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December 4, 2011

Phantom Limb Pain and Cortex Reorganization


Feeling pain in the arm that you lost in an accident? Does your arm you lost in the war itch terribly? This sensation of feeling like a lost limb is still attached to the body is known as a phantom limb pain (PLP). The purpose of this study was to identify plastic changes in the somatosensory and motor cortex in patients with and without phantom limb pain. Most sensations regarding these phantom limbs are painful as if the limb was contorted into an awkward position. Although in many cases the complaint is pain, some patients experiencing a phantom limb experience sensations such as itching, burning, or feeling as though the limb is too short. Although PLP is more common in the early stages following an amputation, some have reported pain for years after. It was previously discovered that PLP had a strong correlation with representational plasticity in the somatosensory cortex; however, its correlation with the plasticity in the motor cortex was unknown. This experiment used methods such as Transcranial Magnetic Stimulation (TMS) of the motor cortex, and neuroelectric source imaging of the somatosensory cortex to study the correlation of plasticity in these cortices.

In this study, participants included five upper-limp amputees experiencing PLP and five upper-limb amputees experiencing no PLP. A German version of the West Haven- Yale Multidimensional Pain Inventory was used to evaluate each patient's stump and limb pain. To test for motor reorganization, focal TMS was delivered from a magnetic stimulator through an 8-shaped magnetic coil. The leads were positioned to cause currents to flow approximately perpendicular to the central sulcus, optimally causing the largest peak-to-peak motor evoked potential in each muscle. In patients experiencing PLP, a map of outputs determined by neuroelectric source imaging of EEGs done showed significantly larger motor-evoked outputs on the side lacking the arm than the side with the remaining arm, whereas excitability in the motor neurons of amputees remained unchanged. Since it was previously known that motor reorganization in amputees takes place at a cortical level, the leap was made that. "It is likely that cortical mechanisms are also responsible for the differences in reorganization observed in both patient groups (Karl, Anke et. al., 2011)."

While these findings support the notion that increased plasticity is present in the motor cortex of PLP patients, the evidence used to support this main point is presented in a very odd fashion. Immediately following this claim about cortical mechanisms and presenting supporting evidence, they state that their results "do not rule out the possibility of additional subcortical reorganization." This statement is saying that other factors could be causing or contributing to the claims being made by their research, thus making the research inconclusive as a whole. Another problem with the research methods is that the patient's amputations all occurred at different times. Some more recent than others, which could have a profound effect on the plasticity levels reached at the time of testing.
All in all the research conducted further supports already claimed notions, while having no real additions of any validity or originality. These limitations could be reduced by choosing patients who's amputations occurred within the same month. The potential that could be reached through studies similar to this are immense, but further research needs to be conducted in order to draw on more valuable conclusions.




The Journal of Neuroscience, 15 May 2001, 21(10): 3609-3618;
Posted by      Madelyn K. at 8:29 PM MST

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