Electroencephalography and Clinical Neurophysiology, 1978, 45:309--318

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© Elsevier/North-Holland Scientific Publishers, Ltd.

T R A N S C O R T I C A L R E F L E X E S AND FOCAL M O T O R EPILEPSY P. CHAUVEL *, J. LOUVEL ** and M. LAMARCHE Unitd de Recherches sur l'Epilepsie, INSERM U-97, 2 ter, rue d'Al~sia, 75014 Paris (France)

(Accepted for publication: November 18, 1977)

In some epileptic patients a passive or voluntary m o v e m e n t can trigger ~ m o t o r seizure. If the epileptogenic focus is located in a circumscribed zone of the primary m o t o r area, mobilization of the corresponding limb can produce a focal electrographic and clinical seizure. This p h e n o m e n o n has been observed on several occasions in man since Jackson (1870) and Gowers (1885), b u t it has been interpreted in many different ways over the years. Particularly because of the technical difficulty of localizing the causal lesion, the p h e n o m e n o n has, for example, been called extrapyramidal epilepsy (Spiller 1927) and related to paroxysmal choreoathetosis (Mount and Reback 1940). In man, it was ultimately recognized and classified as ' m o v e m e n t epilepsy' (Stevens 1966). More recently, we have been able to reproduce these clinical manifestations in the monkey with a chronic epileptogenic focus in the f o o t area of the m o t o r cortex (Chauvel and Lamarche 1975; Chauvel et al. 1975; Lamarche and Chauvel 1978). We have stressed the crucial role of the proprioceptive afferents (more precisely of muscular origin) in triggering and stopping these focal m o t o r seizures. Various types of stimuli were f o u n d to be effective, b u t all of them involved either sudden or repeated muscular stretching. A single brief stimulus of this kind evoked an ECoG 'spike' in the epileptogenic focus that in some cases was immediately followed b y a muscle * Attach6 de Recherches ~ I'INSERM. ** Allocataire de Recherches D G R S T .

jerk at the periphery (Lamarche and Chauvel 1975). It is thus conceivable that a transcortical reflex may be the basic element accounting for all these phenomena. The present paper will argue in favour of this possibility b y examining the electrophysiological features of the afferent pathway of such a reflex, o f its cortical transfer, and of its efferent pathway. We shall also discuss the implications this might have for the physiopathology of the m o t o r epilepsies.

Methods The experiments were conducted in 5 monkeys (Macaca n e m e s t r i n a and fascicularis) in which an epileptogenic focus was created by subpial injection of alumina cream ('Phosphalugel') according to the m e t h o d of Kopeloft et al. (1942). The alumina cream was injected into the f o o t area of the primary m o t o r cortex which had previously been delimited through cortical electrical stimulation of the anaesthetized trepanated animal. In the postoperative period the corresponding limb was observed to be slightly hypotonic. No tendon hyperreflexia was observed in any of the animals. The first ECoG and clinical signs of the i n d u c e d m o t o r epilepsy appeared approximately 6 weeks after the alumina cream injection. The seizures continued for several months and, in one case, for several years. The course of this t y p e of experimental epi-

310 lepsy varied from one animal to the next, b u t in all cases there was an alternation of periods dominated by the localized myoclonic jerks of epilepsia partialis continua, and periods characterized by more frequent Jacksoniant y p e seizures (cf. Chauvel and Lamarche 1975).

Recording At the onset of the clinical signs, transcortical muttilead electrodes were implanted in both hemispheres. Each electrode consisted in a linear array of 5 contacts. The distance between two successive contacts was 1 mm. The upper one was on the cortical surface while the deeper ones recorded from grey or white matter, depending on the geometry of the gyri and whether the electrode track was perpendicular, oblique or parallel to cortical layers. Usually 10 such electrodes were concentrated around the focal region and in the corresponding area o f the contralateral hemisphere to record ictal and interictal activities. The electrode leads were connected to sockets fastened to the skull by means of a fibreglass helmet. EMGs were recorded with 2 fine needles, insulated except at the tip, inserted in the muscle 5--10 mm apart at the time of recording. Electrical activities were recorded on a storage oscilloscope or on paper. EMGs were then processed (Averager Devices, Neurolog System) for presentation in histogram form.

