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Pain receptors

All pain receptors can be described as free nerve endings. There are thermal, chemical and mechanical pain receptors. They can be found in epidermis and on inner surfaces like periosteum and joint surfaces. Remote internal surfaces are poorly provided with pain receptors and will spread sensations of aching, chronic pain only if tissue is damaged in these areas.

Pain receptors do not get accustomed to stimulus. In some cases, excitation of pain fibers grows as the ache stimulus continues, causing a condition known as hyperalgesia.

Nociceptors are the free nerve endings of neurons whose cell bodies are located outside the spinal column in the dorsal root ganglion. Their names are based upon their look at the sensory ends. These endings look like the twigs of small undergrowth.

Two major varieties of nociceptor, A? and C fibers, transfer fast and slow pain respectively. Thinly medullated type A? fibers, which convey signals at rates of between 1.2 to 10 meters per second transfer fast pain. This type of pain is percepted in a tenth of a second of submission of the pain stimulus. It is a pricking, acute, sharp pang and includes thermal and mechanical pain. Slow pain is mediated by sluggish and unmyelinated ("bare") type C pain fibers that drive signals at rates less than 1.2 meters per second. This type of pain is felt as an aching, sore, burning pain.

Conduction of pain signals in the CNS

The feeling of pain arises when the nociceptors are stirred; they send signals with the help of sensory neurons in the spinal cord. These neurons secrete glutamate which is the main exicitory neurotransmitter that conveys signals from one neuron to another. The signals go to the thalamus, where an ache perception arises. The signal moves from the thalamus to the somatosensory cortex in the cerebrum, where the pain is restricted to a small area, and the individual feels the pain.

There are 2 ways to send the sensation of pain in the CNS meaning the neospinothalamic tract transmitting fast pain and the paleospinothalamic tract sending slow pain.

• Fast pain is sent via type A? fibers to cease on lamina marginalis (lamina I) of the dorsal horn. Then the second order neurons of the neospinothalamic tract take off and stimulate long fibers crossing the midline through the grey commissure and ascending to the contralateral anterolateral columns. These fibers finish in the thalamus, on its Ventrobasal Complex. Third order neurons correlate with the somatosensory cortex from there. If A? fibers are stirred together with tactile receptors, fast pain can be localized easily.
• Slow pain is sent via slower type C fibers to membranes II and III of the dorsa horns, called in Latin substantia gelatinosa. Second order neurons take off and end in membrane V in the dorsal horn, as well. Neurons of the third order then join fibers from the fast pathway, crossing to the opposite side through the grey commissure, and going upwards through the anterolateral pathway. These neurons end generally in the brain stem, with one tenth of fibers stopping in the thalamus, and the rest stopping in the pons, mesencephalon and medulla. Localizing slow pain is not an easy task.

Anesthesia

Patrick Wall and Ron Melzack proposed the gate control theory of pain which asserts that pain is "gated" by painless stimuli such as tremor. Thus, patting a contused knee seems to relieve pain by preventing its spreading to the brain. Ache is also blocked by signals that come down from the brain to the spinal cord to restrain (and in other cases increase) incoming pain information.

The analgesia scheme consists of 3 major parts which are the periaquaductal grey matter in the midbrain, the nucleus raphe magnus in the medulla, and the pain suppressing neurons within the dorsal horns of the spinal cord, which help to restrain pain-transmitting neurons located in the spinal dorsal horn.

There are several varieties of opioid receptors in the body that react to the binding of the endorphins of the body. These receptors, which exist in a variety of regions in the body, inhibit burning of neurons that would otherwise be stimulated to do so by nociceptors.