Pain in the residual limb is often confused with the phantom phenomenon yet it actually refers to the pain felt in the physical area above the level of amputation (Hill, 1999). However, phantom limb sensation (PLS) is described as any non-painful sensation that is presented where the limb is no longer present (Hill, 1999; Wilkins, McGrath, Finley & Katz, 1998). Conversely, phantom limb pain (PLP) is characterized as burning, tingling, throbbing, cramping, squeezing, shocking or shooting pains experienced where the limb is no longer present (Modirian, Shojaei, Soroush & Masoumi, 2009). For pain in particular, many treatments have been created to ease the pain, but none have been successful at curing the pain (Modirian et al., 2009). One particularly popular treatment option is that of mirror treatment.
2007;11:428-436 Chan BL, Witt R, Charrow AP, Magee A, Howard R, Pasquina PF, et al. Mirror therapy for phantom limb pain. N Engl J Med 2007;357:2206-2007 MacLachlan M. McDonald D, Waloch J. Mirror treatment of lower limb phantom pain: a case study. Disabil Rehabil.
When a person suffers from an extreme disease or injury, they can experience both physical and mental pain. In the case of Phantom limb, the physical pain can be intensified as it exists in a limb that is no longer there. Not only does this make curing it a lot more difficult, it can also result in serious mental anguish. Phantom limb sufferers not only go through the torment of having a limb amputated, they then undergo further misery as their brain plays tricks on them. Phantom limb is the experience of feeling a limb that has been amputated.
Damaged cells discharge their intracellular components, releasing substances, notably ATP, potassium ions (K+) and acetyl chloine (ACh). Some of these contents act on nociceptors directly, triggering an action potential which will end up in the brain. Other components released from the cells can sensitize the terminals, making them hypersensitive to further stimuli. This allows a pain signal to be transmitted when a seemingly insignificant concentration of, for example ATP (released in millimolar quantities), is introduced to the extracellular space. Prostaglandins, of which many pain receptors are especially sensitive, are produced at the site of injury.
A disproportion of pro-inflammatory and anti-inflammatory cytokines is known to be a contributory cause of pain and pain behavior. Embedded into psychoneuroendocrine and immunological feedback control systems, cytokines are able to perpetuate a vicious connection between local inflammation and systemic pain behavior (pain/sickness behavior), contributing towards chronification of nonspecific musculoskeletal pain. TNF-α (through NF-κB in astrocytes) causes release of CCL-2, which interacts positively with both NMDA and AMPA receptors in neurons. This adversely affects central descending pain modulation leading to failure of resolution state. Moreover; Co-localization of IL-1β and NMDA receptors on neuron, and, phosphorylation of NMDA on being stimulated by IL-1 explains direct role of immune system in establishing nociceptive neuronal circuit.
Psychological Relationship between the Sensory Affective Dimensions of Pain Pain can be described in a number of different ways, but is determined by the perception of pain that they are experiencing. “Pain is something that comes from our experiences and develops due to stimulation and human interaction. It involves concepts such as location, feelings of unpleasantness and having the sensation of pain. Pain becomes possible because of a psychological development that begins at birth” (Challies). The sensory pain is the quality of the pain experienced in a particular location and is often described as a sensational form of hurt.
The main cause of chronic back pain has not been identified, but there are many suggested issues that are believed to contribute to chronic back pain. Symptomology: Simple musculoskeletal back pain has symptoms of pain in the lumbrasacral area of the back (Jackson & Simpson, 2006). The upper thighs and knees are also known to be affected (Jackson & Simpson, 2006). This pain is usually described as a dull pain (Jackson & Simpson, 2006). Spinal nerve root pain is localised down the leg, and usually continues below the knee and into the feet (Jackson & Simpson, 2006).
Trigger points are known as tender nodes of degenerated muscle tissue causing local and radiating pain that may be bound to a single muscle or to several muscle groups. Their structure consists of small-circumscribed hyperirritable foci in muscles and fascia, often found within a firm or taut band of skeletal muscles. Trigger points may also occur in ligaments, tendons, joint capsule, skin, and periosteum. When palpating a trigger point, a local or referred pain pattern may be elicited causing a variety of symptoms including pain, muscle weakness, decreased joint motion, paresthesia, along with autonomic symptoms. Trigger points which are located in the head and neck can cause proprioceptive instabilities such as problems with balance, dizziness, and tinnitus.
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