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Migraine is a neurological disorder characterized by paroxysms of head pain accompanied by trigeminovascular system activation and autonomic dysfunction. Diagnosis is currently based on clinical diagnostic criteria. Though physiological differences exist between migraineurs and non-headache controls, true physiological biomarkers have been elusive, especially for the full clinical spectrum of migraine, inclusive of chronic, episodic, and probable migraine. We used edge-light pupil cycle time (PCT) as a probe of the pupillary light circuit in migraine, paired with clinical assessment of migraine characteristics, and compared these to non-headache controls. We found significantly increased PCT in probable, episodic, and chronic migraine, compared to controls. Additionally, increased PCT correlated with the presence of craniofacial autonomic symptoms, linking pupillary circuit dysfunction to peripheral trigeminal sensitization. The sensitivity of PCT, especially for all severities of disease, distinguishes it from other physiological phenotypes, which may make it useful as a potential biomarker.
Learn More >Pain catastrophizing is reliably associated with pain reports during experimental pain in healthy, pain-free subjects and in people with chronic pain. It also correlates with self-reports of clinical pain intensity/severity in a variety of disorders characterized by chronic pain in adults, adolescents and children. However, processes, through which it exerts its effects are yet unclear. In this paper, our primary aim was to synthesize neuroimaging research to open a window to possible mechanisms underlying pain catastrophizing in both chronic pain patients and healthy controls. We also aimed to compare whether the neural correlates of pain catastrophizing are similar in these two groups. PubMed and the Web of Science were searched for magnetic resonance imaging (MRI) studies that explored neural correlates of pain catastrophizing. Twenty articles met the inclusion criteria. The results of our review show a connection between pain catastrophizing and brain areas tightly connected to pain perception (including the somatosensory cortices, anterior insula, anterior cingulate cortex and thalamus) and/or modulation (eg, the dorsolateral prefrontal cortex). Our results also highlight that these processes – in relation to pain catastrophizing – are more pronounced in chronic pain patients, suggesting that structural and functional brain alterations (and perhaps mechanisms) related to pain catastrophizing may depend on prior and/or relatively stable/constant pain experience. However, we also found methodological issues and differences that could lead to divergent results. : Based on our results, pain catastrophizing might be related to salience detection, pain processing, and top-down attentional processes. More research is recommended to explore neural changes to specific types of catastrophizing thoughts (eg, experimentally induced and/or state). Furthermore, we provide ideas regarding pain catastrophizing studies in the future for a more standardized approach.
Learn More >Few studies have investigated the associations of comorbid migraine with other painful physical symptoms (PPS) in patients with major depressive disorder (MDD) at the two-year follow-up point. This study aimed to investigate this issue.
Learn More >Patients with a complex regional pain syndrome (CRPS) in the upper limb show a sensory and motor impairment of the hand. Decreased intra-cortical-inhibition (ICI) of the motor representation of the affected hand muscle and decreased somatosensory hand representation size were related to maladaptive plasticity.
Learn More >Migraines with aura have been associated with suicide in adolescents and young adults, but the association between suicide and migraine frequency has not been determined. This study investigated suicidal ideation and suicide attempts among patients with varying frequencies of migraines, with and without auras. This cross-sectional study analyzed 528 patients aged between 20 and 60 years from a headache outpatient clinic in Taiwan. All patients completed a set of questionnaires, including a demographic questionnaire, the Migraine Disability Assessment questionnaire, the Hospital Anxiety and Depression Scale, the Beck Depression Inventory, and the Pittsburgh Sleep Quality Index. Suicide risk was evaluated by self-reported lifetime suicidal ideation and attempts. Patients were divided into low-frequency (1-4 days/month), moderate-frequency (5-8 days/month), high-frequency (9-14 days/month), and chronic (≥15 days/month) migraine groups. The association between migraine frequency and suicidality was investigated using multivariable linear regression and logistic regression. The rates of suicidal ideation and suicide attempts were the highest for chronic migraine with aura (ideation: 47.2%; attempts: 13.9%) and lowest in migraine-free controls (2.8%). Migraine frequency was an independent risk factor for suicidal ideation and attempts in patients with aura (both < 0.001), but not in patients without auras. Migraine aura and depression were associated with higher risks of suicidal ideation and suicide attempts in patients with migraine. High migraine frequency has a correlation with high suicide risk in patients who experience an aura, but not in other patients with migraine.
