

Nav1.7, or ectopic activity due to alteration in HCN2), it is more likely that a specific constellation of many sensory symptoms and signs might Protein Tyrosine Kinase inhibitor better predict underlying mechanisms. Patient reported outcomes, as well as quantitative sensory testing, or a combination of both, are beginning to be used to analyze sensory profiles in neuropathic pain patients and distinct subgroups of patients can be detected who are characterized by different specific sensory profiles (Baron et al., 2009, Bouhassira et al., 2005 and Scholz et al., 2009). In a large group of patients with diabetic peripheral neuropathy and postherpetic neuralgia, a sensory profiling approach revealed five subgroups of patients with distinct pain-related sensory phenotypes (Baron et al., 2009). For example, patients who suffer from considerable burning Terminal deoxynucleotidyl transferase pain and paresthesias but

minimal mechanical allodynia and thermal hyperalgesia and who additionally show numbness as a prominent finding probably have sensory terminal deafferentation in the skin with little or no central sensitization. A length-dependent dying-back or atrophy of sensory terminals innervating the extremities together with ectopic activity in heat nociceptors, best explains these findings. Patients with spontaneous burning pain in combination with dynamic mechanical allodynia and minimal negative symptoms (no reduced thermal threshold), reflects the presence of relatively preserved and sensitized nociceptors in the skin together with central sensitization (Baron et al., 2009). A major goal is to identify the most relevant and discriminatory aspects of the pain phenotype that most robustly reflect different mechanisms or combinations of mechanisms.