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Evoked potentials following unilateral ECT. II. The flash evoked potential
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Electroencephalography and Clinical Neurophysiology, 1980, 4 8 : 4 9 0 - - 5 0 1 © Elsevier/North-Holland Scientific Publishers, Ltd.
EVOKED P O T E N T I A L S FOLLOWING U N I L A T E R A L ECT. II. THE FL A SH EVOKED POTENTIAL A. KRISS, A.M. HALLIDAY, ELISE HALLIDAY and R.T.C. PRATT Medical Research Council, Institute of Neurology, National Hospital for Nervous Diseases, Queen Square, London WC1 (England) (Accepted for publication: July 18, 1979)
The preceding study showed that there were no significant asymmetries of the SEP following administration of ECT to one side o f the head (Kriss et al. 1980). In the present study the effects of unilateral ECT on the flash VEP were investigated, as evidence from previous studies (Corletto et al. 1966a, b) suggested that, at least following bilateral ECT, the VEP was attenuated for a short time during the immediate post-ictal period. No consistent hemisphere differences have been fo u n d when the flash VEP has been recorded one or more hours after unilateral t r e a t m e n t (Small et al. 1970; Small and Small 1971). Small and Small (1971) did, however, c o m m e n t on non-significant 'latency changes' (the published data appear to show increased latencies) which were reported as being more p r o m i n e n t on the d o m i n a n t side regardless of which hemisphere received the treatment.
Method The flash response was recorded in 16 patients (mean age 54.9 years, range 29--74 years) undergoing a course of unilateral ECT for the t r e a t m e n t o f depression. In 14 the recordings were made following right ECT and in 3 following left ECT. One patient was recorded after both right- and left-sided treatments on separate occasions. Eleven o f the 16 patients had received a number o f recent unilateral treatments (mean 4.5, range 1--12).
Silver/silver chloride electrodes were attached to the scalp with collodion. Three electrodes were placed on a line 5 cm above the inion, with one on the midline and two 5 cm either side of the midline. An electrode 12 cm above the nasion served as a c o m m o n reference. In addition the left and right occipital electrodes were also each referred to a pre-auricular electrode on the ipsilateral side. Vertical eye movements and the ERG were m o n i t o r e d using an electrode sited immediately below the right orbit and referred to the c o m m o n reference. The photic stimulus had an intensity of 125 × 106 cd/m 2. Stimulation at a regular rate of 2/see was carried out with the lamp placed 22 cm from the patient's eyes. While their eyes were open patients were instructed to fixate the centre of the lamp. During the pre-treatment control period, alternate runs were recorded with the eyes open and closed, allowing a short break between the two conditions. Stimulation was continued through the closed lids t h r o u g h o u t anaesthesia, during the fit and the comatose post-ictal period. As soon as the patient was able to cooperate fully the alternating eyes-open, eyes-closed routine was resumed. The flash trigger was recorded along with the EEG on an 8-channel Precision Instruments tape recorder running at a speed of 3.75 in./sec (frequency range DC to 1 kHz). The recording amplifiers had a time constant of 0.3 sec with a flat response to 2 kHz. Averaging of the response occurring in the 320 msec following the stimulus was
FLASH
VEP FOLLOWING
UNILATERAL
ECT
carried out off-line, from tape, using a PDP-12 computer. Before and after treatment, when the patient was awake and cooperative, each average was made up of 100 responses. During anaesthesia, the fit and the comatose recovery period, the number of responses in each average was reduced to 50. The EEG discharge and the accompanying convulsive movements during the fit were visually assessed and the electrographic duration of seizure activity was measured from the point at which the shock was delivered. Details concerning administration of the treatment were described in the preceding study (Kriss et al. 1980) and elsewhere (Halliday et al. 1968).
Results Visual inspection of the EEG showed that 15 of the 17 seizures were characterized by bilateral polyspike and slow wave activity with larger amplitude slow waves and more intense spiking on the treated side. One patient had a seizure of unusually short duration which appeared to be symmetrical while another patient had unusual seizure activity consisting of a mixture of fast (atypical spikes?) and alpha frequency activity on the treated side and alpha, beta and theta activity on the untreated side. Two patients had an initial generalised jerk following the shock and no other obvious convulsive movements although the EEG showed the typical pattern of asymmetrical polyspike and slow wave activity. Fig. 1 shows the pre-ECT responses with eyes open of 14 patients who later received right ECT. The responses shown were obtained from the lateral occipital electrodes 5 cm to the left and right of the midline. Although there was some variability in wave form, amplitude and latency when comparing the VEPs of different patients, most had a response with a prominent positive component peaking at around 130 msec with the eyes open, but about 10 msec later with eyes closed (Pi4Q.
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This P140 component was usually followed by a negative peak of varying amplitude and latency. Other components were less consistently present with some responses having a small early positive peak at about 40-60 msec. The lowermost responses in Fig. 1 are group averages obtained by summing the individual VEPs. Fig. 2 shows the VEP at various stages of the recording in a patient who received right ECT. Before treatment, with the eyes closed, a prominent Pi&IS component was seen which was of similar amplitude and latency on either side of the midline. During the initial stages of anaesthesia (EEG pattern 1, Kiersey et al. 1951), just under 2 min after intravenous methohexitone, the P140 was attenuated while the early positivity (P50) became more accentuated and moderately increased in latency. Three minutes after the seizure a striking asymmetry was apparent, with no response on the treated side while on the untreated side and at the midline a response was clearly present, which was moderately increased in latency with respect to the control pre-ECT run. By 8 min after treatment the VEP had returned on the treated side, but was still slightly smaller and later than contralaterally. At the end of the recording both amplitude and latency asymmetries had resolved but a bilateral latency increase with respect to the pre-treatment response persisted. Fig. 3 shows the group average responses of the 14 patients who received right ECT. In computing these responses allowance has been made for the different number of trials averaged at the various stages of the recording. The ‘recovery period’ represents the time from the end of the seizure to the point at which all patients had recovered consciousness and were able to obey commands. As some patients recovered more quickly than others, the last few responses of the recovery period included some from patients who were conscious but had their eyes closed. For the first response after the recovery period all patients had their eyes open.
492
A. KRISS ET AL. Left
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Fig. 1. Individual flash VEPs with eyes open recorded in 14 patients before right ECT. The lowermost VEPs are group averages obtained by summing the individual responses. The records were obtained from occipital electrodes placed on a line 5 cm above the inion and 5 cm to the left and right of the midline respectively, referred to a common midfrontal electrode placed 12 cm above the nasion. In all figures negativity is upwards and time scale shows 10, 50 and 100 msec marks.
