IWAYAMA, KAORU

KAKO, MAKOTO

KAWASHIMA, HISAHIKO

MORI, KAZUO

Kyoto University Research Information Repository

TitleInteraction Between Transmitted Spike-and-wave Dischargesand Evoked Visual Responses at the Secondary FocusProduced by Tungstic Acid Gel in CatsAuthor(s)MORI, KAZUO; KAKO, MAKOTO; IWAYAMA, KAORU;KAWASHIMA, HISAHIKOCitation日本外科宝函 (1968), 37(2): 265-271Issue Date1968-03-01URL http://hdl.handle.net/2433/207454RightType Departmental Bulletin PaperTextversionpublisherKyoto University原著Interae:tion Between Transmitted Spike-and-wave Discharges and Evoked Visual Responses at the Secondary Focus Produced by Tungstic Acid Gel in Cats hy KAZUO MORI, MAKOTO KAKO, KAORU IWAYAMA and HisAHIKO・KAWASHIMAFrom the Dept. Neurosurgery, Kyoto University School of Medicine (Director : Prof. Dr. HAJIME HANDA) Received for Publication Jan. 10, 1968 INTRODUCTION 265 This report concerns with a part of study of analyzing a function of so cC'.led “mirror focus”． Only a few details are known regarding the underlying mechanisms of the mirror focus, although in clinical and experimental situations, the transmitted paroxysmal dischar-ges in EEG are not infrequently observed at the homologous area contralateral to the original focus. One of the prohlems of most significance is that of deciding the role of the commissural pathway upon the propagation of the discharges from the original focus to the homotopic contralateral one. In our present study, interaction between spike-and-wave discharges transmitted from the ・original focus produced and visual cortical responses elicited by stimulating the optic radiations was observed in order to analyze the neuronal component of cortical elements primarily responsible for the organization of transmitted spike discharges. For the purpose of making animals epileptogenic, tungstic acid gel produced hy BLUM’s method (1960) 3> was topically applied to the left striate ccrtex in cats. As has been pointed out by BLACK et al. (1967) 2>, this method provided the advantage of pro-duoing a strictly localized epileptogenic lesion. METHOD Experiments were performed on 16 cats. The animals were anesthetized with ether to allow canulation of the trachea and placed in a stereotaxic head holder, then paralyzed with gallamine triethiodide (Flaxedil) and artificially respired. A piece of blotting paper 3-4 mm in diameter soaked in the tungstic acid gel was applied to the left striate cortex. As occasion demanded, 2 3 hours after the application of the drug when an atypical spike-and-wave complex (hereafter designated as ASWC) appeared in ECG, the drug soaked blotting paper was removed to prevent the establish-:!tili 日本外科宝函第37巻第2号mcnt of well matured sustained tonic clonic paroxysms. Silver wire electrodes were placed on the dura over the homotopic area (the right striate cortex) contralateral to the produced focus to record the evoked potentials as wel as elsewhere to record th~ ~！ectrocortic9gram (f:S:G). Electrodes, used for stimulation, consisted of a pair of enameled stainless stel wires which were stereotaxically inserted into the optic radiations of the right side. The exact location of these stimulating electrodes was ascertained histologically after the completion of a series of experiments. Square monophasic pulses (30 to 100 microseconds in duration, and between 0. 3 to1. 0 milliamperes) were given at a rate of one every 2 sec. Evoked potentials were observed o~dloscopically and they were stored on magnetic tape. Subsequently, wave (or component) 4 and 5 of visual cortical responses were m匂－sured, averaged and correlated graphically with other data and comparison was made to the mean amplitude obtained from the total experiments. Seizure activity was recorded with a conventional EEG machine. The temporal relation between evoked respons白， recordedoscillographically, and transmitted ASWC was established by utilizinεone EEG channel as a stimulus maker. On account of the remarkable variations of the amplitude of the evoked potentials even when no apparent changes in ECG could be observed, the comparison was made with the mean amplitude of a large number of responses. Mean amplitude of responses evoked during phases when AS＼νC was absent and during periods up to one second before the beginning of spike component of AS＼νc and two seconds after its termination were taken as the control. RESULTS 1. ECG activity after topical application of tungstic acid gel Prior to the development of a well organized rapid paroxysmal activity in ECG, atypical spike-and-wave complex (ASWC) appeared at an 紅白 wheretungstic acid gel had been applied topically and lasted for ・. ..