Motor Cortex Stimulation for Intractable Pain

Richard K. Osenbach, M.D.


Neurosurg Focus. 2006;21(6) 

In This Article

Physiological Mechanisms of MCS

More than four decades ago it was noted that nonnoxious peripheral stimuli produced excitation of neurons in a restricted area of the somatosensory cortex while simultaneously inhibiting neurons in a much larger area.[18] It was postulated that this inhibitory receptive field played an important role in spatial analysis through which precise localization of a stimulus could be determined. It is believed that this inhibitory influence, driven by nonnoxious afferent input, can attenuate the output of nociceptive neurons. It has been hypothesized that one of the essential features of deafferentation pain is loss of this inhibitory field due to aberrant connections within the portion of the somatosensory system that mediates nonnoxious input to nociceptive neurons.[7] Loss of this inhibitory field is thought to result in a divergence of excitation and a reduction of spatial discrimination that is manifested clinically as abnormal sensory phenomena such as allodynia, dysesthesias, and hyperalgesia.

Although various theories have been proposed, the actual mechanism(s) underlying the effects of MCS remain unclear. What is known is that there are highly organized reciprocal neuronal circuits between the primary motor and somatosensory cortices, and that these connections appear to transmit primarily nonnoxious information such as feedback from target muscles. This may explain in part the observation that some patients perceive paresthesias in the painful area during MCS. Tsubokawa and Katayama[31] have postulated that MCS may produce its analgesic effect through orthodromic and/or antidromic activation of these fourth-order antinociceptive neurons, and that such activation secondarily results in inhibition of hyperactive nociceptive cortical neurons. The result is restoration of the previously discussed inhibitory surrounding field that is clinically manifested as analgesia. It has also been shown in experimental animals that MCS can result in inhibition of hyperactive deafferented neurons in the spinal cord, brainstem, and thalamus, and may help explain the benefit of MCS in patients with peripheral deafferentation.[13,26]

Additional physiological studies of MCS obtained using positron emission tomography have shown that stimulation produces an amplification of regional cerebral blood flow in multiple cortical and subcortical sites, including the thalamus, cingulate gyrus, orbitofrontal cortex, and brainstem, indicating activation of these areas.[8,9,24] Peyron et al.[24] have documented increases in regional cerebral blood flow during MCS in the ipsilateral thalamus, where corticothalamic connections from motor and premotor areas predominate. However, the magnitude of increase in regional cerebral blood flow appears to be greatest in the anterior cingulum, insular cortex, and brain stem. In fact, a correlation between the degree of increase in cingulate blood flow and pain relief has been noted, suggesting that MCS may provide pain relief not only by suppression of hyperactive deafferented neurons but also by modulation of limbic pathways. Positron emission tomography studies have shown that MCS does not result in activation of the somatosensory cortex or produce changes in blood flow in motor pathways caudal to the site of stimulation, with the exception of the ipsilateral thalamus. In studies in which positron emission tomography scans were used, investigators have suggested the possibility that MCS may produce at least some effect through activation of the brainstem's periaqueductal gray structures. If the latter were true, then DBS applied to periaqueductal or periventricular gray structures might be expected to result in some degree of analgesia. Unfortunately, DBS targeting of either the periaqueductal or periventricular gray region has not been terribly effective for the treatment of neuropathic pain. Because such pain dominates most of the conditions for which MCS has been beneficial, it would seem less likely that activation of endogenous opioid pathways would be a major contributor to the mechanistic effects of MCS.

It would certainly appear that successful treatment with MCS does not require an intact somatosensory system. Indeed, deafferentation by definition implies an interruption in afferent somatosensory input. However, it does seem that a necessary but perhaps not sufficient requirement for obtaining pain relief with MCS is the presence of a relatively intact corticospinal system. Katayama and associates[10] found no correlation between somatosensory function and response to MCS in a series of 31 patients with poststroke pain. However, there was a high degree of correlation between the presence of preserved motor function and pain relief. The MCS was successful in 13 (72%) of 18 patients who had either normal motor function or only very mild weakness. Indeed, of the 15 patients who derived long-term benefit from MCS, 13 (87%) had well-preserved motor function. Of the 31 patients studied, muscle contraction in response to MCS was obtained in 20, and of these, 14 (70%) achieved long-term pain relief. Conversely, only one (10%) of 10 patients in whom muscle contractions could not be elicited obtained sustained pain relief. There was no difference in effect between patients with thalamic and suprathalamic pain. Therefore, it would appear that, at least in patients with deafferentation pain originating at or rostral to the level of the thalamus, motor responses are required to achieve adequate long-term pain control with MCS. On the other hand, an intact motor system does not guarantee success, because 30% of the patients in this series failed to achieve good pain control despite the ability to elicit motor contractions.


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