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Phantom Limb Syndrome

Phantom limb syndrome and phantom limb pain is characterized by the sensation that an amputated limb exists, is functional, and is in pain.  The sensation of pain is understandable, given that severed pain nerves could be assumed to continue firing randomly.  However, the sensation that the limb is functional, with a "known" sense of shape, position and orientation, does NOT make sense: arm position, for example, is based on sensory feedback from muscles tensed or not tensed to specific degrees, so how can severed nerves that sense the tension in muscles fire and not fire in a coordinated fashion so that the illusion of a coherently behaving limb be maintained?  Certainly the limb may feel larger, smaller, longer, or shorter than the original limb, but the sensation is that it has a definite size.

What should really cue one to the fact that something unusual is taking place is the "mirror box" treatment for certain kinds of phantom limb pain.  Some kinds of phantom limb pain come from a phantom limb as being  "paralyzed" into an orientation that, if the actual limb was present, would generate the same kind of pain that is felt as coming from the phantom limb.  In short, not only is the phantom limb perceived as being in a specific position and orientation, the feeling of pain coming from the limb is consistent with that orientation.  The sensations of orientation and pain are "in sync" and consistent.  The treatment consists of placing the good and amputated portions of the patient's body into a box with a mirror that makes the patient "see" a whole limb proceeding from the stump from which is perceived that the phantom limb comes from.  The patient is instructed to put the good limb into the painful position, but practice "unbending" the amputated limb from that same position, unbending the good limb in step with the sensations "felt" by moving the amputated limb.  The goal is to exercise mental control over a limb that doesn't exist, but using visual cues that would be "in sync" with how the phantom limb is perceived.  This appears to be a very successful treatment, with one patient being able to "telescope" the painful portion of his arm "into" his body so that it felt that his hand was attached to his shoulder!  He apparently accomplished this by practicing removing the limb from the mirror box, yielding a sensation that his arm was getting shorter until it disappeared.

Researchers from Vanderbilt have detected some growth of axons from neurons adjacent to the neurons that would normally handle sensations from the missing limb.  For instance, the neurons handling sensations from the arm are physically adjacent to those handling sehe face, leading some researchers to conduct experments which revealed patients that report feeling sensations from missing arms when their faces were touched.   The fact that axons grow from connected neurons to "unconnected" neurons is significant enough to warrant the hope in some researchers that regrowing spinal cords is possible.  However, how can longer axons that feed signals from neurons governing the face to neurons governing the arm establish connections so coherently and consistently that the illusion of an intact and functional limb is generated and maintained?  Attempts to relieve phantom limb pain based on the assumption that the severed nerves are firing randomly have not been met with much success when the nerves themselves were removed or numbed.  Treatment by drugs that operate on the brain and mind seem to have more success, indicating that the phenomenon is closer to the brain than to the former location of the now-missing peripherals. 

The cause of the axon growth is itself puzzling: cells grow and divide to fill in for cells that die based on chemicals that only occur within cells.  The surrounding cells receive those chemicals only when the cell dies, and thus constitutes the signal to start dividing.  We are familiar with calluses and the fact that broken bones are stronger at the breaks than before.  That is because when one cell dies, only one cell is required to divide to replace the dead cell.  However, because the signal to divide comes from chemicals that are scattered willy-nilly when the cell dies, several surrounding cells receive the chemical signal simultaneously.  Because there is no coordination between cells, more than one divides, so that one dead cell is replaced by multiple new ones.  The multiplicity of new cells causes the extra skin of the callus, as well as the extra cells at the bone break that make it stronger.  However, if neuron cell growth (not division) occurs because of chemical signals, then how can the chemical signal from a severed nerve cell at the elbow make its way to the adjoining neurons in the brain?  Presumably, if the damage was done out at the limb, then the chemicals will leak out at the cut, out there at the appendage, not in the brain at the main body of the neuron where the "sensing" is being processed.

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