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Neurogenic bladder (NB), also known as neurogenic lower urinary tract dysfunction, due to central and/ or peripheral nervous system diseases, is one of the most challenging problems in urology. Various disorders or injuries (e.g., stroke, Parkinson’s disease, multiple sclerosis, spinal cord injury) affecting the nervous system may cause chronic bladder dysfunction, whose type depends on central or peripheral nervous system damage level and intensity. The bladder can become underactive (not emptying completely) or overactive (emptying too frequently/ quickly), with urethral sphincter deficiency (evoking incontinence) or overactivity (leading to dyssynergia with partial or complete urinary retention). The pattern of specific dysfunction following neurological disorder is determined by the site and the nature of the lesion [1]. Whereas brain lesions and those above the pontine micturition center typically lead to detrusor overactivity, those below the pons and above the sacral spinal cord may additionally result in detrusor-sphincter dyssynergia. Lesions located below the sacral spinal cord (infrasacral lesions and those involving peripheral innervation) typically present with detrusor underactivity, often with concomitant sphincter deficiency. In the day-to-day clinical practice of dermatology, physicians often consult patients with skin lesions caused by urogenital infections that may further involve the nervous system or are signs of disorders with neural involvement. The infection mechanism includes autoimmune reaction to peripheral nerves, roots and/or central neural pathways or spreading of the infection from cutaneous nerve endings to the corresponding dorsal root ganglia. This leads to alteration of bladder sensation, detrusor contractility, and detrusor-sphincter synergy [2]. The most common disorders that may result in neurogenic voiding dysfunctions with concomitant dermatological lesions include lumbosacral herpes zoster (varicella-zoster virus – VZV), genitourinary herpes simplex (herpes simplex virus – HSV), tabes dorsalis (Treponema pallidum), HTLV-1-associated infective dermatitis (human T cell lymphotropic virus type 1 – HTLV-1), and acquired immunodeficiency syndrome (AIDS, human immunodeficiency virus – HIV). It has been shown that up to one-quarter of VZVinfected individuals who present with involvement of lumbosacral dermatomes may have concomitant neurogenic lower urinary tract dysfunction [3, 4]. Those patients typically complain of urine retention (due to detrusor underactivity or detrusor-sphincter dyssynergia). Retention appears concurrently with or within a few days following the onset of the rash presented in a sacral dermatomal distribution, typically affecting one or more of adjacent S2, S3, or S4 areas [5]. The lesions can be either unilateral or bilateral. Similarly, urine retention is the most common urological finding in patients with genitourinary infection of HSV [6]. Nevertheless, clinicians should keep in mind that because of the specific rash distribution of HSV type 2 in the genital area, most cases of retention are due to severe dysuria caused by direct contact of urine with the blistering urethral mucosa. True neurogenic urinary retention in anogenital HSV infection is a rare finding and occurs in less than 1% of infected patients [6]. The onset of neurogenic dysfunction occurs 1–2 weeks after the onset of a vesicular and painful rash in the anogenital region. Fortunately, neurogenic voiding dysfunctions in both HSVand VZV-infected patients are transient and fully reversible, often within 4–8 weeks, even without dermatology-specific treatment [7, 8]. Micturition disturbances related to neurosyphilis had a high prevalence in the pre-penicillin era but improvements in medical care have made neurosyphilis a rare entity with neurological sequelae even less prevalent. However, in cases of neural involvement (particularly in immunodeficient patients) neurogenic bladder dysfunctions might occur and

Dermatologist and urologist? A neglected relationship in neurogenic voiding dysfunctions