E Azimi1, E A Lerner, S B Elmariah. 1. Department of Dermatology, Cutaneous Biology Research Center, Massachusetts General Hospital and Harvard Medical School, Boston, MA, 02114, U.S.A.
Abstract
BACKGROUND: The contribution of the nervous system to inflammation in general and inflammatory skin disease in particular has been underappreciated. It is now apparent that an intact neural component is required for the conventional clinical manifestations of many inflammatory skin diseases. OBJECTIVES: To investigate the relationship between nerve damage and skin disease. METHODS: Previous individual reports since 1966 were collected systematically and the clinical observations described therein were placed within current concepts of neurogenic inflammation. RESULTS: We reviewed the literature and identified 23 cases of alterations in the appearance or distribution of skin disorders in patients with acquired central or peripheral neural damage or dysfunction. In 19 cases, near or complete resolution of pre-existing skin lesions occurred in areas directly or indirectly supplied by a subsequently injured nervous system. Exacerbation or new onset of skin lesions occurred in only four cases. The neural deficits described included damage within the peripheral or central nervous system resulting in pure sensory, pure motor or combined sensory and motor deficits. CONCLUSIONS: These cases highlight the importance of neural innervation and neurogenic inflammation in the development of inflammatory skin disease and prompt further examination of the use of neural blockade as an adjunctive therapy in the treatment of inflammatory dermatoses.
BACKGROUND: The contribution of the nervous system to inflammation in general and inflammatory skin disease in particular has been underappreciated. It is now apparent that an intact neural component is required for the conventional clinical manifestations of many inflammatory skin diseases. OBJECTIVES: To investigate the relationship between nerve damage and skin disease. METHODS: Previous individual reports since 1966 were collected systematically and the clinical observations described therein were placed within current concepts of neurogenic inflammation. RESULTS: We reviewed the literature and identified 23 cases of alterations in the appearance or distribution of skin disorders in patients with acquired central or peripheral neural damage or dysfunction. In 19 cases, near or complete resolution of pre-existing skin lesions occurred in areas directly or indirectly supplied by a subsequently injured nervous system. Exacerbation or new onset of skin lesions occurred in only four cases. The neural deficits described included damage within the peripheral or central nervous system resulting in pure sensory, pure motor or combined sensory and motor deficits. CONCLUSIONS: These cases highlight the importance of neural innervation and neurogenic inflammation in the development of inflammatory skin disease and prompt further examination of the use of neural blockade as an adjunctive therapy in the treatment of inflammatory dermatoses.