Before ECT clear differences b e t w e e n the eyes-open and eyes-closed conditions were s e e n w i t h P--i-4D b e i n g l a t e r a n d l a r g e r i n t h e latter condition. Analysis of the individual d a t a using correlated 't' tests showed that
there were n o a m p l i t u d e or l a t e n c y differe n c e s b e t w e e n t h e t w o sides b e f o r e t h e s h o c k , b u t t h e r e was a s i g n i f i c a n t (P < 0 . 0 5 ) b i l a t e r a l latency difference, of the order of 9 msec, b e t w e e n r e s p o n s e s w i t h e y e s - o p e n (L, 1 2 9 . 6
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493 3 m i n u t e s Post E.C.T
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Fig. 2. Flash VEP at various stages of the recording for a patient who received right ECT. Note marked amplitude and latency asymmetries 3 and 8 min after ECT.
msec; R, 130.3 msec) and eyes-closed (L, 138.9 msec, R, 138.1 msec).' The average peak-to-peak amplitude of the eyes-closed responses (L, 23.4 ttV; R. 22.3 pV) was greater than that for the responses with eyes o p e n ( L , 2 0 . 2 ttV; R , 2 1 . 4 t t V ) , b u t t h e d i f f e r ence between the two failed to reach signifi-
cance at the 0.05 level. During barbiturate a n a e s t h e s i a PT-4~ o n b o t h s i d e s w a s s i g n i f i c a n t l y l a t e r b y 8 m s e c {P <: 0 . 0 5 ) a n d s m a l l e r by 9pV (P< 0.01) when compared to the eyes-closed condition before anaesthesia. A v e r a g e r e s p o n s e s o b t a i n e d d u r i n g t h e seizure were difficult to interpret due to the
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A. KRISS ET AL.
Group Average 14 Patients Right E.C.T.
Left side
Approximate recording time (minutes}
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Fig. 3. Group average responses of 14 patients who received right ECT showing the changes in the flash VEP occurring during the recording session. C and O indicate responses averaged with the eyes closed and opened, respectively. Note differences in amplitude and latency between eyes-open and -closed conditions and the depressed activity on the right after ECT.
c o n f o u n d i n g effects o f the high voltage backg r o u n d activity p r e s e n t during this period. Nevertheless, P 5 0 was d e t e c t a b l e in half the recordings while P--l-4-0 seemed t o be p r e s e n t in a b o u t a third.
F o r the first few averaging runs o f the postictal p e r i o d the V E P was bilaterally depressed and t h e n r e t u r n e d a s y m m e t r i c a l l y , recovering faster on t h e u n t r e a t e d Side. Within a b o u t 2 rain after the s h o c k there were significant
FLASH VEP FOLLOWING UNILATERAL ECT Group Average 14 patients Eyes open
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Fig. 4. Comparison of first and last group average VEPs with eyes open for the 14 patients receiving right ECT. A persistent latency increase of P140 was found for the response recorded on both sides"after ECT. left/right differences in both amplitude (P 0.02) and latency ( P < 0.05) with P140 on the treated side being, on average, 5 p V smaller and 12 msec later than on the untreated side. These asymmetries progressively resolved with a tendency for amplitude to recover faster than latency. Analysis of the individual data showed that the average duration of the ~ asymmetry, measured to the point at which it returned to its pre-ECT left/ right ratio, was 9.8 min (S.D. 4.9) for amplitude and 14.6 min (S.D. 6.8) for latency. However, the group average responses showed a more persistent tendency for peaks to be smaller and more rounded on the treated side due to the 'smearing effect' resulting from adding individual responses with different rates of recovery. Fig. 4 compares the first and last responses with eyes open for the group data. A significant (P < 0.01) bilateral latency increase of 10 msec was seen to persist at the end of the recording. Fig. 5 shows the group average responses of the 3 patients who received left ECT. Similar but converse changes are seen with the left side being the more profoundly affected by the treatment. No significant correlation was found
495 between the initial P]4~0 latency and the number of previous treatments. There was also no significant relationship between either duration of EEG seizure activity, shock size or time to eye opening after ECT and the duration of either amplitude or latency asymmetries. It is nevertheless of interest to note that the only patient who did n o t show evidence of any asymmetry had a short-lasting seizure with atypical symmetrical epileptic activity in the EEG. In order to assess response variability the recordings of 5 patients (4 R ECT, 1 L ECT) were re-averaged using a computer program which calculated and displayed the amplitude variance of each ordinate. No significant d i f ference was found between the two sides as far as variance was concerned. It is therefore improbable that the amplitude asymmetry after the seizure was due to a greater a m o u n t of response variability or to the increased noise level associated with slow wave activity on the treated side. Lastly, the ERG exhibited no significant changes in either the ampl!tude or latency of the 'a' and 'b' waves when a comparison was made of these measures before and after treatment.
Discussion The results of this study have shown the flash VEP to be altered by several factors, some related and some unrelated to the treatm e n t procedure. Even before anaesthesia the major positive peak (P--]4~0) was significantly later and had a non-significant tendency to be larger when stimulation was performed with the eyes closed. During barbiturate anaesthesia this c o m p o n e n t showed a further moderate increase in latency and was greatly attenuated. Immediately following unilateral ECT the entire response was bilaterally depressed and subsequently returned asymmetrically, with the untreated side recovering faster. On average, both amplitude and latency asymmetries had resolved within 15 min of the shock,
496 Group
A. K R I S S ET AL. Average Approximate recording time (minutes)
S Patients Left
E.C.T.
Lelt side
Right side
4-0
(0 4-5
C 0
4-- 10 J
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4-- 15
4-0
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1. . . . . . . . .
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~1-80
Fig. 5. G r o u p average for t h e 3 p a t i e n t s w h o received left ECT s h o w i n g t h e changes of t h e flash V E P o c c u r r i n g d u r i n g t h e r e c o r d i n g session. N o t e t h e o p p o s i t e p a t t e r n of a s y m m e t r y c o m p a r e d to right ECT (Fig. 3) w i t h m o r e persistent d e p r e s s i o n o f activity o n t h e left a f t e r t r e a t m e n t .
