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Giant cell arteritis (GCA) is a condition that can cause irreversible visual loss if untreated. While corticosteroids remain the mainstay of treatment to prevent visual loss, the type, dose, route, and duration of corticosteroid treatment of GCA remain controversial. Our study surveyed neuro-ophthalmologists to determine commonly prescribed dosages of corticosteroids for the treatment of GCA with or without visual loss. For patients with acute visual loss, 52% would use intravenous (IV), 46% would use IV or oral and 2% would use oral corticosteroids. Seventy-three per cent would use 500 to 1000 mg IV methylprednisolone in this group. For patients with GCA without acute visual loss, 67% would use the oral route, 30% would use IV or oral, and 3% indicated they would use IV route of treatment. Seventy-five per cent would use 1.0 to 1.5 mg/kg oral prednisone in this group. Our results suggest a majority but not a complete consensus for route and dose of corticosteroid treatment in GCA and confirm conventional recommendations for high dose IV corticosteroids for GCA with visual loss and lower dose oral regimens for GCA without visual loss. [ABSTRACT FROM AUTHOR]

Optic nerve sheath fenestration (ONSF) is a well-known, relatively safe, and effective surgical treatment for visual loss related to papilledema. Visual loss following ONSF is uncommon but can occur from direct surgical trauma, ischemic optic neuropathy, orbital or intrasheath hemorrhage, or arterial occlusion. Transient severe (e.g., light perception (LP) or no light perception (NLP) visual loss) after ONSF is uncommon but has been reported. We describe a case of LP vision following uncomplicated ONSF with orbital imaging demonstrating significant postoperative inflammation and slow recovery after intravenous steroid treatment. We discuss the various mechanisms for this phenomenon after ONSF. To our knowledge, this is the first clinico-radiologic description with follow up and recovery of this postoperative complication of ONSF to be reported in the English language ophthalmic literature. [ABSTRACT FROM AUTHOR]

A 42-year-old Algerian man presented for binocular oblique diplopia, hypersomnolence with drop attacks, bilateral hearing loss, and thoracic pain. He had a right thalamomesencephalic hemorrhage due to an underlying cavernous malformation treated with subtotal surgical resection. On neuro-ophthalmic examination, the patient had a left relative afferent pupillary defect and a right oculosympathetic efferent pupillary defect (i.e., Horner syndrome) in addition to other thalamomesencephalic eye and neurologic signs (right fourth nerve palsy, hearing loss, hemiparesis, and thalamic pain). Clinicians should recognize the localizing value of this unique constellation of mesencephalic afferent and efferent pupillary defects. [ABSTRACT FROM AUTHOR]

We describe a case of unusual ocular movement with features of both the Heimann–Bielshowsky Phenomenon and Ocular Neuromyotonia that might suggest that they share some common pathophysiology or be on a spectrum of abnormal firing of ocular motor cranial nerves. We are the first to propose such a relationship. [ABSTRACT FROM AUTHOR]

Simultanagnosia is a well-known neurologic symptom characterized by the inability to conceptualize the whole picture despite being able to see individual elements within a visual scene. The pathophysiology involves a lesion to the bilateral parieto-occipital lobe. We report two unusual cases of simultanagnosia and juxtaposed homonymous visual field loss involving aqueductal stenosis–related obstructive hydrocephalus and cardiac arrest due to Brugada syndrome. Clinicians should be aware that simultanagnosia can be the presenting symptom of neuro-ophthalmic disease. [ABSTRACT FROM AUTHOR]