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|LETTERS TO EDITOR
|Year : 2019 | Volume
| Issue : 4 | Page : 1122-1123
Miller Fisher Syndrome Following Tetanus, Diphtheria, and Pertussis (Tdap) Vaccine
Rajat Garg1, Shyam S Moudgil2
1 Department of Internal Medicine, St. John Hospital and Medical Center, Detroit, Michigan, USA
2 Department of Internal Medicine and Neurology, St. John Hospital and Medical Center, Detroit, Michigan, USA
|Date of Web Publication||10-Sep-2019|
Dr. Shyam S Moudgil
25195 Kelly Road, Suite B, Roseville, Michigan - 48066
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Garg R, Moudgil SS. Miller Fisher Syndrome Following Tetanus, Diphtheria, and Pertussis (Tdap) Vaccine. Neurol India 2019;67:1122-3
Vaccines are generally safe and are widely administered without significant adverse effects. Neurological complications following vaccination are rare and often represent a self-limiting, monophasic, benign event. We report a case of Miller Fisher syndrome (MFS) following administration of a combined vaccine against tetanus, diphtheria, and pertussis (Adacel®).
A 50-year-old woman was hospitalized with a 7-day history of blurry vision, diplopia, and gait unsteadiness. She also reported fatigue, excessive sleepiness, and paresthesia of both hands. Her symptoms progressively worsened and she required hospitalization. She denied a preceding viral or diarrheal illness. Five days prior to the onset of her symptoms, she had sustained a laceration over the right leg for which she was administered a combined vaccine against tetanus, diphtheria, and pertussis. The past medical history included endometriosis, noise-related hearing loss, and depression. Her only medication was citalopram.
On arrival, she was alert and oriented to person, place, and time. She had moderate ptosis of upper eyelids bilaterally. Pupils were mid-dilated and nonreactive. Eyes were conjugate. Ocular motility was profoundly impaired with minimal horizontal and absent vertical eye movements [Figure 1]. Fundus examination revealed sharp disc margins. There was no pallor or edema. The remainder of the cranial nerve examination was normal except for impaired hearing bilaterally. Motor strength was normal. Vibratory sensation was reduced over toes. Deep tendon reflexes were absent in upper extremities and at knees. Ankle reflexes were hypoactive. Gait was unsteady and she was unable to tandem walk.
|Figure 1: (a-c) Initial presentation – Bilateral moderate ptosis, dilated pupils, impaired right (a) and left (c) lateral gaze; (d-f) 4-weeks follow-up – resolution of deficits with complete recovery|
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Cranial magnetic resonance imaging (MRI) did not demonstrate any abnormality. Hematological and biochemical workup was unremarkable. Tensilon test failed to improve ptosis or ocular dysmotility. Cerebrospinal fluid (CSF) studies revealed elevated proteins without pleocytosis. There were no oligoclonal bands in CSF. Serum anti-GQ1b IgG antibody was detected in high titers of 299 (Ref range: 0–50). Serum anti-GD1b and anti-GM1 antibodies were negative. She was treated with plasmapheresis. Over the next 2–3 days, she developed tachycardia and increased somnolence which lasted for 3–4 days. With treatment, she showed a slow and steady improvement with a return to baseline functional status over the next few weeks [Figure 1].
Miller fisher syndrome is a rare variant of Guillain–Barre syndrome (GBS) characterized by a triad of ophthalmoplegia, ataxia, and areflexia. It is usually preceded by a viral or diarrheal illness. Anti-GQ1b antibodies are present in 80–85% of patients with MFS. A wide variety of phenotypic variation has been described with the presence of either less extensive (incomplete) or more extensive (with additional features) subtypes. Additional features include hypersomnolence, ptosis, mydriasis, other cranial nerve dysfunction, paresthesia, and autonomic dysfunction. Our patient had most of these additional features despite the classical triad of ophthalmoplegia, ataxia, and areflexia. Clinical manifestations are attributed to the presence of anti-GQ1b antibodies that attack GQ1b ganglioside expressed abundantly in oculomotor nerves, reticular formation, muscle spindles, and dorsal root ganglion neurons. The exact mechanism of phenotypic variation as seen in patients with MFS is not clearly understood. It may be related to the variation of expression sites of the GQ1b antigen among different individuals, accessibility of antibodies to these sites, and finer specifications of these antibodies. Hypersomnolence, as seen in our patient, is related to the affinity of an anti-GQ1b antibody to GQ1b ganglioside present in the retricular formation. Mydriasis is an uncommon symptom. Cases of isolated mydriasis have been reported in patients with elevated anti-GQ1b antibody, and immunopathogenicity related to the presence of GQ1b ganglioside in the ciliary ganglion has been postulated to cause mydriasis.
Standard treatment of the syndrome involves removal or neutralization of neurotoxic antibodies either by plasmapheresis or intravenous immunoglobulins. Unlike other autoimmune conditions, patients with Guillian–Barre syndrome (GBS) and its variants do not respond to corticosteroids. Better understanding of the disease and its pathogenesis may lead to the development of new and effective therapies in the future.
A viral or bacterial infection precedes most of these cases. On thorough investigation, no other antecedent event could be identified in our patient except for the exposure to Tdap vaccine. Since she had developed the symptoms 5 days after receiving the vaccine, a strong causal association is proposed. Cases of GBS and rarely MFS have been associated with various vaccinations, particularly after influenza vaccine. An association between the H1N1 vaccine and GBS has been clearly shown. A few cases of atypical GBS and MFS have also been reported with other vaccines including Tdap. Kramer et al. reported the first case of MFS after Tdap vaccination; their patient, however, was seronegative for anti-GQ1b antibodies. The mechanism of autoimmune disorders following immunization is not clear. Molecular mimicry, an aberrant immune function, and genetic predisposition are the possible explanations. In addition, vaccine-induced anti-GM1antibodies have been implicated in vaccine-associated GBS.
To our knowledge, this is the first report of a seropositive MFS following Tdap vaccination. This case also highlights the significance of a careful and accurate history taking in identifying an antecedent event leading to the patient's presentation. Further research is warranted to explore the vaccine-related induction of anti-GQ1b antibody.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
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Conflicts of interest
There are no conflicts of interest.
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