Nociception (synonym: nocioception or nociperception) is defined as "the neural processes of encoding and processing noxious stimuli."[1] It is the afferent activity produced in the peripheral and central nervous system by stimuli that have the potential to damage tissue.[2][3] This activity is initiated by nociceptors, (also called pain receptors), that can detect mechanical, thermal or chemical changes above a set threshold. Once stimulated, a nociceptor transmits a signal along the spinal cord, to the brain. Nociception triggers a variety of autonomic responses and may also result in the experience of pain in sentient beings.[3]
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Mechanical, thermal, and chemical stimuli are detected by nerve endings called nociceptors, which are found in the skin and on internal surfaces such as the periosteum or joint surfaces. The concentration of nociceptors varies throughout the body, mostly found in the skin and less so in deep internal surfaces. All nociceptors are free nerve endings that have their cell bodies outside the spinal column in the dorsal root ganglia and are named according to their appearance at their sensory ends.
Nociceptors have a certain threshold; that is, they require a minimum level of stimuli before they trigger a signal. Once this threshold is reached a signal is passed along the axon of the nerve into the spinal cord.
In some conditions, excitation of pain fibers becomes greater as the pain stimulus continues, leading to a condition called hyperalgesia.
Before reaching the brain, the spinothalamic tract splits into the lateral, "neospinothalamic" tract and the medial, "paleospinothalamic" tract.[4]
Fast pain travels via type Aδ fibers to terminate on the dorsal horn of the spinal cord where they synapse with the dendrites of the neospinothalamic tract. The axons of these neurons travel up the spine to the brain and cross the midline through the anterior white commissure, passing upwards in the contralateral anterolateral columns. These fibres terminate on the ventrobasal complex of the thalamus and synapse with the dendrites of the somatosensory cortex. Fast pain is felt within a tenth of a second of application of the pain stimulus and is a sharp, acute, prickling pain felt in response to mechanical and thermal stimulation. It can be localised easily if Aδ fibres are stimulated together with tactile receptors.
Slow pain is transmitted via slower type C fibers to laminae II and III of the dorsal horns, together known as the substantia gelatinosa. Impulses are then transmitted to nerve fibers that terminate in lamina V, also in the dorsal horn, synapsing with neurons that join fibers from the fast pathway, crossing to the opposite side via the anterior white commissure, and traveling upwards through the anterolateral pathway. These neurons terminate throughout the brain stem, with one tenth of fibres stopping in the thalamus and the rest stopping in the medulla, pons and periaqueductal grey of the midbrain tectum. Slow pain is stimulated by chemical stimulation, is poorly localized and is described as an aching, throbbing or burning pain.[5]
The body possesses an endogenous analgesia system, which can be supplemented with analgesic drugs to regulate nociception and pain. There is both an analgesia system in the central nervous system and peripheral receptors that decreases the grade in which nociception reaches the higher brain areas. The degree of pain can be modified by the periaqueductal gray before it reaches the thalamus and consciousness. According to gate control theory of pain, this area can also reduce pain when non-painful stimuli are received in conjunction with nociception.
The central analgesia system is mediated by 3 major components: the periaquaductal grey matter, the nucleus raphe magnus and the nociception inhibitory neurons within the dorsal horns of the spinal cord, which act to inhibit nociception-transmitting neurons also located in the spinal dorsal horn.
The peripheral regulation consists of several different types of opioid receptors that are activated in response to the binding of the body's endorphins. These receptors, which exist in a variety of areas in the body, inhibit firing of neurons that would otherwise be stimulated to do so by nociceptors.
The gate control theory of pain, proposed by Patrick David Wall and Ronald Melzack, postulates that nociception (pain) is "gated" by non-nociception stimuli such as vibration. Thus, rubbing a bumped knee seems to relieve pain by preventing its transmission to the brain. Pain is also "gated" by signals that descend from the brain to the spinal cord to suppress (and in other cases enhance) incoming nociception (pain) information.
When nociceptors are stimulated they transmit signals through sensory neurons in the spinal cord. These neurons release the excitatory neurotransmitter glutamate at their synapses.
If the signals are sent to the reticular formation and thalamus, the sensation of pain enters consciousness in a dull poorly localized manner. From the thalamus, the signal can travel to the somatosensory cortex in the cerebrum, when the pain is experienced as localized and having more specific qualities.
Nociception can also cause generalized autonomic responses before or without reaching consciousness to cause pallor, diaphoresis, tachycardia, hypertension, lightheadedness, nausea and fainting.[6]
Nociception has been documented in non-mammalian animals, including fishes[7] and a wide range of invertebrates,[8] including leeches,[9] nematode worms,[10] sea slugs,[11] and fruit flies.[12] As in mammals, nociceptive neurons in these species are typically characterized by responding preferentially to high temperature (40º Celsius or more), low pH, capsaicin, and tissue damage.
The term nociception was coined by Charles Scott Sherrington to make clear the difference between the physiological nature of nervous activity signalling tissue damage and the psychological response of pain to this physiological event.[13]
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