Stimulation The proprioceptive afferent fibres were activated through electrical stimulation of the tibial nerve in the popliteal fossa through surface bipolar electrodes. This technique, first described b y Hoffmann (1934) in man, and developed in m o n k e y by Roll et al. (1973) permits, at threshold, a selective activation of group I fibres in a mixed nerve. The adequate localization of the stimulating electrodes and the appropriate stimulus intensity were determined according to the ability to elicit a n H reflex in the soleus muscle. Intensities were directly given by the

P. CHAUVEL ET AL. constant current stimulator (Neurolog System, Devices). Several controls were done (including tests on the experimenters themselves) to ensure that these current intensities did n o t cause any tactile or painful sensation. The observation of EMG responses in the soleus and in flexor muscles led us to assume that, in our conditions, flexor reflex afferents were not involved, even at the highest intensity used (10 mA). The stimulating electrodes and the leg position (in half extension) were maintained unchanged during the whole duration of each session (about 10 min). Cortical stimulation (via an electrical shock delivered between two leads of the same electrode) were achieved with the usual techniques.

Resul~

Each shock delivered to the tibia] nerve elicited a complex cortical response together with a series of distinct EMG bursts in the soleus.

(A ) The cortical evoked response The response to single shock stimulation of the tibia] nerve, in bipolar transcortical recording, was either biphasic or triphasic, depending on the stimulus strength. Weak stimulation (near threshold for the H reflex) elicited an evoked potential having all the characteristics of a primary response: a latency of a b o u t 10 msec (9.5--10.5 msec), a positive phase lasting 20 msec, of 200--300 pV in amplitude, and a longer (40 msec) negative phase of a b o u t 100 ~V. This response was recorded on both sides, which is n o t surprising, considering that proprioceptive projections to the m o t o r cortex are bilateral (see Albe-Fessard and Liebeskind 1966}. With stronger stimuli (generally eliciting a maxima] H reflex} the response became triphasic. The positive phase had the usual latency and amplitude of an evoked potential, as described above. Superimposed on the negative phase, was a biphasic negative-positive potential of large amplitude (1--2 mV)

T R A N S C O R T I C A L R E F L E X E S AND EPILEPSY

and long duration (100--120 msec). This had all the distinctive features of an epileptic 'spike' (Fig. 1). The transition between the usual evoked potential and this 'evoked spike' was analysed by gradually increasing the stimulus strength: when the shock was raised from 6 to 10 mA, the latency of the high voltage negative-positive response grew shorter and shorter until finally the response followed directly and abruptly the positive phase of the primary evoked potential (Fig. 2). Although it could vary at threshold intensities, no relation could be established between spike amplitude and the above-threshold stimulus intensity: in this respect, the spike exhibited some properties of an all-or-none phenomenon. In most c~ses such a spike was only observed on the side of the focus. Increasing the stimulus strength did not change the normal pattern of the contralateral response (Fig. 2). Nevertheless in some cases, a small amplitude spike appeared contralaterally to the focus, some 10 msec later, on the other hand, the latencies of the primary evoked potentials on both sides were unchanged. Although we have no direct evidence, the difference in latencies of the spikes may indicate that the contra-

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lateral one was partly due to a callosal transfer from the focus (Fig. 1). It was thus possible to distinguish, near a m o t o r focus, the epileptic spike from the c o m p o n e n t which was actually evoked by proprioceptive input. The evoked potential appeared normal and seemed to trigger the spike.

