Functional differentiation of skeletal muscles

According to BUCHTHAL the histogram of duration and voltage from the motor unit of biceps brachii muscles gives only one peak respectively as can be seen in Fig. 14 in his paper which reports the data covering the experiment on 1,268 motor units. However, his histogram seems to be made of the spikes led off from several motor units because the histogram shows no much fluctuations in voltage as 50&#956;V to 1,000&#956;V and in duration as 1 msec to 20 msec. Therefore, if observations are actually based on a single motor unit, two peaks may reasonably be expected on the histogram, because two kinds of the motor units, kinetic (phasic) and tonic, have respective individual characteristics of their own shikes The histological observation shows that many white and red muscle fibers are intermingled with each other even in one single fasciculus, and it is supposed that the fasciculus does not correspond to a single motor unit. Moreover, the shape of the spikes, which was formerly considered as a motor unit, is not a pure diphasic form, but irregular and polyphasic ones, and also electromyographically a single motor unit controls the area of more than 10mm in width (BUCHTHAL). From these facts, it is probable that the histogram by BUCHTHAL was made of the spikes composed of muscle fibers belonging to several different motor units. Our observations done by the above stated method showed clearly the pure diphasic spikes. Therefore, we are of the opinion that these spikes obtained by our method are led off from only one or from a few muscle fibers belonging to the same motor unit. These spikes are lower than 550&#956;V in voltage and shorter than 5.5 msec in duration and every individual spikes show uniform diphasic pattern. There exist two kinds of spike groups, in the histogram one which is composed of high voltage with short duration (1.0-1.5 msec.), and the other of low voltage with long duration (2.0-4.0msec.). The former may be of kinetic (phasic) motor unit and the latter is of tonic motor unit, because the white muscle fibers with a larger diameter may have a higher voltage than the red and the white fibers that perform rapid contraction may show shorter duration in wave form. In the two cases having spinal cord tumors, two kinds of spikes with respective and individual characteristics were observed in the same EMG. These will be two different kinds, kinetic (phasic) and tonic motor units. In the case of amyotrophic lateral sclerosis, two kinds of spikes appeared, but since both of them were of short duration, they might be considered to be of kinetic (phasic) motor unit (or its intermediate motor unit). Furthermore, since its histological findings revealed that the red muscle fibers were all atrophied and degenerated and showd only white muscle fibers to be normal, it is obvious that the kinetic (phasic) motor unit with a shorter duration is derived from white muscle fibers. Therefore, in our opinion the widely accepted concept that spikes including even irregular wave forms all belong to the motor unit seems not to be true, but these spikes seem to represent a combination of several pure spikes though not so many, and those muscle fibers belonging to the same motor unit appear to be intermingling themselves in a relatively wide area. The reason for this contention may be explained as follows. If the muscle fibers belonging to the same motor unit were agglomerated, clearcut diphasic spikes should appear even with a fairly big electrode, and if the accepted concept be true, these spikes can never be picked up at the distance so far apart as 2.0cm. or 2.5cm. (0.5-1.2cm. by BUCHTHAL) as has been possible in our experiments. Furthermore, the histogram composed only of these pure spikes reveals two peaks, and therefore, we believe it is reasonable to say that these two peaks indicate the existence of kinetic (phasic) and tonic motor units. As a small number of motor units located in between these two peaks can be recognized, these are believed to be the muscle fibers possessing an intermediate stainability as revealed in the histological examination. However, further studies are required before giving any definitive conclusion on this point.</p

Ein Neues Verfahren zur Messung der Bakteriziden Fähigkeit des Vollblutes

Das oben erwahnte Verfahren hat vor den anderen Methoden besonders die Vorzuge, 1) da&#946; man dadurch zu einem sicheren Resultat gelangen und gleichzeitig auch jedes Datum mit exakten Ziffern zum Ausdruck bringen kann, 2) da&#946; bei diesem Verfahren keineswegs erforderlich ist, eine bestimmte Anzahl von Keimen einschlie&#946;ende Bakterienaufschwemmung herzusteHen und auch Kontrollversuch anzustellen, 3) da&#946; es von den Fehlern des Mischverhaltnisses zwischen der Bakterienlosung und dem Blut nicht so erheblich beeinflu&#946;t wird, und 4) da&#946; man durch dieses Verfahren gleichzeitig mehrere bakterientotende Faktoren untersuchen kann. Ferner hat dieses Verfahren auch den Vorzug, da&#946; es praktisch sehr einfach auszufuhren ist und nur 6 Stunden nach der Blutentnahme bereits das Ergebnis liefert. Es gestattet ferner, die bakterizide Kraft des Blutes gleichzeitig bei 6 - 8 Menschen zu untersuchen, was mich zur Uberzeugung fuhrt, da&#946; es in der Klinik hochgeschatzt werden wird. Auch das Verfahren und die ebenfalls vom mir aufgestellte Formel zur zusammenfassenden Beurteilung kann man nach meinem Erachten durch entsprechende Veranderungen einiger Faktoren ohne jede Schwierigkeiten auch fur andere Bakterienarten anwenden. Man wird wohl gegen eine einzige Lucke dieses Verfahrens, da&#946; die mikroskopische Untersuchung und die Berechnung allzu verwickelt zu sein scheint, Einwand erheben, eine Lucke, zu deren Schlu&#946; jedoch nur eine kurzfristige Ubung erfordert wird, durch welche die mikroskopische Untersuchung innerhalb 30 Minuten, die Berechnung nur in 5 Minuten vollendet werden kann. (Zur Berechnung bedarf es einer Gauss'schen Logarithmentafel.) Obgleich das geschilderte Verfahren noch viele, genauere Prufungen erheischende Punkte in sich einschlie&#946;t, mu&#946; es hier, wenn auch in Grundzugen, jetzt schon angefuhrt werden,. da ich der festen Uberzeugung bin, da&#946; es im Vergleich zu den bisherigen Methoden ein dem wirklichen Wert der Bakterizidie des Vollblutes im lebenden Organismus viel naheres Resultat liefert.</p