FLASH VEP FOLLOWING UNILATERAL ECT b u t a latency increase, c o m m o n to both sides, persisted b e y o n d the end of the 0.5 h recording session. The VEP changes associated with eye closure agree with those reported by others (Van H o f 1960; Gastaut and Regis 1965; Domino 1967; J o n k m a n 1967). It is likely that several factors are responsible for causing these changes. Following lowering of the eyelids the retinal adaptation level is altered towards the scotopic state and this has been reported to selectively enhance c o m p o n e n t 5c (180 + 40 msec) of the major positive c o m p o n e n t (wave 5) (Gastaut and Regis 1965). Furthermore, while eye closure reduces the intensity of light entering the eye, a factor known to increase latency (Vaughan 1966; Creutzfeldt and Kuhnt 1967) it also results in dilation of the pupils, which is reported to increase the amplitude of the VEP (Bergamini and Bergamasco 1967). Enhancement of the response may also occur from the change in hue towards red (Perry and Childers 1969) due to transillumination of the eyelids. Although there was evidence that early components may persist during the seizure, was not detectable in the majority of recordings. It is difficult to c o m m e n t on the cause of these alterations during this phase of the recording as no clear distinction can be made between the attenuating effects of the anaesthetic and the effects of the seizure itself. Rodin et al. (1966} claimed that all c o m p o n e n t s of the flash VEP tended to persist during the clonic stages of seizures induced by the convulsant drug megimide, when this was administered without prior anaesthetic, and concluded that neural elements responsible for the response were not involved in seizure activity. However, these authors reported that the VEP was not discernible for about 1 min after the end of the fit and suggested that hypoxic mechanisms may be responsible for this. The finding that the VEP following ECT also is definitely, but transiently, attenuated agrees with the reports of Corletto et al. (1966a, b) w h o recorded the response after bilateral ECT. These authors,
497 however, did not report any latency changes, nor did they c o m m e n t on the symmetry of the response. In the present study, clear VEP asymmetries were found in the immediate post-ictal period, which usually resolved within 0.5 h following the shock. It is therefore not surprising that some previous investigations failed to show definite hemisphere differences (Small et al. 1970; Small and Small 1971) when the flash response was recorded more than 1 h after unilateral treatment. The present findings demonstrated clearly that the treated side was always the most profoundly affected. This is in contrast to the non-significant trend reported by Small and Small (1971) where latency changes were more prominent on the dominant side regardless of which hemisphere received the treatment. The present investigation was concerned with electrophysiological effects of ECT and their time course and it was n o t feasible to assess patients for concomitant neurological defects. A separate study was performed, however, in which patients were examined during the immediate post-ictal period and the findings have been reported elsewhere (Kriss et al. 1978b). In brief, transient neurological deficits referable to the treated hemisphere were found to occur over a similar time period to the VEP changes. Among these were h o m o n y m o u s hemianopia lasting on average 10 min and both visual and tactile inattention persisting usually for just under 15 min following treatment. The flash VEP asymmetries seen after unilateral ECT are similar to those reported in clinical conditions associated with hemianopic defects, that is, with the side of the lesion having VEP components which are smaller and later (Vaughan et al. 1963; Vaughan and Katzman 1964; Gastaut and Regis 1965; Kooi et al. 1965; Crighel and Botez 1966; J o n k m a n 1967; Oosterhuis et al. 1969; Harding et al. 1970). In this respect the lateralisation of the flash response differs from that for the pattern reversal response (Barrett et al. 1976; Blumhardt et al. 1977). From our studies, it is
498 tempting to postulate an association between the duration of hemianopia and the VEP amplitude asymmetry on the one hand, and the inattention and latency asymmetry on the other. However, such tentative suggestions must await further testing by the concurrent assessment of both VEP and neurological asymmetries in the same patient. In spite of the fact that no significant correlations were found between the duration of VEP asymmetries and either the duration of the seizure, time to eye opening or shock size, it may still be that the more likely factor influencing post-ictal asymmetries is the seizure itself, as post-ictal suppression of the flash VEP is seen after seizures induced by convulsant drugs (Rodin et al. 1966) and an association between seizure and post-seizure activity has been shown for the EEG (Ottosson 1962). The latency increase still present at the end of the recording could have been attributable to the combined effects of anaesthesia, the patients' reduced level of arousal and the effects of ECT itself or to any one or more of these factors. Studies in monkeys have shown that the later components of the flash response may take over 0.5 h to return to their pre-drug status after barbiturate anaesthesia (Hughes 1964). In man, VEP latencies have been reported to be increased in the 'groggy' or cloudy stage after awakening from natural sleep (Shagass and Trusty 1966; Saier et al. 1968). In the present study no information is available on how long the bilateral latency increase took to resolve as no longterm follow-up of the VEP was done. It is of interest to note, however, that Small et al. (1970) commented on a general tendency for VEP peak latencies to be increased the day after treatment. The discrepant behaviour of the visual and somatosensory responses following unilateral ECT suggests fundamental differences in the nature of the responses to these two modatities. As reported elsewhere (Kriss et al. 1980), the SEP showed no consistent hemisphere asymmetries after ECT and patients had no
A. KRISS ET AL. significant left/right differences in their subjective sensory threshold. In an associated study of neurological signs, however, lateralised deficits including hemiparesis and tactile inattention were c o m m o n l y found to occur after unilateral treatment (Kriss et al. 1978b). Previous studies have also found that the somatosensory response may be normal in the presence of inattention and/or hemiplegia (Giblin 1964; Liberson and Scott 1964). On the other hand, the SEP has been found to be profoundly altered in lesions of the dorsal column/medial lemniscal pathway and primary sensory cortex (Halliday and Wakefield 1963; Giblin 1964; Domino et al. 1965; Stohr and Goldring 1969; Williamson et al. 1970). By contrast, the post-ECT flash response was found to be asymmetrical in the present study, paralleling the clinical evidence of visual defects over the same period (Kriss et al. 1978b). Compared to the somatosensory response to electrical stimulation, the origin of the flash response is poorly understood. The latter has been reported to persist in cortical blindness (Crighel and Poilici 1968; Brindley et al. 1969; Spehlmann et al. 1977) and, conversely, to be altered in the absence of frank visual defects (Bergamini and Bergamasco 1967; J o n k m a n 1967; Schneider 1968; Oosterhuis et al. 1969). It is known from animal studies that there are retino-cortical pathways other than the direct geniculo-striate route which are also capable of influencing occipital activity following visual stimulation. In m o n k e y , a response to flash is still recordable over the posterior cortical regions in spite of experimental lesions involving striate and peristriate areas (Cohn 1969; Vaughan and Gross 1969). These less direct pathways involve thalamic association nuclei, midbrain and brain stem structures such as the pretectum, rectum, superior colticulus and reticular formation (Thompson et al. 1963; Buser and Bignall 1967; Rose and Lindsley 1968; Marg 1973; Sprague et al. 1973). Cortical projections from these structures are usually well localized though in the case of the reticular forma-
FLASH VEP FOLLOWING UNILATERAL ECT tion a more diffuse projection is reported (Jasper 1954). Ciganek (1965) concluded, on the basis of the effects on the flash VEP of sleep, anaesthesia and rapid stimulation (Ciganek 1961), and on cross-modality comparisons (Ciganek 1965), that components earlier than 100 msec were localized association area responses and later components reflected activity of the diffuse projection system. If true, this concept might help to explain the VEP changes seen after unilateral ECT, for the diffuse projection pathways have been shown to be intimately involved in producing generalized epileptic discharges (Jasper 1954). EEG seizures seen following unilateral ECT appear to be very similar to the unilateral EEG seizures seen in epileptics (see Kriss et al. 1978a for fuller discussion) in which epileptic activity though generalized has a greater emphasis in one hemisphere (Gastaut et al. 1962). The asymmetry of the VEP after the seizure could reflect the involvement of the generator neurones in the seizure activity itself. Attenuation of evoked activity followed by gradual recovery is characteristically seen in neural tissue involved in epileptic discharges (Jasper 1954).
Summary The flash evoked potential (VEP) was recorded in 16 depressed patients before, during and for 0.5 h following administration of unilateral ECT. In 14 the recordings were made following right ECT and in 3 following left ECT. One patient was recorded after right- and left-sided treatments administered on separate occasions. While the patients were conscious, responses were averaged with eyes open and eyes closed. During anaesthesia, ictus and post-ictal coma the response to repetitive stimulation through closed eyes was recorded continuously in sequential runs. Consistent latency differences between VEPs with eyes open and closed were established in the runs prior to treatment. In post-
499 ictal coma there was a marked asymmetry in the response from the two sides. C o m p o n e n t P-i~0, in particular, was significantly smaller and later over the side which received ECT. On average, these asymmetries lasted less than 15 min following the treatment. A significant latency increase, c o m m o n to both hemispheres, was found at the end of the recording session.
