A common experience is to find that patients’ evaluation of the effectiveness of SCS will wane over the years but that if a technical failure occurs, they demand rapid resolution and often indicate that they had forgotten how bad the original pain was. Assessing the outcome in patients with neuropathic pain syndromes is much more problematic. The response of patients with angina pectoris and PVD to SCS is relatively straightforward because reliable objective measures of ischemia, mobility, and other factors are available to support pain estimates. McMahon FMedSci, FSB, in Wall & Melzack's Textbook of Pain, 2013 Assessment of Outcome Initial positive results were also observed in patients with aphasia ( Cherney et al., 2010). Integrity of efferent fibers and stimulation substrate seems to be an important predictor in stroke recovery. Meanwhile, small phase II studies were performed, with improvement of upper limb function in conjunction with physical therapy ( Brown et al., 2008 Huang et al., 2008 Levy et al., 2008). The first results with epidural stimulation came from Katayama and colleagues (1998), who stimulated patients with poststroke pain and found some functional recovery of the hemiplegic upper limb in 19% of patients. Most data come from noninvasive repetitive TMS and tDCS studies. Different aspects of motor learning will be improved by either motor or sensory cortex stimulation ( Meehan et al., 2011). The same holds true for noninvasive transcranial stimulation ( Reis and Fritsch, 2011). Most interestingly, the functional enhancement persists even after cessation of stimulation ( Plautz et al., 2003) with concurrent rehabilitation measures. Another explanation would be an inhibition of deafferented areas, which approximates to Tsubokawa’s original concept in patients with poststroke pain. This can be interpreted as supportive reorganization, because the previous stroke was recent. Subthreshold stimulation over the motor or speech area improves function after cortical or subcortical infarctions, either by changes in cortical excitability or by interhemispheric disinhibition ( Harvey and Nudo, 2007). Rasche, in Handbook of Clinical Neurology, 2013 Rehabilitation In the next section, studies are presented that provide more specific information on how altered cerebral pain modulation might amplify the processing and experience of pain. In conclusion, the enhanced brain activation in response to experimental pain stimuli confirms patients’ reports of increased pain sensitivity. When the perceived intensity is equated between patients and controls rather than stimulus intensity, brain activation is not generally different in patients ( Giesecke et al 2004). In an interesting study, Lawal and colleagues (2006) found enhanced activation even in response to subliminal esophageal stimulation in IBS patients, perhaps suggesting that at least part of the amplification is related to non-psychological factors. Increased brain activation indicates that the nociceptive signal is amplified somewhere along the pain transmission pathways, although it does not pinpoint the mechanism of amplification.
In line with the generalized hyperalgesia that is observed in many of these patients, activation of pain-processing regions is typically increased when stimuli are used that are of the same intensity as in the healthy control group (e.g., Verne et al 2003, Cook et al 2004, Giesecke et al 2004, Pukall et al 2005). Such studies have been performed predominantly in patients with so-called functional pain syndromes, including fibromyalgia, IBS, and vulvovestibulitis. Instead of imaging brain activation associated with clinical pain, it would be more practical in many instances to use acute experimental stimuli to probe the pain-processing circuitry in patients with chronic pain.
McMahon FMedSci, FSB, in Wall & Melzack's Textbook of Pain, 2013 Cerebral Processing of Experimental Pain in Chronic Pain States
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