υi・ ・ ε．， c・H・.。ー’ －. r'心.：，－」い一一：－－－－＞－－ー；ー，~べ！「；F司，a”‘’a句，.＿，.＿』喝、，幡、｛’～・F一一，，~－吋一一戸P 岬＿＿＿＿，，，ー申－・1・－’…ー一一』・｝九『h…｛一白一……『一一、J' ・－·－～－·《p、－－·－－、~ ·日 -・＇・ー、、，、旬、，T旬、園、ー－一一 ～－－ィ －ー.一一__, ・，vFig. 1 Before and after section of the corpus calosum ・。 andS indicate original and 提condary(projected J side respectively. several hours with a gradual incr聞記 infre・ quency and amplitude ASWC was also ob-served at the homotopic area contralateral to the original focus (the projected secondary area). The ASWC from the projected se・ condary area was always preceded by that from the original area, and the temporal relation between the two was calculated as approximately 10-20 msec. As has been reported in elsewhere, transection of the corpus callosum resulted in the disappearance of the projected secon・ dary ASWC completely remaining ASWC from the original area unchanged (Fig. 1 and ~）. SECONDえRYFOCUS AND EVOKED 孔じTlVITY '2()7 Fig. 2 Sucesive brain slices of the cat from Fig. 1. The corpus callosum is discon-nected in al slices. Fig. 3 Prim;iry visual cortical re叩。n盟 elicitedby the electrical stimulation of the optic radiations in cat. Positive up and nega-tive clown. Time marks 1 m田c.2. Interaction of ASWC and evoked potentials observed at the projected secondary focus Fig. 3 shows a typical primary visual cortical response recorded from one of the animals in this series which consists of four successive surface positive spikes followed by a negative wave. The component 4th (C-4) of the response was measured from the point of its initiation to the positive peak and the component 5th (C :i) was measured from the base line to its negative peak (in this and the following Fig., the positive de-flection of the evoked response always indicates upward shift from the base line and vice versa). The results of interactions between the projected ASWCs and the primary visual responses (VRs) are shown in Fig. 4. In our experimental conditions, ¥'R showed con-siderable variations in its components and the changes in amplitude were observed during various phases of the projected ASWC. However, characteristically, increase in amplitude of VR was observed without fail from immediately before (about 0. 5 sec prior to) the appearance of ASWC. In Fig. 5, changes in the overall amplitude of VRs were plotted in relation to the time course of a projected discharge and zero time is indicated by the beginning of the initial negative phase of spike in ASWC. Fig. 5 and 6 show changes in the mean amplitude of C-・I and C 5 recorded before, during and after the appearance of ASWC respectively. It is indicated that the mean amplitude of both C 4 and C 5 recorded immediately prior to the onset of ASWC was '.!):-; 日本外科宝函第37巻第2号園 園 園田圃圃． 園－1~ o ~o 2.0 圃TIME IN SECONDS 園 圃園園田Fig. 4 Alterations in visual responses recorded at the s即）ndary~ focus~ occurring during diferent phases of the projected A日VClin同 ti. Augmentation of potentials up to approximately 0. 5 sec before the onset of ASWC was observed. Numbers indicate time at which伊tentialswere evoked (zero time ト representingan onset of the initial rising phase of spike component of ASWC) and minus indicat円 thatpotential was evoked prior to the onset of ASWC. significantly ！日rgeras compared with that recorded during the control periods. Especially the augmentation of potentials was much more prominent in C 4, where it was found that the mean amplitude was approximately 33 % I日明日 than that noted during periods of control (Fig. 5) , whereas （、 5 remained to show about 10 % increase of the mean amplitude (Fig. 6). DISCUSSION Visual evoked responses have been widely used in the study of factors modulating or changing in responsiveness in specific sensory pathways. However, studies of a number of investigators have indicated that only C 1, the first positive spike of the primary visual cortical response, represents presynaptic radiation activity and there remains some questions as to whether C 2 and C 3 are reflections of presynaptic or postsynaptic events. Although many authors agree that both C 2 and （、；treflect postsynaptic cortical activity, several investigators have presented evidence that C 2 and C 3 also represent activity in presy・ naptic radiation fibers (Chang and Kaada 19506> ; Chang 19525> ; Bremer and Stoupel 19503>). SECONDARY FOCUS AND EVOKED ACTIVITY 150 Comp. 4 ???。?