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Year : 2003  |  Volume : 51  |  Issue : 2  |  Page : 283-

Recurrent Miller Fisher syndrome

I Derakhshan 
 Cincinnati & Case Western Reserve Universities, 415 Morris st., suite 401, Charleston, WV, 25301, USA

Correspondence Address:
I Derakhshan
Cincinnati & Case Western Reserve Universities, 415 Morris st., suite 401, Charleston, WV, 25301

How to cite this article:
Derakhshan I. Recurrent Miller Fisher syndrome .Neurol India 2003;51:283-283

How to cite this URL:
Derakhshan I. Recurrent Miller Fisher syndrome . Neurol India [serial online] 2003 [cited 2023 Sep 28 ];51:283-283
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I read with interest Dr. Sitayalakshmi and colleagues' article on recurrent Miller Fisher syndrome (MFS).[1] Their contribution in reporting a case of relapsing MFS is acknowledged and timely, but more could have been surmised from their case than that which came in their brief report, as follows:

First, is the fact that the second attack in their patient occurred without an antecedent intestinal syndrome, which occurred in the first attack. This raises the issue of chance occurrences of confounding factors that to my knowledge has never been fully addressed in relationship to Guillain Barre Syndrome and its allied conditions.[2]

Second, is their statement as to wide �acceptance that serum anti-GQ1b IgG is associated with ophthalmoplegia in patients with MFS�, if by that they imply that this test is needed to make a positive diagnosis. The latter is not uniformly present,[3] neither is there any documentation that such results are not secondary to the pathology affecting the brain or the spinal cord. Such an interpretation explains those aspects of the syndrome that appears �peripheral� in nature; such as the sensory and motor neuropathy, as detailed elsewhere.[2] Indeed, more recent findings corroborating the latter conclusion in a more contemporary setting are already on record. Yuki and colleagues have recently reported white matter lesions in a case of motor axonal neuropathy that falls within the family of syndromes now under consideration.[4]

Third, is their silence as to the possible relationship between this family of syndromes and multiple sclerosis, remembering that remission and exacerbation is the hallmark of the latter condition. It is vital to realize that a normal MRI in a symptomatic patient does not mean absence of a lesion in the white matter as the term �normal appearing white matter� confirms. And, and that the very first case of MFS (serendipitously) showing CNS involvement could easily have been missed had the CT through the midbrain was off by only 2-3 millimeters.[2]


1Sitajayalakshmi S, Borgohain R, Mani J, Mohandas S. Recurrent Miller Fisher syndrome: a case report. Neurol India 2002;50:365-7.
2Derakhshan I. Yuki N. Guillain-Barre, Fisher, Bickerstaff syndromes: nature versus well established ideas. J Neurol Neurosurg Psychiatry 2000;69:703-4.
3Ryo M, Saito T, Kunii N, Hasegawa H, Kowa H. [A case of chronic inflammatory demyelinating polyneuropathy with recurrent ophthalmoplegia, persistent conduction block, antibody activity against gangliosides GM1].Rinsho Shinkeigaku 1994;34:702-6.
4Sekiguchi K, Susuki K, Funakawa I, Jinnai K, Yuki N. Cerebral white matter lesions in acute motor axonal neuropathy. Neurology 2003;61:272-3.