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: Vestibular migraine (VM) is one of the most common causes of recurrent vertigo, but the neural mechanisms that mediate such symptoms remain unknown. Since visual symptoms and photophobia are common clinical features of VM patients, we hypothesized that VM patients have abnormally sensitive low-level visual processing capabilities. This study aimed to investigate cortex abnormalities in VM patients using visual evoked potential (VEP) and standardized low-resolution brain electromagnetic tomography (sLORETA) analysis. : We employed visual stimuli consisting of reversing displays of circular checkerboard patterns to examine "low-level" visual processes. Thirty-three females with VM and 20 healthy control (HC) females underwent VEP testing. VEP components and sLORETA were analyzed. : Patients with VM showed significantly lower amplitude and decreased latency of P1 activation compared with HC subjects. Further topographic mapping analysis revealed a group difference in the occipital area around P1 latency. sLORETA analysis was performed in the time frame of the P1 component and showed significantly less activity (deactivation) in VM patients in the frontal, parietal, temporal, limbic, and occipital lobes, as well as sub-lobar regions. The maximum current density difference was in the postcentral gyrus of the parietal lobe. P1 source density differences between HC subjects and VM patients overlapped with the vestibular cortical fields. : The significantly abnormal response to visual stimuli indicates altered processing in VM patients. These findings suggest that abnormalities in vestibular cortical fields might be a pathophysiological mechanism of VM.
Learn More >Lower limb pain, whether induced experimentally or as a result of a musculoskeletal injury, can impair motor control, leading to gait adaptations such as increased muscle stiffness or modified load distribution around joints. These adaptations may initially reduce pain but can also lead to longer-term maladaptive plasticity and to the development of chronic pain. In humans, many current experimental musculoskeletal-like pain models are invasive, and most don't accurately reproduce the movement-related characteristics of musculoskeletal pain. The main objective of this study was to measure pain adaptation strategies during gait of a musculoskeletal-like experimental pain protocol induced by phase-specific, non-invasive electrical stimulation. Sixteen healthy participants walked on a treadmill at 4 km/h for three consecutive periods (BASELINE, PAIN, and POST-PAIN). Painful electrical stimulations were delivered at heel strike for the duration of heel contact (HC) using electrodes placed around the right lateral malleolus to mimic ankle sprains. Gait adaptations were quantified bilaterally using instrumented pressure-sensitive insoles. One-way ANOVAs and group time course analyses were performed to characterize the impact of electrical stimulation on heel and forefoot contact pressure and contact duration. During the first few painful strides, peak HC pressure decreased on the painful side (8.6 ± 1.0%, < 0.0001) and increased on the non-stimulated side (11.9 ± 0.9%, < 0.0001) while HC duration was significantly reduced bilaterally (painful: 12.1 ± 0.9%, < 0.0001; non-stimulated: 4.8 ± 0.8%, < 0.0001). No clinically meaningful modifications were observed for the forefoot. One minute after the onset of painful stimulation, perceived pain levels stabilized and peak HC pressure remained significantly decreased on the painful side, while the other gait adaptations returned to pre-stimulation values. These results demonstrate that a non-invasive, phase-specific pain can produce a stable painful gait pattern. Therefore, this protocol will be useful to study musculoskeletal pain locomotor adaptation strategies under controlled conditions.
Learn More >Previous studies targeting inter-individual differences in pain processing in migraine mainly focused on the perception of pain. Our main aim was to disentangle pain anticipation and perception using a classical fear conditioning task, and investigate how migraine frequency and pre-scan cortisol-to-dehydroepiandrosterone sulfate (DHEA-S) ratio as an index of neurobiological stress response would relate to neural activation in these two phases. Functional Magnetic Resonance Imaging (fMRI) data of 23 participants (18 females; mean age: 27.61± 5.36) with episodic migraine without aura were analysed. We found that migraine frequency was significantly associated with pain anticipation in brain regions comprising the midcingulate and caudate, whereas pre-scan cortisol-to DHEA-S ratio was related to pain perception in the pre-supplementary motor area (pre-SMA). Both results suggest exaggerated preparatory responses to pain or more general to stressors, which may contribute to the allostatic load caused by stressors and migraine attacks on the brain.
