The Role of the Nervous System in the Pathophysiology of Psoriasis: A Review of Cases of Psoriasis Remission or Improvement Following Denervation Injury

Abstract

As most efforts in the last decade have focused on the immunologic basis of inflammatory skin disease, there has been less emphasis on the role of the nervous system in the disease process of psoriasis. Evidence in support of the neurocutaneous pathway has come from observations of patients experiencing unilateral improvement and even complete remission following nerve damage in the affected dermatomal region. The aim of this review was to investigate the role of neuropeptides in the intricate pathophysiology of psoriasis. The PubMed database was searched for individual case reports or case series that reported clearance or significant improvement in psoriatic disease in patients following documented nerve injury. A total of 11 cases were found that reported improvement of psoriatic lesions in areas afflicted by central or peripheral nerve injury. The most common causes of denervation were inadvertent surgical interruption, cerebrovascular accident, and poliomyelitis. In four cases the patients eventually regained neurologic function, which was associated with a recurrence of skin lesions. In cases of permanent nerve damage, there was remission of psoriasis. The cases reported in the literature to date provide clinical evidence that absence of neural input leads to psoriasis improvement, suggesting a crucial role of the nervous system in the pathophysiology of psoriatic disease. In fact, neuropeptides such as nerve growth factor, substance P, calcitonin gene-related peptide, and vasoactive intestinal peptide may be important contributors of psoriatic disease and potential targets for future therapies.

Unilateral Remission of Psoriasis Associated with a Spinal Arteriovenous Malformation

“…To date, several case reports have described psoriatic lesions with acquired central or peripheral nerve damage that exhibited unilateral local clearance or improvement (2). Consistent with those clinical reports, another study using a murine model of psoriasis demonstrated that loss of cutaneous innervation via traumatic nerve injury resulted in reduction of the clinical symptoms of psoriasis (3).…”

What about physical contacts between epidermal keratinocytes and sensory neurons?

“…Identifying these mechanisms could shake up the established dogma regarding sensory perception as well as contribute to a better understanding of skin diseases with psychic participation, such as psoriasis. The existence of psoriasis remission or improvement following denervation injury could support this hypothesis …”

Neuropsychiatric comorbidity among adolescents with psoriasis

“…Upon secretion from nerve endings, NGF can bind to keratinocytes’ NGF receptors, thus promoting keratinocytes’ de‐differentiation and hyperproliferation . Furthermore, these mediators promote vasodilatation and innate and adaptive local neurocutaneous inflammation, which contribute to psoriasis pathogenesis . Additionally, higher concentrations of NGF, SP and CGRP are found in psoriasis lesions than in healthy skin …”