Rdsumd Potentiels dvoquds visuels aprds dlectrochoc unilatdral. H Le potentiel dvoqud visuel (PEV) a dtd enregistrd chez 16 malades d~primds avant, pendant et durant 0,5 h qui suivait l'application unilatdrale d'dlectrochocs. Chez 14 malades, les enregistrements furent r~alis~s apr~s dlectrochocs droits et dans 3 cas, apr~s dlectrochocs gauches. Chez un patient, l'enregistrement a dt~ pratiqud apr~s traitements fi droite et fi gauche, appliques ~ des occasions distinctes. Pendant que les patients dtaient consients, les rdponses dtaient moyenn~es sdpardment avec les yeux ouverts et ferm~s. Durant l'anesthdsie, la crise et le coma post-critique, des sdquences de rdponses ~ la stimulation rdpdtitive dtaient continuellement enregistrdes, les yeux dtant fermds. Des differences de latence stables furent observdes entre les PEVs recueillis avant traitement, selon que les yeux dtaient ouverts ou ferm~s. Durant le coma post-critique, une asym~trie nette a ~td constat~e entre r~ponses recueillies d'un c6td ou de l'autre. La composante P140 en particulier, dtait significativement plus petite et plus tardive du cStd ayant subi l'dlectrochoc. En m o y e n n e ces asymdtries duraient moins de 15 min apr~s le traitement. Une augmentation significative de latence, identique des deux cStds, fut trouv~e fi la fin de la pdriode d'enregistrement. We would like to thank Dr. Geoff Barrett for programming assistance and Mr. Jack Pitman for technical support.
500 References Barrett, G., Blumhardt, L., Halliday, A.M., Halliday, E. and Kriss, A. A paradox in the lateralization of the visual evoked response. Nature (Lond.), 1976, 261: 253--255. Bergamini, L. and Bergamasco, B. Cortical Evoked Potentials in Man. Thomas, Springfield, Ill., 1967. Blumhardt, L.D., Barrett, G. and Halliday, A.M. The asymmetrical visual evoked potential to pattern reversal in one half field and its significance for the analysis of visual field defects. Brit. J. Ophthal., 1977, 61: 454--461. Brindley, G.S., Gautier-Smith, P.C. and Lewin, W. Cortical blindness and the functions of the nongeniculate fibres of the optic tract. J. Neurol. Neurosurg. Psychiat., 1969, 32: 259--264. Buser, P. and Bignall, K.E. Non-primary sensory projections on the cat neocortex. Int. Rev. Neurobiol., 1967, 10: 111--165. Ciganek, L. The EEG response (evoked potential) to light stimulus in man. Electroenceph. clin. Neurophysiol., 1961, 13: 165--172. Ciganek, L. A comparative study of visual and auditory EEG responses in man. Electroenceph. clin. Neurophysiol., 1965, 18: 625--629. Cohn, R. Visual evoked responses in brain injured monkey. Arch. Neurol. (Chic.), 1969, 21: 321--329. Corletto, F., Gentilomo, A., Rosadini, G., Rossi, G.F. e Zattoni, J. Studio comparativo dell'attivit~ elettroencefalografica 'spontanea' ed 'evocata' da singoli stimoli visivi durante il coma da elettroshock. Riv. Neurol., 1966a, 36: 327--337. Corletto, F., Gentilomo, A., Rosadini, G., Rossi, G.F. et Zattoni, J. Correlations entre niveau de conscience, EEG et potentiels ~voquSs chez l'homme. Rev. neurol., 1966b, 115: 5--14. Creutzfeldt, O.D. and Kuhnt, U. The visual evoked potential: physiological developmental and clinical aspects. Electroenceph. clin. Neurophysiol., 1967, Suppl. 26: 29--41. Crighel, E. and Botez, M. Photic evoked potentials in man in lesions of the occipital lobes. Brain, 1966, 89: 311--316. Crighel, E. and Poilici, I. Photic evoked responses in patients with thalamic and brain stem lesions. Confin. neurol., 1968, 30: 301--312. Domino, E.F. Effects of preanesthetic and anesthetic drugs on visually evoked responses. Anesthesiology, 1967, 28: 184--191. Domino, E.F., Matsuoka, S., Waltz, J. and Cooper, I.S. Effects of cryogenic thalamic lesions on the somesthetic evoked response in man. Electroenceph. clin. Neurophysiol., 1965, 19: 127--138. Gastaut, H. and Regis, H. Visually-evoked potentials recorded transcranially in man. In: L.D. Procter
A. KRISS ET AL. and W.R. Adey (Eds.), The Analysis of Central Nervous System and Cardiovascular Data Using Computer Methods. NASA, Washington, D.C., 1965: 7--34. Gastaut, H., Roger, J., Faidherbe, J., Ouahchi, S. and Franck, G. Non-jacksonian hemiconvulsive seizures. One-sided generalized epilepsy. Epilepsia, 1962, 3: 56--68. Giblin, D.R. Somatosensory evoked potentials in healthy subjects and in patients with lesions of the nervous system. Ann. N.Y. Acad. Sci., 1964, 112: 93--142. Halliday, A.M. and Wakefield, G.S. Cerebral evoked potentials in patients with dissociated sensory loss. J. Neurol. Neurosurg. Psychiat., 1963, 2: 211--219. Halliday, A.M., Davison, K., Browne, M.W. and Kreeget, L.C. A comparison of the effects on depression and memory of bilateral ECT and unilateral ECT to the dominant and non-dominant hemispheres. Brit. J. Psychiat., 1968, 114: 997--1012. Harding, G.F.A., Thompson, C.R.S. and Panayiotopoulos, C. Evoked response diagnosis in visual field defects. Proc. Electrophysiol. Technol. Ass., 1970, 16: 159--163. Hughes, J.R. Responses from the visual cortex of unanesthetized monkeys. Int. Rev. Neurobiol., 1964, 7: 99--152. Jasper, H.H. Electrophysiology and experimental epilepsy. In: W. Penfietd and H.H. Jasper (Eds.), Epilepsy and Functional Anatomy of the Human Brain. Churchill, London, 1954: 183--238. Jonkman, E.J. The Average Cortical Response to Photic Stimulation. Thesis. University of Amsterdam, 1967. Kiersey, D.K., Bickford~ R.G. and Faulconer, A. Electroencephalographic patterns produced by thiopental sodium during surgical operations: description and classification. Brit. J. Anaesth., 1951, 23: 141--152. Kooi, K.A., Guvener, A.M. and Bagchi, B.K. Visual evoked responses in lesions of the higher optic pathways. Neurology (Minneap.), 1965, 15: 841--854. Kriss, A., Halliday, A.M., Halliday, E. and Pratt, R.T.C. EEG immediately after unilateral ECT. Acta psychiat, scand., 1978a, 58: 231--244. Kriss, A:, Blumhardt, L., Halliday, A.M. and Pratt, R.T.C. Neurological asymmetries immediately after unilateral ECT: J. Neurol. Neurosurg. Psychiat., 1978b, 41: 1135--1144. Kriss, A., Halliday, A.M., Halliday, E. and Pratt, R.T.C. Evoked potentials following unilateral ECT. I. The somatosensory evoked potential. Electroenceph, clin. Neurophysiol., 1980, 48: 481--489: Liberson, W.T. and Scott, D. Evoked potentials in
FLASH VEP FOLLOWING UNILATERAL ECT hemiplegic patients. Electroenceph. clin. Neurophysiol., 1964, 17: 451--472. Marg, E. Neurophysiology of the accessory optic system. In: R. Jung (Ed.), Visual Centres in the Brain. Handbook of Sensory Physiology, Vol. VII/3, Part B. Springer, Berlin, 1973: 103--111. Oosterhuis, H., Ponsen, L., Jonkman, E. and Magnus, O. The average visual response in patients with cerebrovascular disease. Electroenceph. clin. Neurophysiol., 1969, 27: 23--34. Ottosson, J.O. Seizure characteristics and therapeutic efficiency in electroconvulsive therapy. J. herr. ment. Dis., 1962, 135: 239--251. Perry, N.W. and Childers, D.G. The Human Visual Evoked Response. Thomas, Springfield, Ill., 1969. Rodin, E., Gonzalez, S., Caldwell, D. and Laginess, D. Photic evoked responses during induced epileptic seizures. Epilepsia, 1966, 7: 202--214. Rose, G.H. and Lindsley, D. Development of visually evoked potentials in kittens: specific and non-specific responses. J. Neurophysiol., 1968, 31: 607--623. Saier, J., Regis, H., Mano, T. et Gastaut, H. Potentiels ~voqu~s visuels et somesth~siques pendant le sommeil de l ~ o m m e . Brain Res., 1968, 10: 431--440. Schneider, J. Tumeurs c~r~brales et potentiels ~voqu~s. Rev. neurol., 1968, 118: 443--458. Shagass, C. and Trusty, D. Somatosensory and visual evoked response changes during sleep. In : J. Wertis (Ed.), Recent Advances in Biological Psychiatry, Vol. VIII. Plenum Press, New York, 1966: 321-334. Small, I.F. and Small, J.G. EEG, evoked potential and DC responses with unilateral ECT. J. nerv. ment. Dis., 1971, 152: 396--404. Small, J.G., Small, I.F., Perez, H.C. and Sharpley, P. EEG and neurophysiological studies of electrically induced seizures. J. nerv. ment. Dis., 1970, 150: 479--489. Spehlmann, R., Gross, R.A., Ho, S.U., Leestma, J.
