The distinction between absence petit mal and psychomotor seizures

THE DISTINCTION

BETWEEN ABSENCE PETIT MAL AND PSYCHOMOTOR

SEIZURES

LEVER F. STEWART, Department of Neurology, University of Virginia School of Medicine and The Neurological Service, University of Virginia Hospital, Charlottesville, Virginia, USA.

SUMMARY A brief discussion of the manifestations of limbic lobe discharge as opposed to discharge in neocortical temporal lobe structures is given. The opinion is expressed that, apart from certain characteristic limbic auras, the manifestations of psychomotor epilepsy are those of inactivation of brain stem mechanisms subserving consciousness. A brief discussion of other manifestations of inactivation of brain stem mechanisms subserving various other functions, as seen in other clinical patterns of epileptic discharge, follows. Hippocampal sclerosis is put forth as the cause rather than the result of seizures in both the juvenile and the adult age groups. It is proposed that limbic lobe structures have a low threshold for initiating epileptic discharge when injured, are predisposed to injury and give rise to discharge which has preferential access to brain stem structures. It is stated that petit mal absences and psychomotor attacks are clinically indistinguishable. The further opinion is expressed that the 3 per second wave and spike EEG pattern associated with petit mal is an epiphenomenon dependent upon the maturational stage of development of the brain at the time when the causative lesion responsible for epilepsy is acquired. The view that the 3 per second wave and spike pattern is a direct correlate of the clinical manifestations of epilepsy, in those patients who show this pattern, is challenged. It is concluded that the pattern is the result of rostral brain stem discharge acting upon the cortex. The view is offered that two factors are necessary for the development of epilepsy: (1) an adequate pathological basis in the form of a cerebral lesion and (2) a greater or lesser predisposition toward inadequate biochemical mechanisms tending to check or control the spread of seizure discharge, the latter being in all probability at least partially genetically determined. It is concluded that triggering cortical foci exist in nearly all cases of epilepsy, though the participation of brain stem structures is essential to explain many of the clinical and EEG manifestations of the attack.

INTRODUCTION A recent review of “Basic Mechanisms of the Epilepsies” states that “most of these studies are needle in the haystack searches, whose empirical strategy and ultimate goals lack conceptual clarity. There is a quixotic flavor to these quests, with epileptic neurones for windmills and micro-electrodes for lances.” “The enormous efforts going into some of these pseudorelevant investigations might well be devoted to a more systematic analysis of normal structure-function relations . . . 99 It goes on to say, “We already know that major differences in structure among brain areas are paralleled by differences in susceptibility to epileptic activity. The reasons for this should more readily be revealed by study of normal brain than of the capricious and uncontrolled manifestations of induced seizure foci.” Finally, “Much of the reported work reflects an emphasis upon technique rather than thoughtful analysis of the real problems of epilepsy and of the ways in which epilepsy can contribute to a knowledge of brain mechanisms” (1). No clinician accustomed to dealing with patients who suffer from epilepsy can fail to have been struck by the close similarity between the clinical attack patterns of absence petit mal and psychomotor epilepsy. Traditionally, the first of these two types of seizures is regarded by most authorities, in the larger proportion of cases, to be arising primarily from brain stem structures; while the second is regarded as originating in the cortex of one or other temporal lobe. The widely differing electroencephalographic manifestations accompanying these two clinical patterns of attack have done much to lend support to these views. Twenty years ago, it was pointed out that the clinical symptomatology in cases of so-called “idiopathic” 185

epilepsy is indistinguishable from that encountered in “psychomotor” epilepsy. Attention was also called to the fact that the lesions found in psychomotor epilepsy are histologically identical to the cortical sclerosis described in classical idiopathic epilepsy and are found in the convexity of the temporal lobe, its infero-medial aspect, the perifalciform and, particularly, rhinencephalic structures (2). This paper is an attempt to reexamine the traditional concepts relating to these two common forms of epilepsy in the light of rather less orthodox views of the origin and significance of their clinical attack patterns and accompanying electroencephalographic correlates.