(B) The EMG responses The EMG bursts recorded from the soleus (extensor) ipsilateral to the stimulus were characterized by a variety of specific components. Their time of occurrence, relative to that of the evoked responses and a comparison of these results with those obtained on the normal side (contralateral stimulation and contralateral recording) suggest certain hypotheses as to the origin of the bursts. (1) Description of the bursts (Fig. 3). There were 4 successive bursts. The first c o m p o n e n t occurred very early (latency 12 -+ 1 msec) and was very brief. It corresponded to the monosynaptic reflex as usually recorded under these stimulation conditions, that is, to the H response first described in man and later in the m o n k e y (Hoffmann 1934; Magladery and McDougall

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Fig. 1. Electrical stimulation of the right tibial nerve elicits both ipsi- and contralateral responses on the primary m o t o r area. The latencies of both responses are similar; however, the amplitude of the contralateral evoked potential is significantly greater. With a stimulus strength of 6 mA, an epileptic spike may appear which grows during the negative phase of the contralateral evoked potential. When the stimulus strength is raised to 10 mA, the spike is more constant and appears earlier (second traces). The typical biphasic aspect of this spike, identical to a spontaneous spike (extreme right trace), is shown with a slower sweep-speed (right traces). Note that a small negative wave is recorded from the ipsilateral m o t o r cortex, about 10 msec after the onset of the contralateral spike.

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Fig. 2. Left: latencies of both ipsi- and contralateral cortical responses to tibial nerve stimulation are identical; however, the amplitudes vary (gains are identical for both traces). Middle and right: when stimulus strength is raised from 4 mA to 10 mA, the latency of the spike is shorter and the negative wave of this spike abruptly follows the positive phase of the evoked potential. 1 9 5 0 ; Paillard 1 9 5 5 ; Roll et al. 1973). I ~ a m p l i t u d e varied with t h e s t i m u l u s s t r e n g t h a n d it gradually d i s a p p e a r e d w i t h the a p p e a r a n c e o f t h e M r e s p o n s e , t h e earlier m u s c l e r e s p o n s e due to activation of the a motor axons of the extensor muscle. T h e s e c o n d c o m p o n e n t was also b r i e f (20 m s e c ) b u t with a m e a n l a t e n c y o f 40 m s e c ( 3 5 - - 4 5 msec). It a p p e a r e d t o be c o r r e l a t e d with t h e p r e s e n c e o f t h e e p i l e p t o g e n i c f o c u s since it usually did n o t o c c u r on t h e n o r m a l side. We called this t y p e o f b u r s t El. Its a m p l i t u d e was largest with w e a k s t i m u l a t i o n , eliciting an H r a t h e r t h a n an M r e s p o n s e . T h e third b u r s t h a d a m e a n l a t e n c y o f 80 m s e c a n d was m a r k e d l y l o n g e r ( 7 0 - - 9 0 msec). It was also linked t o t h e p r e s e n c e o f t h e f o c u s since it was n e v e r elicited b y s t i m u l a t i o n o f t h e tibial nerve c o n t r a l a t e r a l t o t h e h e a l t h y h e m i s p h e r e . B o t h t h e p r o b a b i l i t y o f occurr e n c e a n d t h e a m p l i t u d e o f this r e s p o n s e , w h i c h we called E2, were d e p e n d e n t on t h e strength of stimulation. It appeared with w e a k stimuli ( w h e n t h e H r e s p o n s e was

Fig. 3. Muscular events associated w i t h cortical e v o k e d spike. R e c o r d i n g f r o m soleus. X axis = t i m e in msec; Y axis = n u m b e r o f EMG spikes per 2 msec ( s t i m u l a t i o n a r t i f a c t is suppressed). Histograms are b u i l t u p b y s u m m i n g t h e results o f 32 trials. In t h e u p p e r h i s t o g r a m , t h e first c o m p o n e n t includes M a n d H r e s p o n s e s ( t h e t w o p e a k s can b e d i s t i n g u i s h e d ) . T h e s e c o n d c o m p o n e n t is s u p p o s e d t o b e t h e t r a n s c o r t i c a t reflex associated w i t h t h e evoked p o t e n t i a l , w h e r e a s t h e t h i r d o n e w o u t d b e linked t o t h e spike itself. In t h e l o w e r histogram, o b t a i n e d w i t h s t r o n g e r stimuli, t h e H reflex has d i s a p p e a r e d a n d o n l y t h e M r e s p o n s e r e m a i n s in t h e first c o m p o n e n t . T h e s e c o n d o n e is t h e n very small, w h e r e a s t h e third is m u c h larger. No i n t e r p r e t a t i o n could b e given for t h e f o u r t h one, w h i c h is m u c h less c o n s t a n t , i.e. it is a l m o s t i n e x i s t e n t in t h e u p p e r h i s t o g r a m :

