ArticleCase reports in ophthalmological medicine2026
Papilledema With Facial and Vestibulocochlear Nerve Involvement in Idiopathic Intracranial Hypertension: An Unusual Case.
Article in Case reports in ophthalmological medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Idiopathic intracranial hypertension (IIH) is defined by elevated intracranial pressure in the absence of an intracranial mass or cerebrospinal fluid abnormality and is commonly associated with papilledema. Although cranial nerve involvement may occur, simultaneous facial and vestibulocochlear nerve dysfunction is rare and may lead to diagnostic confusion. Case Presentation: A 42-year-old obese woman with metabolic comorbidities developed acute right-sided peripheral facial palsy preceded by facial pain and accompanied by severe headache, pulsatile tinnitus, and blurred vision. A 5-day course of oral prednisolone for presumed Bell's palsy yielded no improvement. Ophthalmologic referral on Day 7 revealed bilateral Frisén Grade I papilledema with normal automated perimetry and absence of visual field defects. Neurological examination confirmed House-Brackmann Grade III facial palsy, and audiometry demonstrated bilateral high-frequency sensorineural hearing loss (right worse than left). After systematic exclusion of cerebellopontine angle lesions, demyelinating disorders, infectious neuritis, and venous sinus thrombosis, brain MRI showed a Grade IV sellar arachnoidocele and a neurovascular contact of the right facial nerve (Chavda Grade I). Lumbar puncture on Day 12 documented an opening pressure of 36 cm H Conclusion: This case broadens the phenotypic spectrum of IIH, showing that facial and vestibulocochlear neuropathies are reversible with pressure reduction. Yet, progressive visual field loss may ensue despite stable papilledema, revealing the optic disc as an unreliable proxy for neuronal integrity. Only spectral-domain OCT-by quantifying inner retinal layer loss-can expose silent axonal degeneration and must therefore become the cornerstone of long-term monitoring, independent of clinical appearance.
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