Studies on Allergic Genesis of Idiopathic Epi­lepsy

In such animals not having any organic changes in their brains during the initial stage showed a descendence of convulsive threshold. abnormal findings in their electroencephalogram and ascending activity of ChE. But what is the cause of these functional changes? First, from the fact that though there was no organic changes, they were sensitized and reiniected by a known antigen, which is obviously an antigen-antibody reaction. Second, from the fact that we got a histological.change, which was acknowledged as C.L.A. changes by increasing the concentration of these solution and the number of injections, it could be thought that these functional changes were caused by what I called latent C.L.A.. That is, it seems it could be thought that it would give functionally a permanent hypersensitivity, which is called convulsive arrangement. Furthermore, a similar histological findings as seen in old epileptics were made experimentally after prolonged and repeated injections of very diluted antigens. I believe it can be said, also from this histological point that they are experimental epileptics. But I am not trying to say that idiopathic epilepsy is the same allergic disease as asthma. If it was so, it should offer clinically a problem of eosinophilia in the blood of epileptics. But actually there is no eosinophilia in epileptics. Also, in adult epileptics, convulsive attacks is not often seen soon after introduction of antigens. Consequently, my theory that epilepsy is allergic, does not mean that allergy is the direct cause of epileptic attacks. What I mean is, the causal genesis of idiopathic epilepsy is hypersensitivity of nerve cells in the brain. This hypersensitivity was attained as a tissue reaction by some allergic mechanism without any organic changes. This functional change gives the nerve cell a hypersensitive state, which becomes the base of the beginnihg of convulsion. Its inducement of attack could be water stagnation in the body, anemic state of the brain, alkalosis, or introduction of allergens. In short, the cause of attack does not always come from allergic reactions.</p

On the March of the Cerebellar Epi­leptic Convlsion in Dogs

1) Cerebellar convulsion was identical with the cerebral cortical epileptic convulsion and the number of cases in which the march of spasm was observed were quite the same as that of cases in which convulsion occurred at the same time on the whole body. 2) No convulsion occurred by stimulation of the vermis cerebellaris and also convulsions occurred very rarely by that of the cerebellar nuclei. 3) In cases having the march of spasm caused by stimulation of the lobus lunatus anterior, spasm began in the fore limb, while by stimulation of the lobus lunatus inferior and lobus semilunaris spasm started mainly in the hind limb on the side of stimulation. 4) In the case of stimulation of cerebellum, the pathway of the impulse to the opposite side was considered to be the communication between both cerebellar hemispheres and both thalami and thus the march of spasm spread from one side of the body to the other side. 5) No march of cerebellar epileptic convulsion occurred without the cerebral motor cortex. 6) After the removal of both sides of the cerebral motor cortex no march occurred, but the general convulsion occurred. 7) No convulsion occurred by stimulation of the cerebellar hemisphere after the removal of both thalami or both nuclei lenticulares. 8) The march of convulsion occurs by close cooperation of the pyramidal and extrapyramidal tracts. It seems that for the impulse of the convulsion the extrapyramidal tract plays an important role, while for the start of the convulsion, that is, march of spasm pyramidal tract plays the main role.</p

