A study of the response of pleurocephalic oedema of the optic disc (papilloedema due to idiopathic intracranial hypertension) to treatment

Abstract

Summary I diopathic intracranial hypertension (IIH) is a disorder of unknown etiology that predominantly affects obese women of childbearing age. The primary problem is chronically elevated intracranial pressure (ICP), and the most important neurologic manifestation is papilloedema , which may lead to progressive optic atrophy and visual loss. Papilloedema is an optic disc (OD) swelling that is secondary to elevated ICP. It almost always presents as a bilateral phenomenon and may develop over hours to weeks. Papilloedema can be monitored using qualitative and quantitative methods. Visual field assessment was documented as the most sensitive in the detection of visual loss in cases of papilloedema, with statistically greater sensitivity in comparison with visual acuity and contrast sensitivity testing. Optical coherence tomography (OCT) is a potential tool to quantify changes in the degree of papilloedema and to monitor the efficacy of treatment interventions. However, the clinical interpretation of the thickness of the peripapillary retinal nerve fiber layer (PRNFL) is difficult in the setting of ODoedema associated with visual field loss, since there may be swelling of some axons with atrophy of neighboring axons, confounding the relationship between PRNFL thickness and corresponding visual field sensitivity. This is where evaluation of the thickness of the Ganglion cell complex (GCC) may be helpful. Loss of neurons in the setting of optic disc oedema would be likely to be detected in the macula, where the ganglion cell layer (GCL) would become thinner over time as atrophy takes place. Results in studies in which a correlation between the degree of papilloedema and visual field loss were evaluated are contradictory. Our study included 10 eyes of 5 Egyptian female patients aging from 14 to 45 years with a recent clinical diagnosis of IIH based on the modified Dandy criteria and pleurocephalic oedema. The exclusion criteria were a refractive error more than +/- 5.00 diopters sphere and +/- 3.00 diopters cylinder and other ocular pathologies affecting PRNFL thickness, e.g. glaucoma. Patients were studied serially during the course of a follow-up period of six months. Each patient was examined on presentation then at 3 and 6 months. The present study showed that PRNFL thickness abnormalities evaluated by OCT in cases of papilloedema due to IIH are associated with perimetric threshold alterations at baseline. Therapeutic improvement of these parameters is accompanied by recovery in visual field indices. The most common visual field defects documented in patients with papilloedema were an enlarged blind spot, arcuate defects, nasal steps, global constriction and lower nasal localized field defects. Our study suggested that SD-OCT imaging can be included as a noninvasive quantitative method of measuringPRNFL thickening in pleurocephalic oedema and monitor the response to treatment, even in cases without visual loss.

Our study also suggested that GCC thickness evaluation at the macula and perimacular area; can also be used as a useful tool for detection of early axonal loss especially in cases where both oedema and axonal loss are occurring simultaneously, and to differentiate whether the decrease in the PRNFL thickness is due to resolving disc oedema or due to an ongoing damage to the axons.