The antinociceptive system. Endogenous mechanisms of pain control

Представлен обзор современных данных по изучению антиноцицептивной системы и эндогенных механизмов обезболивания. Контроль болевой чувствительности осуществляется многими структурами ЦНС, каждая из которых функционирует как самостоятельное образование. В комплексе все они входят в состав сложной системы антиноцицепции, аналогично тому, как ощущение боли является результатом интегративной функции ЦНС. Данное сообщение посвящено анализу роли информации, поступающей по толстым миелиновым волокнам в задние рога спинного мозга и нисходящих тормозных влияний на уровне задних рогов спинного мозга. Охарактеризованы структуры, влияющие на антиноцицепцию. На уровне спинного мозга обнаружены два механизма подавления боли - это сегментарный контроль и система нисходящего тормозного контроля. По современным данным обезболивающие эффекты объясняются не только сегментарным контролем, но и включением надсегментарных механизмов контроля, в т.ч. и гуморальных. Центральные структуры головного мозга оказывают не только нисходящее влияние на спинальном уровне, но и модифицируют болевые сигналы в местах их переключения в различных структурах головного мозга. Нисходящая ингибиторная система тесно взаимосвязана с тремя нейротрансмиттерными системами: опиатной, норадренергической и серотонинергической. Возникновение боли зависит не только от интенсивности ноцицептивного повреждения, но и от состояния различных звеньев антиноцицептивной системы. На основании знаний о патогенезе острой боли, структуре и функции антиноцицептивной системы дается определение понятия «боль». This review focused on the antinociceptive system and endogenous mechanisms of pain control. Multiple structures of the central nervous system control the pain sensitivity, and each of them functions as an independent entity. Together they constitute a complex system of antinociception consistent with that the sensation of pain is provided by integrative functioning of the central nervous system. This review analyzed the role of information delivered through thick myelin fibers to posterior horns and descending inhibitory effects at the level of the posterior horns. Two pain relief mechanisms were found at the spinal level, the segmental control and the descending inhibitory control system. According to current data anesthetic effects are explained not only by the segmental control but also by involvement of suprasegmental control mechanisms, including humoral ones. Central structures both exert downstream effects at the spinal level and modify pain signals at the locations where they switch over in various cerebral structures. The descending inhibitory system is closely interrelated with three neurotransmitter systems, the opiate, noradrenergic and serotonergic ones. Emergence of pain depends on both the intensity of nociceptive damage and on the condition of multiple parts of the antinociceptive system.Based on studying the pathogenesis of acute pain and the structure and function of antinociceptive system the authors provided a definition for the term of pain.

Features of the alteration of poststimulus thresholds of the pain and its subjective characteristics in patients with neuropathic pain in the process of empatho-technique

In the work there are presented results of the investigation offeatures of the alteration of thresholds of the post-stimulus pain and its subjective characteristics in patients with phantom pain syndrome and psychogenic pain in the process of empatho-technique. There was studied the role ofpsychophysiological autoregulation in the restoration of sensitivity in patients undergone to amputation of lower extremities. The use of empatho-technique was found to allow not only to significantly reduce the intensity ofphantom, and psychogenic pain, but to fully restore sensitivity to ultrasonic stimuli in the psychogenic pain and significantly eliminate cases of its disturbance in the phantom pain. It is assumed that the reducing influence of empatho-technique on the intensity of the perception ofpain can be realized by means of activation of the antinociceptive system, enhancement of its inhibitory effect on the painful stimulus, as well as decline in the activation of the nociceptive system, with a subsequent decrease in the intensity of sensations ofpain and restoration of sensitivity.

Dissociating the neural mechanisms of pain consistency and pain intensity in the trigemino-nociceptive system

Background Individual differences in pain perception to a standardized nociceptive input are a well-known phenomenon within pain research. Brain structures known to play a crucial role in pain modulatory processes are the rostral/subgenual anterior cingulate cortex (sACC) as well as the periaqueductal gray (PAG), which belong to the endogenous antinociceptive system. However, the exact mechanisms possibly leading to this high level of variance in pain perception are still a matter of debate. Methods Pain perception within the trigemino-vascular system was investigated in 37 healthy volunteers using functional magnetic resonance imaging. Results Behavioral results show high levels of variance being inversely correlated to mean pain ratings as well as to an increase in BOLD signal intensity within the sACC. In addition, higher sACC activation was coupled with activation in the PAG the lower the level of intra-individual variance. Conclusion This study gives first indications that coupled BOLD response within brain structures of the antinociceptive system seems to rather not code pain intensity within the trigemino-nociceptive system but the stability of volunteers’ pain ratings. Intrinsic mechanisms may modulate the pain perception in the trigemino-vascular system, which is highly involved in headache disorders.

Quantitative Sensory Testing in Cluster Headache: Increased Sensory Thresholds

To determine if recently reported changes in sensory thresholds during migraine attacks can also be seen in cluster headache (CH), we performed quantitative sensory testing (QST) in 10 healthy subjects and in 16 patients with CH. Eight of the patients had an episodic CH and the other eight a chronic CH. The tests were performed on the right and left cheeks and on the right and left side of the back of the hands to determine the subjects' perception and pain thresholds for thermal (use of a thermode) and mechanical (vibration, pressure pain thresholds, pin prick, von Frey hairs) stimuli. Six patients were examined in the attack-free period. Three were also willing to repeat the tests a second time during an acute headache attack, which was elicited with nitroglycerin. The healthy subjects performed the experiments in the morning and evening of the same day to determine if sensory thresholds are independent of the time of day. If they were, this would allow estimation of the influence of the endogenous cortisone concentration on these thresholds. The control group showed no influence of the time of day on the thresholds. There was a significant difference in pain sensitivity between the back of the hands and the cheeks ( P < 0.05): higher thresholds were found on the back of the hands. The thresholds generally exhibited little intersubject variability, indicating that QST is a reliable method. There was also a significant difference between the test areas in the patient group ( P < 0.001): the cheeks were also more sensitive than the back of the hands. In comparison with reference data of healthy volunteers, the detection thresholds were increased in the patients on both test areas. These were statistically significant for warmth, thermal sensory limen (TSL), heat and pressure on the back of the hands ( P < 0.04) and for the warmth and TSL thresholds on the cheeks ( P < 0.05). There were no differences in the thresholds regardless of whether the patients were examined in or outside of a cluster bout. Furthermore, we found no cutaneous allodynia in the three patients tested during an attack. The increased sensory thresholds on the cheeks as well as on the back of the hands are in agreement with an increased activation of the patients' antinociceptive system. The seasonal variation and the temporal regularity of single attacks as well as the findings in imaging studies indicate that the hypothalamus is involved in the pathophysiology of CH. In view of the strong connectivity between the hypothalamus and areas involved in the antinociceptive system in the brainstem, we hypothesize that this connection is the reason for the increased sensory thresholds in CH patients found in our study.

Dinamics of somatosensory generated potentials in myofascial pain syndromes

In pronounced pain syndrome the most important functional shifts (the generators of pathologically increased excitement) by recording somatosensory generated potentials arc revealed at higher levels than in slight tenderness. At the same time in slight painfulness tenderness a great number of the generators of mild activity arc found, showing insufficient activity of antinociceptive system. After treatment a number of the generators of pathologically increased excitement decrease, at the same time the migration to the caudal parts of nervous system occurs. The neurophysiologic basis for possible worsening myofascial pain syndromes is created.