Muscular Contraction following rapid Electrical Stimulation of Central Nervous System

1891 ◽  
Vol 17 ◽  
pp. 178-180
Author(s):  
John Berry Haycraft

(Abstract)Kronecker, Hall, Schäfer, Horsley, and others have found, when stimulating the spinal cord with rapid induced currents (ten, twenty, thirty, forty times per second), that the muscles always responded by giving a curve showing oscillations of one invariable period, no matter what the period of the stimulation may have been. With rapid stimulation, the muscles in the hands of the first named observers gave oscillations of twenty a second, in the hands of the latter observers of ten a second. These results are to be explained in the following way. When the central nervous system is stimulated, the muscles contract but never smoothly, for local fascicular movement, as the author has elsewhere shown, always occurring. These cause the registering apparatus to oscillate at its own period, just as any swinging body may be kept in motion by occasional disturbances. We can thus explain how each observer obtained the same number of oscillations every time he stimulated the nervous system; it was because he used the same recording apparatus each time. We can also see that the different periods observed by different observers are due to the fact that they each used a different recording apparatus. The author finds that on changing the recording apparatus (lever or tambour) the tracing obtained can be changed at will, and is practically a tracing of the oscillating period of the instrument used.

In the study of the phenomena of anaphylaxis there are certain points on which some measure of agreement seems to have been attained. In the case of anaphylaxis to soluble proteins, with which alone we are directly concerned in this paper, the majority of investigators probably accept the view that the condition is due to the formation of an antibody of the precipitin type. Concerning the method, however, by which the presence of this antibody causes the specific sensitiveness, the means by which its interaction with the antibody produces the anaphylactic shock, there is a wide divergence of conception. Two main currents of speculation can be discerned. One view, historically rather the earlier, and first put forward by Besredka (1) attributes the anaphylactic condition to the location of the antibody in the body cells. There is not complete unanimity among adherents of this view as to the nature of the antibody concerned, or as to the class of cells containing it which are primarily affected in the anaphylactic shock. Besredka (2) himself has apparently not accepted the identification of the anaphylactic antibody with a precipitin, but regards it as belonging to a special class (sensibilisine). He also regards the cells of the central nervous system as those primarily involved in the anaphylactic shock in the guinea-pig. Others, including one of us (3), have found no adequate reason for rejecting the strong evidence in favour of the precipitin nature of the anaphylactic antibody, produced by Doerr and Russ (4), Weil (5), and others, and have accepted and confirmed the description of the rapid anaphylactic death in the guinea-pig as due to a direct stimulation of the plain-muscle fibres surrounding the bronchioles, causing valve-like obstruction of the lumen, and leading to asphyxia, with the characteristic fixed distension of the lungs, as first described by Auer and Lewis (6), and almost simultaneously by Biedl and Kraus (7). But the fundamental conception of anaphylaxis as due to cellular location of an antibody, and of the reaction as due to the union of antigen and antibody taking place in the protoplasm, is common to a number of workers who thus differ on details.


1945 ◽  
Vol 22 (1-2) ◽  
pp. 63-74
Author(s):  
JOSEPH BARCROFT ◽  
D. H. BARRON

