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Integumentary and Musculoskeletal System Case Study: Pain
The mechanism of phantom limb pain is yet to be identified. However, several theories that explain its development are currently present. First of all, it is believed that phantom pain occurs due to the emergence of neuromas. Those often develop after the amputation as a result of the abnormal growth of damaged nerve fibers (McCance & Huether, 2014). However, people with the missing limbs since birth can also experience phantom pain. This fact suggests the presence of a center responsible for these sensations, which may form due to the changes in cortical reorganization and neurological pathways. For example, the damage affecting peripheral nerves can lead to the degeneration of the C-type nerve fibers in the posterior horn of the spinal cord, with the A-type fibers subsequently expanding to this location. In case such situation takes place, the inputs from the latter can be represented as harmful stimuli, resulting in the emergence of phantom pain (Benzon et al., 2014).
Pain receptors (nociceptors) react to the factors that may cause damage to the body and can be divided into several groups depending on the stimulus that results in their response. The first of them are the so-called mechanonociceptors, which respond to the mechanical deformation, e.g. a needle prick or plucking of the skin with tweezers. On the other hand, their mechanothermal variety also reacts to the extreme increase or decrease in temperature (McCance & Huether, 2014). Finally, the chemical nociceptors react to such stimuli as spices and environmental irritants such as smoke. Moreover, all of the listed receptors incorporate different types of nerve fibers, which determine the properties of their axons. In particular, the mechanonociceptors contain the A-delta fibers that are characterized by a high speed of signal transmission. They are lightly myelinated, having a myelin sheath that covers central axis-cylinder, and are responsible for the sensation of fast, acute pain, being stimulated by the mechanic and mechanothermal nociceptors (McMahon et al., 2013). On the other hand, the C-fibers do not have a myelin sheath and transmit signals at relatively low speed, resulting in the dull pain. They are of a polymodal nature, being affected by the receptors of all types. Additionally, it is possible to identify the heavily myelinated A-beta fibers, which are primarily responsible for tactile senses. They do not transmit pain signals but play a part in their modulation (McCance & Huether, 2014).
By taking into account that the patient experiences phantom limb pain, it is possible to assume that the mechanism of its development involves the A- type nerve fibers. The primary reason for this statement is the fact that A-fibers contain myelin, which makes them suitable for the innervations of the body parts that experience considerable functional load, including skeletal muscles and, therefore, limbs (McMahon et al., 2013). Moreover, as it was mentioned before, one of the theories describing the nature of the phantom pain is based on the deterioration of the C-fibers in the spinal cord, with their subsequent replacement of those belonging to the A-type. It should be noted that the transmission of pain occurs due to the presence of specific substance that is usually produced by the A-delta and C-fibers. However, after the peripheral nerve injury, for example, after the severe trauma or amputation, it is primarily provided by the A-beta fibers, i.e. the ones that replace the deteriorated C-fibers. In turn, this fact results in the leads to excessive stimulation of the spinal cord, which usually occurs only in the presence of harmful stimuli of different nature (Benzon et al., 2014). Therefore, the patient experiences the sensation of pain in the missing limb.
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