PURPOSE: To demonstrate whether the magnetic resonance imaging (MRI) localization of the abnormal enhancement of the optic nerve can be related to the pain or pattern of visual field loss associated with acute optic neuritis. DESIGN: Retrospective observational series and MRI review from a referral neuro-ophthalmology service. PARTICIPANTS: Seventy-three women and 23 men with acute optic neuritis who had high resolution gadolinium-enhanced fat-suppressed MRI within twenty days of the onset of visual loss. METHODS: The presence of eye or other fifth cranial nerve (V(1)) pain, and pain with eye movement ipsilateral to the affected optic nerve or no eye pain was recorded. The neuroradiologist reviewed the MRI, masked to the affected eye, and recorded the length and segment (orbital, canalicular, intracranial, or combination of segments) of abnormal optic nerve enhancement. The presenting visual field defects were characterized as diffuse, central, arcuate, nasal or temporal. MAIN OUTCOME MEASURES: The types of pain and patterns of field loss were correlated with the segments of optic nerve enhancement in the affected eye. RESULTS: Five patients had nerves that did not enhance and were excluded from the outcome analysis. In the 91 patients with abnormal enhancement, 70 experienced eye/V(1) pain, 67 had pain with eye movement and 17 patients had no pain. Enhancement of the orbital optic nerve occurred in 66 patients, 93.9% who had eye/V(1) pain and 92.4% who had pain with eye movement. In the 25 patients with enhancement of the canalicular, intracranial or both segments, without orbital involvement, 32% had eye/V(1) pain and 24% had pain with eye movement. No pain occurred in 3% with enhancement of the orbital segment and in 60% with enhancement of the other optic nerve segments. The length of enhancement moderately correlated with eye/V(1) pain (r = 0.49, P = 0.01) and pain with eye movement (r = 0.37, P = 0.01). Patients with enhancement longer than 10 mm had pain five times (P = 0.004) more frequent than did those with enhancement <or=10 mm. There was no significant specific pattern of field loss associated with a particular location of enhancement, except temporal field loss occurred in 25% of intracranial lesions (P = 0.04). CONCLUSION: When optic neuritis involved the orbital segment of the optic nerve, eye or other V(1) distribution pain (94.3% vs. 32%) and pain with eye movement (91.4% vs. 24%) were significantly more frequent. In contrast, pain was absent 20 times more often when the orbital segment was not involved (60% vs. 3%). Except for temporal field loss in eyes with intracranial nerve lesions, no pattern of visual field loss appeared to correlate with the location or length of abnormal optic nerve enhancement.
PURPOSE: To demonstrate whether the magnetic resonance imaging (MRI) localization of the abnormal enhancement of the optic nerve can be related to the pain or pattern of visual field loss associated with acute optic neuritis. DESIGN: Retrospective observational series and MRI review from a referral neuro-ophthalmology service. PARTICIPANTS: Seventy-three women and 23 men with acute optic neuritis who had high resolution gadolinium-enhanced fat-suppressed MRI within twenty days of the onset of visual loss. METHODS: The presence of eye or other fifth cranial nerve (V(1)) pain, and pain with eye movement ipsilateral to the affected optic nerve or no eye pain was recorded. The neuroradiologist reviewed the MRI, masked to the affected eye, and recorded the length and segment (orbital, canalicular, intracranial, or combination of segments) of abnormal optic nerve enhancement. The presenting visual field defects were characterized as diffuse, central, arcuate, nasal or temporal. MAIN OUTCOME MEASURES: The types of pain and patterns of field loss were correlated with the segments of optic nerve enhancement in the affected eye. RESULTS: Five patients had nerves that did not enhance and were excluded from the outcome analysis. In the 91 patients with abnormal enhancement, 70 experienced eye/V(1) pain, 67 had pain with eye movement and 17 patients had no pain. Enhancement of the orbital optic nerve occurred in 66 patients, 93.9% who had eye/V(1) pain and 92.4% who had pain with eye movement. In the 25 patients with enhancement of the canalicular, intracranial or both segments, without orbital involvement, 32% had eye/V(1) pain and 24% had pain with eye movement. No pain occurred in 3% with enhancement of the orbital segment and in 60% with enhancement of the other optic nerve segments. The length of enhancement moderately correlated with eye/V(1) pain (r = 0.49, P = 0.01) and pain with eye movement (r = 0.37, P = 0.01). Patients with enhancement longer than 10 mm had pain five times (P = 0.004) more frequent than did those with enhancement <or=10 mm. There was no significant specific pattern of field loss associated with a particular location of enhancement, except temporal field loss occurred in 25% of intracranial lesions (P = 0.04). CONCLUSION: When optic neuritis involved the orbital segment of the optic nerve, eye or other V(1) distribution pain (94.3% vs. 32%) and pain with eye movement (91.4% vs. 24%) were significantly more frequent. In contrast, pain was absent 20 times more often when the orbital segment was not involved (60% vs. 3%). Except for temporal field loss in eyes with intracranial nerve lesions, no pattern of visual field loss appeared to correlate with the location or length of abnormal optic nerve enhancement.