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TitleTHE INFLUENCE OF THE MIDBRAIN TRANSECTIONAND PHENOBARBITAL ADMINISTRATION ON THEEXPERIMENTAL TRAUMATIC COMA
Author(s) MATSUMOTO, SATOSHI
Citation 日本外科宝函 (1960), 29(5): 1059-1090
Issue Date 1960-09-01
URL http://hdl.handle.net/2433/207159
Right
Type Departmental Bulletin Paper
Textversion publisher
Kyoto University
原著
THE INFLUENCE OF THE MIDBRAIN TRANSECTION AND PHENOBARBITAL ADMINISTRATION ON THE
EXPERIMENTAL TRAUMATIC COMA
by
SA TOSill MATSUMOTO
From the !st Surgical Division, Kyoto University Medical School (Director : Prof. Dr. CmsATO ARAKI) Received for publication July. 12, 1960
I. INTRODUCTION
1059
A transient reversible disorder of consciousness immediately following head
injury is called cerebral ooncussion. Accompan:-,ring signs of cerebral concussion are
paleness of skin, cold sweating, hypothermia or change of respiratory and circulatory
functions simultaneously. Of all the phenomena due to head injury, the most
important is the reversibleness of functional disorders in the nervous system.
There are three hypotheses concerning the etiology of cerebral concussion. 1) Transient anoxia or h:-,・poxia in the central nervous system resulting from
cerebrovascular changes caused by head injuries.
2) Functional, reversible reaction of the central nervous system to mechanical
stress which may be associated with no morphologic changes. This may be descri-
bed as“molecular reaction of the nervous system”． 3) The existence of organic change in the central nervous system caused by
mechanical stress. As to the location of lesions in the brain in case of cerebral concussion, there
are two hypotheses.
a) The lesions in the nervous system brought on by mechanical stress are not
localized in some sp巴cificpart, but diffuse throughout the central nervous system
(DENNY-BROWN & RUSSEL, 1941, RAND & COURVILLE, 1946).
b) In cerebral concussion, lesions may be localized mainly in the brain stem,
though the influences spread secondarily to the cerebrum and spinal cord.
The latter theory is based upon the di~turbance of consciousness from inflamm-
ation, neoplas1n and operative procedures in the diencephalon or midbrain.
Recently there are many experiments affirming the latter theory, in which
when an experimental localized lesion is made in the reticular formation or the
surrounding tissue of the midbrain or medulla oblongata by va1匂usexperimental
methods, there may appear the transient disturbance of consciousness (MORISON &
DEMPSEY, 1942, IsmI, 1944, PENFIELD & JASPER, 1947, M0Ruzz1 & MAGOUN, 1949,
1060 日本外科宝函第29巻第5号
MAGOUN, 1950, 1952, JASPER et al., 1952, PENFIELD, 1952, HAYASHI, 1959, MATSUMURA,
1959). Microscopic hemorrhage in the brain tissue due to mechanical stress may te
important in the discussion of the etiology of cerebral concussion. It had betn
shown by 0Gosm (1948), Kuno (1949) and others that there are hemorrhagic foci
in cases of initial or secondary coma from head injury not only in the cerebrum
but also in the midbrain, though not出 frequent. In the present study, the author
has studied the interrelation of the nervous function between cerebrum and brainstem
in the case of experimental cerebral concussion in cats. First of all, air impact by
m伺 nsof air rifle discharge was given against the exposed dura overlying the
parietal cortex in a cat whose midbrain had been transected intercollicularly already
dy BREMER’s method ( 1935) . That is, the nervous connection between cephalic and
caudal parts of the brain at the intercollicular plane was interrupted perfectly by
making “cerveau isole”， and then air impact was given over the parietal region.
Secondly, phenobarbital was injected in an amount not enough to produce a
change in clinical features, but enough to have some paralytic in臼uenceon the
mesencephalic reticular formation, and then air impact was given in the same
manner as in the first.
Thirdly, the experimental cats receiving preliminarilyi:>oth midbrain trans伐tion
and phenobarbital injection in the same manner as in the first and the second
experiments were given air impact injury over the parietal region thereafter.
II. EXPERIMENT AL METHODS
1. Animals :
Unanesthetized adult male or female cats weighing from about 1.8kg to 4.2kg
were used for experiments. Vagus nerve and carotid artery were maintained intact throughout the operation.
Inhalation ether narcosis by open drop method was used only initially for head・
fixation, midbrain transection and insertion of electrode in the brain.
2. Procedure of the operation :
(1) General procedure :
Each cat was fixed on a hammock in prone position. In some cases the four limbs were allowed加 hangdown naturally.
The median sk.in incision of the head was done from nasal tip to occipital
protuberance. Both temporal muscles were separated from the skull by blunt dissection.
In the occipital region was made a bone window which was long in the frontal
plane and narrow in the sagittal plane. The posterior end of the window reached
the tentorium. Then the dura was incised, exposing the occipital cortex of this area through the window in the skull.
The above procedures were preliminaries to midbrain tran忌e~·tion. After making
midbrain transection the skull window was白lledand cm・ered with temporal muscles
THE INFLUENCE OF THE MIDBRAIN TRANSECTION 1061
and skin. This procedure of opening and closing the skull window was done on
all cats of all four groups of experiments.
(2) Method of midbrain transection : The midbrain transection was done following BREMER. That is, through the
skull window in the occipital region the occipital cortex was exposed and moistened
with saline. Then the occipital lobe was pushed away anterocranially b? means
of a brain spatula inserted toward the tentorial incisura horizontally along the
superior wall of tentorium. On reaching the tentorial incisura the cerebral spatula
was raised to vertical and then the midbrain was transected intercollicularly throug-
hout.
The ventral line of incision in the midbrain was terminated at the anterior
limit of the pons, which was just behind the outlet of oculomotor nerve.
In order not to contuse the cerebral falx or GALEN’s vein during midbrain
transection, the bilateral transection was done separately.
Vascular injury of the ventral brainstem should be minimi苧dand the basilar
ar白ryshould be maintained intact. After midbrain transection the occipital skull
window was repaired with temporal muscles and scalp.
L・3 2 －ι
l )
(A)
2 －ι
2 ゐ(B)
Fig. 1 EEG BEFORE A:--.!D AFTER THE MIDBRAIN-TRANSECTION (Fronto-occipital bipolar leads) ~ : Before Transection B : After Transection
1062 日本外科宝函第29巻 第5号
R-Transeo七．
↓
B.P.o
50
』＿＿，.6”
L-Transeo七．
Fig. 2 CHANGE OF THE RESPIRATION AND BLOOD PRESSURE BEFORE AND AFTER THE MIDBRAIN-TRANSECTION
Whether the midbrain was perfectly transected or not could be known by the
changes of EEG, clinical findings (particularly ocular signs) and postmortem disse・
ction. There were the spindle burst waves of EEG, extreme myosis, immobility
of the eye balls and fixed downward gaze. The light reflex of the pupils disapp-
eared generally. There was generalized muscular rigidity, transient or permanent
after midbrain transection. Following midbrain transection there were prominent
changes in blood pressure and respiration ; that is, transient hypertension, bradyca・
rdia, spastic apnea, oligopnea or tachypnea (Fig. 1, Fig. 2).
