Local injection of physostigmine 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 lies in the sympathetic nerves of the affected area and that non‐dermatomally distributed vitiligo has its primary disturbance in the melanocyte itself, where an autoimmune mechanism is suspect. Results of therapy supported this hypothesis by showing that topical corticosteroid is effective only in the latter, while the former reacts to oral nialamide. It is proposed that non‐dermatomally distributed vitiligo be referred to as Type A and dermatomally distributed vitiligo as Type B.