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Electroencephalography and Clinical Neurophysiology, 1978, 4 4 : 6 6 4 - - 6 6 8 © Elsevier/North-Holland Scientific Publishers Ltd.

Clinical note PROVOKED VISUAL IMPAIRMENT IN MULTIPLE SCLEROSIS STUDIED BY VISUAL EVOKED RESPONSES* HANS E PERSSON and C H A R L O T T E SACHS

Departments o f Clinical Neurophysiology and Neurology, Karolinska Sjukhuset, S-104 Ol Stockholm (Sweden) (Accepted for publication: November 4, 1977)

It is a well-known clinical observation that exercise, increase in body temperature and emotional stress may provoke temporary visual impairment in patients with multiple sclerosis (MS) (see e.g. McAlpine et al. 1972). Transient reduction in visual acuity after exercise was first described by U h t h o f f (1889), and this finding has since been repeatedly demonstrated (Brickner 1950; McAlpine and Compston 1952; Edmund and Fog 1955; Ricklefs 1961; Goldstein and Cogan 1964; Thomson 1966). In a recent study (Perkin and Rose 1976), it was shown that transient visual blurring from exercise occurred in 11% of 125 investigated patients with demyelinating optic neuritis. The pathogenesis of these temporary exacerbations is obscure. A critical reduction in the blood supply to the optic nerves has been suggested as a possible explanation (Franklin and Brickner 1974; Brickner 1950; Earl 1964). Alternatively, the mechanism may be an increase in body temperature or change in electrolyte concentration, which directly or indirectly influences the neuronal transmission in the optic nerve fibers (for ref. see Halliday and McDonald 1977). Since the first study by Halliday et al (1972), several investigators have demonstrated that the visual evoked response (VER) elicited by checker-board pattern-reversal is valuable in diagnosing optic neuritis (Halliday et al. 1973a,b; Asselman et al. 1975; Hennerici et al. 1977). The characteristic abnormality, although not specific, of the VER in demyelinating optic neuritis is a delay in the peak of the major positive component. In the acute phase of the disease the amplitude of the evoked potential is usually reduced, but returns to normal with clinical recovery, while the prolonged latency remains. A notable feature of this recovery is the parallelism of the changes in visual acuity and evoked response amplitude (Halliday et al. 1973b). It may be surmised that similar changes in the VER could be correlated to the provoked

* This study was supported by grants from the Swedish Medical Research Council (Project No 04X-5179) and the Swedish MS-foundation.

transient reduction in visual acuity observed in patients with MS. The present paper reports correlative findings in the VER and the visual impairment provoked by exercise in two patients with multifocal demyelinating disease.

Methods

Stimulation Pattern-reversal stimulation was obtained with a commercially available device (Medelec TV-patterngenerator). A black and white checker-board pattern was presented on a standard 26 inch TV-set in front of the patient at a distance of 1.5 m. The whole stimulating field corresponded to a visual angle of 15.2 ° and each square subtended a visual angle of 48'. The average luminance of the TV-screen was 47 cd/m 2 with a contrast between squares of 50%. Monocular stimulation of each eye was used with a pattern-reversal frequency of 2 c/sec.

Recording The visual evoked responses were recorded between 2 electrodes applied to the scalp at Oz and Fz. The EEG was fed into a preamplifier with low and high frequency filters set at 0.8 and 80 c/sec, respectively. Responses to 128 reversals were averaged. Analysis time was 200 msec. The latency of the responses was defined as the time from the pattern-reversal to the point of maximal positivity. The amplitude was measured from the preceding negative peak to the trough of the major positive wave. The reproducibility of the latency in consecutive recordings was found to be good i.e. less than 5 msec, which is our laboratory standard. The variability of the amplitude was low, since the standard deviations of control measurements before and one day after the actual experiment fell within our laboratory standard.