(3) The method of phenobarbital injection :
Phenobarbital was dissolved in the solution provided directly before making
injection in the lateral radial or ulnar cutanous vein slowly, for a total dose of 20
mg per kg. ( 4) Insertion of the superficial and deep electrodes into the brain :
Lead electrodes for surface EEG consisted of four steel needles inserted to the
THE INFLUENCE OF THE MIDBRAIN TRANSECTION 1063
surface of dura at following four points through the skull which was widely freed
of the temporal muscles.
a) Frontal point which is 5～lOmm rostral from the coronal suture, 5～lOmm
lateral from the midline of the skull (right and left side).
b) Occipital point which is 5～lOmm caudal from the coronal suture and
5～lOmm lateral from the midline of the skull (right and left side).
Deep electrodes were made of stainless steel wire of about 0.2mm in diameter, each of which was insulated and fixed to each other by means of vinyl chloride
ト＼い75
Transverse Section at the Level of
0.2mm. in front of the Interaural Line.
？＼し78
Transverse Section at the Level of
0.2皿 infront of the Interaural Line.
？い.8-1
Transverse Section at the LeYel of
l.7mm. behind the Interaural Line.
Fig, 3 SITES OF THE SUBCORTICAL ELECTRODES (TRANSVERSE SECTION OF THE MIDBRAIN 1
1064 日本外科宝函第29巻第5号
except for 2～3mm length at the tip. The bipolar electrodes were separated about 2～3mm from each other. When suitable craniectomy in the parieto凹cipitalregion had been done, the HoRsLEY-CLARKE’s stereotaxic instrument was placed on the head of the cats, and the bipolar electrode was inserted into the midbrain which was marked by GERARD’s map at the point : 0.2mm, 4.0mm, 3.0mm, this being the
reticular formation of the midbrain (GERARD et al., 1936). After the experiments had been done the brain was taken out, fixed and
subjected to KLUEVER-BARRERA’s stain, then the insertion lesions of the deep electrodes were con白rmed(Fig. 3). Surface and deep EEG were recorded with SAN-EI 2 channel
portable electroencephalograph. (5) Measurement of blood pressure and respiration : Records were made on a kymograph by a mercur~’ manometer for blood
pressure, and by a balloon under a wide band fastened around the chest for respir-
ation. 3. The method of the air impact : A small hole about 6mm in diameter was made in the parietal region of the
skull, 7～9mm lateral from the cranial midline. Then a steel pipe lOmm in length was inserted tightly into the small, well adapted parietal cranial hole. The muzzle of the air rifle was attached to this steel pipe tightly, then air impact was deliver叙1on the exposed dura vertically (Fig. 4) .
The energy of air impact force was about 9,800 erg. b~’ 1 pump method, 29, 400 erg. by 2 pump method on the average, which was measured b~・ the potential energy of pendulum movement i】ydelivering air impact on a certified weight hanging vertically. There appears a swelling of cerebrum out of the skull window of the occipital region following air impact, but the cerebral swelling may be minimized when the occipital skull window had been repaired well with temporal muscles and scalp. The cases in which the swelling or intracranial bleeding following air impact seemed marked were excluded in all experiments.
4. Criteria of the experimen・同lcoma:
In an animal the presence or absence of consciousness is a matter for conjecture. Therefore, the state ↓
, ... "' of consciousness in experimental cats was judged indirectly according to _ nociceptive reflex and postural reflex ・ 1 ・
(ARAKI, 1956）.羽Teshould like to
classify the general responsiveness
of animals from the modification of
GrRNDT (1932) and MATSUNAGA’s
(1959) criteria. Dura Sku.Ll
J:'neumatio Gw‘
(1) Unresponsiveness of III degree or comatose state :
Fig. 4 DIAGRAMMATIC DRAWING OF THE AIR IMPACT APPARATUS USING A PNEUM-ATIC GUN
THE INFL DENCE OF THE MID BRAIN TRANSECTION 1065
.Ur llJ戸時
B.p
60
。 」』＿.＿＿＿，＿＿ー6・
Fig. 5 CHANGE OF THE RESPIRATION AND BLOOD PRESSURE (GROUP I; UNRESPONSIVENESS-III)
Nearly all of nocice~tive reflexes
or vital reflexes such as corneal, pinna
reflexes, light re日exesare absent either
comフletelyor partially ; vomiting reflex by pharyngeal stimulus is lost, transient
apnea, hyper『 orhypotension, hyper and
hypotonus of muscles are present (V
& VI degree on GIRNDT’s scale).
(2) Unresponsiveness of I and II degrees:
Postual reflex, spontaneous move-
ment and response to smell stimuli are
disturbed. Movements avoiding pressure
or pain stimuli partially remain. There
are moderate changes of respiration
such as transient apnea on air impact (3) Intact responsiveness :
B.P
同
＇・Fig. 6 CHANGE OF THE RESRIRATION
AND BLOOD PRESSURE (GROUP I ; UNRESPONSIVENESS I-II)
(II-IV degree on GIRNDT’s scale).
The animal shows no distinct di百erencein spontaneous movement, postural reflex
and so on before and after the air impact (less than I degree on GrnNDT’s scale).
III. EXPERIMENTS
1. The examination of the reaction in Group I (Control Group) which received
no procedure but air impact after the occipital skull window was made, that is, the determination of the intensity of adequate air impact to produce coma in 100% of
】
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ness
Unrespons
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Unrespons.
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Unrespons.
Ill
(GROUP I : 2 PUMP-METHOD)
｜ ！ P叫 三T百7ττ一一Respiration I Pulse I : nむ aιL』onI I 一！GagRe臼exI I Tonus of
I I Size I to I u " ! Ear lobe I "' I n~何｜I I I I Heflex i I I Hel1ex I Extremities I I I Light i一一 • ~~flex I ｜一一ー ｜ N臥判 A*11 100／一丁雨戸「 nor；~1~一一！ -+ ；トー工－「＋丁－「「 norm. T ··~：：…： 3.s1同 iB*21 ー（2811) I + 1 Mydr.*6→Myos.ペー（2011)l -(2叫ー（24")Iー（30") I一（3011)I hyper*s-nor川 皿
N臥 561 A I 50/m 1120/m j norm. j + I + I + : + I + I norm I 2.81匂｜ B I ー附 I + I M肉→norm. ! ｜一（60")1 一（90")1 一c420") I -02011) I ・ No. 60 I A ! 24 /m い40/mI norm. : + I + I + I + L土」,..__ ! I I I Mydr. I I I I ' I
3.:kg ! B Iー（2511〕 I+ I Mが I I -(30")1 -c2011) iー（40'') I I hy附→hypo. i 1 1 1 norm. 1 1 1 1 ! '
~~A1 ·· …－下両Im[ norm.-1---+-1－＋－下－：「！っ 「7十つ函7 1可ムぷ－4f1勾 B ［一16511) I + I mydr. I I一（8011)1 ー（35＂） ー（8511) I J hyper.-norm. ! Ill
N~］A ! 1~·0ん 下両「 附 m 「工丁円一千一一｜ ＋ ｜ ＋下つm － 3.Sl同 IBーr-（］門 j + / mydr. ！ 卜c40")1 -(70") I -c 45") I I N.0;r工了 66/m ! 150/m J つ戸－－！ + I + ! + I + 1 + ! 3.Zl同 IB I一160勺 ：+ myos.→附m. I 卜（24叫－α1011)Iーcao") I I
Unrespons.
hyper.*9→hypo.
bypu.→norm.
norm.
norm.
REFLEXES OR RESPONSES TESTED Table Ia
pricking of nose tip 村 mydr.: mydriasis
hyper.→norm.
