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Discussion

The mechanism of action of ECT is still unknown, although several observations have been made regarding the effect of ECT on pain processes. King and Nuss (25) and McDaniel (26) both postulated that massive quantities of neurotransmitters are released during ECT that induce changes in CNS post-synaptic receptors throughout the nervous system. The neurotransmitters affected include serotonin, dopamine, norepinephrine (27), substance P, neuropeptide Y, somatostatin, TSH, and CRH (26). Other neuromodulators, including enkephalin, immune-reactive dynorphin, and beta-endorphins, have also been implicated in the effects of ECT on pain (26,32,33). King and Nuss (25) and Abdi et al (32) have postulated that the electrical current transmission through the thalamus and hypothalamus which occurs during bilateral ECT alters pathways for pain sensation and perception. Wasan et al (27) suggested that disrupted affective processing of pain in CRPS leads to enhanced receptive fields, intensified pain perception and increased pain sensory input. ECT may interrupt this inappropriate processing of pain by disrupting the memory for pain. In addition, Wasan et al (27) have postulated that ECT may stimulate the lateral thalamic structures involved in descending pain inhibition. Fukui et al (33) have studied the effect of ECT on regional cerebral blood flow. They found that patients with chronic neuropathic pain have decreased blood flow to the thalamus. After treatment with ECT, one of their patients had increased regional cerebral blood flow to the thalamus and a dramatic reduction in pain.

Functional changes in the brains of CRPS patients have been described with functional MRI (fMRI). Maihofner et al (34) have shown that activation of the contralateral SI, bilateral SII, and insular cortex all contribute to the encoding of non-painful stimuli. Deactivation of the ipsilateral SI and the primary visual cortex was found in CRPS patients. However, CRPS patients with allodynia have widespread cerebral fMRI activation that includes the ipsilateral and contralateral SI, the primary motor cortex, the contralateral parietal association cortex, bilateral SII, insula, and frontal cortex as well as the anterior and posterior cingulate cortex. Deactivations were detected in the ipsilateral superior frontal cortices, contralateral inferior frontal cortices, visual cortices, and the contralateral temporal and posterior insular (vestibular) cortices. In addition, Maihofner et al (35) have also used magnetic source imaging to show that the brain reorganizes with pain in CRPS, particularly in the primary somatosensory cortex, and recovers from cortical reorganization when CRPS pain is reduced. Therefore, it is possible that ECT may trigger the recovery process of the brain that has been reorganized by CRPS pain to its original form. Because our patient’s symptoms did not immediately completely improve, it can be postulated that ECT may begin the process that restores the brain to its normal functional somatotopic processing capacity, but it may require a prolonged period of time to completely recover.

Conclusion

Further controlled randomized studies will be necessary to elucidate possible mechanisms involved in ECT for the benefit of severe refractory CRPS.

Attached Files

Treatment of CRPS with ECT- Wolanin Gulevski and Schwartzman - painhysicianjournal 2007.pdf (139.0 KB, 149 views)