r e c o r d e d ) a n d i n c r e a s e d w i t h s t r o n g e r stimuli t h a t elicited t h e M r e s p o n s e (Fig. 4). T h e f o u r t h b u r s t had an a p p r e c i a b l y

TRANSCORTICAL REFLEXES AND EPILEPSY R .Tib.n.Stim.

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Fig. 4. E E G ( m o t o r c o r t e x ) and EMG (limb e x t e n s o r ) recordings following stimulation of tibial nerve. Left : a weak stimulation (4 m A ) elicits a c o m p l e x m y o graphic response: 1 - typical triphasic H reflex (peak at 12 msec); 2 - "transcortical r e f l e x " (latency: 40 msec); 3 - late response (80 msec) associated with t h e epileptic cortical spike. Middle: a stronger stimulus (6 m A ) is f o l l o w e d b y a m y o g r a p h i e response t h e pattern of which is slightly m o d i f i e d : 1 - the first c o m p o n e n t is n o w m o s t l y due to direct activation o f m o t o n e u r o n e fibres (M response); 2 - t h e short latency transcortical reflex is strongly r e d u c e d ; 3 - the late response is greatly enhanced. N o t e that t h e latencies o f the epileptic spike (negative cortical wave) and o f this late response are b o t h reduced. Right: stimulation (6 m A ) o f t h e tibial nerve ipsilateral t o t h e focus elicits t h e e x p e c t e d M response in the muscle whose nerve is stimulated, whereas early and late transcortical c o m p o n e n t s are small o r inexistent.

longer and more variable latency, of the order of 160--180 msec. It occurred less constantly than the other 3 types and did n o t appear to be directly related to the stimulus strength. It may correspond to a secondary postural adjustment following the other perturbations just described. It must be emphasized that, if M and H responses were constant from session to session, the probability of occurrence and the amplitudes of E1 and E2 seemed to be closely correlated with the level of excitability of the focus: they were maximal in the period just preceding a seizure and, on the contrary, they usually disappeared in the post-ictal state. (2) Correlations with the evoked response. Latency and amplitude correlations could be established between the phases of the evoked

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Fig. 5. Muscular responses elicited by stimulation of m o t o r c o r t e x close to the focus (upper traces) or contralateral to the focus ( l o w e r traces). A single shock (0.3 msec, 2 m A ) on the non-epileptic side is foll o w e d by a single muscular response (extensor and f l e x o r are co-activated), whereas the same stimulus applied w i t h i n the focal area elicits a double m y o graphic response.

spike as described above and the EMG bursts. The latency of the first burst (H or M burst) was completely independent of the cortical response. The E1 b u r s t had a relatively constant latency regardless of the stimulus strength. It began a b o u t 10 msec after the end of the positive phase of the primary evoked potential. In contrast, the latency of the E2 burst was inversely related to the stimulus strength, b u t within certain limits: in no case was the latency shorter than 65--70 msec, while the amplitude was directly related to the stimulus

