Pains are subject to obvious, well-documented, and striking top-down influences. This is in stark contrast to visual perception, where the debate over cognitive penetrability tends to revolve around fairly subtle experimental effects. Several authors have recently taken up the question of whether top-down effects on pain count as cognitive penetrability, and what that might show us about traditional debates. I review some of the known mechanisms for top-down modulation of pain, and suggest that it reveals an issue with a relatively (...) neglected part of the cognitive penetrability literature. Much of the debate inherits Pylyshyn’s stark contrast between transducers and cognition proper. His distinction grew out of his running fight with Gibson, and is far too strong to be defensible. I suggest that we might therefore view top-down influences on pain as a species of transducer calibration. This provides a novel but principled way to distinguish between several varieties of top-down effect according to their architectural features. (shrink)

Discussions concerning the modularity of the pain system have been focused on questions regarding the cognitive penetrability of pain mechanisms. It has been claimed that phenomena such as placebo analgesia demonstrate that the pain system is cognitively penetrated; therefore, it is not encapsulated from central cognition. However, important arguments have been formulated which aim to show that cognitive penetrability does not in fact entail a lack of modularity of the pain system. This paper offers an alternative way to reject the (...) modularity of the pain system, which is independent from, but consistent with, the presence of cognitive penetration. It is proposed that, given the current knowledge regarding the functioning and the structure of the pain system, there are good reasons to accept that certain central cognitive mechanisms are part of the pain system. It is argued that such a ‘cognitive constitution’ of the pain system entails that the pain system is not modular. (shrink)

BackgroundThe Basal ganglia (BG) played a crucial role in the brain-level mechanisms of chronic pain disorders. However, the functional changes of BG in chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) are still poorly understood. This study investigated the BG subregions’ resting-state functional connectivity (rs-FC) in CP/CPPS patients compared with healthy controls.MethodsTwenty eight patients with CP/CPPS and 28 age- and education-matched healthy males underwent clinical measurements and 3T brain MR imaging, including T1-weighted structural images and resting-state functional imaging. The data were analyzed (...) by the seeded-based rs-FC analysis. Then, a machine learning method was applied to assess the feasibility of detecting CP/CPPS patients through the changed rs-FC.ResultsCompared with healthy males, patients presented decreased rs-FC between the BG subregions and right middle cingulate cortex, and correlated with pain (r = 0.51, p-uncorrected = 0.005) and urinary symptoms (r = –0.4, p-uncorrected = 0.034). The left superior temporal gyrus and right supramarginal gyrus showed decreased rs-FC with the BG subregions as well. The area under the receiver operating characteristic curve of 0.943 (accuracy = 80%, F1-score = 80.6%) was achieved for the classification of CP/CPPS patients and healthy males with support vector machine (SVM) based on the changed rs-FC.ConclusionThese findings provide evidence of altered BG subregions’ rs-FC in CP/CPPS, which may contribute to our understanding of the BG’s role in CP/CPPS. (shrink)

Health care providers are expected both to relieve pain and to provide anticipatory guidance regarding how much a procedure is going to hurt. Fulfilling those expectations is complicated by the cognitive modulation of pain perception. Warning people to expect pain or setting expectations for pain relief not only influences their subjective experience, but it also alters how nociceptive stimuli are processed throughout the sensory and discriminative pathways in the brain. In light of this, I reconsider the characterization of placebo analgesia (...) as pharmacologically inert and the use of it as deceptive. I show that placebo analgesia exploits the same physical mechanisms as proven analgesics and argue that it should be utilized to relieve pain. Additionally, I describe factors to help identify situations in which clinicians have the obligation to disclose the potential for pain coupled with ways of mitigating the risk of high-intensity pain by setting positive expectations. (shrink)

To cause pain, it is not enough to deliver a dose of noxious stimulation. Pain requires the interaction of sensory processing, emotion, and cognition. In this paper, I focus on the role of cognition in the felt intensity of pain. I provide evidence for the cognitive modulation of pain. In particular, I show that attention and expectation can influence the experience of pain intensity. I also consider the mechanisms that underlie the cognitive effects on pain. I show that all the (...) proposed mechanisms of pain modulation affirm the view that cognition impacts the sensory and discriminative aspects of pain. I conclude that pain perception is a cognitively penetrated phenomenon. (shrink)

Fibromyalgia is a chronic pain syndrome characterized by dysfunctional processing of nociceptive stimulation. Neuroimaging studies have pointed out that pain-related network functioning seems to be altered in these patients. It is thought that this clinical symptomatology may be maintained or even strengthened because of an enhanced expectancy for painful stimuli or its forthcoming appearance. However, neural electrophysiological correlates associated with such attentional mechanisms have been scarcely explored. In the current study, expectancy processes of upcoming laser stimulation (painful and non-painful) and (...) its further processing were explored by event-related potentials (ERPs). Nineteen fibromyalgia patients and twenty healthy control volunteers took part in the experiment. Behavioral measures (reaction times and subjective pain perception) were also collected. We manipulated the pain/no pain expectancy through an S1–S2 paradigm (cue-target). S1 (image: triangle or square) predicted the S2 appearance (laser stimulation: warmth or pinprick sensation). Laser stimuli were delivered using a CO2 laser device. Temporal and spatial principal component analyses were employed to define and quantify the ERP component reliability. Statistical analyses revealed the existence of an abnormal pattern of pain expectancy in patients with fibromyalgia. Specifically, our results showed attenuated amplitudes at posterior lCNV component in anticipation of painful stimulation that was not found in healthy participants. In contrast, although larger P2 amplitudes to painful compared to innocuous events were shown, patients did not show any amplitude change in this laser-evoked response as a function of pain predictive cues (as occurred in the healthy control group). Additionally, analyses of the subjective perception of pain and reaction time indicated that laser stimuli preceded by pain cues were rated as more painful than those signaling non-pain expectancy and were associated with faster responses. Differences between groups were not found. The present findings suggest the presence of dysfunction in pain expectation mechanisms in fibromyalgia that eventually may make it difficult for patients to correctly interpret signs that prevent pain symptoms. Furthermore, the abnormal pattern in pain expectancy displayed by fibromyalgia patients could result in ineffective pain coping strategies. Understanding the neural correlates of pain processing and its modulatory factors is crucial to identify treatments for chronic pain syndromes. (shrink)

ABSTRACTIndividual differences in fear generalisation have been proposed to play a role in the aetiology and/or maintenance of anxiety disorders, but few data are available to directly support that claim. The research that is available has focused mostly on generalisation of peripheral and central physiological fear responses. Far less is known about the generalisation of avoidance, the behavioural component of fear. In two experiments, we evaluated how neuroticism, a known vulnerability factor for anxiety, modulates an array of fear responses, including (...) avoidance tendencies, towards generalisation stimuli. Participants underwent differential fear conditioning, in which one conditioned stimulus was repeatedly paired with an aversive outcome, whereas another was not. Fear generalisation was observed across measures in Experiment 1 and Experiment 2, with overall highest responding to the CS+, lowest to the CS− and intermediate responding to the GSs. Neuroticism had very little impact on fear generalisation, in line with the idea that fear generalisation is largely an adaptive process. (shrink)