DEFINITIONS Clinically, a petit mal absence attack has been defined by the Committee on Classification of the International League Against Epilepsy as beginning suddenly with an alteration or loss of awareness and/or responsiveness without gross convulsive movements. There may be, in addition, what is clinically termed a blank stare, brief upward rotation of the eyes, interruption of activity and maintenance of posture. It ends quickly, is usually brief, but may vary in duration. One must distinguish between temporal lobe, psychomotor and limbic lobe seizures. Temporal lobe seizures are those arising in temporal lobe neocortex and carry such focal signatures as highly structured auditory and vibual hallucinations, manifestations of deja vu and jamais vu, distortions of visual and/or auditory perspective, dysphasia, depersonalization, autoscopy 9 “forced thinking” and certain “fugue” states, Psychomotor seizures (automatisms) clearly differ from temporal lobe seizures arising focally in neocortex, in that during them, as is the case during the petit ma1 absence,

consciousness is impaired even though a grand mal seizure does not develop. This would seem to indicate bilateral cerebral or, more likely, brain stem involvement. Though consciousness may be impaired in non-limbic, temporal lobe neocortical discharge in some cases in which the attack does not progress to become a grand mal seizure, it seems probable that the degree of this impairment is relative and largely due to the patient’s preoccupation with the subjective content of his seizure. Even in these situations he can often recall what transpired in the external environment during the attack, whereas this is seldom the case following a psychomotor seizure. The so-called “focal” manifestations of psychomotor automatisms really often do not represent evidence of local epile@ic discharge at all, but rather continuance of normal motor activity of a low order of complexity in a situation in which brain stem mechanisms subserving the maintenance of consciousness are impaired. Such common manifestations of the psychomotor attack as mumbling, fumbling and disrobing may be used to illustrate this point. The motor activity seen in these attacks is frequently in context with the situation that obtains and often represents a continuation of motor activity initiated prior to the onset of the seizure (3), though the protracted continuation of this activity may no longer be appropriate. No clinical distinction is possible between a petit mal absence attack and a psychomotor seizure (3,4) nor does it seem likely that any fundamental physiological distinction exists. Both patterns of attack are commonly preceded by a’ rising epigastric aura as a focal manifestation of limbic lobe discharge. The distinction between the clinical seizure patterns of absence petit mal and psychomotor automatism is made on the basis of the patient’s age: if a child he is presumed to have petit mal (though such does not always prove to be the case from the EEG point of view); if an adult he is presumed to have psychomotor epilepsy. The limbic lobe, consisting of the uncus, amygdala, hippocampus, hippocampal gyrus, dentate gyrus and cornu Ammonis, is the site of cortical representation of visceral function, hence olfactory and gustatory auras, lip-smacking, chewing and swallowing movements, rising epigastric auras, changes in pupillary size, blood pressure, heart rate, skin color, diaphoresis, piloerection, sensations of fear and other subjective and objective manifestation of visceral activity are the manifestations of focal discharge in this area. Discharge from the limbic lobe would seem to have preferential access to brain stem structures (5). Further clarification of the distinction between limbic lobe and psychomotor seizures is indicated. It may be said that, in a large proportion of cases, the triggering focus of more general epileptic discharge, due to involvement of brain stem structures, lies in the limbic lobe in patients suffering from psychomotor seizures. Such clinical evidence of limbic lobe discharge as lip-smacking and chewing and swallowing movements (presumably resulting from the patient experiencing a gustatory aura) are the only focal manifestations of psychomotor epilepsy in most cases. The more striking features of the attack, which accompany these focal manifestations and often persist for a time following their discontinuation, are those of the psychomotor automatism proper, in which the patient manifests evidences of impaired