Learn More >There has been accumulating evidence on sex disparity in incidence, prevalence, symptomology, and burden of migraine. Several neuroimaging studies on migraine patients attempted to unravel the mechanisms of the disease, yet very few of them examined the sex-related differences. Here, we will first discuss some of the reported neuroimaging patterns that discriminate females from males in migraine. We will then re-examine the salient neuroimaging findings in migraine and discuss them in relation to sex-related influences. Finally, we will discuss some of the intriguing recent data suggesting the presence of sex-specific traits in migraineurs. These findings may have potential implications for future neuroimaging studies to identify underlying correlating patterns in the brain to (1) explain the neural basis for higher prevalence of migraine in women, and (2) better understand migraine-specific changes during different stages of life in both men and women.
Learn More >Evidence supports the benefits of resilience among older adults with chronic pain. While numerous factors confer resilience, research has largely examined these measures in isolation, despite evidence of their synergistic effects. Conceptualizing resilience from a multisystem perspective may provide a deeper understanding of adaptive functioning in pain. Sixty adults (ages 60+ years) with chronic low back pain completed measures of physical function, pain intensity, disability, and a performance-based task assessing back-related physical functioning and movement-evoked pain (MEP). Depressive symptoms, quality of life, and general resilience were also evaluated. To examine multisystem resiliency, principal components analysis (PCA) was conducted to create composite domains for psychological (positive affect, hope, positive well-being, optimism), health (waist-hip ratio, body mass index, medical comorbidities), and social (emotional, instrumental, informational support) functioning measures, followed by cluster analysis to identify participant subgroups based upon composites. Results yielded four clusters: Cluster 1 (high levels of functioning across psychological, health, and social support domains); Cluster 2 (optimal health and low psychosocial functioning); Cluster 3 (high psychological function, moderate-to-high social support, and poorer health); and Cluster 4 (low levels of functioning across the three domains). Controlling for sociodemographic characteristics, individuals with a more resilient phenotype (Cluster 1) exhibited lower levels of disability, higher quality of life and psychological functioning, and greater functional performance when compared to those with a lower degree of personal resources (Cluster 4). No significant cluster differences emerged in self-reported pain intensity or MEP. These findings signify the presence of resiliency profiles based upon psychological, social, and health-related functioning. Further examination of the additive effects of multiple adaptive behaviors and resources may improve our understanding of resilience in the context of pain, informing novel interventions for older adults.
Learn More >Informing patients about potential adverse events as part of the informed consent may facilitate the development of nocebo-driven drug adverse events (nocebo side effects). To investigate whether informing about the nocebo effect using a short information sheet can reduce nocebo side effects. A total of = 44 participants with weekly headaches for at least 6 months were recruited using the cover story of a clinical trial for a headache medicine. In reality, all participants took a placebo pill and were randomized to the nocebo information group or the standard leaflet group. Participants were instructed to read the bogus medication leaflet entailing side effects information shortly before pill intake. The nocebo group additionally received an explanation about the nocebo effect as part of the leaflet. Questionnaires were completed at baseline, 2 min, and 4 days after the pill intake. We conducted general linear models with bootstrap sampling. Baseline symptoms were included as a covariate. Most participants (70.5%) reported nocebo side effects at 2 min. Participants who received the nocebo information ( = 24) reported less nocebo symptoms than the control group ( = 20) (estimated difference: 3.3, BCa 95% CI [1.14; 5.15], = 0.01, Cohen's = 0.59). Baseline symptoms, perceived sensitivity to medicine, and side effect expectations each moderated the group effect (estimated difference in slope: 0.47, BCa 95% CI [0.19; 0.73], = 0.001, = 0.75; 1.07 [0.27; 1.61], = 0.006, = 0.73; 1.57 [0.38; 2.76], = 0.02, = 0.58). No group differences were found at 4-day follow-up. After revealing the actual aim of the study, 86% of the participants evaluated the nocebo information to be helpful in general. Results provide the first evidence that informing about the nocebo effect can reduce nocebo side effects.
