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Neurology India
Medknow Publications on behalf of the Neurological Society of India
ISSN: 0028-3886 EISSN: 1998-4022
Vol. 51, Num. 2, 2003, pp. 283

Neurology India, Vol. 51, No. 2, April-June, 2003, pp. 283

Letter to Editor

Recurrent Miller Fisher syndrome

I. Derakhshan

Formerly, Associate Professor of Neurology, Cincinnati & Case Western Reserve Universities, 415 Morris st., suite 401, Charleston, WV, 25301, USA. E-mail: idneuro@hotmail.com

Code Number: ni03091

Sir,

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

REFERENCES

1. Sitajayalakshmi S, Borgohain R, Mani J, Mohandas S. Recurrent Miller Fisher syndrome: a case report. Neurol India 2002;50:365-7.
2. Derakhshan I. Yuki N. Guillain-Barre, Fisher, Bickerstaff syndromes: nature versus well established ideas. J Neurol Neurosurg Psychiatry 2000;69:703-4.
3. Ryo 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].RinshoShinkeigaku 1994;34:702-6.
4. Sekiguchi K, Susuki K, Funakawa I, Jinnai K, Yuki N. Cerebral white matter lesions in acute motor axonal neuropathy. Neurology 2003;61:272-3.

Authors' Reply

S. S. Jayalakshmi, R. Borgohain, S. Mohandas
Department of Neurology, NIMS, Punjagutta, Hyderabad.
E-mail: sita_js@hotmail.com

Sir,

We would like to reply to the three points raised as follows. 1. Our patient with recurrent Miller-Fisher syndrome (MFS) had no antecedent illness during the second episode as mentioned in the case report.1 Antecedent infection is not always present and it has been found in 60-80% of patients with Guillian Barre syndrome and those with anti-GQ1b IgG antibody syndrome.2,3 2. Though it has been found that serum anti GQ1b Ig G antibodies is associated with MFS, antiGQib IgG antibodies may not be uniformly present as mentioned. 3. It has been mentioned in the letter that "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". Our patient had definite neuropathy as evidenced by the prolonged F wave responses, reduced motor conduction velocities and absent sensory nerve action potentials in the upper and lower limbs. The nerve biopsy showed segmental demyelination. Hence the possibility of multiple sclerosis cannot be considered.

REFERENCES

1. Sitajayalakshmi S, Borgohain R, Mani J, Mohandas S. Recurrent Miller Fisher syndrome: a case report. Neurol India 2002;50:365-7.
2. Caudie C, Vial C, Bancel J, Petiot P, Antoine JC, Gonnaud PM. Antiganglioside autoantibody profiles in Guillain-Barre syndrome. Ann Biol Clin (Paris) 2002; 60:589-97.
3. Odaka M, Yuki N, Hirata K. Anti-GQ1b IgG antibody syndrome: clinical and immunological range. J Neurol Neurosurg Psychiatry. 2001;70:50-5.

Copyright 2003 - Neurology India. Also available online at http://www.neurologyindia.com

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