Faculty Bibliography

Eight patients with malignant gliomas were monitored with clinical examinations to study the effects of the combination of intravenous administration of carmustine and infraophthalmic intra-arterial administration of cisplatin on retinal and optic nerve function. Three patients developed a severe macular retinal pigment abnormality in the eye ipsilateral to the intra-arterial infusion. Electrophysiologic studies disclosed no evidence of a generalized disturbance in the photoreceptors, middle retinal layers, or retinal pigment epithelium. In contrast to previous studies involving patients whose visual loss was caused by vaso-occlusive lesions in the retina and optic nerve, our study involved patients with clinically significant maculopathy, that was not vascular in origin and that developed after treatment with carmustine and cisplatin. We suggest that the deficit may result from a localized retinal pigment disturbance in the macula

The management of patients with isolated oculomotor nerve palsies (OMPs) who have normal pupils and no other signs of neurological disease is a controversial issue. A more precise delineation of the clinical course of isolated OMPs may help to determine whether neuroradiologic evaluation is indicated in these cases. We studied 41 patients with isolated third cranial nerve palsies, emphasizing the times of progression and resolution of the oculomotor nerve dysfunction. The average interval from onset to development of maximal ophthalmoplegia failed to differentiate between a microvascular etiology (3.3 days) or posterior communicating artery aneurysm (3 days). Of the 28 patients with diabetic or idiopathic palsies, regardless of pupillary involvement, 68% had improvement of the oculomotor paresis within 4 weeks, 96% within 8 weeks, and 100% within 12 weeks of the onset of symptoms. Our study suggests that patients with pupil-sparing OMPs should be considered for extensive neuroradiologic evaluation only if there is deterioration or failure to improve within 4 to 8 weeks

Four patients with macroprolactinomas treated with bromocriptine had tumor growth and visual loss despite marked reduction in their serum prolactin levels. Explanations for this dissociation of tumor growth and prolactin measurement might include noncompliance. Patients treated with bromocriptine require periodic examination by computed tomographic scan or magnetic resonance imaging and neuro-ophthalmological evaluation in addition to monitoring of serum prolactin

Fourteen patients, 12 of whom were women, with an age range from 26 to 56 years, presented with progressive or recurrent optic neuropathy, despite conventional doses of corticosteroid, and laboratory evidence of collagen vascular disease. The visual loss was severe and most had an acuity less than 20/200. Megadose corticosteroid therapy improved the vision in 11 of the 12 patients. Continued oral prednisone and cytotoxic drugs were necessary to maintain vision in nine patients. Patients with autoimmune optic neuropathy must be differentiated from cases with idiopathic optic neuritis or multiple sclerosis to facilitate the appropriate therapy

Thirty-eight patients (39 eyes) with optic nerve sheath meningiomas were entered into a treatment plan and were followed up for at least three years. Eighteen eyes were simply observed because they had minimal functional deficit or the eye was blind. Radiation was used on six eyes with documented progressive visual loss that still had useful vision. Surgery was initially used in an attempt to remove optic nerve sheath meningiomas but was abandoned except in exceptional cases. Total surgical removal of the tumor was carried out in ten eyes with loss of vision and in which the meningioma was growing. Surgery for subtotal or complete removal of the tumor followed by radiation was carried out in five eyes exhibiting aggressive growth of the tumor. This treatment plan has helped us to treat patients with optic nerve sheath meningiomas in an orderly way

The authors managed 38 consecutive cases of nontraumatic vascular shunts involving the cavernous sinus. Selective angiography demonstrated 12 carotid cavernous fistulas (CCFs) and 26 dural arteriovenous shunts (DAVSs). Visual disability occurred from glaucoma, venous retinopathy, optic neuropathy, or diplopia. Ten patients with slow-flow shunts and minimal dysfunction were treated medically to lower intraocular pressure (IOP) and/or instructed in manual compression of the internal carotid artery, ipsilateral to the lesion, using the contralateral hand. Percutaneous intraarterial embolization using detachable balloons, isobutylcyanoacrylate, or polyvinyl alcohol particles was successful in 16/18 DAVSs and 9/10 CCFs. The neuro-ophthalmic signs resolved in these 25 cases. Complications occurred in five patients. These included a transient hemiparesis, twelfth nerve palsy, unilateral nasal field loss, a pseudoaneurysm causing a third-nerve paresis, and temporary cavernous sinus thrombosis. Conservative therapy in mild cases and embolization in cases with visual disability or progressive signs are warranted