Ebook Central pain syndrome - Pathophysiology, diagnosis, and management (2/E): Part 2
➤ Gửi thông báo lỗi ⚠️ Báo cáo tài liệu vi phạmNội dung chi tiết: Ebook Central pain syndrome - Pathophysiology, diagnosis, and management (2/E): Part 2
Ebook Central pain syndrome - Pathophysiology, diagnosis, and management (2/E): Part 2
TreatmentDeep brain stimulationDespite initial optimistic reports, it has become clear that deep brain stimulation (DBS) is not as successful as was i Ebook Central pain syndrome - Pathophysiology, diagnosis, and management (2/E): Part 2initially 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 aro Ebook Central pain syndrome - Pathophysiology, diagnosis, and management (2/E): Part 2und the third ventricle, including CM-Pf and the junction of the third ventricle and the sylvian aqueduct (rostral ventral PAG, caudal ventral PVG). CEbook Central pain syndrome - Pathophysiology, diagnosis, and management (2/E): Part 2
P is generally treated by contralateral Vc stimulation, which is effective only unilaterally. The internal capsule (posterior limb) may be used if thaTreatmentDeep brain stimulationDespite initial optimistic reports, it has become clear that deep brain stimulation (DBS) is not as successful as was i Ebook Central pain syndrome - Pathophysiology, diagnosis, and management (2/E): Part 2sm of actionThe 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 variabilit Ebook Central pain syndrome - Pathophysiology, diagnosis, and management (2/E): Part 2y of the axons' orientation limits the value of computational models of DBS.PAG/PVGYoung and Chambi (1987) used a double-blind, placebo-controlled stuEbook Central pain syndrome - Pathophysiology, diagnosis, and management (2/E): Part 2
dy design and found no evidence that PAG/PVG-induced analgesia in humans is mediated by an opioid mechanism. In a study, low-fl-20 Hz) and high-frequeTreatmentDeep brain stimulationDespite initial optimistic reports, it has become clear that deep brain stimulation (DBS) is not as successful as was i Ebook Central pain syndrome - Pathophysiology, diagnosis, and management (2/E): Part 2ith SCI pain, and one with tabes dorsalis, despite a modest-to-significant increase in CSF endorphin levels (Amano el al. 1982): thisincrease was interpreted as a psychological response. Actually, the contrast medium (metrimazide) used for the ventriculography, not PVG DBS, appears to be responsible Ebook Central pain syndrome - Pathophysiology, diagnosis, and management (2/E): Part 2 for the elevated estimation of betaendorphins (Fessler el al. 1984).Aziz’s group found that pain suppression is frequency-dependent (Nandi el al. 200Ebook Central pain syndrome - Pathophysiology, diagnosis, and management (2/E): Part 2
3, Nandi and Aziz 2004). During 5-35 Hz PVG stimulation, the amplitude of thalamic field potentials (FPs) was significantly reduced, and this was assoTreatmentDeep brain stimulationDespite initial optimistic reports, it has become clear that deep brain stimulation (DBS) is not as successful as was i Ebook Central pain syndrome - Pathophysiology, diagnosis, and management (2/E): Part 2epending on duration of stimulation) was seen in FP reversal upon switching off the stimulator. The FPs were of ver}' low frequency (0.2-0.4 Hz) in Vc: their amplitude was much stronger OFF or with ineffective (50 Hz) stimulation than with analgesic 5-35 Hz stimulation. This suggested a fairly direc Ebook Central pain syndrome - Pathophysiology, diagnosis, and management (2/E): Part 2t neuronal circuit between PVG and Vc mediated by reticulospinal neurons. All patients were also stimulated in Vc, alone or simultaneously with PVG. TEbook Central pain syndrome - Pathophysiology, diagnosis, and management (2/E): Part 2
