$23 evoked by a similar binocularly presented checkerboard stimulus with contrast borders. Potential profiles were constructed, and reference-independent component latencies were defined as the occurrence time of maximal 'field power'. Both stimulus conditions evoked occipitally positive components of similar latency but component amplitudes evoked by stereoscopic stimuli were significantly smaller, and they showed a more anterior scalp location. Further analysis of the data as source derivations confirmed these findings. Neural activity patterns of longer duration were analyzed over time, and it was found that the topographical differences between stereoscopic and contrast stimuli were not restricted to the occurrence between times of components, but prevail over long durations. These topographical data suggest that the time course of the activation patterns is similar but that the underlying neural generators are different. The finding of more anteriorly located potential peaks evoked by stereoscopic stimuli may be interpreted as an indication that more neurones in area 18 than in the primar 3 visual cortex are activated by stereoscopic stimuli.
W 2.05 T O P O G R A P H I C VEP MAPPING IN CORTICAL VISUAL IMPAIRMENT.
P.K.H. Wong, J.E. Jan and K. Farrell (Vancouver, Canada) The value of the traditional visual evoked potential (VEP) and electroretinogram is well recognised in the assessment of visual impairment due to disorders of the eye and optic nerve. How~ ever. their role in the assessment of blindness due to retrochiasmatic causes is less clear, particularly in the case of flash VEP. Because it is often not possible to use pattern reversal stimuli in young children, particularly when they have multiple neurological handicaps, we determined if flash VEP combined with topographic mapping provided additional information. Twenty-three children (ages 1.3-13.5 yrs) in whom cortical visual impairment was diagnosed were studied. None had significant or predominant pre-chiasmatic disease. All had neurological and ophthalmologic examinations, EEG and CT scan in addition to VEP mapping (VEPM). All had significant as sociated neurological problems, including mental retardation, cerebral palsy and epilepsy. The anatomic substrate of their impairment was determined, based on clinical and CT findings. Three VEPM patterns were identified which correlated well with the anatomic localizations. Our preliminary data suggest that this technique can be used to distinguish between involvement of the optic radiation (geniculo-calcarine pathways), striate cortex and secondary visual association areas.
W 2.06 PATTERN EVOKED POTENTIALS IN CHILDH O O D OPTIC NEURITIS.
A. Kriss, F. Cuendent, D. Francis, A.M. Halliday, W.I. McDonald and D. Taylor (London, UK) Pattern reversal evoked potentials to a checkerboard of 50 minute checks were recorded in 10 patients who had had an attack of childhood optic neuritis (mean age at attack 10.6 yrs, range 7 12 yrs). Patients were recorded, on average, 48 months (range 1 week-89 months) following the attack. Six patients (60%) had responses from each eye which were entirely within normal limits. In the 4 patients with abnormal findings recordings were made from 6-88 months after the onset of the attack. Two patients had definitely delayed responses (one unilateral, the other bilateral). In another patient latencies from each eye were within normal absolute limits but the interocular latency difference was at the upper limit of norm al (8 msec). In the fourth patient, recorded 72 months after the attack, responses were not recordable from one eye and were normal from the other eye. This relatively low incidence of abnormality following childhood optic neuritis contrasts with the much higher incidence of abnormality ( > 90%) following optic neuritis in adulthood.
W 2.07 H Y P E R V E N T I L A T I O N (HVI A N D T H E PATI'ERN-REVERSAL VISUAL EVOKED POTENTIAL (VEP) IN PATIENTS WITH MULTIPLE SCLEROSIS (MS). H.D. Davies. W.M. Carroll and I~2L. Mastaglia (Perth, Australia) The effect of HV on the VEP has been studied in 13 MS patients with visual in volvement and 7 normal subjects. In 9 MS subjects, monocular half-field (HF) VEPs were recorded from a transverse chain of occipital electrodes before, during and after 4-5 min of HV. In the other 4, monocular full field VEPs were recorded from a mid-occipital electrode. End-tidal pCO 2 during HV fell by a mean of 18 mmHg in the MS subjects and 17 mmHg in controls. In controls, the HF P100 latency changed by a mean of - 2 . 3 msec ( + 1 to - 7 msec after HV. Seven MS subjects had an identifiable HF P100 prior to HV and its latency fell by a mean of 12.6 msec ( - 3 to - 2 2 msec) after HV. The Pl00 latency change was significantly different in the MS and control groups (p < 0.001). In one MS subject, a P100 was identifiable only after HV. In 2 MS subjects P100 amplitude increases greater than in any of the controls occurred with HV. The findings suggest that HV can influence conduction in the visual pathway in patients with MS. Such effects are likely to be mediated through an increase in extracellular pH or secondary reduction in ionised calcium levels. The possibility that some of the VEP changes may be the