Abstract
Local injection of physostigmine in humans revealed that dermatomally distributed vitiligo was associated with a dysfunction of the sympathetic nerves in the affected skin and that non-dermatomally distributed vitiligo was not. These observations led to the hypothesis that the primary disturbance of dermatomally distributed vitiligo lay in the sympathetic nerves of the affected area and that non-dermatomally distributed vitiligo had its primary disturbance in the melanocyte itself, where an autoimmune mechanism was suspect. Results of therapy supported this hypothesis by showing that topical corticosteroid was effective only in the latter, while the former reacted to oral nialamide. It was proposed that non-dermatomally distributed vitiligo be referred to as Type A and dermatomally distributed vitiligo as Type B.