John KEESEY¹ and Johan AARLI^2
1Department of neurology, UCLA, Los Angeles, California, USA.  jkeesey AT ucla.edu
²Department of Neurology, University of Bergen, Norway.  JohanAarli AT neuro.uib.no

From the first descriptions of myasthenia gravis (MG) in the late 19th century, speculation about the cause of MG has centered on the possibility of some curare-like factor circulating in the blood.  The transfer of transient myasthenic symptoms for a myasthenic mother to her newborn reinforced this speculation.  However, it was not until 1960, when William Nastuk and co-workers noted that serum complement correlated with the clinical course in MG, and Arthur Strauss and colleagues described anti-skeletal-muscle antibodies in the sera of some MG patients, that a paradigm shift occurred from prior exclusive focus on the neuromuscular junction to a broader consideration of the relevance of immunological mechanisms in myasthenia.  These findings coincided with an even greater scientific revolution pioneered by Macfarlane Burnet towards cell-mediated and away from chemical immunology.  The dominant immunological question of the decade 1955-1965, however, was whether human autoimmune diseases actually existed.  During the next decade, 1965-1975, various diseases were accepted as being autoimmune in character, and although comparatively rare, MG became prominent among them because of a known antigen, the acetylcholine receptor, and an excellent experimental model.

12th Annual Meeting of the International Society for the History of the Neurosciences   (ISHN)
Los Angeles, California, USA, 19-23 June 2007