*1 A: Before Air Impact 町 B: At Air Impact 判 Nosetip Reflex : Flight reflex from 判 FlightReflex : Flight reflex from pricking of forelimb 町 norm.: normal in size or in tonus *7 myos. : myosis 崎 hyper.:hypertonus of muscles *9 hypo.: hypotonus of muscles
(GROUP I : I PUMP-METHOD) REFLEXES OR RESPONSES TESTED Table lb
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' 0 ~ I B I -(IO') I + I 詰（ トイ ー（17')I I 合
Nペ75I A I町 m I町 mI norm. I + I + I + I + I + 11. I
_ 3.~配下ナゴ止とリ竺~n~·1 ＿~－~~_j －~－ 」一一土－·－L土－~竺；~·~~l~L 土L 田氏＇＜＞，：，.＿84l A I 18伽い80/mI norm. i + I + I + 1 + t + I norm. I Un向。ns.
。九g I B Iーc20") I + I 111凶 →norm. + [ -(3011)1 -(2511) j ー（例 I I hy附→
N~~9；τ1 寸20/m 1180/m j ……一一一｜+ + .I + ! + I + ！ － ·－~~~~ 3.SJ同 IB I + I + j norm. j + ! + J + I + I + I hyper.→norm.
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Unrespons.
Unrespons.
Unrespons.
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hyper.→norm.
Intact
Response
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日本外科宝函
animals: When the air impact was done by
means of 2 pump air method for
makng cerebral concussion, the cat’s
reaction was found to be unresponsiv-
eness III (coma) in all cases, which was
accompanied by transient hypertension
and apn白（Tab.Ia, Fig. 5). On the other hand, when the air
impact was done by means of 1 pump
air method, there reulted 3 cases of
unresponsiveness III out of a total of 5
cats ; 1 case of unresponsiveness I-II,
and another 1 case of intact responsi-
veness (Tab. lb, Fig. 6). As shown in
Fig. 6 (Unresponsiveness I-II) there was
transient hypertension and dyspnea but
the oligopnea was not as severe as in
Fig. 5 (Unresponsiveness III).
In almost all cases, whether the
experimental procedure was made by 1
or 2 pump method, there appeared a
transient muscular hypertonia of extr-
emities following air impact.
From the above it may be conclude-
d that adequate stimulation to cause
cerebral concussion h? impact energy was more than 1 pump method and
less than 2 pump method, so we have
decide the 2 pump method as a suffic-ient intensity of stimulation for cerebral
concussion.
2. Group II (The group of midbト
ain transection) :
The air impact was given lηγmeans
of 2 pump method, after allowing a
lapse of at least 30 minutes, usually 60
min. after the procedure of midbrain
transection. The result was that the
air impact which was of a strength
adequate to produce coma in 100% of
the animals in Group I, produced coma
only in 4 cases (33%). In the cases of
1068
．Ha回目ロム吋Fd回Zの凶。司．Ha出回
足HU回同kpHZ4HN〉Zω問。叶aH。
z
(GROUP II : UNRESPONSIVENESS l -ll OR INTACT RESPONSE)
i I 1'up1Js I I ・ I I 1 I I i一 一 1 1 rneal I Pj Gag I Flight I Muscular I I Respiration I Pulse I I Reaction I I or I I I I f I I Size f to f ef!ex IE町 lobe[Reflex I Reflex f Tonus f ness ｜ ｜ ｜ ｜ 1空ht I i R旦日exI I I I
No01{AfB－両ん／45/m[zoo岬一雨戸l~yos. I+ I ー i + i ＋ 「 ＋ I + !norm./ hyper.→norm.下一瓦：；一一ー 一 一
目
川 E C / 30/m 1 1町 m ) / myos. j 一＋ I + I + ! + I norm. / Response
I i I i I I I norm. I + : I I I I No. 771 A i B 1160/m 42/m:l80/ml210/mlnorm. I ＇..： ~！山川 ＋ i (ri広ht) + I + I + i + lnorm. I 会 ｜ ｜ ｜ ｜ ｜ ｜川U唱 ー I I I I I I ! I ' ! I I ;·i~1加 f I neft) : I I J I I
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♀ I 1 1 I I I norm. I ! ! 1 I I I
2.8判 c ! 12/m i 120/m I 町 dr. I ー ｜ ＋ ｜ ＋ ｜ ＋＋ ｜
No. 86f A I B /180/m 30/mf180/mf180/m1norm.; ♀ ト_J__ー」ー」一一一斗 I l一一」
2.4 kg I c ； 一 ~2D ＇＇つ） I 120/m f myd
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1.9' l匂／ C 24/m / 170/m
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3.51同［ C I 36/m / 180/m , myos. [
N札 93[A I B f 150/rn 60/m 180/ml 70/m norm. I mycs. 合トー」ー←一一一 ト一一－＇－ 一l一一一～1
2.¥.1 J氾I c I 町 m i 町 m i myos.
Responsiveー
Unrespons.
I -ll
Intact
hyper.
REFLEXES OR RESPONSES TESTED Table II b
Response
Intact
Unrespons.
I -ll
+ jnorm. j hyper.→norm.
[norm. I hyper→norm.
I hy附→norm
hyper.→norm.
norm ＋
＋
＋
＋
＋
＋
＋
＋
｜＋｜－ ｜ I - I + !
r. I＋「－ I + I
｜ 一 ！ ＋ ｜
＋ r myd
+ ; + I + I + jnorm. I hy阿 ｜+ j + 1 + / + I hyper. :
+ I + [ + ¥norm.¥ hyper.→norm. !
[ + I + J + I + .I norm.
I + I + I + I + lnorrn. / hy阿→norm.
－一丁工「てよ「－工「孟l 防…ーm -
Response
Unrespons.
I -Il
Intact
＋ ＋ ＋ norm
】｛）自由
Response
Intact
Response
i; : , . oo c:1 二
＋
；＋｜
1070 日本外科宝函第29巻第5号
unresponsiveness III there appeared on one hand transient hypertension which proc-
eeded to hypotension with bradycardia and on the other hand tonic apnea which proceeded to oligopnea (Fig. 7).
In the cases of intact responsiveness the blood pressure was increased or decre-
ased but slightly. There was no change of the pulse pressure, but in some cases there was玄aspingrespiration (Tab. Ila, Ilb, Fig. 8).
3. Group III (The group receiving phenobarbital intravenously) : About 20-30 min. after injecting
a definite dose of phenobarbital intrave-
nously ther,e appeared spindle burst wa-
ves or high voltage slow waves in the EEG, but there were no clinical signs indicating sleep.
The air impact was delivered about
↓Air Impact
20～30 min. after taking phenobarbital. B.P
The unresponsiveness III was seen in 7
cases, unresponsiveness I II in 2 cases, and intact responsiveness in 3 cases out of a初旬lof 12 cases.
The influence on respiration and blood circulation resembled that in Grouu I (Tab. Illa & IIlb).
4. Group IV (Intravenous phenoba-rbital plus midbrain transection) :
Phenobarbital injection was done
about 30 min. after intercollicular
ぬ
言肯」一一
Fig. 7 CHANGE OF THE RESPIRATION AND
BLOOD PRESSURE (GROUP II, UNRE-SPOSIVENESS III)
Air Impact
B.P. J.
B.P.