501 and Norcross, K.A. Visual evoked potentials and post mortem findings in a case of cortical blindness. Ann. Neurol., 1977, 2: 531--534. Sprague, J.M., Berlucchi, G. and Rizzolatti, G. The role of the superior colliculus and pretectum in vision and visually guided behaviour. In: R. Jung (Ed.), Visual Centres in the Brain. Handbook of Sensory Physiology, Voi. VII/3, Part B. Springer, Berlin, 1973: 27--101. Stohr, P.E. and Goldring, S. Origin of somatosensory evoked scalp responses in man. J. Neurosurg., 1969, 31: 117--127. Thompson, R.F., Johnson, R.H. and Hoopes, J.J. Organization of auditory, somatic sensory and visual projection to association fields of cerebral cortex in the cat. J. Neurophysiol., 1963, 26: 343--364. Van Hof, M.W. Open-eye and closed-eye occipitocortical response to photic stimulation of the retina. Acta physiol, pharmacol, neerl., 1960, 9: 443--451. Vaughan, H.G. The perceptual and physiologic significance of visual evoked responses recorded from the scalp in man. Vision Res., 1966, 6 (Suppl. 1): 203--223. Vaughan, H.G. and Gross, C.G. Cortical responses to light in unanesthetized monkeys and their alteration by visual system lesions. Exp. Brain Res., 1969, 8: 19--36. Vaughan, H.G. and Katzman, R. Evoked response in visual disorders. Ann. N.Y. Acad. Sci., 1964, 112: 305--319. Vaughan, H.G., Katzman, R. and Taylor, J. Alterations of visual evoked response in the presence of homonymous visual defects. Electroenceph. clin. Neurophysiol., 1963, 15: 737--746. Williamson, P.D., Goff, W.R. and Allison, T. Somatosensory evoked responses in patients with unilateral cerebral lesions. Electroenceph. clin. Neurophysiol., 1970, 28: 566--575.
Electroencephalography and Clinical Neurophysiology, 1980, 4 8 : 4 9 0 - - 5 0 1 © Elsevier/North-Holland Scientific Publishers, Ltd.
EVOKED P O T E N T I A L S FOLLOWING U N I L A T E R A L ECT. II. THE FL A SH EVOKED POTENTIAL A. KRISS, A.M. HALLIDAY, ELISE HALLIDAY and R.T.C. PRATT Medical Research Council, Institute of Neurology, National Hospital for Nervous Diseases, Queen Square, London WC1 (England) (Accepted for publication: July 18, 1979)
The preceding study showed that there were no significant asymmetries of the SEP following administration of ECT to one side o f the head (Kriss et al. 1980). In the present study the effects of unilateral ECT on the flash VEP were investigated, as evidence from previous studies (Corletto et al. 1966a, b) suggested that, at least following bilateral ECT, the VEP was attenuated for a short time during the immediate post-ictal period. No consistent hemisphere differences have been fo u n d when the flash VEP has been recorded one or more hours after unilateral t r e a t m e n t (Small et al. 1970; Small and Small 1971). Small and Small (1971) did, however, c o m m e n t on non-significant 'latency changes' (the published data appear to show increased latencies) which were reported as being more p r o m i n e n t on the d o m i n a n t side regardless of which hemisphere received the treatment.
Method The flash response was recorded in 16 patients (mean age 54.9 years, range 29--74 years) undergoing a course of unilateral ECT for the t r e a t m e n t o f depression. In 14 the recordings were made following right ECT and in 3 following left ECT. One patient was recorded after both right- and left-sided treatments on separate occasions. Eleven o f the 16 patients had received a number o f recent unilateral treatments (mean 4.5, range 1--12).
Silver/silver chloride electrodes were attached to the scalp with collodion. Three electrodes were placed on a line 5 cm above the inion, with one on the midline and two 5 cm either side of the midline. An electrode 12 cm above the nasion served as a c o m m o n reference. In addition the left and right occipital electrodes were also each referred to a pre-auricular electrode on the ipsilateral side. Vertical eye movements and the ERG were m o n i t o r e d using an electrode sited immediately below the right orbit and referred to the c o m m o n reference. The photic stimulus had an intensity of 125 × 106 cd/m 2. Stimulation at a regular rate of 2/see was carried out with the lamp placed 22 cm from the patient's eyes. While their eyes were open patients were instructed to fixate the centre of the lamp. During the pre-treatment control period, alternate runs were recorded with the eyes open and closed, allowing a short break between the two conditions. Stimulation was continued through the closed lids t h r o u g h o u t anaesthesia, during the fit and the comatose post-ictal period. As soon as the patient was able to cooperate fully the alternating eyes-open, eyes-closed routine was resumed. The flash trigger was recorded along with the EEG on an 8-channel Precision Instruments tape recorder running at a speed of 3.75 in./sec (frequency range DC to 1 kHz). The recording amplifiers had a time constant of 0.3 sec with a flat response to 2 kHz. Averaging of the response occurring in the 320 msec following the stimulus was
FLASH
VEP FOLLOWING
UNILATERAL
ECT
carried out off-line, from tape, using a PDP-12 computer. Before and after treatment, when the patient was awake and cooperative, each average was made up of 100 responses. During anaesthesia, the fit and the comatose recovery period, the number of responses in each average was reduced to 50. The EEG discharge and the accompanying convulsive movements during the fit were visually assessed and the electrographic duration of seizure activity was measured from the point at which the shock was delivered. Details concerning administration of the treatment were described in the preceding study (Kriss et al. 1980) and elsewhere (Halliday et al. 1968).