Learn More >The use of alcohol and prescription opioids is common among people in pain and poses significant public health burdens. This review identifies factors associated with motivation to use alcohol and prescription opioids in the context of pain. Pain-relevant, cognitive-affective, transdiagnostic vulnerability factors-expectancies/motives, pain catastrophizing, pain-related anxiety, distress intolerance, anxiety sensitivity, and perceived interrelations-were selected from theoretical conceptualizations of pain and substance use. Searches conducted in PubMed, PsycINFO, and Embase returned 25 studies that examined associations between identified variables of interest and the use of alcohol and prescription opioids in the context of pain. Consistent with a larger literature on pain and substance use, the studies included in this review demonstrated that people with chronic pain are motivated to use alcohol and opioids in response to negative affect and hold expectancies/motives for coping with pain. Vulnerabilities that engender difficulty managing aversive internal states (distress intolerance and anxiety sensitivity) and maladaptive responses to pain (pain-related anxiety and pain catastrophizing) also were implicated in motivation for alcohol and opioid use. Although one study found that pain-related anxiety was associated with co-use of alcohol and opioids, no studies examined simultaneous use. Future research directions that can explicate causal associations, identify patterns of alcohol and opioid co-use, clarify the role of pain in cessation processes, and inform treatment development are discussed.
Learn More >To evaluate the relationship between opioid use and specific personality traits among individuals with chronic pain stratified by morphine equivalent doses (MEQ).
Learn More >Opioid doctor shopping has not yet been investigated in patients followed in tertiary care settings. This study aimed at assessing the prevalence of opioid doctor shopping among patients with chronic non-cancer pain (CNCP) (ie, pain lasting ≥3 months) attending multidisciplinary pain clinics in Quebec, Canada.
Learn More >Chronic pain is associated with long term plasticity of nociceptive pathways in the central nervous system. Astrocytes can profoundly affect synaptic function and increasing evidence has highlighted how altered astrocyte activity may contribute to the pathogenesis of chronic pain. In response to injury, astrocytes undergo a shift in form and function known as reactive astrogliosis, which affects their release of cytokines and gliotransmitters. These neuromodulatory substances have been implicated in driving the persistent changes in central nociceptive activity. Astrocytes also release lactate which neurons can use to produce energy during synaptic plasticity. Furthermore, recent research has provided insight into lactate's emerging role as a signaling molecule in the central nervous system, which may be involved in directly modulating neuronal and astrocytic activity. In this review, we present evidence for the involvement of astrocyte-derived tumor necrosis factor alpha in pain-associated plasticity, in addition to research suggesting the potential involvement of gliotransmitters D-serine and adenosine-5'-triphosphate. We also discuss work implicating astrocyte-neuron metabolic coupling, and the possible role of lactate, which has been sparsely studied in the context of chronic pain, in supporting pathological changes in central nociceptive activity.
Learn More >Over the past year our attention has inevitably been on the coronavirus pandemic, the health and welfare of our families, patients, and office staffs as well as the re-opening of our dental practices. In addition, the opioid crisis continues, is very likely to worsen as a result of the pandemic and continues to be a challenge to Dentistry. National public health issues and healthcare disparities continue and have created a global concern for providing evidence-based, adequate pain management in the dental setting. We have brought together a group of national thought leaders and experts in this field who will share their insights on the current state of opioid prescribing in Dentistry and describe some of the exciting work being done in advancing pain management. The learning objectives for this conference proceedings were: Describing the implications of current public health concerns for safe and effective pain management in dental medicine.Identifying risk factors and understanding the current guidelines for the use of opioid and non-opioid medications in dental medicine.Analyzing the interprofessional collaborations necessary for effective pain management in dental medicine.Recognizing the challenges and opportunities brought about by the COVID-19 pandemic for the dental profession.Applying evidence-based strategies for managing the complex pain patient in the dental setting.Appraising new and future modalities for the assessment and management of orofacial pain.
Learn More >Complex Regional Pain Syndrome (CRPS) is characterised by pain, autonomic, sensory and motor abnormalities. It is associated with changes in the primary somatosensory cortex (S1 representation), reductions in tactile sensitivity (tested by two-point discrimination), and alterations in perceived hand size or shape (hand perception). The frequent co-occurrence of these three phenomena has led to the assumption that S1 changes underlie tactile sensitivity and perceptual disturbances. However, studies underpinning such a presumed relationship use tactile sensitivity paradigms that involve the processing of both non-spatial and spatial cues. Here, we used a task that evaluates anisotropy (i.e., orientation-dependency; a feature of peripheral and S1 representation) to interrogate spatial processing of tactile input in CRPS and its relation to hand perception. People with upper limb CRPS ( = 14) and controls with ( = 15) or without pain ( = 19) judged tactile distances between stimuli-pairs applied across and along the back of either hand to provide measures of tactile anisotropy. Hand perception was evaluated using a visual scaling task and questionnaires. Data were analysed with generalised estimating equations. Contrary to our hypotheses, tactile anisotropy was bilaterally preserved in CRPS, and the magnitude of anisotropic perception bias was comparable between groups. Hand perception was distorted in CRPS but not related to the magnitude of anisotropy or bias. Our results suggest against impairments in spatial processing of tactile input, and by implication S1 representation, as the cause of distorted hand perception in CRPS. Further work is warranted to elucidate the mechanisms of somatosensory dysfunction and distorted hand perception in CRPS.
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