he PVG FPs were independent of both the pain scores and the state of stimulation of Vc. In nonresponders, there was no flattening in the slow-wave thaTreatmentDeep brain stimulationDespite initial optimistic reports, it has become clear that deep brain stimulation (DBS) is not as successful as was i Ebook Central pain syndrome - Pathophysiology, diagnosis, and management (2/E): Part 2wmTc-HMPAO SPECT fitted to standard Talairach space at a 10% threshold. All patients were scanned ON- and OFF-DBS with an interval of 2 days, 4-7 months after surgery, and results compared. A wide array of cortical and subcortical regions were cither activated or deactivated without a common thread Ebook Central pain syndrome - Pathophysiology, diagnosis, and management (2/E): Part 2among patients. Considering just the 30% threshold suggestive of very large rCBF differences and only effects during stimulation versus no stimulationEbook Central pain syndrome - Pathophysiology, diagnosis, and management (2/E): Part 2
, their patient 1 (PVG DBS) showed right SI/M1 (3.3%) and left PFC (0.2%) plus brainstem (0.5%) hypoperfusion, patient 2 no anomaly, and patient182r. TreatmentDeep brain stimulationDespite initial optimistic reports, it has become clear that deep brain stimulation (DBS) is not as successful as was i Ebook Central pain syndrome - Pathophysiology, diagnosis, and management (2/E): Part 2rs tried to link these rCBF changes to areas thought to be involved in analgesia, but the findings do not lend themselves to any kind of reasonable analysis.VcVc DBS does not activate the endogenous opioid system (or other descending fiber tracts) (see full discussion in the first edition of this bo Ebook Central pain syndrome - Pathophysiology, diagnosis, and management (2/E): Part 2ok: Canavero and Bonicalzi 2007a). Since the thalamocortical loop works more like a non-linear dynamic system that is not solely based on a firing-ratEbook Central pain syndrome - Pathophysiology, diagnosis, and management (2/E): Part 2
e code, DBS may actually work by rebalancing a skewed oscillator)' pattern (Chapter 26).Neurometabolic studies have been published. These studies repoTreatmentDeep brain stimulationDespite initial optimistic reports, it has become clear that deep brain stimulation (DBS) is not as successful as was i Ebook Central pain syndrome - Pathophysiology, diagnosis, and management (2/E): Part 2(pain condition), the lowest metabolic rate was in the infarcted thalamus; some areas showed decreased glucose consumption in the otherwise normal ipsilateral cortex. A second PET during DBS (off-pain condition) revealed markedly decreased glucose metabolism in most brain regions. Rezai et al. (1999 Ebook Central pain syndrome - Pathophysiology, diagnosis, and management (2/E): Part 2) scanned (fMRI) two patients who had steady-burning CP due to traumatic SCI (a third had PNP). PVG DBS - in contrast to Vc DBS - did not activate SI,Ebook Central pain syndrome - Pathophysiology, diagnosis, and management (2/E): Part 2
but the cingulate cortex (compare with Vim DBS for tremor). Low-frequency stimulation of PVG led toactivation of the medial thalamus (compare with NaTreatmentDeep brain stimulationDespite initial optimistic reports, it has become clear that deep brain stimulation (DBS) is not as successful as was i Ebook Central pain syndrome - Pathophysiology, diagnosis, and management (2/E): Part 2 At paresthesia-evoking intensities Vc DBS resulted in the activation of SI in all three pain patients. In most cases, areas of cortical activation corresponded to the homuncular somatotopy of paresthesias (3 V, 75-100 Hz, 150-200 (is). With no paresthesias, SI was not activated. In addition to SI, Ebook Central pain syndrome - Pathophysiology, diagnosis, and management (2/E): Part 2there was activation of thalamus, S1I and insula. In a similar study, Duncan el al. (1998) submitted five patients with neuropathic pain (perhaps inclEbook Central pain syndrome - Pathophysiology, diagnosis, and management (2/E): Part 2