314 strength. In this respect the E2 burst seemed to vary in parallel with the negative-positive evoked spike, whose latency decreased and whose amplitude increased as the stimulus became stronger. This evidence suggests that E2 is under cortical control and, more specifically, that it could be causally related to the evoked spike. (3) Results of cortical stimulation. With the same cortical electrode leads as previously used to record the evoked potential, we could deliver stimuli to the brain and activate efferent pathways, as indicated by the occurrence of EMG bursts in the corresponding flexor and extensor muscles. In this way, the efferent conduction times from the cortex to the periphery could be measured. By comparing these values with the latencies of the bursts evoked by tibial nerve stimulation, it might be possible to determine whether the E, and E2 bursts are due to transcortical reflexes. The results were as follows. Stimulation of the m o t o r cortex in the vicinity of the epileptogenic focus elicited 2 EMG bursts in the contralateral extensor (triceps surae) and flexor (tibialis anterior) muscles. The first burst had a latency of 12 msec and lasted 10-20 msec; the second had a latency of 45--50 msec and was appreciably longer (approximately 50 msec) (Fig. 5). Stimulation of the contralateral motor cortex through a symmetrical pair of electrodes elicited a single brief (10--20 msec) EMG burst with a short latency (12 msec) in the corresponding triceps surae and tibialis anterior. The later response described above was never observed on this side. Thus, from comparing the latencies of the evoked potential and of the evoked spike after peripheral stimulation with the efferent conduction times, it appears that both E1 ~md E2 could be due to a transcortical reflex. Discussion

In the first place the concept of 'evoked spike' must be discussed. Clinical and experi-

P. CHAUVEL ET AL. mental data have shown (Amantea 1920; Clementi 1929} that in the vicinity of an acute focus in a primary projection area, specific stimuli evoke large amplitude spikes. In contrast, the possible relationship between a spike and a classic evoked potential in chronic foci are n o t clearly understood. Is the spike an exaggerated form of the evoked response, in which case one could speak of a 'paroxysmal evoked potential'? Or is it a superimposed activity triggered by the afferent impulses b u t leaving the primary response unaffected? Several analyses have been p u t forward, both in man (Buser et al. 1972; Gastaut and Broughton 1972) and in natural (Naquet et al. 1975) and experimental (Amand et al. 1973; Lamarche and Chauvel 1975) animal models. In earlier studies a m p l i t u d e changes affecting specifically one of the components of the evoked response, generally the latest one, were described; however, it is most often exceedingly difficult to determine from these studies which part (if any) of a complex spike is due to the primary evoked potential. The interest of our model is precisely that it makes possible the dissociation of two components in the evoked response: ( a ) a n early activity which does not differ in its latency, diphasic pattern, duration, or amplitude from the normal evoked potential that can be recorded on the symmetrical healthy cortex; (b) a later response whose features are very similar to those of a spontaneous spike. It thus seems that, in this model at least, the evoked response is n o t modified by the existence of the focus; it may be considered as a triggering excitation that activates the focus to produce the spike, which thus develops relatively late on the negative phase of the primary response. With stronger stimulation, the lag between the evoked potential and the spike decreases and the spike then seems to integrate itself into the primary response without modifying the amplitude or duration of the initial positive phase.

TRANSCORTICAL REFLEXES AND EPILEPSY

Mechanisms of spike production The existence of close relationships between the evoked potential and the spike does not necessarily mean that the spike arises from the evoked potential by means of a purely cortico~cortical activation, or even less by intrafocal or perifocal activation. It might just as readily be assumed that the 2 successive responses result from the impact of 2 distinct afferent volleys. The existence of direct lemniscal proprioceptive pathways (Phillips et al. 1971) and of indirect pathways via the cerebellum (Murphy et ah 1975) makes this a plausible hypothesis. It might also be supposed that the primary evoked response produces a corticofugal volley which projects via a rather long loop back onto the focal region to give rise to the spike. This loop could, for example, 'be activated by inputs travelling from cerebral cortex via pons to dentate, and back via the ventro-lateral nucleus of thalamus to the same cortical system', as suggested by Murphy et al. (1974, 1975). However, the fact that the delay between the evoked potential and the spike is variable would be better explained by the activation of an intracortical network that secondarily would trigger the synchronous discharge of an unstable neuronal pool, rather than by a two-fold stimulation via two different pathways or by the involvement of a closed loop. Our results can thus be compared to those obtained with acute strychnine (Towe and Mann 1973) or penicillin foci in the sensorimotor cortex. In the penicillin preparation, weak stimulation of the nucleus ventralis lateralis (VL) triggers in the pyramidal neurones within the focus a two-fold response consisting of a complex excitatory postsynaptic potential (EPSP) followed, some 30--50 msec later, by a paroxysmal depolarization shift (PDS) (Prince 1969). Each PDS has a corresponding spike on the surface ECoG. Although these 2 models are very different, it is interesting to note that in the penicillin model also, raising the stimulus strength leads to a decrease of the time interval between the

