Fellows' Journal Club: Hyperintense Optic Nerve Heads on Diffusion-Weighted Imaging: A Potential Imaging Sign of Papilledema

BACKGROUND AND PURPOSE:Changes at the optic nerve head on DWI in the presence of papilledema have not been systematically studied. The purpose of this study was to evaluate if hyperintensity of ON heads on DWI is associated with papilledema.MATERIALS AND METHODS:In this retrospective study, 19 patients (4 men, 15 women; median age, 32 years) with papilledema and 20 control participants (7 men, 13 women; median age, 48 years) who had undergone prior MR imaging of the brain were identified. Two neuroradiologists blinded to the diagnosis independently reviewed the DWI for the presence of hyperintense signal at the ON head of each eye. If present, they graded the signal as mild or prominent. Groups with and without papilledema were compared for the prevalence of ON head hyperintensity by using the Fisher exact test, with analyses performed both for groups of patients and for individual eyes. Presence of ON head hyperintensity was also studied as a function of Frisen papilledema grade on fundoscopy, when available.RESULTS:Hyperintensity of the ON heads on DWI was significantly associated with papilledema (P = .001). For the 2 readers, hyperintensity at both ON heads was 26.3% and 42.1% sensitive and 100% specific in the detection of papilledema. The presence of unilateral ON head hyperintensity was not specific for papilledema and was invariably graded as mild when seen in the control group. Patients with higher papilledema grades had a higher prevalence of hyperintensity at the ON heads.CONCLUSIONS:Hyperintensity of the ON heads on DWI can serve as a useful imaging marker for papilledema, especially if bilateral. Its absence, however, does not exclude papilledema.

Papilledema is defined as swelling of the optic disc secondary to increased intracranial pressure, often occurring in the setting of intracranial space-occupying lesions, intracranial inflammation, venous sinus thrombosis, hydrocephalus, and idiopathic intracranial hypertension (pseudotumor cerebri).^1–3 Although MR imaging is primarily used in an attempt to elucidate the cause of the papilledema, MR imaging may, at times, provide the first indication of underlying papilledema, particularly in those patients with headache in whom fundoscopic examination has not yet been performed or has not been able to detect papilledema given its less-than-perfect sensitivity because of factors such as patient cooperation and examiner skill.^4,5 This ability of MR imaging to identify otherwise unsuspected papilledema is especially important in patients with idiopathic intracranial hypertension, in whom the diagnosis often hinges on the recognition of papilledema.Several signs relating to papilledema have been described on MR imaging, including flattening of the posterior sclera, intraocular protrusion of the prelaminar ON, orbital ON tortuosity, distention of the perioptic subarachnoid space with fluid, prelaminar ON enhancement with gadolinium, and empty sella. Although these signs have been found to be present in affected patients, the reported sensitivity and specificity of the signs are variable. Although some studies have indicated that MR imaging can identify papilledema with sensitivity and specificity of more than 90%, other studies have indicated that almost all of these signs (with the exception of altered globe configuration at the ON head) may be observed in control participants, making them nonspecific.^6–8 An additional imaging sign of papilledema could improve the diagnostic ability of MR imaging in patients with headache. We have anecdotally observed hyperintensity of the ON head on DWI in some cases of clinically proven papilledema. Although this has been previously described in a case report,² the ability of this sign to distinguish patients with papilledema from healthy control participants has not been systematically studied.The purpose of this study is to evaluate whether hyperintensity of the ON head on DWI is statistically more likely to occur in patients with clinically proven papilledema than in unaffected control participants.