(BQ) Part 2 book “Central pain syndrome - Pathophysiology, diagnosis, and management” has contents: Deep brain stimulation, cortical stimulation, deep brain stimulation, drug dissection, imaging studies, neurophys iological studies, intraspinal druginfusion, and other contents. | Section 3 Chapter 12 Treatment Deep brain stimulation Despite initial optimistic reports, it has become clear that deep brain stimulation (DBS) is not as successful as was initially hoped. The clinical data do not fit with promising animal findings, and large discrepancies are noted between the results of different neurosurgical groups. The targets for DBS include thalamic Vc nuclei and/or the posterior limb of the internal capsule, the caudal medial thalamic areas around the third ventricle, including CM-Pf and the junction of the third ventricle and the sylvian aqueduct (rostral ventral PAG, caudal ventral PVG). CP is generally treated by contralateral Vc stimulation, which is effective only unilaterally. The internal capsule (posterior limb) may be used if thalamic tissue is unavailable (., after an infarct or encephalomalacia). Some groups simultaneously stimulate the PVG area and Vc (Fig. ). Mechanism of action The mechanism or mechanisms of action of DBS are largely unknown, but it is increasingly clear that it depends on the electrical excitation of neural elements and not on their suppression, with antidromic activation playing a starring role (Montgomery 2010). Unfortunately, the variability of the axons’ orientation limits the value of computational models of DBS. PAG/PVG Young and Chambi (1987) used a double-blind, placebo-controlled study design and found no evidence that PAG/PVG-induced analgesia in humans is mediated by an opioid mechanism. In a study, low(1–20 Hz) and high-frequency (50 Hz) stimulation of the PAG neither produced relief nor reproduced pain in eight patients with thalamic CPSP, one with tumor thalamic CP, one with SCI pain, and one with tabes dorsalis, despite a modest-to-significant increase in CSF endorphin levels (Amano et al. 1982): this 182 increase was interpreted as a psychological response. Actually, the contrast medium (metrimazide) used for the ventriculography, not PVG DBS, appears to be responsible for the .
