LAUSR

I read with interest the investigation of vestibular responses in internuclear ophthalmoplegia (INO) by Choi et al.1 While the data are robust, I am concerned that the explanations do not conform with prior reports. Similar to Choi et al., my colleagues and I studied initial horizontal vestibulo-ocular reflex (VOR) in 6 patients with INO and showed reduced VOR gains for both adduction and abduction.2 Because the horizontal VOR pathway is crossed, low contralesional VOR gain is attributable to damage to fibers of passage between contralateral medial vestibular nucleus and ipsilateral abducens nucleus, without implicating deranged signals from posterior canals. Similarly, adaptation to adduction paresis refers to pulse-step mismatch of abducting saccades and cannot explain reduced contralesional horizontal VOR.3 In our study,2 horizontal VOR latencies were normal, implying integrity of direct VOR. Undamaged fibers in medial longitudinal fasciculus (MLF) or extrafascicular pathways can still initiate the VOR without delay, albeit at lower gain. Variability in horizontal VOR gain is due to the extent of MLF damage. If the same premise is applied to the vertical system, posterior canal signals in the MLF would be variably affected. Ipsilesional anterior canal excitation is preserved because signals are extrafascicular. Damage to inhibitory pathways carrying disfacilitation signals in the MLF would not contribute to preserved ipsilesional or reduced contralesional anterior canal VOR.4