Results Visual inspection of the EEG showed that 15 of the 17 seizures were characterized by bilateral polyspike and slow wave activity with larger amplitude slow waves and more intense spiking on the treated side. One patient had a seizure of unusually short duration which appeared to be symmetrical while another patient had unusual seizure activity consisting of a mixture of fast (atypical spikes?) and alpha frequency activity on the treated side and alpha, beta and theta activity on the untreated side. Two patients had an initial generalised jerk following the shock and no other obvious convulsive movements although the EEG showed the typical pattern of asymmetrical polyspike and slow wave activity. Fig. 1 shows the pre-ECT responses with eyes open of 14 patients who later received right ECT. The responses shown were obtained from the lateral occipital electrodes 5 cm to the left and right of the midline. Although there was some variability in wave form, amplitude and latency when comparing the VEPs of different patients, most had a response with a prominent positive component peaking at around 130 msec with the eyes open, but about 10 msec later with eyes closed (Pi4Q.
491
This P140 component was usually followed by a negative peak of varying amplitude and latency. Other components were less consistently present with some responses having a small early positive peak at about 40-60 msec. The lowermost responses in Fig. 1 are group averages obtained by summing the individual VEPs. Fig. 2 shows the VEP at various stages of the recording in a patient who received right ECT. Before treatment, with the eyes closed, a prominent Pi&IS component was seen which was of similar amplitude and latency on either side of the midline. During the initial stages of anaesthesia (EEG pattern 1, Kiersey et al. 1951), just under 2 min after intravenous methohexitone, the P140 was attenuated while the early positivity (P50) became more accentuated and moderately increased in latency. Three minutes after the seizure a striking asymmetry was apparent, with no response on the treated side while on the untreated side and at the midline a response was clearly present, which was moderately increased in latency with respect to the control pre-ECT run. By 8 min after treatment the VEP had returned on the treated side, but was still slightly smaller and later than contralaterally. At the end of the recording both amplitude and latency asymmetries had resolved but a bilateral latency increase with respect to the pre-treatment response persisted. Fig. 3 shows the group average responses of the 14 patients who received right ECT. In computing these responses allowance has been made for the different number of trials averaged at the various stages of the recording. The ‘recovery period’ represents the time from the end of the seizure to the point at which all patients had recovered consciousness and were able to obey commands. As some patients recovered more quickly than others, the last few responses of the recovery period included some from patients who were conscious but had their eyes closed. For the first response after the recovery period all patients had their eyes open.
492
A. KRISS ET AL. Left
side
Right
side
' . . . . I . . . . ' .... I"
P.S. D.Ba.
G.L. D. Bu. E.M.
A.M.
/
D.H. R.H.
110.V
J.L. G.S. E.H. K.S.
R.S.
R.W
Group
Average
Fig. 1. Individual flash VEPs with eyes open recorded in 14 patients before right ECT. The lowermost VEPs are group averages obtained by summing the individual responses. The records were obtained from occipital electrodes placed on a line 5 cm above the inion and 5 cm to the left and right of the midline respectively, referred to a common midfrontal electrode placed 12 cm above the nasion. In all figures negativity is upwards and time scale shows 10, 50 and 100 msec marks.
Before ECT clear differences b e t w e e n the eyes-open and eyes-closed conditions were s e e n w i t h P--i-4D b e i n g l a t e r a n d l a r g e r i n t h e latter condition. Analysis of the individual d a t a using correlated 't' tests showed that
there were n o a m p l i t u d e or l a t e n c y differe n c e s b e t w e e n t h e t w o sides b e f o r e t h e s h o c k , b u t t h e r e was a s i g n i f i c a n t (P < 0 . 0 5 ) b i l a t e r a l latency difference, of the order of 9 msec, b e t w e e n r e s p o n s e s w i t h e y e s - o p e n (L, 1 2 9 . 6
FLASH VEP FOLLOWING U N I L A T E R A L ECT Pro E.C.T I ....
'
493 3 m i n u t e s Post E.C.T
Anaesthesia
.... I" " .... I .... ' .... I"
I ....
I
' ....
I'"
......... I..
'""l
....
' ....
l"
.... [ .... , .... [.
I ....
, ....
I. . . . .
I ....
, ....
I.
Right E.C.T. 8 minutes Post E.CT f ....
~ ....
I**'
' ....
I ....
' ....
3 0 minutes Post E.CT I"
I ....
' ....
I""J'
....
I ....
'
Eyes closed
.... I*
I I ....
, ....
I..
..... I .... p.... I, 0
100
2 0 0
3 0 0 m s e c
Fig. 2. Flash VEP at various stages of the recording for a patient who received right ECT. Note marked amplitude and latency asymmetries 3 and 8 min after ECT.
msec; R, 130.3 msec) and eyes-closed (L, 138.9 msec, R, 138.1 msec).' The average peak-to-peak amplitude of the eyes-closed responses (L, 23.4 ttV; R. 22.3 pV) was greater than that for the responses with eyes o p e n ( L , 2 0 . 2 ttV; R , 2 1 . 4 t t V ) , b u t t h e d i f f e r ence between the two failed to reach signifi-
cance at the 0.05 level. During barbiturate a n a e s t h e s i a PT-4~ o n b o t h s i d e s w a s s i g n i f i c a n t l y l a t e r b y 8 m s e c {P <: 0 . 0 5 ) a n d s m a l l e r by 9pV (P< 0.01) when compared to the eyes-closed condition before anaesthesia. A v e r a g e r e s p o n s e s o b t a i n e d d u r i n g t h e seizure were difficult to interpret due to the
494
A. KRISS ET AL.
Group Average 14 Patients Right E.C.T.
Left side
Approximate recording time (minutes}
Right side
I ....
' ....
I ....
' ....
I ....
' ....
<-0
I'
<--5 C 0 < - 10 Anaesthe~i~l <--15
Fit
Period
<-0
<-'5
<-- I0
4-15
(/ ( (c I .........
I .........
I
......... 1.
I .........
0
I .........
I00
I .........
200
t.
<-20
<--25
4--30
300reset
Fig. 3. Group average responses of 14 patients who received right ECT showing the changes in the flash VEP occurring during the recording session. C and O indicate responses averaged with the eyes closed and opened, respectively. Note differences in amplitude and latency between eyes-open and -closed conditions and the depressed activity on the right after ECT.
c o n f o u n d i n g effects o f the high voltage backg r o u n d activity p r e s e n t during this period. Nevertheless, P 5 0 was d e t e c t a b l e in half the recordings while P--l-4-0 seemed t o be p r e s e n t in a b o u t a third.
F o r the first few averaging runs o f the postictal p e r i o d the V E P was bilaterally depressed and t h e n r e t u r n e d a s y m m e t r i c a l l y , recovering faster on t h e u n t r e a t e d Side. Within a b o u t 2 rain after the s h o c k there were significant
FLASH VEP FOLLOWING UNILATERAL ECT Group Average 14 patients Eyes open
Left side
,----,
. . . . .
w ,
. . . . . . . .
