Biology 202
1998 Second Web Reports
On Serendip

Until the mid 1980's, it was widely believed that once neural pathways were placed during fetal development, these pathways did not change and were not altered in any recognizable way (3). However, recent studies have shown that the brain has a high degree of plasticity into adulthood, which allows it to continually respond to changes in stimuli (4). A study done by Flor, et al., in 1995 showed a relationship between the amount of cortical reorganization and the magnitude of phantom limb pain. Data indicated that PLP is related to, and may be a consequence of, plastic changes in the primary somatosensory cortex, and that the shift of the cortical map following amputation might be a potential neurophysiological basis of PLP (6).

Further studies in 1998 investigating the re-mapping component in the brain were conducted by researchers at the University of Toronto and The Toronto Hospital. The study recruited amputees who experienced phantom pain for surgery to map the sensory areas in the brain. During the mapping process, the conscious patients reported sensations they felt when certain areas of the thalamus were stimulated. Patients reported phantom sensations when areas of the thalamus were stimulated that formally were innervated by neurons from the missing arm, and also when areas on the stump were stimulated that activated these reorganized regions in the brain. Neurons were shown to continue to carry out their original roles, but with different sources of activation (7).

While persuasive, the aforementioned experimental conclusions are well critiqued by Ronald Melzack who argues against looking to the somatosensory cortex or thalamus as the only cause of phantom pain in his April 1992 Scientific American article. He states: Such changes in the somatosensory thalamus or cortex could explain why certain feelings arise in limbs that no longer exist or can no longer transmit signals to the brain. Nevertheless, alterations in this system cannot by themselves account for phantoms and their pain. If this explanation were sufficient, removal of the affected parts of the somatosensory cortex or thalamus would solve both problems (1).

Melzack goes on to suggest that much more of the cerebrum, or the cerebral hemispheres, is involved with PLP, and introduces the concept of "neurosignature" or "neuromatrix (1). Melzack defines a neurosignature as a "network of neurons, that, in addition to responding to sensory stimulation, continuously generates a characteristic pattern of impulses indicating that the body is intact and unequivocally one's own" (1). Melzack states that the "matrix of wholeness" established in the brain will continue to operate even in the absence of sensory inputs, and would create an impression of having a complete and whole body even when a limb has been removed (1). I think that the concept of neuromatrix has great similarity to the idea of "corollary discharge." Defined by Dr. Paul Grobstein as a mechanism by which one part of the nervous system sends information to another area of the nervous system, the corollary discharge is an internal communication network. Dr. Grobstein asserts that the nervous system may contain a corollary discharge record of pattern generators that causes a person to have the sensation of a phantom limb and even allows him or her to state the orientation and position of the missing limb (9).

Pain-related phenomena may be due, in part, to inconsistencies between the corollary discharge signals sent to the brain for processing and those sent by the sensory system. Corollary discharge signals are used to define expectation, and when the sensory input does not match this expectation, the nervous system sends out a signal that says "there is something wrong" which may be felt as pain in the phantom limb. Melzack also describes the pain phenomena through his neuromatrix. He states that the neuromatrix is prewired to "assume" that the limbs can move, and that when they do not, stronger and more frequent messages may be sent to the muscles, and is perceived as pain (1). Interesting findings regarding treatment of phantom limb pain also indicate that more than the somatosensory cortex is involved with the pain felt by phantom limb sufferers. In the past, the success rate for treatment of phantom pain has been negligible, with only about one percent of treated amputees reporting any relief lasting for a year. However, recently, the use of electromyographic and temperature feedback has proven effective for patients with cramping and burning phantom pain. The aim of the treatment is to teach amputees to unconsciously keep their phantom limb as warm as their intact limb (8). This treatment may somehow allow the corollary discharge and sensory system signals to agree with one another or may allow the patient to resist fighting his or her prewired neuromatrix. It also suggests further study of the integration of perception and reality with regard to phantom limb pain management. Another unconventional pain management technique is continuous electrical stimulation through electrodes surgically implanted into the thalamus. This technique blocks neuronal activity in the thalamus that may be the cause of some phantom pain (10).

Although I think that this treatment definitely is on the right track, the only time that electrical blocking will prove effective is when it is used to correct the difference in information and signaling sent by the corollary discharge and sensory system to the brain. For example, instead of a blanket inhibition of neuronal firing, stimulation should also occur when normal movement by the person would usually require movement of the missing limb. Therefore, if a person with a missing right arm started walking, stimulation of the sensory neurons that coincided with the movement of the arms would also occur - thereby correcting the difference in information between the corollary discharge and the sensory system. The stimulation would basically send a "false" sensory signal to the cortex telling it that the arm indeed was moving, even when it was not. Then, when the person were no longer walking, inhibition of neuronal firing would commence. In conclusion, I think that Melzack's theories and findings are valid. He incorporates what research has found on cortical rearrangement without fingering a single source as the cause of phantom limb pain. Melzack opens the doors to looking at the neuromatrix and corollary discharge signals in the brain and the influence that these prewired expectations may have on the body, especially pain. These ideas are the key to providing long-term pain management for PLP patients.

References

1. Melzack, Ronald, Scientific American. "Phantom Limbs"

2. Katz, Joel, "Phantom Limb Pain. (Commentary)"

3. Yang, Tony T., Gallen C., Schwartz, B., Bloom, F.E., Ramachandran, S. Cobb, "Sensory Maps in the Human Brain," Nature, vol. 368, 14 April 1994: 592-593.

4. "Cortical Reorganization and the 'Phantom Limb'"

5. "Plasticity"

6. Flor, H., Elbert,T., Knecht, S., Wienbruch, C., Pantev, C., Birbaumer, N., Larbig, W., Taub, E., "Phantom Limb Pain as a Perceptual Correlate of Cortical Reorganization Following Arm Amputation," Nature, vol. 375, 8 June 1995: 482-483.

7. "New Piece to Puzzle in Phantom Pain Mystery: Media Release from the University of Toronto"

8. Sherman, Richard, "The Use of Electromyographic and Temperature Biofeedback for Treatment of Cramping and Burning Phantom Limb Pain"

9. Grobstein, Paul, Class Lecture. Neurobiology and Behavior. Bryn Mawr College. February and April 1998.

10. "Phantom Pain Not Imagined," The University of Toronto


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