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Phantom pain is a painful perception that an individual experiences relating to a limb or an organ that is not physically part of the body, either because it was removed or was never there in the first place. Sensations are reported most frequently following the amputation of a limb, but may also occur following the removal of a breast, tongue, or internal organ. Phantom eye syndrome can occur after eye loss. The pain sensation and its duration and frequency varies from individual to individual. Phantom pain should be distinguished from other conditions that may present similarly, such as phantom limb sensation and residual limb pain. Phantom limb sensation is any sensory phenomenon, except pain, which is felt at an absent limb or a portion of the limb. It is estimated that up to 80% of amputees experience phantom limb sensations at some time of their lives. Some experience some level of this phantom feeling in the missing limb for the rest of their lives. Residual limb pain, also referred to as stump pain, is a painful perception that originates from the residual limb, or stump, itself. It is typically a manifestation of an underlying source, such as surgical trauma, neuroma formation, infection, or an improperly fitted prosthetic device. Although these are different clinical conditions, individuals with phantom pain are more likely to concomitantly experience residual limb pain as well. The term "phantom limb" was first coined by American neurologist Silas Weir Mitchell in 1871. Mitchell described that "thousands of spirit limbs were haunting as many good soldiers, every now and then tormenting them". However, in 1551, French military surgeon Ambroise Paré recorded the first documentation of phantom limb pain when he reported that "for the patients, long after the amputation is made, say that they still feel pain in the amputated part". Signs and symptoms The symptomatic course of phantom pain is widely variable, but the onset often presents within the first week after amputation. The reported pain may be intermittent and lasting seconds to minutes, but can be continuous with acute exacerbations. The duration of symptoms varies among individuals, with some reporting decreased pain over time and others reporting a more stable or even increasing trajectory. Sensations may be described as shooting, stabbing, squeezing, throbbing, tingling, or burning, and sometimes feels as if the phantom part is being forced into an uncomfortable position. While the sensation often affects the part of the limb farthest from the body, such as the fingers or toes, other body parts closer to the brain, such as the arm or leg, can still experience similar sensations. It is thought that phantom pain more commonly involves the part of the limb farthest from the body because of its larger cortical representation within the somatosensory cortex. Overall, the sensations may be triggered by pressure on the remaining part of the limb, emotional stress, or changes in temperature. Causes Individuals may experience phantom pain following surgical or traumatic amputation of a limb, removal of an organ, or in instances of congenital limb deficiency. It is most commonly observed after amputation, although less frequent cases have been reported following the removal of a breast, tongue, or eye. Phantom pain is seen more often in older adults as compared to individuals with congenital limb deficiency or amputation at an early age. It has also been reported that individuals with a prior history of chronic pain, anxiety, or depression are more likely to develop phantom pain than those without these risk factors. Pathophysiology The neurological basis and mechanisms for phantom pain are all derived from experimental theories and observations. Little is known about the true mechanisms causing phantom pain, and many theories highly overlap. Historically, phantom pains were thought to originate from neuromas located at the stump tip. Traumatic neuromas, or non-tumor nerve injuries, often arise from surgeries and result from the abnormal growth of injured nerve fibers. Although stump neuromas may contribute to phantom pains, they are not the sole cause. The reason is because patients with congenital limb deficiency can sometimes also experience phantom pains. This finding suggests that there is also a central mechanism responsible for generating painful sensations. Currently, theories are based on altered neurological pathways and maladaptive changes within the peripheral nervous system, spinal cord, and brain. Peripheral mechanisms Neuromas formed from injured nerve endings at the stump site show increased sodium channel expression and are able to spontaneously fire abnormal action potentials. This increased activity of Aδ and C fibers, which are involved in pain and temperature sensation, can contribute to phantom pain. However, it has been noted that pain still persists once the neuromas have ceased firing action potentials or when peripheral nerves are treated with conduction blocking agents. The peripheral nervous system is therefore thought to have at most a modulation effect on phantom limb pain. Spinal mechanisms In addition to peripheral mechanisms, spinal mechanisms are thought to have an influencing role in the development of phantom pain. Peripheral nerve injury can lead to the degeneration of C fibers in the dorsal horn of the spinal cord, and terminating A fibers may subsequently branch into the same lamina. If this occurs, A fiber inputs could be reported as noxious stimuli. Substance P, involved in the transmission of pain signals, is usually expressed by Aδ and C fibers, but following peripheral nerve damage, substance P is expressed by Aβ fibers. This leads to hyperexcitability of the spinal cord, which usually occurs only in the presence of noxious stimuli. These changes to the nerve fiber inputs may also lead to an expansion of the neuronal receptive fields, such that previously non-noxious stimuli are now interpreted as noxious. This process of hyperexcitability and receptive field changes is broadly referred to as central sensitization. It is also known that increased expression of glutamate and NMDA, coupled with decreased inhibition from GABAergic neurons, further contributes to the mechanism of central sensitization. However, because patients with complete spinal cord injury have experienced phantom pain, there must also be an underlying central mechanism within the brain. Central mechanisms Under ordinary circumstances, the genetically determined circuitry in the brain remains largely stable throughout life. For much of the twentieth century, it was believed that no new neural circuits could be formed in the adult mammalian brain, but experiments from the 1980s onward cast this into doubt. For instance, functional MRI studies in amputees have shown that almost all patients have experienced cortical remapping. After amputation, cortical remapping is the process by which area.... Discover the Jennifer Schulz popular books. Find the top 100 most popular Jennifer Schulz books.