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Introduction: Onychomadesis occurs when the nail plate separates from the nail matrix and nail bed, eventually leading to shedding of the nail. This condition has been attributed to viral infections, autoimmune disorders, drug side effects, and physical trauma. A subset of patients has a recurrent form of onychomadesis without a clear trigger; this phenomenon is not well characterized in the literature. Case Presentation: We present a case series of pediatric and adult patients with recurrent toenail onychomadesis in order to better characterize the disorder and explore possible etiologies, risk factors, and treatments. Discussion/Conclusion: For the cases herein, we propose microtrauma associated with footwear as the underlying etiology given the periodicity of nail shedding, exclusion of other etiological factors, and presence of predisposing risk factors in certain patients. Many patients saw improvement with application of urea 40% cream, suggesting this can be a valuable part of a treatment strategy, in addition to minimizing injury to involved digits.

Trichodynia refers to the painful sensation of the scalp related to the complaint of hair loss. Originally suggested to be distinguishing for telogen effluvium and related to hair loss activity and follicular inflammation, further studies have found trichodynia to be common in androgenetic alopecia as well and coexisting with psychopathologic findings. The respective studies failed to demonstrate correlations between trichodynia and quantifiable hair loss activity, nor histopathologic evidence for follicular inflammation. A symptomatic scalp is a frequent condition in specific dermatological conditions of the scalp. By definition of exclusion, we are not dealing with trichodynia in these cases. It is conceivable that neuropeptides are key players between the central nervous system and the skin immune and microvascular system. Such mechanisms would explain the noxious effects of both external stimuli and emotional distress in eliciting cutaneous nociception. Since we have begun to understand the diverse etiologies of trichodynia, and a single term does not measure up to this circumstance, it may be wiser to describe the condition depending on the type of scalp sensation and its specific disease association. Further studies are warranted into the neural/endothelial/follicular interactions both in hair growth and shedding and the psychosomatic diseases of the hair and scalp.