Joel S. Glaser

Fluorescein angiography in the diagnosis of giant cell arteritis.

Clinical data and fundus fluorescein angiograms were analyzed from 35 patients with acute (onset less than four weeks) anterior ischemic optic neuropathy. Nineteen of the 35 patients (54%) had nonarteritic disease, and 16 patients (46%) had giant cell arteritis confirmed by biopsy. Patients with arteritis had higher erythrocyte sedimentation rates, larger cup/disk ratios, and delayed fluorescein dye appearance and choroidal filling times. Three additional patients with cranial arteritis confirmed by biopsy, but without visual loss, had angiographic characteristics similar to patients with arteritic ischemic neuropathy. We consider fluorescein angiography a valuable diagnostic adjunct in identifying patients with giant cell arteritis.

Magnetic Resonance Imaging of Optic Nerve Meningiomas: Enhancement with Gadolinium-DTPA

Six patients with optic nerve sheath meningiomas were studied with gadolinium-diethylenetriaminepentaacetic acid (Gd-DTPA)-enhanced magnetic resonance imaging (MRI) to evaluate intracranial extension. The intraorbital and intracranial tumors were isointense to cortical gray matter on T1-weighted studies without contrast in all patients. After Gd-DTPA, three patients showed mild enhancement of the intraorbital tumor, whereas five of six patients showed vivid enhancement of the intracranial tumor. In four cases, the intracranial extension could not be definitely seen on MRI without Gd-DTPA. Two patients had proton density and T2-weighted studies; in each case, the intraorbital tumor remained nearly isointense. The intracranial tumor was suggested in one patient on T2-weighted studies, but was poorly defined. Gadolinium-DTPA has proved valuable in detecting intracranial extension of optic nerve meningiomas that are not well visualized on standard MRI without contrast.

Pseudotumor cerebri from cranial venous obstruction.

Dural sinus hypertension from cerebral venous outflow impairment is a cause of pseudotumor cerebri. The authors documented six such patients: two with unilateral neck dissection, one with surgical ligation of the dominant sigmoid sinus, two with thrombosed central intravenous catheterization, and one with dural sinus thrombosis. The site of cerebral venous outflow obstruction was variable and identified in three patients with computed tomography, conventional magnetic resonance imaging, magnetic resonance angiography, and/or angiography. Magnetic resonance angiography used in two patients characterized the venous flow pattern and identified the site of obstruction, confirming magnetic resonance angiography as an effective noninvasive blood flow technique in diagnosing and following these patients. Three patients were treated successfully with medical therapy and one patient with optic nerve fenestration. The two patients with thrombosed central venous catheters had serious systemic illnesses and suffered permanent visual loss.

Magnetic Resonance Imaging of Radiation Optic Neuropathy

Three patients with delayed radiation optic neuropathy after radiation therapy for parasellar neoplasms underwent magnetic resonance imaging. The affected optic nerves and chiasms showed enlargement and focal gadopentetate dimeglumine enhancement. The magnetic resonance imaging technique effectively detected and defined anterior visual pathway changes of radionecrosis and excluded the clinical possibility of visual loss because of tumor recurrence.

Optic Neuropathy in Hodgkin's Disease

Hodgkins disease is a rare cause of infiltrative optic neuropathy, which typically evolves late in the disease course. We managed an unusual case of isolated optic neuropathy in a 21-year-old man occurring during clinical remission from Hodgkins disease. Radiotherapy and treatment with high-dose systemic corticosteroids resulted in dramatic improvement in vision. Even without other evidence of recurrent disease, acute-onset optic neuropathy in a patient with a history of a lymphoproliferative disorder should raise the question of a reemergence of the malignancy.

Myasthenic Sustained Gaze Fatigue

Sustained gaze fatigue was found in two patients whose diplopia was the first manifestation of myasthenia gravis. Although ocular excursions initially appeared full, a slow drift toward the primary position occurred during sustained extreme gaze. This motility pattern signifies pathologic extraocular muscle fatigue and strongly implicates myoneural junction disease. When myasthenia gravis is suspected, the presence of sustained gaze fatigue provides a tentative clinical diagnosis to be confirmed by pharmacologic testing.