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2 responses, the lag becoming practically zero with maximal VL stimulation (Matsumoto et al. 1969). Again, such a fluctuation is hardly compatible with the involvement of precise circuits involving, e.g., a subcortical region. It rather suggests a purely intracortical mechanism.

Significance of the E1 muscle burst Since the cortex is at one and the same time the site of projection of proprioceptive afferents and the origin of the cortico-spinal tract, it could be assumed that the E1 response is a reflex, bearing in mind what has been described under other conditions, in the anaesthetized animal, as the 'pyramidal reflex' (Buser and Ascher 1960; Patton et al. 1962). More recently, it has indeed been possible to demonstrate a 'transcortical reflex' of proprioceptive origin that also reverberates on the primary motor area. This was achieved in the unanaesthetized monkey trained to carry out a specific task (Evarts 1973; Tatton et al. 1975). Similar responses were observed in man (Melvill~lones and Watts 1971). This reflex could be revealed by voluntary muscle contraction (Upton et ai. 1971), reinforced by a certain kind of training (Milner-Brown et al. 1975; Marsden et al. 1976), and considerably modified by the presence of a parkinsonian type of motor disturbance (Lee and Tatton 1975; Tatton and Lee 1975). The neuronal organization of the mammalian motor cortex is indeed such that a cell receiving afferent impulses of muscular origin projects in turn to the very same muscle from which these impulses originate (Brooks 1971; Goldring and Ratcheson 1972; Asanuma 1975). Such a structural coupling between input and output is the anatomo-functional substrate of a transcortical reflex. In our opinion the E1 response can reasonably be considered as the analogue of this long-loop reflex; the lag between the cortical evoked response and the muscle response makes this hypothesis very plausible (Conrad et al. 1974). If this is the case, one would have to assume that the existence of the epi-

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leptogenic focus abolishes an inhibitory control that is normally exerted over this reflex arc, thus considerably enhancing a response which is generally inapparent in the untreated animal.

Significance o f the E2 muscle burst Given the relatively strict relationships between the spike and the E2 burst (the fact that both are either present or absent, their temporal relationships, etc.), E2 might be thought to represent the myoclonic jerk itself, i.e., the m o t o r phenomenon associated with the typical epileptiform spike response. However, it should b e recalled that in the nonepileptic animal or subject who has undergone special training, electromyographic bursts with approximately the same latency as E2 have been demonstrated (the V3 response described by Milner-Brown et al. 1975; the M3 response of Tatton et al. 1975). Ought V3 and M3 and, on the other hand, E2 to be considered as of the same nature, with the presence of the epileptogenic focus again being responsible not for adding a supernumerary response b u t more simply for amplifying a normally subthreshold reflex? It is difficult to answer this question because so little is known a b o u t the mechanism by which the spike is produced (see above discussion). If the spike results from a purely intracortical reactivation and if E2 is indeed linked to the spike, then E2 is definitely n o t comparable to V3 or M3, which are presumed to depend on a pathway involving the cerebellum (Angel and Lemon 1975; Milner-Brown et al. 1975; Murphy et al. 1975). If that is the case, then it must be said that the two types of response overlap or mask each other because of their similar latencies, although they are very different in origin. Transcortical reflexes and motor epilepsy It is likely that such transcortical reflexes play a role n o t only in triggering short myoclonic jerks b u t :also in maintaining longer seizures. The efferent :activity responsible for the myoclonic jerk is manifested by the contrac-