50
。
~す』－
Fig. 8 CHANGE OF THE RESPIRATION AND BLOOD PRESSURE <GROUP II, INTACT RESPONSE)
寸回目
HZ同，Fd円Z。問。】U
J司同四冨門口回HNKFHZ・HaMNkpzm円。叶aHOZ
I ' IN五点tfol I I 1 Pupils :Corneal I or "I G昭 IFlight I Muscular : Respon-R叩 ration j Pulse 「~· Re両日／Reflex !Ea巾 belRe~eバ Reflex I Tonus siveness
I I to Light! IRe自ex I I I
1 ；~／m 150/m ; 150/m 120/m ' norm norn~~ i 十＋｜ ＋ ｜ ＋ 「工丁 ＋ I norm~ ，－~~孟.－ri my<lr. ! i I I I I : 、I lψ1 I I I I I hyper i
i-(180匂 rtif.resp.): + I myos. Iー（90")I Iー（20011)1ー（240り｜ー（300り｜↓ ｜¥27011 spont.res./ i I .r, I I I I I I I l ’！ I I I I I I ' norm. I I norm. I ' I I ) I
3伽 18/m 180/m 150/m I norm. 附 m. + + + I + I + + ; norm. 附 m I
｜ー C4D"!Iー(10川 ー（山）｜ h rer. I mydr. . I 1 I I
norm I I n。rm. 1
150/m ; norm. I norm. I + I + i + + + I + r norm. I norm. ! m:i:,dr. I i I I I I hyper. I myos. ' 1 I-(13'1）卜 (13り｜ー（1511)I ↓ ！
1 1 1 ' nor町l.norm. i I I I
norm. 附 Ill : + i + 1 + i + + I + 1 norm i norm. I 一「• -r・寸一一「一i一一日 一一(10り｜｜↓
1 norm.
norm. J+ .I + [ ・＋－； ↓て ＋ ,I + norm. , n… mydr. I I I 1 : hyper. ↓｜ー（30")Iー（2511)I一（50"I -(4011) ＇ ↓
norm. I I norm
…戸工 7 「「「＋ ＋… j norm. I I ,o' 1-( I hyper. I －て10＂）ー （601 -(80り｜ー cao11)Iー（30川↓ l
I I I nor】11. I
日1「十 日三主三i~~1:m. li~~＇ I I 5 ~ ； 一（ I I I hyper. ー（2511)Iー（25'l: -( 20り｜｜ー（30り｜」
I I I I I norm.
UNRESPONSIVENESS皿〕
4
3
E
4・8
K
0
1
F
D
N
a
Unrespons.
Unrespons.
Ill
Unrespons.
Unrespons.
III
Ill
1c;J{QUP Ill REFLEXES OR RESPONSES TESTED
＋
＋
川】｜
150/m 30/m
Table Illa
一（JOり
30/Jn I
一（35り
120/m
' A判 B*2No.42
♀
3叫¥'o.43 I ♀ ｜
3拘！
一同
批
ヨロl＋
r
I
一
y
m
M
O
町
n
l川l
ii
一川ー－
nu
－nv
BI
＋一
ι一＋
m
－
一m一
ω－
一ω一
川
一
一
ι
AU
－
PO
。。、ーノ
90
III
Um百 pons.
III
Unrespons.
開山
Unrespons.
mydr
120/m norm.
myos.
m
，，F’一
nu uυ
？にo.57
♀
'.?.'.?kg
No.71 i
合 1
3.lkg
No.85 A B
合
2.8kg
No.89 I
合 1
:2.5kg
B
B
B
C句
c
c
A
A
A
＋
＋
90/m
ー（4511)
30/m
ー（20り
160/m
m
，，，
pnv
q3
B
c
c
A
c
A 1 B
目。吋H
－
m山
吋 C: At Air Impact *2 B : After Phenobarbital Injection
一（ 10り
*l A . Before I'hcnobarbital Inj巴ctwn
c
ロ叶N
r Respiration l 山 I ~Is l国間協：I ~：！ex IF叫~~：~ar I…ve
:: I斗~Bf~（＝.i~m 1 l~0~20/m i oo＝~9~ ~~ ~ ~可~~11::: A ~ B I竺ア1 ~~γo<m=m I士川：J~ I ~ I：「Y
I －〔10") I + I；立 I+ I + I + I + I + I ::J:・ l 36/m ／ お／m / 1
l印／m / 180/m I norm. I附 m.I + I + / + I + j + ! + I norm. no；~
｜立 ｜＋｜＋丁工I+ I ~－I ：。↓；
回一升浅草附図
鴻NU嚇
鴻印a中
ness
Unrespons.
Unrespons.
Response
I -JI
I -JI
Table Illb
c
Intact B i
Response
Intact
Response
＋
＋ + (tachypnea)
+(gasping)
150/m m
，，，，，，ι AU
今、
υB
c
c
ヮ，6ZFu
b
J
6
？
2 R、『
合 一一
4.01 怒
陥 781A
3 .0~g I
・Ha回目
H
Z司Hhd回Z
。問。司吋出問旨Hロ回同Nkrロム斗同〉HLω問。、吋同（）げム
一 ｜恥esp竺｜二！！！！一ド竺：~i1s 1roe認~I℃：；l高＇~~：1 ニ：~ I ~~~B~＇C" 150/:0l
一 一 ←I -(?O") I + J :J：~ I 一｜一（叶叶叶(180")1 ：主~： i
No.821 ·~一 le ~：~~120／了l:'J一？一一一l一一（40") I + t :x:.・ L土…いり 1-c叫（120")1 :r.:
__ J_ c I 30/m ~1 _1_3ピ…一…－1-l-I+ I ＋止工」t! ：：；：＿~r no_r ~ ？ ！ ； I ＼；！竺｜ユJ ご~工｜ + I＿：竺十二－(3011)
No87~日＼！弓5坦片：Gy~~_1手ご卜：一Ll;i : TT=1 ::1~~I 2.8ペ D_ I -(6011) I + I mydr. ; __ , -1 - I－叶(1~司副ー(lIO";I ::r.・ I
Responsive
ness
Unrespons
REFLEXES OR RESPONSES TESTED Table IVa
No.65
III ♀
Unrespons
Unrespons
而凪
UnrespQns
III
而皿
D判
B
3.lkg
No.83 1
会
♀
♀
日｛）吋
ω
句 C: After Phenobarbital Injection B: After Midbrain Transection ホ2A : Before Midbrain Transection D : At Air Impact
*I
ホ4
(GROUPN : UNRESPONS. I -II OR INTACT RESPONSE.)
e I Pupils… Size [R町1t~.on Retie ・ e; ReflexJ Refl叫 ｜
下~8~；~ . I __ ~竺~~－－ -t:~ － － －~一：士」－三L山 I1山 1150川；mydr.'川一：一I+ : + I + ,J + I hy~er . , norm. I
-1 ~ - I m凶 ＼- i + ~－］－↓丁J I ＝~：＿~： ___ _ I 2伽 ド n~~~ T.工－r~「＋1 千 「·;-r- …竺－川 30／＿~＿ I-24/m i mydr. i五lJ-!+ ; + i + I + I：エl
I 0 /m : ( ri g~.2\l，ふt ) - : + I + ! + I + I
j 200／~；＇ ! nor~ j + [ + ; + [ + I + i norm.
ω叫ん可1~－；引 ：J：：措i ~ -1-i ~ i；；誌t) I + i + : + I ::J:r. i norm.
