Filler Christmas 2012: Yesterday’s World

An early British case of neuromyelitis optica (1850)

BMJ 2012; 345 doi: http://dx.doi.org/10.1136/bmj.e6430 (Published 17 December 2012) Cite this as: BMJ 2012;345:e6430
  1. Sven Jarius, neuroimmunologist,
  2. Brigitte Wildemann, head of division
  1. 1Division of Molecular Neuroimmunology, Department of Neurology, University of Heidelberg, Heidelberg, Germany
  1. sven.jarius{at}med.uni-heidelberg.de

The term neuromyelitis optica (Devic’s syndrome) refers to the co-occurrence of acute myelitis and optic neuritis. Regarded for many decades as a clinical variant of multiple sclerosis, neuromyelitis optica has only very recently been recognized as a disease in its own right with distinct pathogenesis, prognosis, and treatment.

While the history of classic multiple sclerosis has been studied extensively, little is known about the early history of neuromyelitis optica. Here we would like to draw readers’ attention to a now forgotten early British case, which appeared in 1850 in the precursor of the BMJ, the Provincial Medical and Surgical Journal, as part of a series of “Brief notes of medical cases,”1 thus predating Jacob August Lockhart Clarke’s case in the Lancet2 by 15 years and Eugene Devic’s and Fernaud Gault’s disease defining research on neuromyelitis optica by more than 40 years.3

The patient, a labourer aged 40 years at disease onset and “previously in good health,” was seized with a sensation “as if a tight band were encircling his waist” a few days after exposure to “cold and moisture.” This was accompanied by gradually increasing hypoesthesia and loss of power in both lower extremities, finally resulting in paraplegia. In addition, “automatic movements” of the legs occurred. Importantly, his eyesight, “which, prior to this attack, had been good,” gradually failed, culminating in complete and persisting amaurosis of the right eye and transient amaurosis of the left eye. Subsequently, the right arm was also subject to automatic movement. None of the applied treatments standard at that time—including purging; internal application of mercury, strychnine, iodine, and other “remedies”; counter-irritation by means of a seton at the nape of the neck; thermal treatment; and even “electro galvanism”—resulted in clinical improvement. Instead, the patient’s condition grew “rapidly and decidedly worse.” Only after the seton was withdrawn did the symptoms stabilise, although the author regarded the patient’s prognosis as “peculiarly unfavourable.”

This case, which is clinically highly suggestive of neuromyelitis optica, was related by Christopher Mercer Durrant, MD Edin., FRCP Lond. (1814-1901), then physician to the East Suffolk and Ipswich Hospital. Durrant was twice president of the East Anglian branch of the British Medical Association and a prolific writer, whose bibliography includes almost 50 publications in the BMJ and its precursor alone. His obituary in the BMJ described Durrant as an accomplished physician “of the old school.”4

Little was known about inflammatory diseases of the central nervous system at that time. Although Durrant discussed myelitis as a possible cause, he regarded this diagnosis unlikely, mainly due to the absence of fever and convulsions in his patient (symptoms not usually associated with neuromyelitis optica, as we know today). Instead he speculated that “congestion” of the spinal capillaries, excited by “the influence of cold,” might have caused “softening of the spinal cord” by impairing its “nutrition.”

The recent discovery of a novel and pathogenic autoantibody to aquaporin-4 (AQP4-IgG) in patients with neuromyelitis optica has revived interest in the co-occurrence of eye disorders in patients with myelitis.5 6 We believe it is now time to do justice to those who were the first to report on this rare but intriguing coincidence by according them their position in the history of medicine. Durrant’s report is one of the earliest on a case of possible neuromyelitis optica in the Western medical literature and deserves to be remembered.

Notes

Cite this as: BMJ 2012;345:e6430

References