Auditory and visual evoked saccadic latency in multiple sclerosis

E. Young1, T.J. Anderson2, M.R. MacAskill1, R.D. Jones3, G. Caroll2

1Department of Medicine, Christchurch School of Medicine, P.O. Box 4345, Christchurch, New Zealand;
2Department of Neurology, Christchurch Hospital, Private Bag 4710, Christchurch, New Zealand; (e-mail:tim.anderson@chmeds.ac.nz);
3Department of Medical Physics and Bioengineering, Christchurch Hospital, Private Bag 4710, Christchurch, New Zealand

There has been debate regarding the origin of increased latencies of reflexive saccades in patients with multiple sclerosis (MS). In a previous investigation we demonstrated that MS patients (with predominantly cerebellar involvement) were able to reduce the latency of their predictive saccades compared to reflexive saccades to a similar degree as controls but both reflexive and predictive saccades were of significantly longer latency (about 100 ms) than controls. This finding suggested that predictive mechanisms are normal in MS but the increased latency of predictive saccades is likely due to delay in afferent visual information reaching the saccadic motor system. In other words, MS patients perceive target motion later than controls. The aim of the present study was to further investigate the hypothesis that saccadic delay in MS is due to delay in the afferent visual pathway rather than delay within cortical, transcortical or efferent pathways.

We therefore decided to examine visual and auditory evoked reflexive and predictive saccades in patients with MS and to correlate saccadic latency with visual (VEP) and middle latency auditory middle latency (MLAEP) evoked potential latency. A finding of increased latencies of visual evoked saccades but not auditory evoked saccades would support the proposal that the increase in latency of visual evoked saccades was due solely or predominantly to delay within the afferent pathway. Fifteen patents with definite MS (Poser criteria) and 15 age and sex matched controls were recruited. Eye movements were recorded with infrared scleral reflection oculography. Results were as follows:

  1. VEP latency was significantly prolonged as expected in the MS group, 119.4 ms left, and 120.6 ms right) compared to controls (mean, 105.5 and 104.1 respectively, p < 0.03).
  2. Visual reflexive saccade latency was significantly increased in the MS group (mean, 218.6 ms left, 228.8 ms right) compared to controls (mean, 199.4 ms left, p < 0.05; 201.0 ms right; p < 0.03).
  3. There was no difference in MLAEP latency between the MS (Pa mean, 31.3 ms left, and 28.8 ms right) and control groups (mean, 29.1 ms and 29.5 ms respectively).
  4. There was no significant difference in auditory reflexive saccadic latencies between MS (mean, 210.4 ms left and 218.6 ms right) and control subjects (mean, 203.1 ms and 211.0 ms respectively).
  5. Visual predictive saccades were of significantly longer latency than auditory predictive saccades but there was no difference between MS patients and controls for either saccade type.
  6. For both MS and control groups there was no correlation between firstly, VEP and latency of visual evoked reflexive and predictive saccades or secondly, MLAEP latency and latency of auditory evoked reflexive and predictive saccades.

The observations in this study of delayed VEP and visual reflexive saccades but normal visual predictive saccades, and normal MLAEP and auditory evoked saccades, in patients with clinically definite multiple sclerosis suggest that the prolonged latencies of visually evoked saccades in this disorder are predominantly or even solely due to demyelination within the afferent pathway. Comparison studies in patients with optic neuritis are ongoing.