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To assess whether dual therapy with erenumab and onabotulinumtoxinA (BoNTA) was more effective than erenumab alone in chronic migraine.

To summarize the recommendations on the interventional management of subacute and chronic non-radicular low back pain (LBP) from the 21 quality-appraised CPGs identified in the previously published paper: "Quality of Clinical Practice Guidelines on Interventional Management of Low Back Pain: A Systematic Review". By disseminating this information, we aim to facilitate the implementation of these recommendations into clinical practice.

Osteoarthritis of the elbow joint secondary to elbow dysplasia is common in dogs. Intraarticular radionuclide injection is thought to suppress both synovitis and inflammatory pain mediators in the joint which are not directly addressed by current treatments. This dose-finding investigation was a longitudinal, prospective, experimental parallel group, post-test study with repeated measures. Forty-four dogs, with low to intermediate-grade osteoarthritis, received a single injection into their most clinically affected elbow joint and were randomized into three treatment cohorts; 37 MBq, 64.75 MBq, or 92.5 MBq (normalized to the body surface area of a 22 kg dog) of Sn radiocolloid. Dogs were assessed monthly by owners, using the canine Brief Pain Inventory (cBPI), and at 1, 3, 6, 9, and 12 months intervals by investigators. Positive responses to treatment were observed by both owners and clinicians in all dose groups with the medium dose group having the highest and most durable response rate based on cBPI scores. The results of this study support the use of Sn radiocolloid as a primary treatment of osteoarthritis in low to intermediate-grade osteoarthritis of the canine elbow.

Neuropathic pain (NP) is a chronic pain condition resulting from a lesion or disease in the somatosensory nervous system. The aim of this study was to investigate the metabolome in plasma from patients with chronic peripheral, posttraumatic/postsurgical NP compared to healthy controls. Further, we aimed to investigate the correlation between pain intensity and the metabolome in plasma. The metabolic profile in plasma samples from 16 patients with chronic NP and 12 healthy controls was analyzed using a nuclear magnetic resonance spectroscopy method. Information about pain intensity, pain duration, body mass index (BMI), age, sex, and blood pressure were obtained through a questionnaire and clinical examination. Multivariate data analysis was used to identify metabolites significant for group separation and their correlation with pain intensity and duration, BMI, and age. We found 50 out of 326 features in plasma significantly contributing to group discrimination between NP and controls. Several of the metabolites that significantly differed were involved in inflammatory processes, while others were important for central nervous system functioning and neural signaling. There was no correlation between pain intensity and levels of metabolite in NP. These findings indicate that there seems to be peripheral/systemic differences in the metabolic profile between patients with chronic NP and healthy individuals.

The basal ganglia including the subthalamic nucleus (STN) and substantia nigra pars reticulata (SNr) are involved in pain-related responses, but how they regulate pain processing remains unknown. Here, we identify a pathway, consisting of GABAergic neurons in the SNr (SNr) and glutamatergic neurons in the STN (STN) and the lateral parabrachial nucleus (LPB), that modulates acute and persistent pain states in both male and female mice. The activity of STN neurons was enhanced in acute and persistent pain states. This enhancement was accompanied by hypoactivity in SNr neurons and strengthening of the STN-LPB glutamatergic projection. Reversing the dysfunction in the SNr-STN-LPB pathway attenuated activity of LPB neurons and mitigated pain-like behaviors. Therefore, the SNr-STN-LPB pathway regulates pathological pain and is a potential target for pain management.

Migraine and stroke are highly prevalent diseases with a high impact on quality of life, with multiple epidemiological, pathophysiological, clinical, and prognostic areas of overlap. Migraine is a risk factor for stroke. This risk is explained by common risk factors, migraine-specific mechanisms, and non-migraine-specific mechanisms that have a relevant role in patients with migraine with aura (e.g., atrial fibrillation, paradoxical embolism through a patent foramen ovale). Another important link between migraine aura and ischemic stroke is cardiac embolism. Cardioembolism is the most frequent cause of ischemic stroke and increasing evidence suggests that microembolism, predominantly but not exclusively originating in the heart, is a contributing mechanism to the development of migraine aura. In this review, we discuss epidemiological aspects of the association between migraine and ischemic stroke, the clinical presentation of ischemic strokes in patients with migraine, and the differentiation between migrainous and non-migrainous infarctions. After that, we review migraine-specific and non-migraine-specific stroke mechanisms. We then review updated preclinical and clinical data on microembolism as a cause of migraine aura. In the last section, we summarize knowledge gaps and important areas to explore in future research. The review includes a clinical vignette with a discussion of the most relevant topics addressed.

To determine if the degree of baseline fibromyalgia symptoms in patients with rheumatoid arthritis (RA), as indicated by the Fibromyalgia Survey Questionnaire (FSQ) score, predicts RA disease activity after initiation or change of a disease-modifying antirheumatic drug (DMARD).