LETTER TO THE EDITOR
Year : 2015  |  Volume : 10  |  Issue : 4  |  Page : 418-419

Concurrent acute disseminated encephalomyelitis and Guillain–Barré syndrome in a child

Mahmood Dhahir Al-Mendalawi
Department of Paediatrics, Al-Kindy College of Medicine, Baghdad University, Baghdad, Iraq

Date of Web Publication

20-Jan-2016

Correspondence Address:
Mahmood Dhahir Al-Mendalawi
P. O. Box: 55302, Baghdad Post Office, Baghdad
Iraq

Source of Support: None, Conflict of Interest: None

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DOI: 10.4103/1817-1745.174460

How to cite this article: Al-Mendalawi MD. Concurrent acute disseminated encephalomyelitis and Guillain–Barré syndrome in a child. J Pediatr Neurosci 2015;10:418-9

How to cite this URL: Al-Mendalawi MD. Concurrent acute disseminated encephalomyelitis and Guillain–Barré syndrome in a child. J Pediatr Neurosci [serial online] 2015 [cited 2022 Jul 4];10:418-9. Available from: https://www.pediatricneurosciences.com/text.asp?2015/10/4/418/174460

Dear Sir,

I have two comments on the interesting case report by Deshmukh et al.^[1]

First, acute disseminated encephalomyelitis (ADEM) and Guillain–Barre syndrome (GBS) are both parainfectious demyelinating disorders. While ADEM almost always affects the central nervous system (CNS), GBS affects the peripheral nervous system (PNS). The combined demyelinating process, demyelination of both upper motor neuron and lower motor neuron, can occur either sequentially or simultaneously. The attempt to determine the former as a clinical entity is still elusive. Frequently, the demyelination process tends to start with CNS involvement with subsequent PNS pathology, in some cases with a relapsing-remitting course. Three potential mechanisms for the autoimmune etiology of these conditions could be related: (1) They could be caused by a common auto-immunological reactivity against myelin antigens or epitopes present in both CNS and PNS. (2) They could be due to a higher general susceptibility to autoimmune disease, which in some cases might have been caused or exacerbated by immunomodulatory treatment, e.g., b-interferon. (3) Their co-occurrence might be coincidental.^[2]

Second, Fisher syndrome (FS) is an acute polyneuropathy typically characterized by the triad of ataxia, areflexia, and ophthalmoplegia, although it might present with two or even just one of these clinical findings. Similarities between FS and other acute polyneuropathies such as GBS and Bickerstaff brainstem encephalitis suggest that FS is part of a spectrum of autoimmune disorders that may affect the PNS and/or CNS. Anti-GQ1b antibody is present in the serum of more than 85% of patients with FS, but it is not specific to FS.^[3] I wonder why Deshmukh et al.^[1] did not attempt to detect serum anti-GQ1b antibody in their studied patient. Nevertheless, it remains yet unclear why some patients develop FS and others develop classical GBS or one of its variants.

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References

1.	Deshmukh IS, Bang AB, Jain MA, Vilhekar KY. Concurrent acute disseminated encephalomyelitis and Guillain-Barré syndrome in a child. J Pediatr Neurosci 2015;10:61-3.   [PUBMED]
2.	Kamm C, Zettl UK. Autoimmune disorders affecting both the central and peripheral nervous system. Autoimmun Rev 2012;11:196-202.
3.	Snyder LA, Rismondo V, Miller NR. The Fisher variant of Guillain-Barré syndrome (Fisher syndrome). J Neuroophthalmol 2009;29:312-24.