Anatomical Studies on Conduction Pathways of Advcrsive Movement

1. The descending fi bers from the areas 8 and 6 a&#946; reaching the lateral and ventral nuclei of the homolateral thalamus are recognized. They are considered to be the conduction pathways of the adversive movements caused by the stimulations on the areas 8 and 6 a&#946;. 2. The descending fibers from the areas 5, 7, 19 and 22 reaching the head and the tail of the homolateral caudate nucleus are revealed. These fibers are considered to be the conduction pathways of the adversive movement caused by the stimulation on these areas. Moreover, the descending fibers from the areas 7, 19 and 22 reaching the homolateral superior colliculus are recognized. These fibers are also considered to participate in the adversive movement. 3. The fibers from the lateral and ventral nuclei of the thalamus reaching the homolateral superior colliculus, Cajal's interstitial nucleus and reticular formation of the mesencephalon are observed. These fibers are considered to be the conduction pathways of the adversive movement from the thalamus. 4. The caudate nucleus and the lenticular nucleus are connected closely by the numerous fiber bundles crossing the internal capsule. 5. The fibers from the lenticular nucleus which participate in the adversive movements descend through the lenticular fasciculus, Forel's field, the comb-fibers in the cerebral peduncle, substantia nigra and medial lemniscus, and then reach the stratum lemnisci et profundum of the homolateral superior colliculus, Cajal's interstitial nucleus, Darkschewitsch's nucleus, Westphal-Edinger's nucleus, oculomotor nucleus and trochlear nucleus. 6. The tectobulbar tracts from the superior colliculus joined with the both oculomotors, contralateral trochlear, abducens, facial and accessory nuclei, thus they are considered to take part in the adversive movement. 7. The ascending fibers from the dentate nucleus pass through the homolateral brachium conjunctivum and reach the contralateral trochlear and oculomotor nuclei, superior colliculus and the lateral and ventral nuclei of the contralateral thalamus. These ascending fibers are considered to be the conduction pathways of the adversive movement from the cerebellum.</p

Experimental Studies on Adversive Movement

Adversive movement was first reported in 1870 by Fritsch and Hitzig when they said that when gyrus Sylvii was stimulated electrically the eyes moved to the opposite side of the stimulation. Vogt and Foerster made a detailed report on adversive movement, which is a rotary motion of the head, trunk and both eyes. But in their report, they did not make it clear what tracts the stimulation took. Mitsueda, who iS under Hayashi, defined the cortical area of the eye balls and the eye lids. He reported that they were of the extrapyramidal kind. Russel reported that when the cerebellum was stimulated the eye balls moved to the side of the stimulation, but did not say anything about adveraive movements which concerned the movement of the head and the trunk. Therefore, to ascertain the center of adversive movement and its tract the following experiments were performed. For stimulation electrical ones and chemical ones using metrazol (cardiazol) were used. As Ishizuka, who is under Hayashi, has proved excitement is only seen when cardiazol is injected among the nerve cells at a certain concentration, and it is not seen when injected among the nerve fibres.</p

Biochemical studies on the epileptic cerebral cortex

Within the range of our investigations the most important biochemical characteristics in the brain of idiopathic epileptic patients seem to be defect in the production of and the attendant decrease in free amino acids of the brain. On account of these phenomena there seem to occur the acceleration of the ChE activity and a poor utilization of glucose. Of the free amino acids in the brain the combined amount of glutamic acid, glutamine and &#947;-aminobutyric acid (GABA) will occupy the major portion of the total free amino acids found in brain, and thus diminution in the contents of glutamic acid and GABA in the brain of idopathic epileptic patients has quite an important meaning. At the present stage it is not yet possible to give any definitive answer to the question why such decrease occurs but it is believed that the most urgent problem facing us today is the amino acid metabolism that is associated with glutamic acid and the comparative studies of the amino acid metabolism in the epileptic brain to that in the non-epileptic brain are required. The fact that &#947;-amino-&#946;-hydroxybutyric acid (GABOB), the substance that suppresses the central excitation, is decreased seems to indicate biochemically the existence of a defect in the processes of excitation in the brain of idiopathic epleptic patients.</p

On the Adversive Movement of Area 4C of the Motor Cortex

1. Adversive movements were induced by electrical stimulation and metrazol injection on area 4c of the cerebral cortex. 2. The adversive movement from area 4c does not pass through the thalamus, nucleus caudatus, nucleus lenticularis or superior collicuIus, but through direct efferent pathways in the internal capsule. 3. The adversive movement from area 4c passes through the pyramidal tract.</p

Experimental Studies on the March of Spasm During Epileptic Convulsion

March of spasm in epileptic convulsions was first observed by Tackson in 1863, when he said that in certain epileptic convulsions there is a phenomenon, where the convulsion starts from a certain muscle group and gradually spreads to other muscle groups. He called this, &#34;march of spasm&#34; and reported that it spreads according to the arrangement of motor representations in Rolando's area of the cerebral cortex. Since then, many important studies concerning the cerebral motor cortex were performed and reported. Recently, when Erickson had brought out a method in measuring electroencephalographic waves, Jackson's theory has been acknowledged. In Japan, Hayashi and his school has made an extensive study on epileptic convulsion. They used nicotine, cardiazol and others as chemical stimulations and decided the conduction tract of epileptic convulsion in dogs. The characteristic part of chemical stimulation is that, the nelve cells excite themselves when it is injected directly among them in certain concentrations and do not excite themselves when performed among nerve fibers. This was proved by Ishizuka. We used this method in dogs to see what was the mechanism of this phenomenon, &#34;march&#34; which is seen in epileptic convulsions and what tracts they took for conduction. And as its result, we found new facts that the presence of the motor cortex was needed for the march of spasm, and the conduction tract descending from the lenticular nucleus were quite different from Hayashi and his school had previously reported.</p