Nociception refers to a complex interaction of nerve stimuli that result in pain due to mechanical, chemical, or thermal stimuli in pain-sensitive human tissues. The direct pain-inducing stimuli are transmitted to the CNS by specialized sensory nerves, the nociceptors. The centers in the brain responsible for this process form the corresponding pain sensation from the received stimuli from the nociceptors.
What is nociception?
Nociception includes all nerve stimuli that are reported by specialized sensory nerves, the nociceptors, to specific brain centers via afferent fibers. Nociception includes all nerve stimuli that are reported by specialized sensory nerves, the nociceptors, to specific brain centers via afferent fibers. The nerve stimuli themselves are triggered by surrounding cells that are subject to mechanical, thermal, or chemical injury. The damaged cells release messenger substances that are capable of triggering action potentials in the nociceptors, which are reported to the brain for further processing. The responsible brain centers collect the pain stimuli, evaluate them and generate from them a – normally – appropriate pain sensation. Three different types of nociceptors are available to detect the mechanical, chemical and thermal stimuli emitted by cells that are under stress or even destroyed. One is the mechanoreceptors specialized for mechanical stimuli, which have relatively fast conducting A-delta fibers surrounded by a medullary sheath. The second are polymodal nociceptors, which respond to mechanical as well as chemical and thermal stimuli and also have A-delta fibers, although these are only weakly myelinated. The third class of nociceptors are polymodal pain sensors, which have nonmyelinated C-fibers and have a low transmission rate of about 1 meter per second. A-delta fibers, on the other hand, transmit their action potential at about 20-30 meters per second.
Function and task
One of the main functions of nociception is to trigger pain almost instantaneously in the presence of imminent danger. In these cases, nociception enables the generation of pain of a warning nature. The sharp and stabbing primary pain, which occurs completely unexpectedly immediately after a dangerous mechanical, thermal or chemical impact, is usually triggered by specialized mechanoreceptors or by polymodal nociceptors. Both classes of sensory nerves have the fast A-delta fibers. They are capable of generating pain sensations that can trigger reflexive protective responses to avert imminent danger. For example, when accidentally touching the hot stove top, the hand reflexively recoils to avoid imminent burn damage. Impending injuries or injuries that have already occurred, for example from a knife or heavy objects that threaten to crush the foot, also lead to similar reflexive retrieval movements of the hand or foot. In the case of a less acute hazard that does not pose an immediate threat to the body or parts of the body, the polymodal C-fibers take over the sensory reception of the reporting cells, the conversion into neuronal action potentials and the transmission to the CNS. The pain sensation that is generated as a result is less localizable and usually feels duller and more persistent than the stabbing or burning and easily localizable primary pain that occurs, for example, in cuts or burns. Thus, the benefit of this type of pain sensation is mainly to recall such situations from episodic memory in order to avoid similar situations in the future that have proven to be unfavorable to the body. This means that slow C-fiber signals are highly processed in certain centers in the brain and linked to other sensory messages occurring at the same time. This can lead to the fact that certain sensor messages can already trigger pain sensations, although objectively no pain stimulus should be present. The reflex-triggering primary pain is exclusively a surface pain that can be localized relatively well.In contrast, deep pain, which can originate in muscles, bones, or internal organs (visceral pain), is less localizable.
Diseases and complaints
Given the complexity of nociception and the processing of neuronal action potentials from nociceptors into subjective pain sensation, various potential problems may occur. On the one hand, neuronal disturbances in the recording of signals from affected cells by the nociceptors and/or the transmission of the potentials to the CNS may occur. On the other hand, problems in the processing of the sensor signals are also conceivable, leading to an exaggerated or to a reduced pain sensation. A distinction can therefore be made between nociceptive and neuropathic pain. Nociceptive pain occurs, for example, after tissue trauma or in chronic inflammation of internal organs. Chronic back pain and tumor pain are also frequently triggered by changes in the endings of the nociceptors that function as signal receivers. In these cases, impaired functionality of the nociceptors leads to altered pain sensation. Much more common is neuropathic pain, which results in reversible or irreversible pain sensation due to a systemic change in signal processing. The signals from the nociceptors are first processed in the thalamic nuclei and, after further processing in certain regions of the cortex and amygdala, are also confronted with mental associations before they reach consciousness as concrete pain sensations. An example of pathologically exaggerated pain sensation is fibromyalgia syndrome, also known as soft tissue rheumatism. The disease leads to muscle pain, especially in the joints. The opposite of an abnormally exaggerated pain sensation is a greatly reduced pain sensation. It is symptomatic in borderline disorder, a severe mental illness. Sufferers tend to inflict injuries on themselves without feeling pain. Far more common, however, are diseases that are symptomatically accompanied by chronic pain in the neuropathic area. Examples include diabetic polyneuropathy, shingles, multiple sclerosis, and even long-term alcohol abuse.
