Papilledema in an otherwise clinically typical case of Miller Fisher syndrome

Bruce, Carl T.; McClelland, Collin M.; Stavern, Gregory P. Van

doi:10.1016/j.jcjo.2015.04.016

Cited by 6 publications

(6 citation statements)

References 14 publications

(11 reference statements)

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“…Although papilloedema is a well-known association of GBS,7–9 it is often under-recognised and may result in permanent vision loss when severe. It generally improves with improvement in the underlying neurologic deficits associated with GBS, as demonstrated in our case.…”

Section: Discussionmentioning

confidence: 99%

Severe papilloedema with vision loss secondary to Guillain-Barré syndrome

Moloney,

Ong,

Irani

2024

BMJ Case Rep

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We discuss a patient who presented with bilateral VI and VII cranial nerve palsies, symmetric upper and lower limb weakness and areflexia, 2 weeks following an flu-like illness. At presentation, there was no papilloedema, and her visual function was normal. Cerebrospinal fluid analysis and electrophysiology supported the diagnosis of Guillain-Barré Syndrome (GBS). She received intravenous immunoglobulins. She subsequently developed headaches and vision loss. Funduscopy demonstrated severe papilloedema with visual acuity of 6/18 right eye, 6/12 left eye with bitemporal visual field depression. Lumbar puncture revealed elevated opening pressure with high protein and normal cell count. She received acetazolamide. There was resolution of papilloedema and normal visual function at 3 months. Of note, the patient’s body mass index was 17 kg/m2.Our case highlights the rare occurrence of papilloedema in GBS, reiterating the importance of performing funduscopy on patients with any neurological diagnosis. Early detection and prompt management of papilloedema can prevent permanent vision loss.

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Section: Discussionmentioning

confidence: 99%

Severe papilloedema with vision loss secondary to Guillain-Barré syndrome

Moloney,

Ong,

Irani

2024

BMJ Case Rep

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“…Rare cases AIDP and Miller Fisher syndrome have been reported where in addition to the typical findings patients also have papilledema. 6,7 The CSF in patients with Miller Fisher syndrome is usually notable for albuminocytologic dissociation and antibodies against GQ1b. 5 Our patient, however, had preserved reflexes without appreciable ataxia and no such CSF abnormalities making this diagnosis unlikely.…”

Section: Discussionmentioning

confidence: 99%

Pseudotumor Cerebri Syndrome Complicated by Diffuse Ophthalmoparesis and Polyradiculopathy

Nathan

O'Kula

Bausell

et al. 2020

The Neurohospitalist

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Pseudotumor cerebri syndrome (PTCS), also known as idiopathic intracranial hypertension (IIH), is defined by elevated intracranial pressure in the absence of a structural or cerebrospinal fluid (CSF) abnormality. Typical features include headache, visual symptoms, and pulsatile tinnitus. Cranial nerve deficits are seen in a minority of cases, most often sixth nerve palsies. We present a unique cause of PTCS complicated by diffuse ophthalmoparesis and polyradiculopathy. A 27-year-old healthy woman presented with 2 weeks of blurry vision, diplopia, and facial and arm weakness. On examination, she had decreased visual acuity, markedly constricted visual fields in both eyes, with severe bilateral optic disc edema on fundus examination. There was diffuse ophthalmoparesis, right upper and lower facial weakness, and bilateral arm weakness. Magnetic resonance imaging brain revealed optic disc protrusion and a partially empty sella but no other abnormalities. Electromyogram (EMG) was consistent with bilateral C5-6 radiculopathies. Lumbar puncture revealed an opening pressure of 56 cm H2O with otherwise normal CSF constituents. She was treated with high-dose acetazolamide and methylprednisolone followed by optic nerve sheath fenestration. Due to progressive vision loss, she ultimately required ventriculoperitoneal shunting, after which her papilledema, ophthalmoparesis, and facial and arm weakness rapidly improved. This is a unique case of PTCS associated with diffuse ophthalmoparesis and polyradiculopathy. This constellation of abnormalities usually suggests an underlying inflammatory process in the subarachnoid space. However, once this has been excluded, the possibility of PTCS should be considered as early treatment can result in rapid reversal of symptoms and preserve visual function.