1. A method (the needle method) is described for the measurement of the pressure in the stream going through a vessel. 2. In the foetal sheep the needle method applied to the umbilical artery gives substantially the same results as the mercurial manometer applied to the carotid, until about half-way through the gestation period. 3. As gestation proceeds the needle method applied at the first moment at which it can be applied to the umbilical artery (or a branch) gives readings substantially lower, and increasingly lower as gestation proceeds, than does the mercurial manometer read at the first moment at which it can be read. 4. The discrepancy is due to the sum of a number of causes which are discussed, but of these the most important is an actual rise of pressure between the time of delivery and the completion of the dissections contingent on the use of the mercurial manometer. 5. The cause of this is not at present demonstrated, but either or both of two factors may be concerned: (a) a dulling of the central nervous system which weakens the depressor reflex; (b) the establishment of a greater degree of vasomotor tone consequent on the bombardment of the central nervous system with sensory stimuli. 6. The pulse rates in utero and just after delivery of the foetus into a saline bath at 39-40°C. (the umbilical circulation being unimpaired) are not significantly different. 7. The pulse rate quickens up to the 70th-80th day, after which it becomes slower as gestation proceeds. 8. If both vagi be severed, the pulse rate te to quicken throughout gestation. The pulse, therefore, comes increasingly under vagus inhibition from the 80th-90th day onwards. 9. Even after the vagi have been cut after the 120th day (it has not been tried before) adrenalin in sufficient quantity will cause a further quickening of the pulse. 10. The earliest date at which stimulation of the peripheral end of the right vagus was observed to slow the heart was the 77th day. On the 85th day peripheral stimulation of the left vagus also failed, but succeeded on the 101st day. 11. Central stimulation of the left vagus, with the right vagus intact, produced slowing on the 77th day. 12. Slowing of the heart synchronous with rise of arterial pressure has been observed on the 111th day. 13. Slowing of the heart which bears evidence of being reflex has been obtained by raising the blood pressure (clamping the cord) on the 121st day and by injection of adrenalin on the 118th day. 14. Approaching term both the carotid sinus and cardiac depressor mechanisms are functional. 15. Lowering of the blood pressure as the result of stimulation of the central end of the vagus and with both vagi severed can be demonstrated late in gestation.


2008 ◽  
Author(s):  
Jonathan M. Cayce ◽  
Chris Kao ◽  
Jonathan D. Malphurus ◽  
Peter Konrad ◽  
Duco Jansen ◽  
...  

2005 ◽  
Vol 328 (2) ◽  
pp. 177-186 ◽  
Author(s):  
Alim-Louis Benabid ◽  
Bradley Wallace ◽  
John Mitrofanis ◽  
Celine Xia ◽  
Brigitte Piallat ◽  
...  

2019 ◽  
Vol 10 (1) ◽  
pp. 63-71
Author(s):  
Aleksandr A. Kalinkin ◽  
Alexey G. Vinokurov ◽  
Olga N. Kalinkina ◽  
Alexander S. Ilinykh ◽  
Andrey A. Bocharov ◽  
...  

The technique of deep brain stimulation is used to treat patients with various diseases of the central nervous system who are not amenable to conservative therapy, while open interventions in them are associated with a high risk of complications. In the review, we evaluate the efficiency of the deep stimulation of different regions of the brain in some pharmacoresistant forms of diseases.


1963 ◽  
Vol 4 (2) ◽  
pp. 118-130 ◽  
Author(s):  
Hideo UEDA ◽  
Akiyuki YAMADA ◽  
Hitoshi GOTO ◽  
Iwao ITO ◽  
Yutaka TAKABATAKE ◽  
...  

1954 ◽  
Vol 32 (5) ◽  
pp. 498-503 ◽  
Author(s):  
C. W. Gowdey ◽  
A. R. Graham ◽  
J. J. Seguin ◽  
G. W. Stavraky

The effects of dieldrin (hexachloro-epoxy-octahydro-dimethanonaphthalene) were studied in acute experiments on cats and rabbits. When injected intravenously or intra-arterially, it caused excitation of the central nervous system, which resulted in increased reflex excitability, convulsions, bradycardia, and some vasodepression. Dieldrin potentiated the effects of acetylcholine on the central nervous system and on the circulatory system as well as on intestinal motility. These latter manifestations were abolished by section of the vagus nerves, indicating a central action. Dieldrin had no effect on salivary secretion produced either by stimulation of the chorda tympani or by injections of acetylcholine in the decentralized submaxillary gland. Thus, although dieldrin has a marked parasympathomimetic action, this effect is exerted through stimulation of central mechanisms and not peripherally.


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