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HANDBOOK OF PHYSIOLOGY 



NEUROPHYSIOLOGY 



contraction (first clonic jerk). A further period of ex- 

 tinction then follows, longer than the first, and is itself 

 foUovved by another discharge. The cycle continues in 

 this way throughout the whole of the clonic phase 

 until total exhaustion, which is characterized by 

 lasting extinction of both electrical activity and con- 

 vulsions.'^ 



Postictal recovery is slow; it is manifested elec- 

 trically by the appearance of abnormal rhythms, first 

 delta then theta, and from the clinical point of view 

 by coma and an episode of gradually clearing con- 

 fusion. 



This simplified picture of a grand mal seizure might 

 lead one to believe that the fit is limited to a cortical 

 discharge recorded on the EEG and the convulsions 

 observed clinically. This is far from being the case, 

 since all the cerebral neurons discharge at the same 

 time as the cortical cells recorded on the EEG and 

 all the peripheral effector structures are activated 

 at the same time as the skeletal muscles. Thus the 

 whole of the autonomic system is involved in a grand 

 mal seizure, but its efTects are masked by the spectacu- 

 lar nature of the generalized convulsions. We may 

 recall, for example, the fact that the smooth muscu- 

 lature is brought into play, in the pupils, nipples and 

 viscera; that salivary, sweat and vaginal glands are 

 stimulated; and that there are alterations in cardiac 

 rhythm, arterial pressure and vasomotor activity. 

 This widespread action is easily understood since the 

 diffuse projections, which radiate out from the brain 

 stem reticular formation, go not only to the cortex 

 but to all the grey matter of the brain, and because 

 the reticulospinal pathways connect with the auto- 

 nomic preganglionic centers in the brain stem and 

 spinal cord just as they do with the somatomotor 

 centers in these same regions. 



The second mechanism involves active inhibition. 

 It may be supposed that the rhythmical interruption 

 of a grand mal seizure depends not only on neuronal 

 exhaustion, but also on the development of inter- 

 mittent inhibition in ' suppressor' structures. 



Expounding this theory in 1949, Jung (116) sug- 

 gested that the inhibitory structure was the caudate 

 nucleus, for it was from there that he recorded large 

 regular slow waves, coinciding with the episodes of 

 relaxation in the clonic movements and interposed 

 between the fast rhythms recorded from the cortex 

 and the thalamus. This hypothesis agrees well with the 



" However, fatigue is probably responsible only for the 

 progressive slowing of the discharge and not for the rhythmical 

 interruption which depends exclusively on the inhibitory 

 mechanism described later. 



views of Dusser de Barenne et al. (41) who believed 

 that inhibitory neurons situated in the caudate 

 nucleus were acted upon by the various cortical 

 ' suppressor' zones, and that they were efTective 

 through the thalamus and a corticocaudothalamo- 

 cortical circuit. The close relationship between the 

 theories of Jung and of Dusser de Barenne is further 

 demonstrated by the fact that Gastaut & Hunter 

 (66) and Starzl et al. (184) recorded these same slow 

 waves in the intralaminar and mid-line nuclei of the 

 thalamus. 



From these experimental results one may postulate 

 the existence of a thalamocaudate inhilsitory system' 

 ' branched-off in a side-chain' from the nonspecific 

 thalamocortical projection system, a system which 

 may actively inhibit the reticular formation of the 

 thalamus as well as that of the caudal brain stem and 

 thus prevent the discharge of cortical spikes at the 

 same time as the peripheral contraction. 



In other words, the thalamocortical discharge of 

 grand mal responsible for cortical spikes and for 

 reticular ' release' (with its consequent tonic phase) 

 may be equally responsible for putting into action the 

 inhibitory system, the slow wav-es from which rhyth- 

 mically interrupt the discharge of spikes. The slow 

 wave represents not a convulsion wave but a veritable 

 state of neuronal depression linked to a phenomenon 

 of active inhibition (the ' braking' wave of Jung, the 

 phylactic wave of Walter, or the inhibitory wave of 

 Gastaut). 



This theory explains the absence of the true clonic 

 phase in anoxic and strychnine seizures, for in these 

 the telencephalon which incorporates the inhibitory 

 system is functionally depressed or not actively 

 brought into play. It explains why the tonic strychnine 

 convulsions can be interrupted by a clonic phase 

 when large doses of pentylenetetrazol are injected into 

 a slightly strychninized animal (fig. 5). It also ex- 

 plains why the seizures induced by pentylenetetrazol 

 or other analeptics in the diencephalic, mesencephalic 



' The existence of definite connections between the head of 

 the caudate nucleus and the nonspecific formations of the 

 thalamus has been demonstrated by physiological neuronog- 

 raphy (176). Histological proof of these connections were 

 given: a) by Ranson et al. (164, 165) and Papez (154) who 

 showed direct connections (in both directions) between the 

 pallidum and the anterior ventral nucleus of the thalamus 

 (the former receiving fibers from the caudate and the latter now 

 incorporated in the nonspecific system of the thalamus); and 

 A) by Stefens & Droogleever-Fortuyn (185) and Nauta & 

 Whitlock (151) who demonstrated projections between the 

 head of the caudate and the intralaminar and mid-line thalamic 

 nuclei. 