contact with his environment, is slow to respond mentally and physically (if, indeed, he responds at all) to external stimuli and manifests evidences of stereotyped behavior which may well have been initiated appropriately prior to the commencement of the attack, but which are no longer appropriate in context with the situation, by virtue of being protracted to the point where they cease to serve a useful purpose and simply become meaninglessly repetitive. For example, a housewife might be polishing a mirror at the beginning of her attack and continue to do so during the seizure, long after the mirror is clean; or a mechanic removing a tire from an automobile might spin the same wheel lug back and forth on its shaft without removing it completely and getting on with the business of changing the tire. Because of the extensive interconnections between limbic structures and anterior temporal lobe neocortex, clinical evidence of psychomotor activity and of focal epileptic discharge referable to temporal lobe neocortex are sometimes observed in the same seizure, and the EEG frequently shows spiking over the lateral convexity of the temporal lobe, as well as over its mesiobasal aspect, in the inter-ictal state. From an electroencephalographic point of view, the EEG during a psychomotor seizure commonly shows bisynchronous, 2 to 10 cycle per second discharges predominating fronto-temporally. Sharp waves or spikes may be interspersed. Fluctuating asymmetries are common during the attack. Usually, any focal, sporadic spiking prior to the onset of the attack disappears and suppression of electrical activity in all relevant leads may briefly precede the onset of the bisynchronous, rhythmic discharges characterizing the electrographic seizure. This pattern holds true in about eighty-five percent of cases (6) (Fig. 1). The patient was unresponsive during the time represented by the EEG sample. Note the similarity to the three per second wave and spike pattern of petit mal, save for the absence of spikes. In each case, the abnormality is diffuse. If the EEG abnormality remains more or less limited to temporo-limbic structures during a clinical seizure (Fig. 2), consciousness is unimpaired and responsivity and contact with the environment are maintained: i.e., there are no characteristic “psychomotor” manifestations. The arrow at the bottom of the figure indicates the onset of clinical symptomatology as well as the onset of EEG abnormality at T4 The patient complained at this time of feeling sick, nauseated and vertiginous, and of experiencing numbness in the left leg and an unpleasant taste in his mouth. He remained alert and responsive throughout, speech being tmaffected. Where the electroencephalographic concomitants of absence petit mal are concerned, the situation is quite different. Here, clinical evidences of seizure activity are accompanied by the paroxysmal appearance of high amplitude, rhythmic, bisynchronous, generalized, 3 per second wave and spike activity, which ceases at the end of the attack as suddenly as it commenced (Fig. 3). It can, thus, be seen that the basis for making a distinction between absence petit mal and psychomotor automatisms relates largely to the differences between the electroencephalographic patterns observed in association 186

!

Figure 1:

EEG L4,bORATORY. UNIVERSITY OF VIRGINIA HOSPITAL

Diffuse EEG abnormality recorded during a psychomotor

/

187

seizure. See text for explanation.

children (8, 9), though such is not the case in adults (10, 11). If hippocampal sclerosis were the result and not the cause of seizures in adults with limbic lobe or psychomotor attacks, it would be dimcult to understand why all adult epileptics do not show the finding, rather than just those whose seizure foci, clinically and on electroencephalographic examination, correspond to the localization of the pathologic lesion. Furthermore, it would be difllcult to account for the initial seizure in such patients in view of the absence, in most cases, of any other possibly relevant pathological lesion capable of accounting for the development of epilepsy (7). Furthermore, if the hippocampal lesion were not responsible for the epilepsy (psychomotor; limbic lobe) in the adult group, resection of this area in temporal lobectomy would not, contrary to what is the case (1 I), be essential for the abolition of the seizures in most cases. Thus, in the adult, the evidence for a causal relationship between hippocampal sclerosis and psychomotor or limbic lobe epilepsy seems incontrovertible. Of course, the pathological lesion need not always be that of hippocampal sclerosis, for hamartomas and other forms of neoplasm involving the limbic lobe are also well recognized as a cause of psychomotor epilepsy. The lesion of hippocampal sclerosis is also common in the age group whose seizures start before puberty, however (8, 7). Surely hippocampal sclerosis is not a common lesion in

