Acta neurol. scandinav. 59, 324-330, 1979 Department of Clinical Neurophysiology, Glostrup Hospital, Denmark
Visual evoked potential in patients with cerebral asthenopia N.
c. GULMA", P. E. )EAMMERBER6, LISBETHBUSCHJENSEN, K. w. SOMMERBECK AND KIRSTENQ)RB&K
Cerebral asthenopia is often overlooked as a symptom in diffuse brain lesion. An objective correlate of this symptom has so far never been demonstrated. Averaged visual evoked potential (VEP) in 10 patients with asthenopia was compared with 20 normal subjects. Both eyes and each eye alone were stimulated using bipolar recording in the midline and over each of the occipital lobes. There was no difference of latency of the VEPs in the two groups, but the amplitude of the most prominent component was significantly reduced in the patients. There was also a difference in the two groups regarding habituation and lateralisation. No amplitude difference could be found in the somatosensory evoked potential. The amplitude difference in VEP, as an objective correlate of asthenopia, is probably modal specific and suggests involvement of the visual cortex. VEP is unsuitable as a diagnostic tool due to the great overlap between amplitudes in asthenopic patients and control subjects. Key words: Asthenopia - cerebral - occipital cortical lesion sory evoked potential - visual evoked potential
Cerebral asthenopia is an overlooked and unnoticed condition, although the asthenopic disturbances are disabilitating and common in diffuse brain lesion of different etiology (Willanger & Klee 1966, Danielsen et al. 1975). The patients complain that they see changes of different kinds a few seconds after fixation of a stationary object. The object may change form, contour, position, or it may appear to move and there may be monocular diplopia. These changes with time are of central origin and are not due to any abnormality in the eye or difficulty in fixation. As each patient describes the same disturbances with the same latency with marked regularity in repeated test situations, it appears that the asthenopic symptoms are due to disturbances at a rather primitive level in the cerebral organisation of visual perception (Willanger & Klee 1966). Previous investigations of the condition have been based on a phenomenological description given by the patient. This is perhaps why cerebral asthenopia has attracted little interest in the medical profession. We wanted to investigate whether the averaged visual evoked potential (VEP) could be used as an objective dimension in asthenopia. 0001-6314/79/060324-07 $0.2.50/0 @ 1979 Munksgaard, Copenhagen
Table 1. Asthenopic phenomena in 10 patients
Phenomena Macropsi Micropsi Rod appears tilted Change in contour Corona around the rod Diplopia Dimness of vision Pulsation phenomena Rod appears t o move Asthenopic scotoma
No. 2 1 2 2 2 5 4 7 3 1
The range per patient is 1-6 phenomena with a median of 2 phenomena.
MATERIAL AND METHODS Within 12 months 13 patients were found to have asthenopic disturbances, 10 of whom were included in this study. The diagnosis was made among patients during admission to the neurological ward, who for various reasons were investigated by extensive neuropsychological tests, including a test for asthenopia. The test for asthenopia is a modification of the test described by Willanger & Klee (1966). The patient was asked to describe the changes in perception of a vertical white rod, 7 cm long and brightly lit on a dark background, and the latency for the changes was measured. The eyes were investigated several times both separately and together. Only the phenomena which repeatedly occurred with the same latency were registered as asthenopic symptoms. The material consisted of seven males and three females aged 33-57 years (median 50). Four patients suffered from sequels after concussion, three had encephalopathia of unknown etiology, one hereditary grand ma1 epilepsia, one sequels after encephalitis, and one had vertigo of unknown cause. None of the patients had major neurological signs. In the psychological test all of the patients showed a slight to moderate intellectual reduction. In five of the patients refractive errors were found in ophthalmological examination. When corrected, as in the VEP recordings, a normal visual acuity was obtained. Twenty normal persons (10 males and 10 females) served as controls. Eleven had corrected refractive errors. Their ages ranged from 22 to 65 years (median 38), i.e. significantly lower than in the patient group, but the age has no or little influence on the VEP latency or amplitude (Beck e f al. 1975, Celsia & Daly 1977). VEP recordings Platinum needle electrodes were applied to the scalp according to the 10-20 International System and the montage 0,-C,,0,-P, and 0,-P, were used. The input from the electrodes was fed into a amplifier with a bandwidth of 2 Hz to 1 kHz. The output was fed into a digital averager (DISA 14 G 0 1) with an analysis time of 500 msec. Writeouts from the averager were made with a moving coil pen recorder (Clevite brush mark 220). The subject was comfortably seated in a partially darkened room at a distance of 1 m from an oscilloscope monitor which generated an appearing - disappearing pattern consisting of six horizontal green fluorescent lines. The subject was instructed to fixate
326 on a white dot in the center and the stimulus field was seen under an angle of 30". There were given 128 flashes at a frequency of 1 Hz. With the montage 0,-C,recordings were made with simultaneous stimulation of both eyes (1: OU - 0,-C,(l)),with stimulation of the right eye (2: OD - 0,-C,)and of the left eye (3: 0s - 0,-C,). With the montages 0,-P, and 0,-P, both eyes were stimulated (4: OU - 0,-P, and 5: OU 0,-P,). Finally the first recording ,was repeated (6: OU - 0,-C,(2)). During recording 1 and 6, eye movements were detected with electrooculography by continous EEG recording with electrodes placed prefrontally and lateral to the eyes. To reveal signs of drowsiness, EEG was also recorded from 0,-C, and 0,-C3. In all patients and in 15 of the control subjects (median age 44 years) the somatosensory evoked potentials (SEP) were recorded after stimulation of the median nerve at the wrist and with the montages P,-C, or P4-C4 contralateral to the stimulated nerve. The stimulus had a duration of 0.2 msec and an intensity of 5-10 mA which gave a moderate twitch of the thumb. The results were analysed with nonparametric statistic (Mann-Whitney's test for unpaired samples, Wilcoxon's test for paired samples and the chi-s'quare test).
The most prominent component of the VEP was the negative peak N,, which could be easily identified in all the recordings both in the control subjects and in the patients (Figure 1). There was no significant difference as to the
Figure 1. Typical visually evoked potential (VEP) and somatosensory evoked potential (SEP) from a normal subject (M,48y) and from a patient with asthenopia (M,44y). The VEP is recorded from electrodes over the midline between the occipital lobes after stimulation of both eyes. The SEP is recorded from the parietal lobe after stimulation of the contralateral median nerve at the wrist.
327 Table 2 . Peak latency (msec) of visually evoked potentials after stimulation of both eyes with bipolar recording over the occipital lobes (0,Cd Median values and range Peak
Pl Nl P, N2
73 111 227 331
(59-87) (102-130) (161-268) (263-388)
79 111 226 327
(78-82) (96-118) (206-247) (278-362)
Difference NS NS NS NS
Table 3. Amplitude ( p V ) of visually evoked potentials after stimulation of both eyes with bipolar recording over the occipital lobes (Ox-Cx).Median values and range Amplitude
op, PIN1 NlP, P2N2
3.4 14.9 18.1 8.5
(0-8.0) (6.5-22.9) (10.0-35.7) (3.6-18.6)
Asthenopia 0.1 7.5 12.4 9.7
(0-4.4) (2.0-20.0) (5.3-25.0) (3.1-11.5)