Case material Two patients with multifocal demyelinating disease in stable clinical status were studied. Their main

PROVOKED VISUAL IMPAIRMENT IN MS AND VER

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symptoms were optic neuritis and disturbed sensory functions. The diagnosis was verified by the findings of MS-specific patterns in the cerebrospinal fluid proteins with isoelectric focusing (Kjellin and Vesterberg 1974). The patients had no history of any other disease. Case 1. Male, 34 years of age, suffering for 1 year from permanent visual impairment of the right eye (visual acuity: 0.1) and half a year prior to our study, from one period of about 1 month of reduced visual acuity (0.6 as the lowest value recorded) of the left eye. The diagnosis of optic neuritis was based on the findings of pale discs and bilateral central scotomas. He had also had attacks o f hyposensibility of the face and one arm. Case 2. Female, 27 years o f age with several bouts of paresthesia of the limbs since 7 years and during the last 2 years periodical visual impairment and defective color vision of the right eye. The patient had no symptoms from the left eye. Both patients often experienced transient visual impairments (case 1: left eye, case 2: right eye) in connection with exercise, emotional stress or elevated body temperature. At the beginning of this study, the visual acuity was 1.0 of the left eye of case 1 and both eyes of case 2.

A

Procedure

and McDonald 1977). The patients experienced visual impairment from these eyes during exercise. Stimulation o f the left eye in case 2 produced a norreal VER. Diagrams of the VER-amplitudes after stimulation of the eyes with Uhthoff's sign before and after exercise are shown in Fig. 2. The pre-exercise amplitudes were within the normal range and the visual acuity was 1.0. After about 10 rain work on a bicycle ergometer, the visual acuity fell to 0.8 (case 1) and 0.4 (case 2). The amplitudes of the VERs 1 min after exercise had decreased markedly (case 1 to 3 uV; case 2 to 0 ~V). The amplitudes of the VER regained pre-exercise control values after 14 min; at about the same time when the patients reported return of normal sight. At this time the VER-amplitudes corresponded to the lower end of the control amplitude range. The low amplitude of the VER (Fig. 2) 10 min after exercise in case 2, could be due to the patient temporarily not focusing on the stimulating pattern properly. The latencies did not change significantly during test (see Table). The VER of the left eye in case 2 (see Table I) was within the normal range and the visual acuity of that eye was 1.0 during the whole experiment. The VERs recorded on day 2 did not differ significantly from the preexercise controls of day 1. The body temperature measured orally was 37.0°C in the case 1 and 36.8°C in case 2 before exercise. After exertion, the temperature increased to 37.5°C in case 1, but remained unchanged in case 2.

On the first day, pre-exercise VERs were recorded with the subjects comfortably seated in a semidarkened room without previous adaption. Three summations of the VE R were made on each eye. The visual acuity was also measured on each eye. The body temperature was measured using a mouth thermometer. Thereafter, the patients exercised on a bicycle ergometer (about 10 rain) until visual impairment occurred. The visual acuity of each eye and body temperature was thereafter again registered. During the following 25 min, the VERs of the patients were recorded until the responses had regained preexercise pattern. Control VERs were recorded without exercise on the second day.

Results The VER-parameters are presented in the Table. Representative examples of original recordings from case 1 are shown in Fig. 1. In case 1, no response could be recorded after stimulating the right eye, which had permanent visual impairment (visual acuity: 0.1). The pre-exercise VERs registered after stimulating this patient's left eye and the right eye of case 2 displayed markedly prolonged latencies (M : 140 msec and M : 144 msec, respectively) with normal amplitudes (M : 7.7 and M : 6.4, respectively). This VER-pattern has been considered typical although not specific for demyelinating optic neuritis (Halliday

B

C

Fig. 1. VERs from case 1. A: pre-exercise response. B: changes in VER after exercise. The numbers below each response represent time in minutes after exercise. C. Response recorded 24 h later. Horizontal bar, 100 msec; vertical bar, 10 uV.

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Provoked visual impairment in multiple sclerosis studied by visual evoked responses.

664 Electroencephalography and Clinical Neurophysiology, 1978, 4 4 : 6 6 4 - - 6 6 8 © Elsevier/North-Holland Scientific Publishers Ltd. Clinical no...
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