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MJ Kupersmith, HE Fazzone, D Lefton; Optic Neuritis: Correlation of Pain and MRI . Invest. Ophthalmol. Vis. Sci. 2002;43(13):2632.
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Purpose: To demonstrate whether the MRI localization of the lesion can be related to the pain associated with optic neuritis or the pattern of visual field loss. The pain with eye movement (EOM) in optic neuritis is thought to be due to the movement of the affected intraorbital optic nerve, but this has not been verified. The lack of pain on eye movement in this disorder has also not been explained. Methods: The presence of eye or V1 distribution pain and pain with EOM ipsilateral to the acutely affected optic nerve was recorded in 96 patients (73 women, 23 men, mean age 36 years). The location and length of abnormal optic nerve enhancement on MRI were documented. The presenting visual field defects were characterized as diffuse, central, arcuate, nasal or temporal. As recorded in the ONTT, the visual field sensitivity loss was graded according to the mean deviation (minimal if ≷ -3dB and -6dB and -20dB). Results: 71patients experienced eye pain and 67 patients had pain with EOM. 20 patients had no pain. Enhancement of the orbital optic nerve occurred in 68 patients, 91% who had V1 pain (OR 2.84; 95%CI 1.65-4.88) and 88% who had pain with EOM (OR 3.53; 95%CI 1.85-6.74). Enhancement of the canalicular, intracranial or both segments was seen, without orbital involvement, in 23 nerves, and 5 nerves had no enhancement. In these 28 patients, 32% had V1 pain (OR .35, 95%CI .21-.61) and 25% had pain with EOM (OR .28, 95% CI .15-.54). In the patients with enhancement limited to the canalicular (8) and intracranial (8) optic nerve, 2 and 1 had pain with EOM, respectively. Orbital optic nerve enhancement alone produced central (25%), diffuse (33%), arcuate (28%), nasal (3%) and temporal (0%) field defects. Canalicular nerve enhancement alone produced central (50%), diffuse (12%), arcuate (25%), nasal (0%) and temporal (0%) field defects. Intracranial optic nerve enhancement alone produced central (25%), diffuse (12%), arcuate (25%), nasal (0%) and temporal (25%) visual field defects. Nerves with longer segments of enhancement had more eyes with severe field loss (55% vs 32%, p=0.008). Conclusion: The majority of patients with optic neuritis with eye or V1distribution pain or pain with EOM have involvement of the orbital segment of the optic nerve. The absence of pain, particularly with EOM, suggests the disorder is limited to the canalicular or intracranial portions of the optic nerve. Except for temporal field loss in eyes with intracranial nerve lesions, no pattern of field loss appears related to the location or length of abnormal enhancement.
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