:r~ /m ~~； （~i-gh~~l~ft! : - ~ - ¥ + I十 _I + J 70川 I 2001m i 附 m. I + [ + i + I + j + j norm. I 30 /m ： ·；~雨。ムr：~：~ム可＝－1 ~i ~J ＋~ i .↓了日：:[1：~.： · 1___ J__ 130/m ：三？と」一二三己l___ ~J_ __ + I norm. l
190/m I 120/m ¥ norm. j + j + + I + I + J norm.
¥ 54/ 24/m
-I i；工J「二孟一 j my閃一 l 士一（ 」 ！叩－－＝一r~－－ r了！一
目。斗AF
回一分浮い翠川附図
滞日由品市
Intact
Response
Response
Response
Intact
Intact
norm.
REFLEXES OR RESPONSES TESTED
Respiration
、An
ff
一
nvVIlli－－
i
一じ
n
一
一
1
一
／ハUA坐
ムト工工：？
__ I一一一一
i川
90/m
＋
Table IVb
B
（？
c
D
B
No.55
No.5』 ｜
♀
3.2kg I
2.4kg
会
♀
瀦印
1
叩
norm.
Intact
30/m
c
D
A No.63 ----,-
f B 1 ♀
Response
Unrespons.
I -Il hypo.
180/m
c
D
A
D
B
3.0kg
No.BO :
会
THE INFLUENCE OF THE MIDBRAIN TRANSECTION 1075
midbrain transection. Then, air impact was done 30 min. after injecting phen-obarbital. There were no changes in clinical signs before or after injecting pheno-
barbital intravenously.
Muscular rigidity of extr℃mities, immediately following midbrain transection intercollicularly, was observed transiently or permanently in all cases.
If the section of“cerveau isole" was typical, myosis usually occurred, but in some cas田 mydriasisresulted instead of myosis. Perhaps this is because the superior
(1) GROUP-I
(a) 2・pu皿ps血ethod
(b)
;;pも：~
100需6
Unresp. Unresp. Intact III 1・II Response
3
11 1
Unresp. Unresp. Intac包
III I-II Response 品 、‘ ’ の’・一ヤン、 － '• ..、．，
( 3) GROUP-III ,,
58需
7
3
2
Unresp. Unresp. Intact lII I-II ttespunse
(2) GRαJP・II
33 %
3
Unresp. Un resp. Intact III I-II Response
'"
・- 白紙E、
(4) G虫OUP・IVJ、，，
』崎
ι ι
1
Unresp. Unresp. I且tact工II I・II Response
Fig. 9 PROBABILITY OF THE UNRESPONSIVENESS III BY MEANS OF THE AIR IMP ACT
1076 日本外科宝函第29巻 第5号
coliculus and oculomotor nerve tracts <lid not always remain intact.
In this group, unresponsiveness III resulted in 4 cases, unresponsiveness I-II in
1 case, and intact responsiveness in 4 cases out of 9 cases. The pupilary reaction following air impact might be transient myosis or permanent myosis after transient
mydriasis (Tab. IVa, IVb, Fig. 9).
In the ・cerveau isole”ca ts there was occasionally absence of light reflex, or
corneal reflex following air impact. Throughout all experimental groups, in c部 esof
unresponsiveness III or I -II, respiration became gasping or hyperpneic associated
with general excitability, and in some cases irregular oligopnea appeared following apnea after air impact.
5. Cerebral electrical changes in each experimental group : (1) Group I:
a) No. 38 (Unresponsiveness III)
In this case air impact on}he right parietal region has caused an artefact in
all leads which lasts for l～2 sec. Then low voltage and fast waves are present
iooL
l 3
(A)
州川仙川~阿川州W仰帆州州内~
(B) 2・ι
L・3
(C)
2 －』
府内ト
Fig. 10 EEG OF GROUP J, No. 38 (UNRESPONSIVENESS III) A : Before Impact B : At Air Impact C : Zmin. after Impact
THE INFLUENCE OF THE MIDBRAIN TRAJ.'ISECTION 1077
for about 30 sec. About 60 sec. following the end of the above changes, there
appear high voltage and slow waves on EEG which may represent a recovery stage
from cerebral concussion (Fig. 10).
b) No. 75 (Unresponsiveness I-II) The electrical activityア ofthe cortex and brain stem structure following the air
impact are reduced in amplitude with little change in frequency, but at times
essentially no change is produced. High voltage and slow waves of cerebral electrical
potential are present 80 sec. later, which may represent a recovery stage from
concussion (DENIS WILLIAMS & D. DENNY BROWN, 1941). Changes in the・ electrical
activity of brain stem structures largely parallel those in the cortex (Fig. 11).
J.oof"vL一一 昨「何時五cuJ.o-.tt叫 ioularLe&<11) 仏・rも骨。曲。－occip..l.J
Jヘドゾ~(A)
(B) uιT工C.-.tETlC.
(C) RETIC.・且ETIC.
l・3
(D）い
Fig. 11 EEG OF GROUP I, ＼，，。 75(U~HESPONSIVENESS I -II )
A Before Impact
C : 80 Sec. after Impact
B : 10 Sec. after Impact
D : IO min. after Impact
"
1078 日本外科宝函第29巻第5号
c) No. 84 (Unresponsveness II!) The findings of electrical activity of cortex and brain stem appearing immedi-
ately following air impact are generalized flattening. 20 min. later the electrical
activity has almost returned to i臼 formerlevel, parallel wi七hcortical and subcortical
electrical changes (Fig. 12).
(2) Group II :
No. 95 (Unresponsiveness III) Directly following air impact, EEG shows generalized臼atteningand decrease in
frequency. But the spindle burst waves which are present speci日開llyin “cerveau isole" preparations, are difficult to erase by air impact (Fig. 13).
(3) Group III :
a) No. 43 (Unresponsiveness Ill) Following air impact the EEG of the cortex shows flattening but the spindle
lOOJIV lOOJ/"V
I Lーー し一一(R柿 1oul。．蜘tioularL岨曲｝ (Lett Fronto・白。1p.w
．
nu ，，‘
市A
pb
nn －
－
nhw T4
mA
”島”“ 1
・a｛
(Bl
l J
(C)
1・3
引~凶へ~(D)
''y..,,,、Fig. 12 EEG OF GROUP J, '¥Jo. 84 (UNRESPONSIVENESS Jil )
A : Before Impact C : 15 Sec. after. Impact B : At Air lmcact D : 20 min. after Impact
THE INFLUENCE OF THE MIDBRAIN TRANSECTION ,1079
burst waves which were present after injecting phenobarbital intravenously, though
decreasing somewhat in amplitude, remain for a long time (Fig. 14).
b) No. 67 (Unresponsiveness 1-ll) Slow waves and spindle waves in the cortical EEG of this group show flattening
following air impact. The subcortical electrical activity is seen also to be flattened
but on recovery the later electrical activity shows greater depression th~n that of
the cortex (FoLTz et al., 1954) (Fig. 15).
( 4) Group IV : No. 63 (Intact responsiveness)
Following the combined preshot procedures, this group presents typical spindle
waves in cortical electrical activity. The high voltage and low frequency waves
ioo;rv
L一一一一1 Sec,
,(A)
1 －ι
2 3
(l』） 2 －ι
l・3
(C) 2ι
l 3
(ll) 空 ι
Fig. 13 EEG OF GROUP JI, No. 95 (UNRESPONSIVENESS ][)
A : Before Transection B : 60 Sec. Midbrain Transection
ふし＆し
ρLρL
aa
Dゐ
p・
mm
yaATEA
r
r
olvAC
tt
βIrム
aa
c－
m
E
I
Sn
nU山川
l
；
C
D
1080 日本外科宝函第29巻 第5号
in cortical EEG of Group IV are seen more clearlJァ thanin that experiment witb
phenobarbital injection alone. The spindle waves remain even following air impact,
like in the cases of Group II. In this case the EEG does not return to the pattern
before air impact, probably as a result of possible contusion of the occipital cortex
under the skull window at the moment of air impact (Fig. 16). The severity of the
cerebral electrical changes is usually not proportional to the objective signs of
concussion (eg. loss of corneal reflex, respiratory paralysis and rise in blood pressure).
