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Neurophysiology of pain

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Physiology of painEdit

Pain refers to the subjective, unpleasant sensation that accompanies damage or near-damage to tissues, though it can also occur in the absence of such damage if the systems of nociception are not functioning properly. Nociception refers to the system that carries signals of damage and pain from the tissues; it is the physiological event that accompanies pain.[1]

NociceptorsEdit

All nociceptors are free nerve endings that have their cell bodies outside the spinal column in the dorsal root ganglia and are named based upon their appearance at their sensory ends. Nociceptors can detect mechanical, thermal, and chemical stimuli, and are found in the skin and on internal surfaces such as the periosteum or joint surfaces. Deep internal surfaces are only weakly supplied with pain receptors and will propagate sensations of chronic, aching pain if tissue damage in these areas occurs.

Nociceptors do not adapt to stimuli. In some conditions, excitation of pain fibers becomes greater as the pain stimulus continues, leading to a condition called hyperalgesia.

Transmission of nociception to the central nervous systemEdit

There are two ways for nociceptive information to reach the central nervous system, the neospinothalamic tract for "fast spontaneous pain" and the paleospinothalamic tract for "slow increasing pain".[How to reference and link to summary or text]

Neospinothalamic tractEdit

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. [How to reference and link to summary or text]

Paleospinothalamic tractEdit

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.[How to reference and link to summary or text]

Effects in CNSEdit

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, bradycardia, hypotension, lightheadedness, nausea and fainting.[2]

ReferencesEdit


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