with these two types of seizure and to the predominance of petit mal absence attacks in the age group under twenty. An attempt will be made on the basis of the author’s interpretation of the evidence presented in the following pages, to convince the reader that, as is the case with the attack characterized by psychomotor automatisms, in the case of the attack characterized by absence petit mal, the triggering focus lies in the limbic lobe. In both instances, it is the preferential access to brain stem structures of discharge arising in the limbic lobe that precipitates the indistinguishable manifestations of absence in the petit mal attack and impaired contact with the environment, accompanied by purposeless stereotyped activity, in the psychomotor attack.

PATHOLOGY

Let us now turn to a brief consideration of the pathological substratum of epilepsy as it concerns the limbic lobe. The desirability of substituting the term “hippocampal sclerosis” for the more usual “Ammon’s horn sclerosis”, so that those pathological changes characterized by cell loss and gliosis in the end folium are included, has been emphasized by Margerison (7) and that convention will be adhered to in this paper. The lesion of hippocampal sclerosis has generally been regarded as secondary to anoxia resulting from epileptic discharge, rather than causative of such discharge, in 187

Figure 2:

~~~

Figure 3:

EEG abnormality recorded during a limbic lobe seizure. See text for explanation.

EJ?G recorded during an absence petit mal attack. See text for explanation.

188

patients suffering from epilepsy which commences prior to puberty because these patients have had their seizures longest and have had greater opportunity to develop nonspecific hypoxic change in consequence of them. It seems much more likely that the pathology and subsequent seizures are due to uncal herniation sustained at birth with consequent injury to hippocampal structures, either directly or secondary to compromise of the circulation to these structures (12, 7). Similar mechanisms of injury occurring after birth, but before puberty, may be invoked to explain the hippocampal lesion in those cases in which birth trauma is thought not to be a factor. In this age group (postnatal but prepubertal), direct damage sustained in closed head injury may also be a factor. Because many of the patients with hippocampal sclerosis have hypoxic lesions elsewhere in the brain (though not consistently localized to any particular area), it seems reasonable that the threshold of the hippocampal area for giving rise to seizures when damaged (perhaps partly due to its apparent preferential access by neuronal propagation to brain stem structures) is lower than this threshold in other parts of the brain ( 13). It is important to note that in a series of cases exposed to diffuse cerebral hypoxia in consequence of hypotension, the lesion of hippocampal sclerosis was not prominent among those found in the brain (14, 15). It thus seems unlikely that hypoxia resulting from non-specific causes, such as a grand mal seizure, would produce the lesion. Furthermore, it is impossible on this basis to explain the presence of such a lesion in those patients whose seizure pattern (petit mal; psychomotor; limbic) is such as to be unassociated with the development of systemic hypoxia during the attack. Not every patient with a focus of pathological change in the brain need have seizures, because more than focal pathology is needed to produce a fit. It seems reasonable to assume, for epilepsy, that an adequate pathological basis in the brain must be combined with a predisposition toward inadequate mechanisms to contain the spread of seizure discharge (16). Only the second of these two factors is, at least in part, genetically determined and doubtless entirely biochemical in nature. Perhaps it can be regarded as the individual’s inborn “anticonvulsant” mechanism, at least from a teleological point of view (17). Nor need brain trauma at birth be proved in every case of hippocampal sclerosis in the prepubertal age group, though it seems likely to occur. albeit clinically undetected, during nearly every delivery. Thus, the pathophysiological potential for a high incidence of limbic lobe seizures in all age groups exists and is likely to be related to the low seizure threshold that characterizes the limbic lobe and its marked susceptibility to injury. This injury could be sustained directly by uncal herniation at birth or in consequence of closed head injury in later life, or it could be sustained indirectly by compression of the vascular supply to the limbic lobe in any age group. Partial herniation of the uncus through the incisura of the tentorium as a result of supratentorial compression in the infant during birth, when the sutures are open and the plates of the skull slide over one another as the head is compressed in passage through the birth canal, is already a

