LAUSR

P aroxysmal symptoms in multiple sclerosis (MS) consist of brief, stereotyped, self-limited, and predominantly positive focal neurological symptoms (1,2). Examination between attacks can be unremarkable, and hence, they often constitute a diagnostic challenge. Ocular motor paroxysms in MS have been anecdotally reported, and the majority lacks anatomical correlation and quantitative assessment (1,2). We provide detailed ocular motor analysis in a MS patient with paroxysmal monocular adduction, occurring several years after an episode of bilateral internuclear ophthalmoplegia (INO), and associated with a chronic paramedian dorsal pontine demyelinating plaque. A 57-year-old man with relapsing-remitting MS for 16 years presented with a 4-year history of recurrent shortlasting episodes of binocular horizontal diplopia in straight gaze lasting a few seconds and occurring up to 100 times per day. Exercise, heat, hyperventilation, and touch or movement of the eyes/head/limbs had no precipitating effect. The patient was asymptomatic between events. His MS history was remarkable for an episode of bilateral INO 14 years earlier, of which he had subjectively recovered after 1 month (i.e., no diplopia), albeit residual bilateral adduction weakness persisted over the years. Current neuroophthalmological examination showed best-corrected visual acuity of 20/20 in both eyes; color vision was 17/17 in the right eye and 15/17 in the left eye on Ishihara color plates; there was a left relative afferent pupillary defect, and the left optic disc was pale. Alternate cover testing showed a 4-prism diopter esotropia in straight gaze. Quantitative ocular-motor analysis with infrared binocular video-oculography (VO425; Interacoustics, Assen, Denmark; 105 Hz) was performed between and during the diplopia attacks. Between attacks, while fixating a 0.8° central target at a 90-cm distance, there was upbeat nystagmus (mean slow phase velocity, 8°/s) in straight gaze. During 5–30° horizontal saccades, there was bilateral slowing of adducting saccades (mean velocity, 143°/s right-eye, 156°/s left-eye) and abducting nystagmus, consistent with bilateral INO. During an attack, while fixating the central target, apart from continuous upbeat nystagmus, there was intermittent adduction of the left eye lasting w5 seconds at a frequency of 0.05 Hz (Fig. 1 and see Supplemental Digital Content, Video, http://links. lww.com/WNO/A382), with no simultaneous change in pupils’ size, and consistently manifesting as transient diplopia. Brain MRI showed a nonenhancing hyperintense lesion in the paramedian dorsal pons affecting both medial longitudinal fasciculi (MLF), more prominent on the left, already observed in older scans (Fig. 1, middle segment). Other supraand infratentorial nonenhancing lesions were present, apparently not involving oculomotorand/or vision-related circuitries. The patient was diagnosed with paroxysmal adduction of the left eye and started carbamazepine 100 mg twice daily, showing complete resolution of the symptoms (Fig. 1 and Supplemental Digital Content, Video, http://links.lww.com/WNO/A382). Ocular-motor paroxysms in MS have been poorly described and are usually observed in association with other symptoms, including dysarthria and ataxia (1,2). Previous ocular-motor paroxysms described up to date in MS include monocular adduction with head turn, superior rectus and levator palpebra spasm, ocular tilt reaction, ocular flutter, and convergence spasm (1–3). In the case previous to ours describing paroxysmal monocular adduction, objective documentation of the paroxysm was not provided and neuroimaging correlation was lacking (1). Here, we provide videooculographic evidence of the intermittent left eye adduction in the presence of a chronic MLF lesion. Paroxysmal symptoms in MS seem to be either generated by spontaneous ectopic intralesional discharges after an increment of sodium channels after demyelination or by transversely spreading ephatic activation of axons originating from a demyelinated lesion (2,4,5). In our case, the absence of triggering stimuli eliciting the attacks made ephatic mechanisms less likely. On Department of Neurosciences and Mental Health (BM), Santa Maria Hospital, Lisbon, Portugal; Faculty of Medicine (BM), University of Lisbon, Lisbon, Portugal; Neurology Department (AIM, AFJ, LS, JL), Coimbra University Hospital Centre, Coimbra, Portugal; Neuroradiology Department (CN), Coimbra University Hospital Centre, Coimbra, Portugal; and Faculty of Medicine (LS, JL), University of Coimbra, Coimbra, Portugal.