THE P.HVSIOPATHOLOGY OF EPILEPTIC SEIZURES 



335 



evoked by mid-line stimulation, are widely distributed 

 over the two hemispheres and are synchronous and 

 symmetrical on the two sides; their generalized dis- 

 tribution thus resembles that of a grand mal seizure. 



Chemical stimulation of the diencephalic brain 

 stem produces generalized electrical discharges. 

 Murphy & Geilhorn (148) obtained generalized dis- 

 charges by injecting strychnine into the hypothal- 

 amus, and recently Ralston & Ajmone-Marsan (163) 

 provoked bursts of bisynchronous con\ulsant waves, 

 predominantly frontal, by injecting penicillin into 

 the thalamic reticular formation in the mid-line. 

 These bursts could \)e precipitated by electrical stim- 

 ulation of the thalamus and appear in the same terri- 

 tory as the 'recruiting' response. The authors indeed 

 believe that propagation takes place along the non- 

 specific thalamocortical pathways responsible for the 

 recruiting response. 



It is remarkable that generalized cortical discharges 

 provoked by stimulation of the thalamic reticular 

 formation do not persist after cessation of stimulation 

 and are never accompanied by convulsions, and it is 

 even more remarkable that generalized convulsions 

 may be observed in the absence of all cortical electrical 

 discharge. This is the case notably in the tonic seizures 

 which are seen in certain forms of syncope and which 

 appear in the EEG as total electrical silence instead 

 of a generalized seizure discharge, as shown by 

 Gastaut & Fischer- Williams (63). 



It is interesting to note that techniques as unlike 

 each other as those which have been applied to the 

 study of the mechanism of generalized convulsions 

 and of the accompanying bioelectric discharges should 

 lead to similar conclusions: the incrimination of the 

 brain stem reticular formation in the origin of these 

 phenomena, the caudal part for the convulsions and 

 the rostral part for the bioelectric discharges. 



These conclusions obviously invalidate postulation 

 of direct relationships between the discharge of corti- 

 cal neurons and the muscular contractions, since both 

 of these depend upon a third event, namely the reticu- 

 lar discharge. For the same reason, no significant 

 relationships between the convulsive brain waves re- 

 corded from the scalp and the convulsive movements 

 observed at the periphery are to be expected; they are 

 separate both causally and temporally. These con- 

 siderations are further emphasized by the following 

 three observations. 



a) The onset of the EEG discharge and that of the 

 tonic phase of the grand mal fit may ije separated by 

 a relatively long time interval. 



b~) The electrical seizure discharge may occur in- 



dependently of any tonic-clonic manifestations of 

 grand mal, and vice versa. Thus EEG discharges of 

 the grand mal type may appear alone in sleep (8y\ 

 whereas tonic seizures secondary to acute cerebral 

 ischemia are not accompanied by any electrical dis- 

 charge whatsoever. 



f) The EEG discharge and the convulsions, even 

 when they begin together, do not necessarily e\olve 

 in a way which is, so to speak, superimposable. Thus, 

 simultaneous EEG and electromyographic recording 

 show some correlation during the clonic phase but 

 none during the tonic phase (5, 168). 



PETIT M.\L OF MYOCLONIC TYPE. This has bccu induced 

 in man and animals by all the measures capable of 

 provoking grand mal. M\-oclonic jerks'- occur before 

 the convulsive seizure when widespread interference 

 with cerebral function acts in a sufficiently slow and 

 progressive manner (anoxia, oxygen intoxication, 

 hypoglycemia, injection of pentylenetetrazol, picro- 

 toxin, chloralose, bromide of camphor, etc.). One 

 has but to increase the interference and metabolic 

 disturbance slightly in order to witness the appear- 

 ance of a grand mal seizure, following the m\ oclonic 

 jerks. 



However, as in grand mal, focal cerebral lesions do 

 not produce the bilateral myoclonic jerks of petit mal 

 unless they are near the mid-line or unless their action 

 is facilitated by the addition of a mild widespread 

 activator, for example a subcon\-ulsant dose of 

 pentylenetetrazol. 



When the disturbance is severe enough to pro\ oke 

 spontaneous myoclonus with its accompanying mul- 

 tiple spikes, any moderately intense sensory stimula- 

 tion, such as a sound, touch or flash of light, pre- 

 cipitates myoclonus after a very brief latent period. 

 Examples include the myoclonus provoked by sound 

 after sodium .santonin poisoning (189), myoclonus 

 evoked by touch and sound after ingestion of bromide 

 of camphor (149), and the multiple spikes and waves 

 and myoclonus produced by flicker, sound and touch 

 after pentylenetetrazol (52). There is here a further 

 analogy between experimental myoclonic jerks and 



-Jerks in myoclonic petit mal must not be confused with the 

 clonic phase of generalized convulsive epilepsy. The confusion 

 arises mainly out of etymology, but we consider it a source of 

 grave error and the subject is later treated in greater detail. 

 .Suffice it to say here that these jerks are positive phenomena, 

 related to an actual neuronal discharge in the central nervous 

 system, whereas the clonic phase in a generalized fit is a nega- 

 tive phenomenon and represents the momentary interruption 

 of the prolonged tonic discharge of grand mal. 