well documented mechanism of injury to this structure (18, 19, 20, 13).

PHYSIOLOGY The experimental evidence for and against the existence of the “centrencephalic” system and its postulated functional mechanisms, including primary and secondary bilateral synchrony, has already been reviewed (21). Suffice it to say here that the term “centrencephalic” is usually employed interchangeably with “idiopathic” or “cryptogenie”. All of these terms carry with them an etiologic connotation and attempt to explain those cases of absence, myoclonic and akinetic petit mal and grand mal, characterized by a 3 per second wave and spike EEG pattern and occurring in the younger age group in the presumed absence of structural brain disease, in terms of dysfunction arising primarily at the brain stem level. Genetic factors are usually invoked to provide a specific etiologic mechanism to account for the postulated aberrations in brain stem function. The terms “primary” and “secondary” bilateral synchrony are electroencephalographic. Primary bilateral synchrony is a diffuse electroencephalographic correlate of epileptic activity thought to be arising de nouo at the brain stem level. In secondary bilateral synchrony, a cortical focus of epileptic discharge is thought to serve as a triggering mechanism for discharges conducted over pathways to a centrally located neuronal network which then fires centrifugally over bilateral projection pathways to set up bilaterally synchronous, rhythmic discharges over wide areas of the cortex of both hemispheres (22). It has become evident that primary and secondary bilateral synchrony cannot be distinguished electroencephalographically (23, 24, 25). It is important to note, however, that the spread of paroxysmal discharges, following the injection of penicillin into the midbrain and midline thalamic nuclei of the cat, occurs to the cerebral hemispheres only after secondary hippocampal activation. “Centrencephalic” structures do not act as a pacemaker, even though the experimental lesion is confined to these structures (26). Furthermore, the use of depth electrodes in man has demonstrated that hippocampal and amygdaloid structures show a prevailing importance in the triggering off of epileptic crises in both “temporal lobe” and “centrencephalic” cases, thus demonstrating the importance of the rhinencephalic system in so-called centrencephalic epilepsy (27). Finally, a recently reported case of petit mal epilepsy demonstrated “single spikes from the intracranial electrode pair overlying amygdala and hippocampus on one side and slow waves from the homotopic region on the other, “summating” at the scalp with a 3-CPS wave and spike. suggesting “focal hyperexcitability in one temporal lobe, hippocampus, or amygdala and reciprocal hyperpolarization from the contralateral homotopic region, the two processes summating and oscillating at 3-CPS over superficial neocortical structures” (28). It seems likely that the limbic lobe can discharge preferentially and in a caudal direction to brain stem mechanisms 189

responsible for the maintenance of consciousness (as in absence petit mal or psychomotor seizures), those responsible for the maintenance of postural tone (as in akinetic petit mal) or those responsible for motor activity (as in myoclonic seizures or grand mal). This concept seems likely best to account for the occasional case in which a patient will remain conscious during a grand mal fit and those cases of grand mal in which the fit will occasionally consist only of loss of consciousness with falling (consciousness and postural tone mechanisms affected) (4). Post-ictal automatism following a grand mal seizure might best be explained as psychomotor activity in a patient, with epilepsy arising focally in the libic area, in whom the initially induced brain-stem convulsive activity involved mechanisms responsible for motor activity as well as those responsible for the maintainence of consciousness. Involvement of the motor mechanisms has ceased, though that of mechanisms responsible for the maintainence of consciousness persists.