usive of CP) to Vc DBS. All had obtained relief for more than 3 years to reduce a placebo confounding role. Three patients were relieved, while two haTreatmentDeep brain stimulationDespite initial optimistic reports, it has become clear that deep brain stimulation (DBS) is not as successful as was i Ebook Central pain syndrome - Pathophysiology, diagnosis, and management (2/E): Part 2ent with continued stimulation. Their data did not support activation of tactile thalamocortical pathways being the sole mechanism underlying successful Vc DBS. Their most prominent cortical rCBF increase was in ipsilateral anterior insula, both with and without relief, although somewhat stronger wi Ebook Central pain syndrome - Pathophysiology, diagnosis, and management (2/E): Part 2th relief. Patients perceived both par-esthesiae and cold and warmth during stimulation. The close proximity' of microstimulation sites evoking tactilEbook Central pain syndrome - Pathophysiology, diagnosis, and management (2/E): Part 2
e and thermal sensations indicates that bipolar stimulating electrodes could easily stimulate neurons within both the insular and SI pathways. They alTreatmentDeep brain stimulationDespite initial optimistic reports, it has become clear that deep brain stimulation (DBS) is not as successful as was i Ebook Central pain syndrome - Pathophysiology, diagnosis, and management (2/E): Part 2neuropathic pain cases) submitted to Vc/ML stimulation. The first was a paraplegic suffering from unilateral leg pain: he obtained 100% relief after 30 minutes of stimulation. This analgesia disappeared immediately upon cessation of DBS. Follow-up was 9 months. On PET day, he was on amitriptyline, b Ebook Central pain syndrome - Pathophysiology, diagnosis, and management (2/E): Part 2aclofen, diazepam, and oxycodone. The second suffered from spinal arteriovenous malformation (AVM)-rclatcd CP to the left leg. Follow-up was 16 monthsEbook Central pain syndrome - Pathophysiology, diagnosis, and management (2/E): Part 2
. Analgesics were retained for 12 hours before PET. There was 0% relief at followup, but some relief immediately postoperatively (tha-lamotomic effectTreatmentDeep brain stimulationDespite initial optimistic reports, it has become clear that deep brain stimulation (DBS) is not as successful as was i Ebook Central pain syndrome - Pathophysiology, diagnosis, and management (2/E): Part 2ree of stimulation-evoked pain relief and the magnitude of rCBF change in either region of the ACC (BA32-24). Activation of posterior ACC was detected183Section 3: Treatmentafter 30 minutes of DBS, but not at the onset of stimulation, in contrast to the ACC, which was activated throughout the period Ebook Central pain syndrome - Pathophysiology, diagnosis, and management (2/E): Part 2 of DBS. Thus, posterior ACC was not related to direct activation from thala mils, but to other structures. Duncan el al. (1998) also noted that someEbook Central pain syndrome - Pathophysiology, diagnosis, and management (2/E): Part 2
ol their DBS-induced activations were stronger alter 30 minutes ol DBS than al DBS onset. In contrast to this study, patients in Davis’s study did notTreatmentDeep brain stimulationDespite initial optimistic reports, it has become clear that deep brain stimulation (DBS) is not as successful as was i Ebook Central pain syndrome - Pathophysiology, diagnosis, and management (2/E): Part 2(only two responders), paresthesias in different body regions, thus activating different portions of Si 11, or diminishing paresthesias in the course of DBS. Other CBF changes may have involved other cortical and subcortical areas.Other areasMayanagi and Sano (1998) state that “patients with chronic Ebook Central pain syndrome - Pathophysiology, diagnosis, and management (2/E): Part 2 pain of thalamic or spinal origin failed to experience pain relief with hypothalamic DBS like stimulation." Stimulation of the Koellikcr-Fuse nucleusEbook Central pain syndrome - Pathophysiology, diagnosis, and management (2/E): Part 2
, a pontine satellite of the locus coeruleus and the major source of catecholamine-containing fibers to the spinal cord, has been attempted in CP caseGọi ngay
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