Motor Cortex Stimulation for Intractable Pain

Richard K. Osenbach, M.D.


Neurosurg Focus. 2006;21(6) 

In This Article

Evolution of MCS

There is physiological evidence to suggest that the system that mediates nonpainful somatosensory information (such as light tactile sensation, and so on) normally exhibits inhibitory influences on nociceptive neurons at multiple levels of the CNS. This concept is supported by observations that electrical stimulation of peripheral nerves, dorsal columns, or the primary sensory relay nucleus of the thalamus can attenuate nociceptive responses in experimental animals as well as reduce pain in selected patients.[13,26] However, it is well documented that in many patients with deafferentation pain, nonnoxious stimuli produce abnormal pain sensations (for example, allodynia, hyperalgesia, and so on), supporting the suggestion that the normal antinociceptive functions of the somatosensory system that mediate nonnoxious information are dysfunctional. This dysfunction has been attributed to abnormal interactions between the somatosensory system mediating non noxious information and the nociceptive neurons. Not surprisingly, many of the neurostimulation therapies such as SCS that are believed to work through activation of large fiber nonnoxious somatosensory neurons are often ineffective in patients with central deafferentation pain, particularly when applied at or caudal to the level of the lesion. It has been suggested that deafferentation pain may be controlled more effectively by applying stimulation at a level more rostral to the site of deafferentation.

Based on these observations and considerations, Tsubokawa and Katayama[31] began to examine the effects of cortical stimulation for the treatment of thalamic pain. Surprisingly, it was discovered that stimulation of the precentral rather than the postcentral gyrus resulted in more effective inhibition of pain. In fact, stimulation of the primary sensory cortex actually exacerbated the pain in a number of patients. The area that was found to produce the strongest pain inhibition corresponded to the area of the precentral gyrus, from which muscle contractions in the painful area could be elicited. Tsubokawa et al.[32,33] published their initial experience with MCS for the treatment of thalamic and poststroke pain in the early 1990s. Not long afterward, Meyerson et al.[15] reported beneficial effects of MCS for the treatment of trigeminal neuropathic pain. Subsequently, over the last decade MCS has been applied for the treatment of a variety of central and peripheral deafferentation pain syndromes.[3,4,6,11,12,22,25,27,28,30]


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