・ー。~ 50 -1000 + 1000 +1500 円、secFig. 5 Amplitude changes in C－~ of visual respon田sevoked prior to, during and after the onset of AS¥VC. Responses ob-tained during phases when ASWC was absent were taken as the control am] the mean value of responses obtained during control periods was expresed as 10. Then, average amplitud白 forrespon配 Srecorded during various phases of ASWC were calculated in terms of percentage d the control. On ordinate are ploted m白nsand standard deviations to control r白－pan町 anddoted area repr目entsstandanJ deviation of the control responses. コり9150 Comp. 5 ?? ?? ? ? ???．???『? ．? ????．? ?? ?? ?? ? ???， ょ?????????? ? ? ? ?? ???? ?????????? ? ???? ? ー ーャ??? ????????? ???? ??? ????? ?????? ? ? ?????? ???．????? ? ? ? ?? ???? 。? ?。? ?。? ? ?? 。 』? ?-。三E50 一同00 + 1000 ＋目。。w、secFig. 6 Amplitude changes in （、五 ofvisual res-ponses. Note that mean amplitude of C-.) incr白田sprior to the onset cf A討Wじvhowever, this augmenteti口nis les remar-kable as compared with that observed at C-4 Iド1g.5) In contrast, almost al authors agree the Bishop and Clare' identities (19；）~） 1 > that C-4 and C-5 represent the postsynaptic cortical activity of different cortical layers. （仁 －4:activation of groups of cells in middle cortical layers ; C-5 : deporalization of superficial apical dendrites) and this is the reason why we chose to use C 4 and （、 5as indicators. On the other hand, fairly extensive studies have been made regarding the changes in a sensory evoked potential at a cortical epileptogenic focus (primary or original focus) produced by the topical application of various convulsant drugs and many authors have observed the augmentation of negative phase of the evoked responses. This negative potentiation indicates that the action of epileptogenic substances is first exserted upon the superficial cortical structures (probably the dendritic layers) which interfere in the er同・nization of the negative phase of the primary sensory evoked responses. However, scanty data are available regarding interactions between the evoked responses and the projεcted 270 日本外科宝函第37巻第2号seizure discharges transmitted from the original focus (Smith and Purpura, 196011> ; Holubar, 1966n ; Holubar and Fischer, 19678') and we know of no previous observa同tion performed at the projected focus which was produced secondarily by the topical application of tungstic acid gel to the contralateral homotopic area. In our present study, an attempt was made to analyze the effect of projected discharges (AS羽TC)upon the amplitude ofじ－4and C 5 of evoked visual cortical responses and it was observed that augmentation of C-4 was much prominent as compared with that of C-5 when they were evoked immediately prior to the onset of ASWC. Thi5 result strongly !Juggests that, at the projected secondary focus, the neuronal aggregate situated within the middle layus of the cortex are activated primarily by the volleys comming from thで original focus and in contrast to the results obtained at the primary focus, activation of the superficial dendritic layer is only secondary. There are many anatomical and physiological grounds fer believing that most calosal fibu3 arise from the fifth and sixth layers, whereas the terminals of these fibers are mainly distributed as frιe endings in the upper three layus. (Terzuolo et al. 196012>). Considering the changes in the evoked visual cortical responses obtained in our study and basing upon the other data reported in elsewhere (Meri et al. 195710> : Mori et al. 19589>), we postulate that as far as ASWC established by the tcpical application of tungstic acid gel is concerned, the principal bombardment from the produced focus (pri-mary focus) centers via commissural pathways on the neuron populations situated in the middle layers wher巴 callosalaxons ramify terminally and subcortical relay system does not play a major role in the propagation of ASWC. Disappearance of ASWC in the proj伐tedside after section of the corpus callosum (Fig. 1 and 2) also supports this concept. SUMMARY Interactions between the projected secondary discharges and the visual cortical response were observed in unanesthetized cats in an attempt to analyze the undulying mechanisms of the so called "mirror focus’＼ Augmentation in amplitude of both C 4 and C 5 was obsuved when the visual cortical responses were evoked up to about 0. 