Radiculopathy as unusual presentation of idiopathic intracranial hypertension: A case report

Ghali, Azza A.; Al-Malt, Ayman M.

doi:10.1016/j.clineuro.2017.10.021

Cited by 5 publications

(3 citation statements)

References 2 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The clinical syndrome of vision loss, ophthalmoplegia, weakness, and areflexia secondary to intracranial hypertension, here referred to as IHP, has been rarely observed. [1][2][3][4][5][6][7][8][9][10][11][12][13] Optic neuritis and different variants of GBS without elevated intracranial pressure have been reported as well. On review of the cases without elevated intracranial pressure, there is often evidence of inflammation and immune activation as detected by (1) nerve root enhancement on MRI; (2) CSF pleocytosis, and/ or (3) the presence of ganglioside GQ1b or myelin oligodendrocyte glycoprotein (MOG) antibodies.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Intracranial Hypertension Associated With Poly-Cranio-Radicular-Neuropathies

Eaton,

Oguz,

Kazimuddin

et al. 2024

The Neurologist

View full text Add to dashboard Cite

Introduction: We present the case of a gentleman who developed rapidly progressive vision loss, ophthalmo-paresis, and flaccid quadriparesis in the context of severe intracranial hypertension. We reviewed the available cases in the literature to increase awareness of this rare clinical entity. Case Report: A 36-year-old man developed rapidly progressive vision loss, ophthalmo-paresis, and flaccid quadriparesis. He had an extensive workup, only notable for severe intracranial hypertension, >55 cm of H2O. No inflammatory features were present, and the patient responded to CSF diversion. Few similar cases are available in the literature, but all show markedly elevated intracranial pressure associated with extensive neuroaxis dysfunction. Similarly, these patients improved with CSF diversion but did not appear to respond to immune-based therapies. Conclusions: We term this extensive neuroaxis dysfunction intracranial hypertension associated with poly-cranio-radicular-neuropathy (IHP) and distinguish it from similar immune-mediated clinical presentations. Clinicians should be aware of the different etiologies of this potentially devastating clinical presentation to inform appropriate and timely treatment.

show abstract

Section: Discussionmentioning

confidence: 99%

“…The clinical syndrome of vision loss, ophthalmoplegia, weakness, and areflexia secondary to intracranial hypertension, here referred to as IHP, has been rarely observed 1–13 . Optic neuritis and different variants of GBS without elevated intracranial pressure have been reported as well.…”

Section: Discussionmentioning

confidence: 99%

Intracranial Hypertension Associated With Poly-Cranio-Radicular-Neuropathies

Eaton,

Oguz,

Kazimuddin

et al. 2024

The Neurologist

View full text Add to dashboard Cite

show abstract

“…Of the cases, only 2 patients were ultimately diagnosed with PTCS, one of whom was a pediatric patient. 11,13 There are notable limitations in these cases and radiculopathy in suspected PTCS is often associated with other clinical features thus alternative diagnoses for elevated intracranial pressure should be considered. Similar to our patient though, the patients in these cases had improvement in symptoms with interventions to lower the intracranial pressure suggesting that elevated pressure was a primary driver of symptoms.…”

Section: Discussionmentioning

confidence: 99%

Pseudotumor Cerebri Syndrome Complicated by Diffuse Ophthalmoparesis and Polyradiculopathy

Nathan

O'Kula

Bausell

et al. 2020

The Neurohospitalist

View full text Add to dashboard Cite

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.

show abstract