P. CHAUVEL ET AL.

tion and stretching of some muscles: a secondary proprioceptive afferent volley can thus in turn give rise to a transcortical reflex, and so on. The hypothesis that the proprioceptive afferent impulses play such a role in epileptic seizures has already been formulated by Arseni et al. (1967). Moreover, both clinical and experimental investigators are familiar with the fact that the progression of a Jacksonian seizure can be interrupted, both electroencephalographically and clinically, by grasping the limb that is first involved (see Chauvel et al. 1975}. It is thus highly probable that these afferents have a modulating function on the epileptogenic focus. Under these conditions, interrupting the proprioceptive afferent pathways might well lead to a decrease in ictal activity. This is what we are n o w attempting to achieve through a stereotaxic approach.

Summary We described in previous papers that, in the monkey with an alumina focus located in the primary m o t o r area, seizures can be triggered by proprioceptive afferents. It is also known that in man as well as in the monkey performing a specific m o t o r task, these afferents may elicit transcortical reflexes involving the primary m o t o r area. This study deals with the possible role of such long-loop reflexes in triggering myoclonic jerks and in extending the seizures. It is shown that selective stimulation of proprioceptive afferents from the limb connected to the focus results in a complex focal response, called on 'evoked spike'. This cortical response begins with an unaltered evoked potential, followed by a biphasic wave quite similar to a spontaneous epileptic spike. A complex EMG activity is associated with the evoked spike, with an initial burst (40 msec} which is supposed to be the enhancement of a physiological transcortical reflex, and a later discharge (80 msec} which seems closely linked to the pathological wave of the evoked spike, This double activation, at the cortical and at the muscular level, is to be compared

T~tANSCORTICAL REFLEXES AND EPILEPSY

with the results of electrical stimulation of motor areas: a single shock on the non-epileptic side is followed by a single motor response, whereas the same stimulus applied within the focal area elicits a double EMG response. The origins of the two components of the evoked spike and their possible relationship to the early and late EMG reflex discharges are discussed.

R~sum~

Rdflexes transcorticaux et dpilepsie motrice locale Nous avons montr~ dans un precedent travail que, chez le singe porteur d'un foyer l'alumine dans l'aire motrice, les crises peuvent ~tre d~clench~es par les aff~rences proprioceptives. On sait par ailleurs que ces aff~rences peuvent, chez le singe normal mais conditionn~, ~tre ~ l'origine de r~flexes transcorticaux articul~s sur l'aire motrice. On ~tudie ici le rSle ~ventuel de ces r~flexes dans le d~clenchement et l'entretien des crises. I1 est montr~ que la stimulation s~lective des aff~rences proprioceptives ~ la p~riph~rie dans une r~gion qui correspond ~ la localisation du foyer ~voque au niveau de ce dernier une r~ponse complexe appel~e 'pointe ~voqu~e', constitute d'un potentiel ~voqu~ peu remani~ sur lequel se greffe secondairement un accident biphasique du type 'pointe ~pileptique'. L'activit~ EMG associ~e ~ cette pointe ~voqu~e est, elle aussi, complexe. Une bouff~e pr~coce (40 msec) semble correspondre l'exag~ration d'un r~flexe transcortical physiologique, tandis qu'une bouff~e plus tardive (80 msec) paraft ~troitement li~e ~ la composante tardive, pathologique, de la pointe ~voqu~e. Cette double activation du cortex qui se traduit par un double r~flexe transcortical est ~ rapprocher des r~sultats de sa stimulation ~lectrique: du cSt~ sain, un choc isol~ entrai'ne une r~ponse motrice unique, tandis qu'effectu~e au voisinage du foyer, la m~me stimulation entrai'ne une

317

double d~charge myographique. L'origine des diff~rentes phases de la pointe ~voqu~e ainsi que les relations possibles de celles-ci avec les diff~rentes composantes de la r~ponse motrice sont discut~es.

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Transcortical reflexes and focal motor epilepsy.

Electroencephalography and Clinical Neurophysiology, 1978, 45:309--318 309 © Elsevier/North-Holland Scientific Publishers, Ltd. T R A N S C O R T I...
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