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HANDBOOK OF PHYSIOLOCJV 



NEUROPHYSIOLOGY I 



jj) The neuronal reactivity of this desynchronized 

 cortex is normal or diminished, but never augmented 

 (199). Chang (26) also found that strychnine de- 

 creased the excitability of the cortical neurons. One 

 must therefore conclude that strychnine convulsions 

 result in a caudal reticular discharge without any 

 participation in the structures of the telencephalon or 

 even of the thalamus (fig. 2). 



c) Intense tonic contraction with loss of conscious- 

 ness preceded by a few isolated clonic jerks and fol- 

 lowed by a phase of rhythmical clonic convulsions 

 are provoked by different convulsants (analeptics), 

 notably by thujone, beta-ethylbetamethylglutarimide 

 (Megimide) and pentamethylenetetrazol (Metrazol). 

 An electrophysiological study of these convulsions in 

 animals has been made by Gastaut & Hunter (65), 

 Gastaut et al. (71), AJmone-Marsan & Marossero (5) 

 and Starzl et al. (184) with the following results. 



/} During these convulsions' a hvpers\nchronous 

 discharge replaces all normal activity in the di- and 

 telencephalic formations, clearly predominating over 

 the cortex and in the thalamus. This discharge de- 

 creases in importance in the midbrain tegmentum 

 where it is not able to replace local spontaneous ac- 

 tivity. It is practically absent from the rhombencepha- 

 lon and the spinal cord where normal or increased 

 spontaneous rhythms continue. 



2) The responsiveness of the cortex to electrical 

 stimulation (as shown by the threshold and sensitivity 

 of the corticospinal neurons) remains unchanged even 

 when pentylenetetrazol is used in sufficientlv large 

 quantities to induce 'spontaneous' consulsive dis- 

 charges (199). Assessing neuronal excitability by the 

 chronaxic method, Chauchard et al. (27) demon- 

 strated that subconviilsant doses of pentylenetetrazol 

 depressed excitabilitx' of the cortex while increasing 

 that of the brain stem and spinal cord, an action com- 

 parable to that of anoxia. 



One must therefore conclude that pent\lenetetra- 

 zol-induced convulsions are evoked b\- a mechanism 

 which is analogous to that of anoxic seizures, i.e. a 

 'liberation' of the activity of the caudal reticular for- 

 mation because the overlying nervous structures are 

 functionally e.xcluded, having been in\aded by a 

 discharge (fig. 3). 



d) Convulsions have been pro\-oked in animals bv 

 the administration of pentylenetetrazol in stronglv 



' We will comider in this paragraph and the next only the 

 tonic phase of convulsions provoked by analeptics. The rhyth- 

 mic clonic phase which follows the tonic phase depends on 

 the effect of a special inhibitory mechanism, which will be the 

 object of a specicil study later. 



strychninized animals (3, 5). These convulsions are 

 expressed by: 



/) hypersynchronous di- and telencephalic dis- 

 charge of the pentslenetetrazol type and by a reticular 

 discharge in the mesorhombencephalon of strychnine 

 type, these discharges developing completely inde- 

 pendently; 



2) tonic spasm of purely strychnine type not bear- 

 ing any resemblance to pent\lenetetrazoI convulsions 

 or any relation to the cortical pentslenetetrazol dis- 

 charge. 



One must therefore conclude that these seizures 

 result from a caudal reticular discharge of strychnine 

 nature, without the participation of the di- and 

 telencephalic structures acti\ated by pentylenetetra- 

 zol (fig. 4). 



Comparing these different mechanisms, it appears 

 that generalized tonic spasm and isolated clonic con- 

 vulsions depend exclusively on the caudal reticular 

 formation which acts on the effector neurons, and 

 particularly on the motor neurons of the spinal cord, 

 by means of the various reticulospinal and vestibulo- 

 spinal pathways and projections. These pathways, 

 like the structures from which they come, are capable 

 of inhibiting as well as reinforcing muscle tone, but 

 not in the same proportion since only the medial part 

 of the caudal reticular formation is inhibitory, whereas 

 all the rest of the reticular formation and the \'estibu- 

 lar formation is facilitatory (133). It may therefore be 

 supposed that the inhibiting action is less efficacious 

 than the facilitating one and that it is entirely masked 

 when the reticular formation is activated as a whole. 

 These views are consistent with the findings of the 

 classical neurophysiologists of the Sherrington school 

 for when the portion of the reticular system, inhibi- 

 tory as well as facilitatory, lying caudal to a midbrain 

 transection, is liberated from the influence of higher 

 centers, a state of decerebrate rigidity results and not 

 one of hypotonia. The mode of activation of this 

 caudal reticular formation \aries, howe\er, for during 

 the tonic spasms it may represent either a positive 

 phenomenon, a hypersynchronous neuronal discharge 

 or a negati\e phenomenon, a liberation by depression 

 or functional exclusion of the oxerlying structures. 



The lo.ss of consciousness accompanying the con\ul- 

 sions would .seem to depend exclusively on the rostral 

 thalamic reticular formation and the cortex. In man 

 anoxic seizures (in certain syncopes) and pentylene- 

 tetrazol seizures, as indeed all other generalized 

 epileptic seizures, are accompanied by unconscious- 

 ness related to functional exclusion of the thalamo- 

 cortical system which is either depri\"ed of oxygen or 

 occupied by a hypersynchronous discharge. Con- 