5 sec prior to the onset of transmitted seizure discharge (ASWC). However, augmentation of C 4 was more prominent as com-pared with that of C 5 indicating that in contra~t to the results obtained at the original focus, the neuronal aggregate situated within the middle layers of the cortex are activated primarily by the comming volleys from the original fccus. ASWC was transmitted via the commissural pathways and the subcortical relay sys-tem does not play a principal role in the propagation of ASWC. ACKNOWLEDG)<;MENT The author' w1'h tリ expr刷、 theirappreciation to Prok則、rDr. 1-IaJirne I I日ndafor his kind guidance through-out the cour世 d this investigation. This、tudyis "'PP •rted in p 1rt by NIH Grant '¥<>. NB 06553-01. REFERENCES l) Bishop, G. H. and Clare, M. H.：汚Itト oforigin of electric pJtentials in stri:ite cortex. J. Neurophysiol .15 : 201-220, 1952. SECONDARY FOCUS AND EVOKED ACTIVITY 271 2) Black, RG., Abraham, J. and, W1:yd. ・A.A. Jr. : The preparation of tungstic acid gel and 1h 四 mthe production of experimental epilepsy. Epilepsia, 8 : 58-63, 1967. 3) Blum, B. and Liban, E. : Experimental ba回temporalepilepsy in the cat. Discrete epileptogenic l白旧nsproduced in the hippocampus or amygdaloid by tungstic acid gel. Neurolりgy,10 : 546-554, 1960 . .j) Bremer, F. and Stoupel. N. : Interpretation de la response de laire visuelle a une volee d’mflux sensoriels. Arch. int. physiol., 64 : 234-250, 1956, 5) Chang, H.T. : Cortical respon田 tostimulation of lateral geniculate body and the pctent岨tionthere of by continuous illumination of the retina. J.Neurophsiol., 15 : 5-26, 1952. 6) Chang, H. T. and Kaada, B. : An analysis of primary r出向n詑 ofvisual口，rtexto optic nerve stimulation in cats. ]. Neurophysiol., 13 : 305-318, 1950. ' 7) Holubar, J. : Different mode of activation of the penicillin and mirror cortical fci i~ rats. In Comparative and Cellular Pathology of Epilepsy, edited by Z. Servit, Amsterd剖n.204-213, 1966. 8) Holubar, J. and Fischer, J. : Electrophysiological properties of the epileptogenic cortical foci produced by a new cobaltgelatine method in rats. An attempt to correlate the electrophy-,iological, h店tologicaland his-tochemical data. Physiol. Bohemoslov., 16 : :!78-:!8.J, 1967 9) Mori, K., Kaku, M目 andHanda, H. : Changes in slow bioelectr ical potentiab of epileptcgenic foCI pro-duced by tungstic acid gel. Electroencphal. Clin. Neurophysiol., In pre出．10〕 Mori,K., Kako, M., lwayama, K and Yonekawa, Y. : A ca田 withthe “projected" EEG disturbances due to minute unilaterd epileptic f町田 Arch.Jap. chir., 36 : 874-880, 1967. 11) . Smith, G. and Purpura, D.P. : .Electrophysiological studies on epileptogenic lesions of cat cortex. Electroーenceph. din. Neurophysiol., 12 : 59-82, 1960. 12) Terzuolo, L.A. and Adey, W.R. : Sensorimotor cortical activities. In Handbook of Physiology, 817 p. Am Physiol. Soc., Washington, D.C., 1960. 和文抄録Tungstic acid gel による癒痢二次性（鏡）焦点部における視性誘発電位の変動京都大学脳神経外科学教室 （主任：半田 肇教授〉森和夫，加古誠，岩山馨，草島向彦綴痢の鏡焦点の機能の分析に関する研究の一環として，二次位焦点（鏡焦点） の部において主主筆波による視性誘発電位の振幅の変化，及び両者の時間的相関について検討を加えた．即ち Blum(1960）の方法lζ準じて tungsticacid gelを作製し，これを無麻酔猫の左側視領野皮質上におき限局性鰍嫡原性焦点を形成，次いで反対側大脳半球同名部 （右視領野）への痘皇賞波の投射による所謂鋭焦点を形成，一方， 右側視放線の電気刺戟による皮質誘発電位をζの鏡焦点部で記録，atypical spike and wave complex (ASWC）がJ京焦点より二次性焦点lζ伝播した時，視性誘発電位の第四及び第五成分が，いかに修飾されるかを分析した．誘発電位が ASWCの出現Ii'.:先行（ほぽ500msecまで）する時，その第四及び第五成分の振幅の増大をみとめるが，特Ii'.:第四成分の振幅のaugmentationが著明であり， controlの振幅のほぼ1.3倍lζ達するに対し，第五成分の振幅の増大はそれほど著明ではない．乙の事実は原焦点からのvoleyが二次性焦点部の皮質中層の細胞集団を先ず発火させる事を示唆するものである．二次性（鏡）焦点における虚燈波と誘発電位の相関Ii'.:関する研究は非常lζ少なし今回報告の如きtung>ticacid gel による二次性焦点での観察は，著者等の知る限りにおいて,-Ktこなされていない．又従来， 各種薬剤貼布，局所冷却等lこより作製された頗絢の原焦点都では，諸家lζより誘発電位の陰性相の強調が主な変化として認められているが二次性焦点部では正記の如く視!'I：巧発電位の第四陽性成分の鳩大が最も著明である．我々 の今回の成績はまだ，既lζ他紙lζ発表した諸所見と共lζ，tungsticacid gel lとより作製した原焦点から二次性焦点へのASWぐの伝揮は，皮質下relめ nuc-leusを経由せず，直接commisuralpathwanが主役を演ずるとする我々の説を更に支持するものである．

Tungstic acid gelによる癲癇二次性 (鏡) 焦点部における視性誘発電位の変動

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Tungstic acid gelによる癲癇二次性 (鏡) 焦点部における視性誘発電位の変動

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