Sir,We read with great interest the article by Ravikumar et al. who report a case of an extensive psoriatic eruption selectively sparing the lower limb that was previously affected by poliomyelitis.[1] The authors attribute this particular distribution to Koebner phenomenon.[1] They hypothesize that friction and increased weight bearing on the polio-non-affected right lower limb may be the reasons for the preponderance of psoriatic lesions on that limb.[1] Although interesting, this hypothesis seems to be not thoroughly convincing. In fact, we think that a decreased local immune response due to the peripheral nerve damage might be responsible for the almost selective lack of psoriatic lesions in polio area. Our interest in this article was aroused by the possible relationship existing between neurological injuries and selective localization or, on the contrary, sparing of skin disorders on the injured areas. This association should not be limited to the fore-mentioned case, but it could be extended to further analogous clinical scenarios. In particular, in the latest years, we were mostly interested in this topic and observed a large and variegate group of cutaneous diseases, which selectively affected neurologically injured areas.[2] The most striking examples are cases of papillomatosis cutis lymphostatica on polio paraplegic area, recurrent blistering of the fingertips in carpal tunnel syndrome, unilateral bullous pemphigoid on hemiplegic side after cerebral stroke, and unilateral rosacea on facial palsy.[2] Although apparently different, the above-listed cases probably share a common pathogenic mechanism. In fact, in each case, the neurological damage, whichever the cause (polio paraplegic limb, carpal tunnel syndrome, hemiplegic cerebral stroke, facial palsy), could induce a local dysregulation in neuropeptide release.[2] This dysequilibrium would result into a regional cutaneous immune destabilization, in turn favoring the occurrence of opportunistic skin diseases selectively confined on neurologically damaged areas. This concept could be best explained by the overarching, fast-growing pathogenic theory of the immunocompromised cutaneous district (ICD),[34] which indicates a cutaneous site that, once it has previously been “marked” by a damaging clinical event, becomes prone to harboring an opportunistic skin disorder. In Ruocco's original description, ICD-inducing events included Wolf's isotopic postherpetic response, lymphedema, and otherwise damaging injuries (vaccination, radiation, burns, traumas).[3] Subsequently, the list of potentially inciting factors able to make a given cutaneous site an immunodestabilized one has progressively expanded, also including neurological injuries.[2] This immune alteration, depending on the neuropeptides each time involved, can be either defective or excessive.[45] In fact, while the selective localization of an immune-mediated skin disorder, such as bullous pemphigoid or rosacea, on a neurologically impaired area can be explained by a local activation of immunity, the selective sparing of polio area by the generalized psoriasis in the case presented by Ravikumar et al.,[1] could ensue from a local reduction of immunity. The reason why a similar injuring event could result in such opposite clinical consequences still remains obscure and further investigations are necessary to better clarify this knowledge gap. We are sure that the ICD pathogenic concept may be a good guidance for investigators to increasingly comprehend the complex pathomechanisms involved in these singular phenomena.