LAUSR

because of the limited number of patients investigated in each study; thus, large scale studies are needed to answer this crucial question. Finally, pain in postherpetic neuralgia (PHN) has elements of an SFN in terms of severe burning often accompanied by allodynia. However, the PHN pain phenotype with its very localized presentation is distinct from SFN that typically affects distal extremities symmetrically—with known variations. The viral basis of disease pathophysiology per se is known in herpes zoster. However, it is still unclear why some of these patients develop pain and PHN, while others do not. This, together with the clinical phenotype, allows the categorization as small fiber pathology. The review article also underscores two points. First, those pathological findings on additional small fiber tests such as quantitative sensory testing or skin punch biopsy do not prove SFN or small fiber pathology. Second, the absence of pathological findings in such tests does not disprove small fiber impairment or diagnoses such as FMS. In particular, the strategy of investigating patients without obvious pathological findings with additional tests does teach us to consider the immense importance of clinical phenotypes and patients’ pain description when diagnosing SFN or small fiber pathology. Further research is needed to better understand the underlying mechanisms of small fiber degeneration and regeneration and dysfunction and to allow pathophysiological rather than clinical classification of damage to the small nerve fibers. Such a research program could open promising new avenues for mechanism-based analgesic treatment.