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“…Her first spinal tap was 2 weeks into her clinical course; thus, a suspected transient elevation in spinal fluid protein may have been missed, consistent with reports noting a transitory elevation of CSF IgG that correlates with the degree of damage to the blood–brain barrier and therefore the clinical course of the disease (1). An elevation in spinal fluid protein leading to obstruction of the CSF arachnoid granulations serves as one theory for the etiology of papilledema in GBS (2). An alternative theory leans on elevated effective venous pressures at points of CSF outflow noted in hydrodynamic studies in a GBS patient; this is completely independent of the spinal fluid protein level (2).…”

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confidence: 99%

“…An elevation in spinal fluid protein leading to obstruction of the CSF arachnoid granulations serves as one theory for the etiology of papilledema in GBS (2). An alternative theory leans on elevated effective venous pressures at points of CSF outflow noted in hydrodynamic studies in a GBS patient; this is completely independent of the spinal fluid protein level (2). Idiopathic intracranial hypertension (IIH) and MFS were noted to occur coincidentally in one previous report (3); however, the lack of risk factors for IIH (body mass index of 19 kg/m 2 and absence of use of exogenous agents known to cause elevated intracranial pressure) argues against the possibility that she had a co-occurrence of these 2 rare entities.…”

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confidence: 99%

“…The presentation of MFS with increased intracranial pressure has only rarely been reported and has yet to be reported in a case with H. pylori (2,3). The prodrome of diarrhea, nausea, and vomiting; the absence of remote episodes of antecedent gastrointestinal illness; and positive stool and serum studies for H. pylori suggest that it may have been the etiologic agent for MFS in this case.…”

mentioning

confidence: 99%

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Miller Fisher Syndrome With Papilledema and Antecedent Helicobacter pylori Infection

Wawrzusin¹,

Chung²,

Sakla³

et al. 2020

Journal of Neuro-Ophthalmology

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A 16-year-old girl from Guinea (in the United States one year) with a history of malaria treated as a child and mild anemia, developed symptoms of headache, meningismus, malaise, upper then lower extremity weakness, diarrhea, nausea, emesis, and polydipsia resulting in multiple outside emergency department visits beginning 3 weeks before presentation to our institution. One week before her presentation to us, she was noted to have altered mental status and was admitted to an outside hospital. A lumbar puncture provided temporary headache relief and yielded clear cerebrospinal fluid (CSF) with an opening pressure of 55 cm/H 2 O, with one white blood cell, 41 red blood cells, protein 23.4 mg/dL, and glucose 70 mg/dL. She was started on acetazolamide (dose 500-1000 mg daily). She developed syndrome of inappropriate antidiuretic hormone. She had a normal computed tomography of the head and MRI of the spine. MRI of the brain one day after admission revealed flattened posterior globes with bulging papillae and a partial empty sella. Headaches recurred and she complained of blurred vision. Papilledema was noted on ophthalmologic examination and repeat lumbar puncture showed an opening pressure of at least 35 cm/H20 (column max 35 cm/H20 in instrument used), with one white blood cell, protein 32.2 mg/dL, glucose 77 mg/dL, negative venereal disease research laboratory test, and negative Borrelia burgdorferi DNA. A ventriculoperitoneal shunt was placed with intraoperative opening pressure noted to be 50 cm/H 2 O. The CSF testing for Escherichia coli K1, Haemophilus influenzae, Listeria monocytogenes, Neisseria meningitidis, Streptococcus agalactiae, Streptococcus pneumoniae, Cytomegalovirus, Epstein-Barr virus, herpes simplex virus 1, 2, and 6, Parechovirus, Varicella zoster, Lyme's western blot and Cryptococcus was normal. Interferon gamma release assay was negative. Serum testing for HIV, complement levels, antiproteinase 3 antibody, antimyeloperoxidase antibody, and antinuclear antibody were normal. Antidouble stranded DNA was weakly positive. One

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Papilledema in an otherwise clinically typical case of Miller Fisher syndrome

Cited by 6 publications

References 14 publications

Severe papilloedema with vision loss secondary to Guillain-Barré syndrome

Severe papilloedema with vision loss secondary to Guillain-Barré syndrome

Pseudotumor Cerebri Syndrome Complicated by Diffuse Ophthalmoparesis and Polyradiculopathy

Miller Fisher Syndrome With Papilledema and Antecedent Helicobacter pylori Infection

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