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ANTI‐GQ1b ANTIBODIES IN A PATIENT WITH FACIAL NERVE DIPLEGIA WITHOUT OPHTHAMOLPLEGIA
Author(s) -
De Riz M.,
Clerici R.,
Carpo M.,
Siglienti I.,
Conti G.,
Scarpini E.,
Baron P.L.,
Silani V.,
Cappellari A.,
NobileOrazio E.,
Scarlato G.
Publication year - 2000
Publication title -
journal of the peripheral nervous system
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1
H-Index - 67
eISSN - 1529-8027
pISSN - 1085-9489
DOI - 10.1046/j.1529-8027.2000.00513-18.x
Subject(s) - medicine , pharyngeal reflex , diplegia , dysphagia , ataxia , anesthesia , surgery , physical therapy , cerebral palsy , psychiatry
Anti‐GQ1b IgG antibodies are detectable in patients with Miller‐Fisher syndrome and related to the development of ophthalmoplegia. We report a 56‐year‐old woman who was admitted in our Hospital because of peripheral facial nerve diplegia, dysphagia, dysphonia, and areflexia two weeks after a mild upper respiratory infection with fever. Gait with superficial and deep sensation appeared normal. Her mental status was intact. CSF, EMG, and MRI of the cervical spinal cord were normal, while GQ1b antibodies (1:1600), were found in the serum. Starting by day 4 after admission, the patient was treated with six plasma‐exchanges, over a three‐week period. By day 9, facial nerve diplegia, dysphagia, and dysphonia started to improve. By day 35, there were no clinical deficits, and by day 45, deep tendon reflexes were elicitable again. Anti‐GQ1b antibodies returned to the normal range (1:800) six months later. Plasma exchange was dramatically effective in the treatment of this patient. This clinical case shows that anti‐GQ1b IgG antibodies may be detectable in acute demyelinating polyradiculoneuropathy with bulbar signs and without ataxia and ophthalmoplegia.