I. Introductory remarks: Basic mechanisms of pain associated with deep tissues

1991 ◽  
Vol 69 (5) ◽  
pp. 607-609 ◽  
Author(s):  
Ronald Dubner
Keyword(s):  
Central Nervous System ◽  
Chronic Pain ◽  
Nervous System ◽  
Deep Tissue ◽  
Cutaneous Pain ◽  
Chronic Pain Conditions ◽  
Stimulation Of

There are important differences in pain arising from deep tissues in comparison to cutaneous pain. These differences can be partially explained by the unique organization of nociceptive systems activated by stimulation of muscle, joint, or viscera. Recent evidence also indicates that stimulation of deep tissues can produce long-lasting changes in central nervous system excitability and, therefore, may play a prominent role in persistent or chronic pain conditions. These findings have important implications for the treatment of chronic deep tissue pain conditions.

scholarly journals A review of the bioelectronic implications of stimulation of the peripheral nervous system for chronic pain conditions

2020 ◽  
Vol 6 (1) ◽  
Author(s):  
Timothy R. Deer ◽  
Ramana Naidu ◽  
Natalie Strand ◽  
Dawn Sparks ◽  
Alaa Abd-Elsayed ◽  
...  
Keyword(s):  
Chronic Pain ◽  
Nervous System ◽  
Peripheral Nervous System ◽  
Chronic Pain Conditions ◽  
Stimulation Of

Central Nervous System and Pituitary Mechanisms in Dopaminergic Stimulation of Growth Hormone Release in Women

1981 ◽  
Vol 32 (4) ◽  
pp. 213-216 ◽  
Author(s):  
Carlo Ferrari ◽  
Roberto Caldara ◽  
Cristiano Barbieri ◽  
Paolo Testori ◽  
Rosanna Benco ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Growth Hormone ◽  
Nervous System ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Dopaminergic Stimulation ◽  
Stimulation Of

scholarly journals VI. —Anaphylaxis and anaphylatoxins

1923 ◽  
Vol 211 (382-390) ◽  
pp. 273-315 ◽  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Guinea Pig ◽  
Anaphylactic Shock ◽  
The Body ◽  
Muscle Fibres ◽  
Direct Stimulation ◽  
Fundamental Conception ◽  
The Central Nervous System ◽  
Stimulation Of

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.

scholarly journals Catastrophizing Interferes with Cognitive Modulation of Pain in Women with Fibromyalgia

Pain Medicine ◽  
2018 ◽  
Vol 19 (12) ◽  
pp. 2408-2422 ◽  
Author(s):  
Laura D Ellingson ◽  
Aaron J Stegner ◽  
Isaac J Schwabacher ◽  
Jacob B Lindheimer ◽  
Dane B Cook
Keyword(s):  
Central Nervous System ◽  
Chronic Pain ◽  
Nervous System ◽  
Pain Catastrophizing ◽  
Pain Modulation ◽  
Critical Function ◽  
Sensory Stimuli ◽  
Brain Responses ◽  
Increased Risk ◽  
Pain Ratings

Abstract Background Pain modulation is a critical function of the nociceptive system that includes the ability to engage descending pain control systems to maintain a functional balance between facilitation and inhibition of incoming sensory stimuli. Dysfunctional pain modulation is associated with increased risk for chronic pain and is characteristic of fibromyalgia (FM). Catastrophizing is also common in FM. However, its influence on pain modulation is poorly understood. Objective To determine the role of catastrophizing on central nervous system processing during pain modulation in FM via examining brain responses and pain sensitivity during an attention-distraction paradigm. Methods Twenty FM patients and 18 healthy controls (CO) underwent functional magnetic resonance imaging while receiving pain stimuli, administered alone and during distracting cognitive tasks. Pain ratings were assessed after each stimulus. Catastrophizing was assessed with the Pain Catastrophizing Scale (PCS). Results The ability to modulate pain during distraction varied among FM patients and was associated with catastrophizing. This was demonstrated by significant positive relationships between PCS scores and pain ratings (P < 0.05) and brain responses in the dorsolateral prefrontal cortex (P < 0.01). Relationships between catastrophizing and pain modulation did not differ between FM and CO (P > 0.05). Conclusions FM patients with higher levels of catastrophizing were less able to distract themselves from pain, indicative of catastrophizing-related impairments in pain modulation. These results suggest that the tendency to catastrophize interacts with attention-resource allocation and may represent a mechanism of chronic pain exacerbation and/or maintenance. Reducing catastrophizing may improve FM symptoms via improving central nervous system regulation of pain.

Blood Pressure and Pulse Rate in the Foetal Sheep

1945 ◽  
Vol 22 (1-2) ◽  
pp. 63-74
Author(s):  
JOSEPH BARCROFT ◽  
D. H. BARRON
Keyword(s):  
Blood Pressure ◽  
Central Nervous System ◽  
Nervous System ◽  
Pulse Rate ◽  
Umbilical Artery ◽  
The Central Nervous System ◽  
The Right ◽  
First Moment ◽  
Left Vagus ◽  
Stimulation Of

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.

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