PHARMACOLOGY It may be that ethosuximide works in petit mal and primidone in psychomotor seizures, because ethosuximide inhibits the effects of propagated seizure discharge at the brain-stem level and primidone the discharging focus in the cortex. In young people, the system may usually be more sensitive to attack by the first means, and in older persons, by the second. Certainly one has seen cases with the 3 per second wave and spike pattern, and protracted absences or psychomotor seizures, who do not respond to ethosuximide, but do to primidone: usually these patients are in the intermediate, or late adolescent, age group.

EEG The liibic lobe focus can rarely be distinguished from the temporal lobe (neocortical) focus, save by the use of special techniques such as the employment of pharyngeal electrodes, sphenoidal needle electrodes, dural leads, cortical leads or depth electrodes. It seems likely that because of the maturational state of development of the brain at the time when the causative lesion of epilepsy is acquired, some patients will develop the 3 per second wave and spike EEG pattern as an electrographic manifestation of one aspect of their attacks (23), any electrographic evidence of a triggering, focal, cortical discharge being lost in the pattern of nearly instantaneously released, diffuse hypersynchrony (29). At least, this is so for scalp EEG recording. The 3 per second wave and spike pattern would, then, result from the brain stem firing back to the cortex (rostrally). It also seems likely, in many cases, to be an epiphenomenon from the clinical point of view and unlikely to be solely responsible for the patient’s impaired state of consciousness, in view of the fact that many cases have been observed in which patients remain apparently normally alert while the EEG shows diffuse, 3 per second wave and spike activity in all leads (4). The converse has also been observed, and patients may be seen to have clinical petit mal absence in the absence of concomitant EEG abnormality (3).

Petit mal is sensitive to hyperventilation, and psychomotor seizures usually are not, because youngsters are responsive to overbreathing and adults usually are not. In the interictal state, where focal epileptiform abnormalities are looked for in the EEG’s of patients suffering from absence petit mal, these are found in a high percentage of cases and are usually consistent in their location from day to day (4). CLINICAL ASPECTS Any number of case reports in the literature may be adduced to support the thesis that has been propounded, but a few examples may suffice. A patient with “propulsive” P.M. and an EEG pattern of hypsarrhythmia has been reported, in whom removal of a cyst in one temporal lobe cured the seizures (30). In another patient, bilateral, synchronous, symmetrical bursts of 3 per second wave and spike activity appeared in the EEG during the course of a left temporal lobe abscess. In addition, there was a delta wave focus in the left temporal area. Often, the 3 per second wave and spike activity was associated with diffuse, high amplitude, 7 per second theta activity. There was no relationship between the focal delta and the generalized, 3 per second wave and spike activity, but there was a clear relationship between the patient’s state of consciousness and the 3 per second wave and spike pattern. Individual bursts of wavespike activity were associated with clinical manifestations of absence, while protracted runs were associated with what clinically appeared to be P.M. status. After evacuation of the abscess, the patient became free of seizures and the EEG returned to normal (31). In an interesting case of “temporal lobe epilepsy”, characterized by grand mal and petit mal in the absence of any true aura, ferocious outbursts of rage and right temporal slowing and focal seizure activity with secondary, bilaterally synchronous disturbances by EEG; the seizures, the rage attacks and the EEG abnormalities all cleared following temporal lobectomy, which included the amygdala. The picture was attributed to a head injury sustained at age 16 months, but no pathology was found in the speciman excised at the time of surgery (32). A PROPOSED SIMPLIFIED