Original Articles ltal. J. NeuroL Sci. 17:43-54, 1996 Are VEP abnormalities in optic neuritis " 9 (ON) dependent on plaque size. A reappraisal of the physiopathology of ON based on improved MRI and multiple-lead recordings Fuigente T. 1, Thomas A. 1, Lobefalo L. 2, Mastropasqua L. z, Gallenga P.E. 2, Gambi D. I, Onofrj M. t i Istituto di Clinica Neurologica e Scienze del Comportamento, Universitd degli Studi "G. D'Annunzio" 2 Istituto di Clinica Oculistica, Universitd degli Studi "G. D'Annunzio", Chieti, Italy Twenty patients with optic neuritis (ON) described in the previous study [23] underwent serial VEP recordings (us- ing multiple electrode arrays) for two years. The VEPs could be correlated with the lesions revealed by MRI, Visual Field tests and other clinical findings. On the basis of their scalp distribution, they were classified as "really de- layed" VEPs and "pseudo-delayed" VEPs. Real delays could be recorded at the onset of ON or shortly afterwards, and their appearance indicated the recovery of visual function and a good prognosis. Pseudo-delays indicated an alteration in the visual field and, unless a breakthrough of normal or delayed compo- nents appeared in the first three months, following acute ON, indicate a poor prognosis for the recovery of visual function. The pseudo-delayed VEPs were mainly observed in patients with longer lesions revealed by means of LTE-STIR MRI [23]; there was no correlation between VEP latency and the length of plaques. Our findings contradict previous theories on the timing of conduction alterations in ON and multiple sclerosis. Key Words: Visual evoked potentials -- VEP -- Optic neuritis -- Multiple sclerosis. Introduction The discussion of the mechanism of evoked potential (EP) delays by McDonald [14] and Halliday et al. [11] is still considered a starting point in the interpretation of EP abnormalities in demyelinating diseases [7]. Halliday et al. [11] described a loss of visual evoked potentials (VEPs) in the acute phase of optic neuritis (ON). When vision is restored during follow up a small amplitude de- layed VEP is recorded, with its amplitude gradually nor- malising along with the recovery of visual acuity. How- ever, for Halliday et al. [11], the increased latency of de- layed VEPs does not return to normal, and they there- fore conclude that "once established, the latency for a particular patient appears to be a stable phenomenon, unless a further attack of optic neuritis occurs, which may increase the delay". Their findings were used to hypothesize that "the amount of delay depends on some fairly stable anatomical fea- ture, such as the length of the demyelinated fibers in the plaque, while the amplitude recovery may reflect the res- toration of conduction in initially blocked nerve fibers". The restoration of amplitude in the initial phase might parallel "the subsiding of oedema" and later "the repair of the fibers by the development of an abnormally thin myelin layer might play a part". Some doubts on the different VEP findings in multiple sclerosis (MS) described by various authors [1, 2, 11, 13] were also cast by Halliday [12] and Blumhardt [3-6]. These authors pointed out that examination of the pub- lished illustrations of delayed VEPs in MS patients re- vealed obvious wave-form differences between the res- ponses from the affected and asymptomatic eyes of the same patient. Using an array of electrodes, Blumhardt [3- 6] showed that the activity evoked by a full field stimu- lus presented centrally is a compound response resulting from the sum of a number of definable major compo- nents, including N75, P100 (major positive) and N140 components ipsilateral to the stimulating half-field, and of P70, N105 and P135 contralateral to the half-field. In previous studies, we have described the same compo- nents [18-21], but called them N1-P1-N2 and iPl-iN1- iP2 because the fact that we used stimuli of different spatial frequencies, meant that the latency changed. The conclusion drawn in the different papers by Blum- hardt [3-6] is that any of the different VEP components Received 16 August 1994 - Accepted in revised form 29 September 1995 43