IV. DISCUSSION
1. Experimental production of cerebral concussion :
(A) 2 －ι
c•，•巴
l・3
(C)
2 －ι
l・3
(D)
2 －ι
100//V
L l .・c.
内~仇付
、知
’
Fig. 14 EEG OF GROUP Ill, No. 43 (UNRESPO:'-!SIVENESSlll)
A: BefoてePhenobarbital Injection . . C .: JO Sec. after Air Impact B : 20 mm. after Phenobarbital InJectJon D : IO min. after Air Impact
THE INFL DENCE OF THE MID BRAIN TRANSECTION 1081
The most important criter,ion for concussion is the occurrence of brief loss of,
consciousness immediately following a head injury. In addition disturbance of vital
reflexes, and anomalies of resr>iration and circulation are noticed as somatic signs.
In an animal, the presence or absence of consciousness is a matter for conjecture.
The criteria for the existence of consciousness should be somatic signs; that is,
disturbance of nociceptive and posture re日exesetc., or of respiration and circulation
(GrRNDT, 1932, ARAKI, 1956) or EEG change (MEYER, DENNY-BRowN, 1955). There are various methods of inducing experimental concussion, that is,
(1) Acceleration concussion (DENN子 BROWN& RussEL, 1941)
This is produced by a blow on the skull held loosely, an acceleration blow
曲
‘
M
U
－u
－。－＠色町・ua
－L
。
F
U
－。
』
4
・a
－
令
u
fL出
v
g’
α
Aザv 」~石7骨 onto・曲oipitalL・
l・3
(A) R!:TIC.-f!ιTIC.
l・1
(Bl RETIC.-RETIC.
L・3
(C)
且ET工C.-RETIC.
(D)
RETIC • -f!ETIC.
Fig. 15 EEG OF GROUP ill, No. 67 (UNHESPONSIVENESS l -II) A : Before Phe.nobiirbital Injection B : 20 min目 afterPhenobarbital Injection
「： 10sec. after Air Impact D : 10 min. after Air Impact
1082 日本外科宝函第29巻第5号
of 29 feet per second by pendulum etc. By this method concussion can be produced
under the conditi<>n in which the intracerebral pressure is not so high, but the
movement of the head inherent in this method is undesirable for recording.
(2) Percussion concussion (WALKER et al., 1944)
Percussion concussion is produced after the method described by WALKER et al.
A weight is dropped into a column of saline on the exposed dura from a maximum
height of 4 feet 6 inches and rapidly withdrawn by a light cord and pulley. The
measured duration of the blow is 0.1 to 0.2 sec.
(3) Compression concussion (MEYER & DENNY-BROWN, 1955)
Compression concussion is produced b~＇ sharply striking the plunger of a syアringe
｛ム）孟 t令
(ll）己． ι
VVvJ-州~2・ゐ(Cl
1 3
(D)
2ι
相州p
lOOf'V
L一一一一一
''<f'"
～r
1"'V¥t-ペrん、．、
Fig 16 EEG OF W, No. 63 (INTACT RESPONSIVENESS) A : Before midbrain-transection B : 1 min. after midbrain-transection
C : 20 min. after Phenobarbital Injection D : 3 min. after Air Impact
THE INFLUENCE OF THE MIDBRAIN TRANSECTION 1083
designed for this purpose. The sγringe is of 2 cc capacity and filled with air or
saline and screwed into a suitable trephine hole in the skull, which has an outlet
of 1 cm diameter. In this method the concussive stimulus is applied for less than
1/10 of a second.
The concussive stimulus in the present experiments can be classified as “com-pression concussion”. In this method cerebral concussion can be reproduced invariably
with no macroscopic hemorrhage in the cerebrum, and with extemely low death rate (NAGASAKI, 1959).
In the author’s experiments the occurrence of some macroscopic change in the cerebrum at the moment of, air impact cannot be denied, because of the presence
of an artificial skull window over the occipital region, and the possible protrusion
of the brain through it due to the changes in intracranial pressures resulting.
However, the cerebral concussion discussed here maY be functional, the neurolo-
gic disturbance being transient or reversible and may not be secondary to ischemia
of local brain, metabolic disturbance or mechanical destruction of brain matter.
Therefore, the cerebral concussion in this experiment should be considered as gene-
ralized reversible functional disturbance of the nervous system following mechanical
force.
2. Physiological mechanism of traumatic cerebral concussion (biological reacti-
vity against the trauma) :
Often with fairly mild blows, not sufficient, but near to concussion strength,
the animal presents slowing of the heart beat and falling of blood pressure (Fig. 8).
There may appear simultaneously oligopnea or conversely transient tachypnea with
hypersalivation and vomiting. Such subconcussive effects ma~＇ be explained in
general as due to the stimulation of the vagoglossopharyngeal mechanism. If in the same animal the vagi are sectioned, the respiratory, circulatory or other vage-
tative nervous changes disappear, a fact which indicates that those phenomena are
based on the stimulation of such vagoglossopharyngeal mechanisms (DENNY-BROWN
& RussELL, 1941) .
In the EEG can be demonstrated desynchronization or synchronization. But we cannot clear the relationship between the concussive or subconcussive stimulus and
the desynchronization or synchronization of EEG as a result of air impact.
In general the traumatic initial shock may be explained as the phenomenon of
transient reversible disorder of the brain stem function due to head trauma.
However, opinions on the mechanism of a transient reversible change of conscious-
ness are still divided. The one is a transient neuronal paralysis arising from the
brain trauma, the other is the result of excessive stimulation of the central nervous
system at the moment of the blow to the head. The latter opinion may be based on the following phenomena associated with
cerebral concussion. That is :
(1) An immediate generalized muscular spasm spoken of as the tetanic stage
of concussion which maγbe a result of intensive stimulation of the nervous function.
(2) The alterations of respiration consisting of a gasp of short duration with
1084. 日本外科宝函第29巻 第5号
resumption of normal respiration, transient irregular respiration or very transient
or prolonged apnea. These phenomena may be due to a spasm of the intercostal or
diaphragmatic mu包cles. (3) .A transient rising blood pressure occurring immediately or a few seconds
later may be caused bY an intense stimulation of the vasomotor centers which leads
to peripheral vasoconstriction. (4) BradJァcardiamay app伺 ras a result of vagal excitation.
(5) Reflex changes, hypo or a-reftexia.
Furthermore the large potentials recorded by WALKER et al. (1944) with a
voltage divider after a concussive blow may be explained as true neuronal excitation,
:ijut the cerebral concussion following air impact may be accounted for by the
disruption of the nervous function as a result of an abnormal excitation rather
than the mere paralyアsisof the nervous system (ARAKI, 195 7).
On the other hand, cerebral concussion is explained as a direct transient
paralysis of central or peripheral neurons (DENNY-BROWN & RussELL, 1944). The
reversible flattening or synchronization of EEG, arising from cortical injury potential
and the rise in cortical ox~·gen availability are all explained by a transient paralysis
of neurons. The cortical injur~・ potential during concussion shows a remarkable
similarity to the change of the motor stimulation thresholds (SPIEGEJ, et al., 1947).