Right side
, . . . . .
I....,....I ......... I....,....I.
'
....
, . . . . .
"
l
'
"
'
"
'
"
l
"
I......... I ...... I....,....I.
I I0uV
Fig. 4. Comparison of first and last group average VEPs with eyes open for the 14 patients receiving right ECT. A persistent latency increase of P140 was found for the response recorded on both sides"after ECT. left/right differences in both amplitude (P 0.02) and latency ( P < 0.05) with P140 on the treated side being, on average, 5 p V smaller and 12 msec later than on the untreated side. These asymmetries progressively resolved with a tendency for amplitude to recover faster than latency. Analysis of the individual data showed that the average duration of the ~ asymmetry, measured to the point at which it returned to its pre-ECT left/ right ratio, was 9.8 min (S.D. 4.9) for amplitude and 14.6 min (S.D. 6.8) for latency. However, the group average responses showed a more persistent tendency for peaks to be smaller and more rounded on the treated side due to the 'smearing effect' resulting from adding individual responses with different rates of recovery. Fig. 4 compares the first and last responses with eyes open for the group data. A significant (P < 0.01) bilateral latency increase of 10 msec was seen to persist at the end of the recording. Fig. 5 shows the group average responses of the 3 patients who received left ECT. Similar but converse changes are seen with the left side being the more profoundly affected by the treatment. No significant correlation was found
495 between the initial P]4~0 latency and the number of previous treatments. There was also no significant relationship between either duration of EEG seizure activity, shock size or time to eye opening after ECT and the duration of either amplitude or latency asymmetries. It is nevertheless of interest to note that the only patient who did n o t show evidence of any asymmetry had a short-lasting seizure with atypical symmetrical epileptic activity in the EEG. In order to assess response variability the recordings of 5 patients (4 R ECT, 1 L ECT) were re-averaged using a computer program which calculated and displayed the amplitude variance of each ordinate. No significant d i f ference was found between the two sides as far as variance was concerned. It is therefore improbable that the amplitude asymmetry after the seizure was due to a greater a m o u n t of response variability or to the increased noise level associated with slow wave activity on the treated side. Lastly, the ERG exhibited no significant changes in either the ampl!tude or latency of the 'a' and 'b' waves when a comparison was made of these measures before and after treatment.
Discussion The results of this study have shown the flash VEP to be altered by several factors, some related and some unrelated to the treatm e n t procedure. Even before anaesthesia the major positive peak (P--]4~0) was significantly later and had a non-significant tendency to be larger when stimulation was performed with the eyes closed. During barbiturate anaesthesia this c o m p o n e n t showed a further moderate increase in latency and was greatly attenuated. Immediately following unilateral ECT the entire response was bilaterally depressed and subsequently returned asymmetrically, with the untreated side recovering faster. On average, both amplitude and latency asymmetries had resolved within 15 min of the shock,
496 Group
A. K R I S S ET AL. Average Approximate recording time (minutes)
S Patients Left
E.C.T.
Lelt side
Right side
4-0
(0 4-5
C 0
4-- 10 J
\
,,
Anaesthesia
4-- 15
4-0
Recovery Period
4-
5
~-- 10 C C 0 C
~ " I~
0 C 0 C
4-I~0
0
~
25
C I~- . . . . . . . I . . . . . . . . .
I.........
I.
1. . . . . . . . .
0
I . . . . , . . . . I . . . . . . . . . l, 100 200 300msec
~1-80
Fig. 5. G r o u p average for t h e 3 p a t i e n t s w h o received left ECT s h o w i n g t h e changes of t h e flash V E P o c c u r r i n g d u r i n g t h e r e c o r d i n g session. N o t e t h e o p p o s i t e p a t t e r n of a s y m m e t r y c o m p a r e d to right ECT (Fig. 3) w i t h m o r e persistent d e p r e s s i o n o f activity o n t h e left a f t e r t r e a t m e n t .
FLASH VEP FOLLOWING UNILATERAL ECT b u t a latency increase, c o m m o n to both sides, persisted b e y o n d the end of the 0.5 h recording session. The VEP changes associated with eye closure agree with those reported by others (Van H o f 1960; Gastaut and Regis 1965; Domino 1967; J o n k m a n 1967). It is likely that several factors are responsible for causing these changes. Following lowering of the eyelids the retinal adaptation level is altered towards the scotopic state and this has been reported to selectively enhance c o m p o n e n t 5c (180 + 40 msec) of the major positive c o m p o n e n t (wave 5) (Gastaut and Regis 1965). Furthermore, while eye closure reduces the intensity of light entering the eye, a factor known to increase latency (Vaughan 1966; Creutzfeldt and Kuhnt 1967) it also results in dilation of the pupils, which is reported to increase the amplitude of the VEP (Bergamini and Bergamasco 1967). Enhancement of the response may also occur from the change in hue towards red (Perry and Childers 1969) due to transillumination of the eyelids. Although there was evidence that early components may persist during the seizure, was not detectable in the majority of recordings. It is difficult to c o m m e n t on the cause of these alterations during this phase of the recording as no clear distinction can be made between the attenuating effects of the anaesthetic and the effects of the seizure itself. Rodin et al. (1966} claimed that all c o m p o n e n t s of the flash VEP tended to persist during the clonic stages of seizures induced by the convulsant drug megimide, when this was administered without prior anaesthetic, and concluded that neural elements responsible for the response were not involved in seizure activity. However, these authors reported that the VEP was not discernible for about 1 min after the end of the fit and suggested that hypoxic mechanisms may be responsible for this. The finding that the VEP following ECT also is definitely, but transiently, attenuated agrees with the reports of Corletto et al. (1966a, b) w h o recorded the response after bilateral ECT. These authors,
497 however, did not report any latency changes, nor did they c o m m e n t on the symmetry of the response. In the present study, clear VEP asymmetries were found in the immediate post-ictal period, which usually resolved within 0.5 h following the shock. It is therefore not surprising that some previous investigations failed to show definite hemisphere differences (Small et al. 1970; Small and Small 1971) when the flash response was recorded more than 1 h after unilateral treatment. The present findings demonstrated clearly that the treated side was always the most profoundly affected. This is in contrast to the non-significant trend reported by Small and Small (1971) where latency changes were more prominent on the dominant side regardless of which hemisphere received the treatment. The present investigation was concerned with electrophysiological effects of ECT and their time course and it was n o t feasible to assess patients for concomitant neurological defects. A separate study was performed, however, in which patients were examined during the immediate post-ictal period and the findings have been reported elsewhere (Kriss et al. 1978b). In brief, transient neurological deficits referable to the treated hemisphere were found to occur over a similar time period to the VEP changes. Among these were h o m o n y m o u s hemianopia lasting on average 10 min and both visual and tactile inattention persisting usually for just under 15 min following treatment. The flash VEP asymmetries seen after unilateral ECT are similar to those reported in clinical conditions associated with hemianopic defects, that is, with the side of the lesion having VEP components which are smaller and later (Vaughan et al. 1963; Vaughan and Katzman 1964; Gastaut and Regis 1965; Kooi et al. 1965; Crighel and Botez 1966; J o n k m a n 1967; Oosterhuis et al. 1969; Harding et al. 1970). In this respect the lateralisation of the flash response differs from that for the pattern reversal response (Barrett et al. 1976; Blumhardt et al. 1977). From our studies, it is
