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A friend of mine approached me last year, to look into a condition of trigeminal neuralgia, a condition his mother had been diagnosed with. It happens that his mom has celiac disease, an area in which I am very interested.

The above post reminded me that Miller-Fisher syndrome (MFS) has been identified as a variant of Guillain-Barre syndrome. Farah et. al. (1) and others have connected this syndrome with opthalmic division of the trigeminal nerve. MFS is a demyelinating neuropathy, which presents in cycles of opthalmoplegia, areflexia, and ataxia (2). Willison & Veach have identified circulating IgG antibodies to carbohydrate determinants in the blood of acute phase MFS patients (3).

The latter researchers argue for GQ1b antibodies as the resulting from a dynamic that appears to be what is characterized by others as molecular mimicry. They suggest that an unidentified glycoprotein antigen with carbohydrate determinants is at the root of this autoimmune attack on the nerves in question.

Hughes, on the other hand, identifies a variability in the autoantigen (2).

Through MRI, Urushitani et. al. have established a clear connection between spinocerebellar lesions, and cerebellar ataxia, but they express less certainty of the case examined as MFS (4).

It may surprise some of those who monitor this newsgroup to hear that I believe that MFS is one manifestation of neuropathic celiac disease which has been defined separately due to the low level of clinical suspicion for celiac disease.

Sincerely,
Ron Hoggan

References:

  1. Farah et. al. "Miller Fisher syndrome: unique involvement of opthalmic division of trigeminal nerve" Clin Neurol Neurosurg 1995; 97(4): 328-331
  2. Hughes, RA "The spectrum of acquired demyelinating polyradiculoneuropathy" Acta Neurol Belg 1994; 94(2): 128-132
  3. Willison & Veitch "Immunoglobulin subclass distribution and binding characteristics of anti-GQ1b antibodies in Miller Fisher syndrome" J Neuroimmunol 1994; 50(2): 159-165
  4. Urushitani et. al. "Miller Fisher-Guillain-Barre overlap syndrome with enhancing lesions in the spinocerebellar tracts" J Neurol Neurosurg Psychiatry 1995; 58(2): 241-243