User:MoFerqueron/Phantom limb

Phantom limb syndrome
Despite the term "phantom limb" not being coined until 1871 by a physician named Silas Weir Mitchell, there have been earlier reports of the phenomenon. One of the first known medical descriptions of the phantom limb phenomenon was written by a French military surgeon, Ambroise Pare, in the sixteenth century. Pare noticed that some of his patients continued reporting pain in the removed limb after he performed the amputation. For many years, the dominant hypothesis for the cause of phantom limbs was irritation in the peripheral nervous system at the amputation site (neuroma). By the late 1980s, Ronald Melzack had recognized that the peripheral neuroma account could not be correct, because many people born without limbs also experienced phantom limbs. According to Melzack the experience of the body is created by a wide network of interconnecting neural structures, which he called the "neuromatrix".

Pons and colleagues (1991) at the National Institutes of Health (NIH) showed that the primary somatosensory cortex in macaque monkeys undergoes substantial reorganization after the loss of sensory input.

Hearing about these results, Vilayanur S. Ramachandran hypothesized that phantom limb sensations in humans could be due to reorganization in the human brain's somatosensory cortex. Ramachandran and colleagues illustrated this hypothesis by showing that stroking different parts of the face led to perceptions of being touched on different parts of the missing limb. Later brain scans of amputees showed the same kind of cortical reorganization that Pons had observed in monkeys.

Maladaptive changes in the cortex may account for some but not all phantom limb pain. Pain researchers such as Tamar Makin (Oxford) and Marshall Devor (Hebrew University, Jerusalem) argue that phantom limb pain is primarily the result of "junk" inputs from the peripheral nervous system.

Despite a great deal of research on the underlying neural mechanisms of phantom limb pain there is still no clear consensus as to its cause. Both the brain and the peripheral nervous system may be involved.

Research continues into more precise mechanisms and explanations.

Differentiation of Limb Sensations
Phantom Limb Syndrome (PLS) is a sensation that the amputated or missing limb is still attached to the body. This is different from Residual Limb Pain (RLP) that is often experienced by people with amputations. While RLP occurs in the remaining or residual body part, the pain or sensation associated with PLS can be experienced in the entire limb or just one portion of the missing limb. Phantom limb can also present itself in two ways: phantom limb pain or phantom limb sensations. Phantom limb pain is a painful or unpleasant sensation experienced where the amputated limb was. Phantom sensations are any other, nonpainful sensations perceived in the amputated or missing limb area.

Types of Phantom Sensations
There are 3 differentiated types of phantom sensations: Kinetic, Kinesthetic, and Exteroceptive. Kinetic phantom sensations are perceived movements of the amputated body part (i.e., feeling your toes flex). Kinesthetic phantom sensations are related to the size, shape, or position of the amputated body part (i.e., feeling as if your hand is in a twisted position). Exteroceptive phantom sensations are related to sensations perceived to be felt by the amputated body part (i.e., feelings of touch, pressure, tingling, temperature, itch, and vibrations).

An additional sensation that some people with amputations experience is known as telescoping. Telescoping is when you feel as if your amputated limb is becoming more proximal to your body through progressive shortening.

Neural mechanisms
Pain, temperature, touch, and pressure information are carried to the central nervous system via the anterolateral system (spinothalamic tracts, spinoreticular tract, spinomesencefalic tract), with pain and temperature information transferred via lateral spinothalamic tracts to the primary sensory cortex, located in the postcentral gyrus in the parietal lobe, where sensory information is represented somatotropically, forming the sensory homunculus. Somatotopic representation seems to be a factor in the experience of phantom limb, with larger regions in the sensory homunculus typically experiencing more phantom sensations or pain. These areas include the hands, feet, fingers and toes.

In phantom limb syndrome, there is sensory input indicating pain from a part of the body that is no longer existent. This phenomenon is still not fully understood, but it is hypothesized that it is caused by activation of the somatosensory cortex. One theory is it may be related to central sensitization, which is a common experience among amputees. Central sensitization is when there are changes in the responsiveness of the neurons in the dorsal horn of the spinal cord, which deals with processing somatosensory information, due to increased activity from the peripheral nociceptors. Peripheral nociceptors are sensory neurons that alert us to potentially damaging stimuli.

There are theories that the phantom limb phenomenon may relate to reorganization of the somatosensory cortex after the limb is removed. When the body receives tactile input near the residual limb, the brain is convinced that the sensory input was received from the amputated limb because another brain region took over. Reorganization has been thought to be related to sensory-discriminative parts of pain as well as the affective-emotional parts of it (I.e., insula, the anterior cingulate cortex, and the frontal cortices).

Phantom sensations can also occur when there has been a peripheral nerve injury resulting in deafferentation. This causes changes in the dorsal horn of the spinal cord, which normally has an inhibitory effect on sensory transmission.