Learn More >Sensory modulation disorder (SMD) affects sensory processing across single or multiple sensory systems. The sensory over-responsivity (SOR) subtype of SMD is manifested clinically as a condition in which non-painful stimuli are perceived as abnormally irritating, unpleasant, or even painful. Moreover, SOR interferes with participation in daily routines and activities (Dunn, 2007; Bar-Shalita et al., 2008; Chien et al., 2016), co-occurs with daily pain hyper-sensitivity, and reduces quality of life due to bodily pain. Laboratory behavioral studies have confirmed abnormal pain perception, as demonstrated by hyperalgesia and an enhanced lingering painful sensation, in children and adults with SMD. Advanced quantitative sensory testing (QST) has revealed the mechanisms of altered pain processing in SOR whereby despite the existence of normal peripheral sensory processing, there is enhanced facilitation of pain-transmitting pathways along with preserved but delayed inhibitory pain modulation. These findings point to central nervous system (CNS) involvement as the underlying mechanism of pain hypersensitivity in SOR. Based on the mutual central processing of both non-painful and painful sensory stimuli, we suggest shared mechanisms such as cortical hyper-excitation, an excitatory-inhibitory neuronal imbalance, and sensory modulation alterations. This is supported by novel findings indicating that SOR is a risk factor and comorbidity of chronic non-neuropathic pain disorders. This is the first review to summarize current empirical knowledge investigating SMD and pain, a sensory modality not yet part of the official SMD realm. We propose a neurophysiological mechanism-based model for the interrelation between pain and SMD. Embracing the pain domain could significantly contribute to the understanding of this condition's pathogenesis and how it manifests in daily life, as well as suggesting the basis for future potential mechanism-based therapies.
Learn More >Earlier studies have demonstrated that essential fatty acid-derived specialized pro-resolving mediators (SPMs) promote the resolution of inflammation and pain. However, the potential analgesic actions of SPMs in chemotherapy-induced peripheral neuropathy (CIPN) are not known. Recent results also showed sex dimorphism in immune cell signaling in neuropathic pain. Here, we evaluated the analgesic actions of D-series resolvins (RvD1, RvD2, RvD3, RvD4, and RvD5) on a CIPN in male and female mice. Paclitaxel (PTX, 2 mg/kg), given on days 0, 2, 4, and 6, produced robust mechanical allodynia in both sexes at 2 weeks. Intrathecal injection of RvD1 and RvD2 (100 ng, i.t.) at 2 weeks reversed PTX-induced mechanical allodynia in both sexes, whereas RvD3 and RvD4 (100 ng, i.t.) had no apparent effects on either sex. Interestingly, RvD5 (100 ng, i.t.) only reduced mechanical allodynia in male mice but not in female mice. Notably, PTX-induced mechanical allodynia was fully developed in or knockout mice, showing no sex differences. Also, intrathecal RvD5 reduced mechanical allodynia in male mice lacking or , whereas female mice with or deficiency had no response to RvD5. Finally, RvD5-induced male-specific analgesia was also confirmed in an inflammatory pain condition. Formalin-induced second phase pain (licking and flinching) was reduced by intrathecal RvD5 in male but not female mice. These findings identified RvD5 as the first SPM that shows sex dimorphism in pain regulation. Moreover, these results suggest that specific resolvins may be used to treat CIPN, a rising health concern in cancer survivors.
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