CLASSIFICATION OF CLINICAL PATTERNS OF EPILEPTIC DISCHARGE IN TERMS OF THE FUNCTIONAL MECHANISMS POSTULATED The accompanying figure (Fig. 4) illustrates a simple, comprehensible and rational approach to the classification of the overwhelming majority of epileptic seizures. In each case the arrow pointing to grand mal simply serves as an indication of the fact that, regardless of initial seizure pattern, (or where in the cortex the triggering focus of epileptic discharge lies), any clinical manifestation of focal epileptic discharge may progress to a generalized, tonic, clonic motor convulsion. This occurs through the mechanism of the cortical focus triggering brain stem mechanisms responsible for motor activity. These, in turn, then fire “down-stream” to the anterior horn cells of the spinal cord.

FITS STARTING

( nearly

GRAND MAL

+

IN THE CORTEX

FOCALLY all

epilepsy

/ OTHER THAN LIMBIC LOBE FOCAL

GRAND MAL

ABSENCE

4

Figure 4:

\ LIMBIC

LOBE FOCAL

PETIT I~TOR+ MA1

MYOCLONIC AKINETIC

)

PETIT

PETIT

GED MAL

MAL

A proposed, partial classification of the epilepsies. See text for explanation.

CONCLUSIONS

REFERENCES

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This paper is not an attempt to account for etiologically, or to explain physiologically, all known kinds of epilepsy; nor is it an attempt to provide a classification for every clinical and EEG seizure pattern. Rather it is an attempt to explain by a common mechanism those clinical and EEG manifestations of epilepsy which are overwhelmingly in the statistical majority. It seems likely that triggering cortical foci exist in nearly all cases of epilepsy, though the participation of brain stem structures is essential to explain many of the clinical and EEG manifestations of the attack. It also seems likely that in most cases, where diffuse degenerative or metabolic brain disease is not involved, diffuse EEG abnormalities in epilepsy are of a secondary and not a primary bilaterally synchronous nature. “It would therefore seem more reasonable to postulate that most cases of presumed primary brain stem epilepsy are, in fact, examples of secondary bilateral synchrony and that the electroencephalographic irregularities and deviations in clinical attack pattern are the result of triggering lesions situated in the cortex and projecting by predilection to the brain stem, rather than to an adjacent cortical area. Such an assumption does not require the presence of a demonstrable brain stem lesion, where in fact one is seldom found, nor the supposition of a derangement of function in brain stem structures at a biochemical level. While it is true that a cortical lesion is seldom found in patients suffering from “idiopathic” seizure disorders, it should be emphasized that one seldom has the opportunity to look for it. When it is looked for it is often found. It is as reasonable to attribute epilepsy to an undemonstrated cortical lesion as to an indemonstrable brain stem lesion” (21).

13. y;r$

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14.

Adams J H, Brierley J B, Connor R C R, Treip C S. The Effects of Systemic Hypotension Upon the Human Brain. Clinical and Neuropathological Observations in Eleven Cases, Brain 89, 235, 1966 15. Brierley J. The influence of Brain Swelling, Age and Hypotension Upon the Pattern of Cerebral Damage in Hypoxia Proc 5th lnt Cong Neuropath. p 21-28, 1966 16. Martinez-Lage M. Etiology and Pathogenesis of Epilepsy Bol Sot Vasco-Navarra Pediat. 2, 101, 1967 17. s3yjno$;9 C. Excitation and Inhibition in Epilepsy. Brain 82, 18. 19.

Earl K M. Baldwin M, Penfield W. lncisurai Sclerosis and Temporal Lobe Seizures Produced b Hippocampal Herniation at Birth. Arch Neuroi Psychiat. 69,27, ly933 Gastaut H, Toga M, Roger J! Gibson W C. A Correlation of Clinical, Electronencephalo raptuc and Anatomical Findings in Nine A$;psied Cases of “femporal Lobe Epilepsy”. Epilepsia 1, 56,

Acknowledgment

20.

Glaser G H. Limbic Epilepsy in Childhood. J Nerv Mental Dis

This study was supported in part by Public Health Service Training Grant MB 5 120-13.

21.

Stewart L F, Dreifuss F E. “Centrencephalic” Seizure Discharges in Patients with Focal Hemispheral Lesions. Arch Neurol. 17, 60.

144, 391. 1967

191

22. 23. 24. 25. 26. 27.

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28. 29. 30. 31.

32.

192

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with Severe