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Prospective Cohort Study of Daily Alcoholic Beverage Intake as a Potential Trigger of Headaches among Adults with Episodic Migraine.

To determine whether alcohol intake is associated with occurrence of headaches on the following day. In this prospective cohort study, adults with episodic migraine completed electronic diaries every morning and evening for at least six weeks in March 2016-October 2017. Every day, participants reported alcohol intake, lifestyle factors, and details about each headache. We constructed within-person fixed-effect models adjusted for time-varying factors to calculate odds ratios for the association between 1,2,3,4, or 5+ servings of alcohol and headache the following day. We also calculated the adjusted risk of headache the following day for each level of intake. Among 98 participants who reported 825 headaches over 4,467 days, there was a statistically significant linear association (p-trend =0.03) between alcohol and headache the following day. Compared to no alcohol, 1-2 servings were not associated with headaches, but 5+ servings were associated with a 2.08-fold (95% confidence interval [CI] 1.16-3.73) odds of headache. The adjusted absolute risk of headaches was 20% (95%CI 19%-22%) on days following no alcohol compared with 33% (95%CI 22%-44%) on days following 5+ servings. 1-2 servings of alcoholic beverages were not associated with higher risk of headaches the following day, but 5+ servings were associated with higher risk. Key Messages:1-2 servings of alcoholic beverages were not associated with a higher risk of headaches on the following day, but higher levels of intake may be associated with higher risk.Five or more servings were associated with 2.08 times (95% confidence interval 1.16-3.73 the odds of headache on the following day.The adjusted absolute risk of headaches was 20% (95%CI 19%-22%) on days following no alcohol consumption compared with 33% (95% CI 22%-44%) on days following 5+ servings.

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Longitudinal Analysis Supports a Fear-Avoidance Model That Incorporates Pain Resilience Alongside Pain Catastrophizing.

The fear-avoidance model of chronic pain holds that individuals who catastrophize in response to injury are at risk for pain-related fear and avoidance behavior, and ultimately prolonged pain and disability.

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Minimally Invasive Oral Surgery Induction of the FRICT-ION Chronic Neuropathic Pain Model.

An easily induced preclinical trigeminal neuropathic nerve injury model is described here for the study of chronic pain, the model acronym oramen otundum nflammatory onstriction rigeminal nfrarbital erve). In patients, neuropathic pain is thought to be related to vascular alignment or multiple sclerosis along this small trigeminal nerve branch (V2) innervating the maxillary teeth and middle third of the face. With no detectable outward physical signs, the FRICT-ION model is ideal for blinded studies. The acronym FRICT-ION applied relates to the persistence of the trigeminal neuropathic pain model likely due to sliding irritation with normal chewing in the mice. A step-by-step method to induce the mild chronic rodent neuropathic pain model is described here. The surgery is performed orally through a tiny surgical slit inside the cheek crease to align a chromic gut suture irritant along the nerve as it passes into the skull. The model allows testing of non-evoked subjective measures and evoked quantitative mechanical hypersensitivity (allodynia) testing with von Frey filaments through at least 10-14 weeks (100 days). Anxiety and depression behaviors develop within 3-6 weeks relevant to the affective component of chronic pain. While many pain drugs have failed based on testing performed in the acute animal models available, the more stable and easily replicated trigeminal inflammatory compression model is the better suited for understanding both mechanistic and affective components of nerve injury-induced chronic neuropathic pain states as well as the more ideal for preclinical trials of novel non-opioid pain relief therapies.

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Skin Barrier Abnormalities and Immune Dysfunction in Atopic Dermatitis.

Atopic dermatitis (AD) is a common and relapsing skin disease that is characterized by skin barrier dysfunction, inflammation, and chronic pruritus. While AD was previously thought to occur primarily in children, increasing evidence suggests that AD is more common in adults than previously assumed. Accumulating evidence from experimental, genetic, and clinical studies indicates that AD expression is a precondition for the later development of other atopic diseases, such as asthma, food allergies, and allergic rhinitis. Although the exact mechanisms of the disease pathogenesis remain unclear, it is evident that both cutaneous barrier dysfunction and immune dysregulation are critical etiologies of AD pathology. This review explores recent findings on AD and the possible underlying mechanisms involved in its pathogenesis, which is characterized by dysregulation of immunological and skin barrier integrity and function, supporting the idea that AD is a systemic disease. These findings provide further insights for therapeutic developments aiming to repair the skin barrier and decrease inflammation.

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Effects of an Individualized Comprehensive Rehabilitation Program on impaired postural control in women with chronic pelvic pain: a randomized controlled trial.

To assess the effectiveness of an Individualized Comprehensive Rehabilitation Program (ICPR) on impaired postural control, pain, self-perceived health status and functionality in women with CPP.

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Neuromodulation in primary headaches: current evidence and integration into clinical practice.

Neuromodulatory approaches add to our armamentarium of therapeutic tools for the treatment of primary headaches. This review provides a comprehensive overview of current controlled studies on the different neuromodulation techniques and recommendations for clinical practice.

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Treatment with slow-releasing hydrogen sulfide donors inhibits the nociceptive and depressive-like behaviours accompanying chronic neuropathic pain: Endogenous antioxidant system activation.

Therapies to treat chronic neuropathic pain and its associated comorbidities are limited. Recent studies demonstrated that the administration of slow-releasing hydrogen sulfide (HS) donors inhibited chemotherapy-induced neuropathic pain. However, the antidepressant or anxiolytic effects of these compounds and their mechanisms of action during chronic neuropathic pain have not been evaluated.

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Prevalence and socio-demographic characteristics of persons who have never had a headache among healthy voluntary blood donors – a population-based study.

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Loss of nucleus accumbens low-frequency fluctuations is a signature of chronic pain.

Chronic pain is a highly prevalent disease with poorly understood pathophysiology. In particular, the brain mechanisms mediating the transition from acute to chronic pain remain largely unknown. Here, we identify a subcortical signature of back pain. Specifically, subacute back pain patients who are at risk for developing chronic pain exhibit a smaller nucleus accumbens volume, which persists in the chronic phase, compared to healthy controls. The smaller accumbens volume was also observed in a separate cohort of chronic low-back pain patients and was associated with dynamic changes in functional connectivity. At baseline, subacute back pain patients showed altered local nucleus accumbens connectivity between putative shell and core, irrespective of the risk of transition to chronic pain. At follow-up, connectivity changes were observed between nucleus accumbens and rostral anterior cingulate cortex in the patients with persistent pain. Analysis of the power spectral density of nucleus accumbens resting-state activity in the subacute and chronic back pain patients revealed loss of power in the slow-5 frequency band (0.01 to 0.027 Hz) which developed only in the chronic phase of pain. This loss of power was reproducible across two cohorts of chronic low-back pain patients obtained from different sites and accurately classified chronic low-back pain patients in two additional independent datasets. Our results provide evidence that lower nucleus accumbens volume confers risk for developing chronic pain and altered nucleus accumbens activity is a signature of the state of chronic pain.

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Spinal cord NLRP1 inflammasome contributes to dry skin induced chronic itch in mice.

Dry skin itch is one of the most common skin diseases and elderly people are believed to be particularly prone to it. The inflammasome has been suggested to play an important role in chronic inflammatory disorders including inflammatory skin diseases such as psoriasis. However, little is known about the role of NLRP1 inflammasome in dry skin-induced chronic itch.

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