That is, the metrazol convulsion threshold is temporarily raised immediately
followi碍 concussio孔 Fromthese data, the general principle is advanced that the
immediate effect of brain trauma of concussion may be a transient paralysis of neurons (MEYER, DENNトBROWN,1955).
3. The localization of the lesions produced bγhead injury with concussion :
In our experiments, the reflex arcs as an indicator of the experimental cerebral concussion are chiefly localized in the brain stem, but it may be necessan to make
clear whether the impact force a汀cctsclirectl>' the reflex arcs themselves or whether it exerts the initial influence on the upper central nervous system which maγ
regulate the reflex arcs of the brain stem, then seconclaril:-・ affecting the reflex arcs.
In the first place it has been found that phenobarbital has a selective inhibitorv e古田ton the reticular formation of the miclbrain (ho, 1958). Then in Group III,
which had intravenous phenobarbital premedication, the cerebral concussion (llnresp-
c.msiveness Ill) following air impact is more ditlicult to produce than in the case of the control group.
Secondly, there are many studies showing the occasional occurrence・ of transient
coma with some somatic symptoms following man>・ kinds of stimuli in arcas of the brainstem not directly involving re日exarcs, especially in the mesencephalic grey
matter or reticular formation of the midbrain (lsttu, 1944. TAKETOMO & TODA, 1950, YA~UNO, 1954, MATSUNAGA, 1959).
In the third place the functional disturbance of the nervous svstem in cerebral concussion following head j;njury is not localized on ！~’ in the upperル central nervous
system but also extends to spinal reflex arcs. Furthermore the influence on spinal
reflex function in cerebral concussion varies before and after cervical spinal transec-
THE INFL DENCE OF THE lVIIDBRAI>l TRANSECTION 1085
tion （羽TALKER,1944).
In the fourth place GROAT et al. have found that in experimental cerebral‘
concussion sufficient to 9-bolish the corneal or other reflexes, threshold in motor
e百ectis raised momentaril~・ to motor nuclei stimulus and for long periods to
supranuclear pathways stimulus, but the threshold in motor effect to peripheral
motor fibers stimulus does not change (GROAT et al., 1944）、
Thus it may be possible to assume that the air impact force a百ectsthe brail{
stem containing each reflex arc or nucleus not only primarib' by direct mechanical
action but also secondarily by downward spread of some physiological action from
the cortex to the brainstem reflex arcs.
In our experiment (Group II) some cases of decerebrated preparation can show
coma (Unresponsiveness ]I) following percussion concussion. But since in this group
cerebral concussion after air impact can be seen less frequently than in the case
of nontransected animals, the supposition of some descending depressive e百ect
from the cerebrum to the brain stem ma:-・ have to be admitted.
4. Unresponsiveness in Group II :
The air impact sufficient to produce coma in 100% in the group I animals
(control group) caused coma in onl:-・ 33五ofthe 12 cats in Group II. That is, by
breaking the neuro-anatomical tracfa between the cerebrum and brain stem in group
II animals, the occurrence of coma can greatly be reduced after air impact.
EEG findings in “cerveau isole” preparations show that the regular spindle
burst waves with low voltage and slow waves persist enm after cerebral concussion.
The results in group II may be explained by two possible factors.
(1) A descending suppressive impulse promoting the production of coma and
transmitted from the cerebrum toward the brain stem.
(2) Transiently disturbed function of the brain stem caused direct！γb~＇ the
impact force.
The above mentioned finding日 will agree with DENNY-BROWN’s experimental
findings following acceleration concussion (1941). They stated that in the decereb-
rated cat the intensity of the blow requir吋 toinduce coma is higher than in the
intact cat. The：－ナ alsostated that in localized percussion or compression concussion
the effect on the brain stem is not dependent on the forebrain or on other parts
of the brain but on the brain stem itself.
In our experiments this view must be revised, in that the descending suppres-
sive influences from the forebrain are rather more important, because after midbrain
transection air impact coma can surely be induced, but less frequent!:-・ than in the
intact (non-transected) cats.
In general, the muscular tonus of the experimental animals is increased after
decerebration. This may be the result of neuroanatomical exclusion of the motor
inhibitory center in forebrain and release of motor facilitatory center in mescncep-
halon, thus resulting in decerebrate rigiditγ． On the other hand there are other factors involved in the hypertonicitγof
muscles. That is, the muscsular reciprocality between extensor and ftexor, anesthesia
1086 日本外科宝函第29巻 第5号
in the animal, level of the midbrain transection or intensity of the external
stimulus> etc. (SPRAGUE et al., 1954, BACH, 1950, LINDSLEY & MAGOUN, 1948).
In the decerebrate animal the muscular tonus showed increase or decrease
respectively following external stimuli applied to different portions of the midbrain. Furtherrnore a considerable influence is e町ectedby decerebration on the function of
vestibular nucles or cerebellum. The galvanic skin reflex after such mesencephalic
transection becomes hypoactive. That is, the facilitatory center of galvanic skin
reflex can be assumed to be localized only on the rostral side of the plane of
midbrain transection (WANG, STAIN & BRowN, 1956).
The ‘electrical activation of the cortical area takes place also in the midbrain
transected animal in the same waY as in the intact animal after stimulating the
splanchnic nerve. This suggests that there is humoral activation of the cortex
through the rostral portion of pontomesencephalic reticular formation (BoNVALLET
et DELL & HIBEL, 1954).
In general under midbrain transection the anomalies of the motor function,
autonomic nervous function or cortical reactivity do not appear parallel to each other but varγdiversely. In conclusion, the preserved activity of caudal mesen-
cephalon in our experiment may be the result of interruption of the traumatic
suppressive impulses from the cerebrum (descending suppression), which e百ect
disturbed function of the brain stem.
5. Unresponsiveness in the Group III animals :
It has been reported that after injection of phenobarbital in an amount insufficient to produce a change in clinical features (sleep), stimulation of the
mesencephalic reticular formation still shows the cortical arousal reaction, though
somewhat hypoactive, and the recruiting reaction is strengthened. Therefore it
may be concluded that even small doses of phenobarbital depress the reticular ascending system (I TO, 1958) .
In group III coma takes place following air impact in fewer cases than in
group I. Perhaps the reason for this may be as follows : Descending suppressive
impulses from cerebrum toward the midbrain promoting the production of coma
are weakened because of depression of the mesencephalic activating system due to phenobarbital.
6. Analogy of the neurological states between group II and group III :
“Cerveau isole" (intercollicular transection) appears to cause the state of
irreversible sleeping. Nevertheless in “cerveau isole”preparation the olfactory and
optic tracts and rostral portion of the mesencephalic reticular formation are still
maintained, but the arousal reaction in EEG is hard to elicit (ARDUINI, A. & Mo-RUZZI, G., 1952, BREMER, 1937, 1953).
The group III cats having phenobarbital in an amount insufficient to produce a change in the clinical features (sleep) show in the EEG the spindle bursts like those in group II （“cerveau isole”）．
7. lJnresponsiveness in Group IV :
This group had the combined procedures of both group II and the group III.
THE INFLUENCE OF THE MIDBRAI::¥T TRANSE「TIO::¥! 1087
The coma on air impact may be expected to take place much less frequentl~＇. but
in the present experiment it was not so infrequent as was expected (Fig. 9). For
the definite explanation of this fact further study is needed.