498 tempting to postulate an association between the duration of hemianopia and the VEP amplitude asymmetry on the one hand, and the inattention and latency asymmetry on the other. However, such tentative suggestions must await further testing by the concurrent assessment of both VEP and neurological asymmetries in the same patient. In spite of the fact that no significant correlations were found between the duration of VEP asymmetries and either the duration of the seizure, time to eye opening or shock size, it may still be that the more likely factor influencing post-ictal asymmetries is the seizure itself, as post-ictal suppression of the flash VEP is seen after seizures induced by convulsant drugs (Rodin et al. 1966) and an association between seizure and post-seizure activity has been shown for the EEG (Ottosson 1962). The latency increase still present at the end of the recording could have been attributable to the combined effects of anaesthesia, the patients' reduced level of arousal and the effects of ECT itself or to any one or more of these factors. Studies in monkeys have shown that the later components of the flash response may take over 0.5 h to return to their pre-drug status after barbiturate anaesthesia (Hughes 1964). In man, VEP latencies have been reported to be increased in the 'groggy' or cloudy stage after awakening from natural sleep (Shagass and Trusty 1966; Saier et al. 1968). In the present study no information is available on how long the bilateral latency increase took to resolve as no longterm follow-up of the VEP was done. It is of interest to note, however, that Small et al. (1970) commented on a general tendency for VEP peak latencies to be increased the day after treatment. The discrepant behaviour of the visual and somatosensory responses following unilateral ECT suggests fundamental differences in the nature of the responses to these two modatities. As reported elsewhere (Kriss et al. 1980), the SEP showed no consistent hemisphere asymmetries after ECT and patients had no
A. KRISS ET AL. significant left/right differences in their subjective sensory threshold. In an associated study of neurological signs, however, lateralised deficits including hemiparesis and tactile inattention were c o m m o n l y found to occur after unilateral treatment (Kriss et al. 1978b). Previous studies have also found that the somatosensory response may be normal in the presence of inattention and/or hemiplegia (Giblin 1964; Liberson and Scott 1964). On the other hand, the SEP has been found to be profoundly altered in lesions of the dorsal column/medial lemniscal pathway and primary sensory cortex (Halliday and Wakefield 1963; Giblin 1964; Domino et al. 1965; Stohr and Goldring 1969; Williamson et al. 1970). By contrast, the post-ECT flash response was found to be asymmetrical in the present study, paralleling the clinical evidence of visual defects over the same period (Kriss et al. 1978b). Compared to the somatosensory response to electrical stimulation, the origin of the flash response is poorly understood. The latter has been reported to persist in cortical blindness (Crighel and Poilici 1968; Brindley et al. 1969; Spehlmann et al. 1977) and, conversely, to be altered in the absence of frank visual defects (Bergamini and Bergamasco 1967; J o n k m a n 1967; Schneider 1968; Oosterhuis et al. 1969). It is known from animal studies that there are retino-cortical pathways other than the direct geniculo-striate route which are also capable of influencing occipital activity following visual stimulation. In m o n k e y , a response to flash is still recordable over the posterior cortical regions in spite of experimental lesions involving striate and peristriate areas (Cohn 1969; Vaughan and Gross 1969). These less direct pathways involve thalamic association nuclei, midbrain and brain stem structures such as the pretectum, rectum, superior colticulus and reticular formation (Thompson et al. 1963; Buser and Bignall 1967; Rose and Lindsley 1968; Marg 1973; Sprague et al. 1973). Cortical projections from these structures are usually well localized though in the case of the reticular forma-
FLASH VEP FOLLOWING UNILATERAL ECT tion a more diffuse projection is reported (Jasper 1954). Ciganek (1965) concluded, on the basis of the effects on the flash VEP of sleep, anaesthesia and rapid stimulation (Ciganek 1961), and on cross-modality comparisons (Ciganek 1965), that components earlier than 100 msec were localized association area responses and later components reflected activity of the diffuse projection system. If true, this concept might help to explain the VEP changes seen after unilateral ECT, for the diffuse projection pathways have been shown to be intimately involved in producing generalized epileptic discharges (Jasper 1954). EEG seizures seen following unilateral ECT appear to be very similar to the unilateral EEG seizures seen in epileptics (see Kriss et al. 1978a for fuller discussion) in which epileptic activity though generalized has a greater emphasis in one hemisphere (Gastaut et al. 1962). The asymmetry of the VEP after the seizure could reflect the involvement of the generator neurones in the seizure activity itself. Attenuation of evoked activity followed by gradual recovery is characteristically seen in neural tissue involved in epileptic discharges (Jasper 1954).
Summary The flash evoked potential (VEP) was recorded in 16 depressed patients before, during and for 0.5 h following administration of unilateral ECT. In 14 the recordings were made following right ECT and in 3 following left ECT. One patient was recorded after right- and left-sided treatments administered on separate occasions. While the patients were conscious, responses were averaged with eyes open and eyes closed. During anaesthesia, ictus and post-ictal coma the response to repetitive stimulation through closed eyes was recorded continuously in sequential runs. Consistent latency differences between VEPs with eyes open and closed were established in the runs prior to treatment. In post-
499 ictal coma there was a marked asymmetry in the response from the two sides. C o m p o n e n t P-i~0, in particular, was significantly smaller and later over the side which received ECT. On average, these asymmetries lasted less than 15 min following the treatment. A significant latency increase, c o m m o n to both hemispheres, was found at the end of the recording session.
Rdsumd Potentiels dvoquds visuels aprds dlectrochoc unilatdral. H Le potentiel dvoqud visuel (PEV) a dtd enregistrd chez 16 malades d~primds avant, pendant et durant 0,5 h qui suivait l'application unilatdrale d'dlectrochocs. Chez 14 malades, les enregistrements furent r~alis~s apr~s dlectrochocs droits et dans 3 cas, apr~s dlectrochocs gauches. Chez un patient, l'enregistrement a dt~ pratiqud apr~s traitements fi droite et fi gauche, appliques ~ des occasions distinctes. Pendant que les patients dtaient consients, les rdponses dtaient moyenn~es sdpardment avec les yeux ouverts et ferm~s. Durant l'anesthdsie, la crise et le coma post-critique, des sdquences de rdponses ~ la stimulation rdpdtitive dtaient continuellement enregistrdes, les yeux dtant fermds. Des differences de latence stables furent observdes entre les PEVs recueillis avant traitement, selon que les yeux dtaient ouverts ou ferm~s. Durant le coma post-critique, une asym~trie nette a ~td constat~e entre r~ponses recueillies d'un c6td ou de l'autre. La composante P140 en particulier, dtait significativement plus petite et plus tardive du cStd ayant subi l'dlectrochoc. En m o y e n n e ces asymdtries duraient moins de 15 min apr~s le traitement. Une augmentation significative de latence, identique des deux cStds, fut trouv~e fi la fin de la pdriode d'enregistrement. We would like to thank Dr. Geoff Barrett for programming assistance and Mr. Jack Pitman for technical support.
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