V. SUMMARY
The author has studied the interrelation between the cerebrum and the brain
stem of ca臼 havingexperimental cerebral concussion.
An air impact was given on the parietal region of the intact brain in group I
(control) and on that of the brain transected intercollicularly （“cerveau isole”） in
group II. In the group III cats, phenobarbital, which is said to have a paralytic
influence on the mesencephalic reticular formation, was injected in an amount not
enough to produce a change in the clinical signs, and then the air impact was
given in the same manner. In group Iγ，the animals received both midbrain
transection and phenobarbital injection and then the air impact was given. The
strength of the air impact was the same throughout the experiment. Modi白ed
GIRNDT’s classification was used as criteria for the disturbed consciousness, and the
animals with changes severer than grade VI were judged as having the coma.
In addition, blood pressure, respiration, and EEG were recol:'ded simultaneousl;;.
The results of the experiment are as follows.
The air impact which was of a strength to produce coma in 100拓 ofthe
animals in group I (control), caused coma in only 33 % in grou1〕 II(12 cats in
all), 58 % in group III (12 cats in all), and 44 '};] in group IV (9 cats in all).
The animals receiving fairl)' mild blows, not sufficient, but near to concussion
strength, presented signs of parasympathetic hyperactivity.
The mechanism of the coma due to the air impact ma~’ be the disruption of
the nervous function caused bY an abnormal excitation rather than the mere
paralysis of the nervous function.
It might be assumed that the e町ectof air impact not onl~· on the brain stem
but also on the telencephalon and the diencephalon is of importance in the produc-
tion of experimental coma.
Thus there seem to be two factors in the production of the experimental coma
by means of air impact, 1) a descending abnormal suppressive impulse from the
cerebrum toward the brain stem, 2) the disturbed function of the brain stem itself
bv transmission of a mechanical force.
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u. Labyrinthin Reflexe羽Tirkungsst忌rkevon Novonal. Arch. fiir exper. Path. u. Pharmiikol.. 164, 118, 1932.
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4. 644, 1958. 18) Jasper, H.: Diffuse Projection Systems: the Integrative Action of the Thalamic Reticular
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21) Lindsley. 0. S. & Ma邑・oun’H.W. : Reticulospinal Influences on Stretch Re臼ex.J. Neur hy-siol., 11. 5bl. 1948.
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Head. Alteration in Nerve Cells. Arch. Neurol. & Psychiat .. 55. 79. 1946.
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34) Sp】egeLE. A., Spiegel-Adorf, M .. Wycis, II. T. & Mai・ ks, M.: Cerebral Concussion and Convulsive Reactivity. Res. Pub!. Ass. Nerv. Ment. Dis., 26, 84, 1947.
35) Sprague James & Chambers，羽T.: Control of Posture by Reticular Formation and Cerebellum in the Intact, Anesthetized and in the Decerebrated Cat. Amer. J. Physiol., 176, 52, 1954.
36) Walker. A. E. Kollros. J. J. & Case. T. J.: The Physiological Basis of Concussion. J. Neuro-surg., I. 103, 1944.
37) Taketomo, T. & Toda, T. : Coma Puncture (in Japanese). Nιshinkei, 6, 354, 1950. 38) Wang Stein & Brown:
(I) Effects of Transections of Central Neuraxia on Galvanic Skin Reflex in Anesthetized Cats. J. Neurophysiol., 19. 340, 1956.
(2) Brain Stem Reticular System and Galvanic Skin Reflex: in Acute Decerebrate Cats. J. Neurophysiol.. 19, 350, 1956.
(3) Changes in Galvanic Skin Reflex after Acute spinal Transection in Normal and Decerebrate Cats. J. Neurophysiol., 19, 446, 1956.
39) Yabuno, S.: Coma Puncture by Means of Nicotinization. Acta Sch. Med. Univ. Kioto, Jap., 32. 32, 1954.
和文抄録
実験的外傷性昏睡I乙於ける中脳切断及び
PHENOBARBITAL投与の影響
京都大学医学部外科学教室（指導：荒木千里教授）
松 オ二
頭部外傷直後の一過性意識障害（無反応状態）が，
脳の知何なる部分の，如何なる機能異常に起因するか
については，尚議論の多い所である．大別すると，外
力に依ってp 脳全体が障害を受け，その一過性神経異
常利京因であるとする脳全体障害説L 脳幹局所がま
づ障害をうけp これが大脳乃至は脊髄にまで二次的に
影響を及ぼすと考える脳幹障害説とに分けられる．又
両者何れの場合でもP この機能異常が，単なる麻痔に
よっておこるものか，或は逆に機能の異常冗進の結果
での無反応状態であるかについても明確に説明されて
いない．
著者はp 空気筒激法に依って惹起される， Z怖の実験
的外傷性昏睡を分析する為にp 種々なる前処置を行な
ってその影響をみた．まづ，第1群の実験狛では，頭
頂部に加えられた空気筒激でp 全例に一過性昏置が発
現出来る最低筒激カを決定し，第2君事では， Bremer
の方法に随い中脳切断を行い，このあとで第 l苦手と同
一条件下で空気筒激を行なった.J:!Pち，第2苦手に於い
悟
ては，前脳と脳幹との神経連絡をまづ機械的に遮断し
て後，外力を加えた．この為に外力はp 脳幹に対して
は，単に物理的刺戟として作用じたものでありp 少く
とも外力によるP 前脳及び脳幹の聞の神経生理学的作
用の関与は除外出来たわけである．
第3群ではp PHENOBARBITALの少量即ち臨床
症状には変化（睡眠）を来すに足りないが，脳幹網様
織の機能低下を認め得る程度の量を投与後，第 l群同
様空気筒撃を加えた．
第 4群としてはp 第 2＇第 3群の両操作を，同一猫
に加え，然る後第 1群と同僚条件下で空撃を加えた．
昏睡の指標としては，動物である為，意識障害を直
接とりあげることは困難である．
随って，脳幹レベルの変化の指標として， 侵害乃至
整位反射の異常，脳幹深部脳波を用いp 呼吸血圧変化
をも記録し， スp 前脳レベルの変化に対して皮質表面
脳波を記録した．
この結果，第2＇第 3＇第 ーl群は，第 l群に比し，
1090
昏医量発現率は有意の差を以て減少している．この説明
としてp 昏｜陸発現に関与する 2つの神経機能障害が想
像出来た．
l.) 空撃に依り，前脳から脳幹えと下降するP 神経
生理学的調整機能が障害される．この障害は結果から
みると，昏睡発現を助長する．
2) たとえ空撃が頭頂部に加えられるとしても，こ
の物理的外力は脳幹にまで波及するわけで，この結果
脳幹局所の機能障害がおこり，昏睡を発現させる．
上記に説明される神経機能障害はp 結果としてp 侵
害p 整位反射の消失等反射効果の抑制を示すものであ
るがp この抑制が神経機能麻庫に依るものかp 逆に機
能異常充進によるかについては更に検討を要する．
次で第2，第3群の反応態度の類似性をも検討し
fこ．
結論としてF 脳振塗性昏睡は， 1) 脳幹単独の局所
性筒激でもおこり得る．然し， 2) 頭部に加えられた
機械的F街激によって，脳幹よりも上位p 即ち大脳レベ
ルから脳幹に下降して，結果としては昏睡発現を助長
するような，神経調整機能異常も決して無視すること
は出来ない．
