Rejected

Although borderline personality disorder (BPD) is associated with both chronic pain and substance abuse, little research examines how BPD features in chronic pain patients may constitute a risk factor for misuse of prescription opioids, and no prior research has examined which particular component(s) of BPD might put chronic pain patients at risk-an oversight that undermines prevention and treatment of such problematic opioid use. In a cross-sectional study of patients in treatment for chronic pain ( = 147), BPD features were associated with several measures of prescription opioid misuse, even controlling for pain severity and interference. Specifically, the identity disturbances and self-harmful impulsivity facets of BPD were most consistently associated with opioid misuse, and exploratory analyses suggested that these factors may be interactive in their effects. Together, these results suggest that BPD features-especially unstable identity and self-harmful impulsivity-play a unique role in problematic prescription opioid use in chronic pain settings.

Paediatric Multisystem Inflammatory Syndrome temporally associated with SARS-CoV-2 (PIMS-TS), first identified in April 2020, shares features of both Kawasaki disease (KD) and toxic shock syndrome (TSS). The surveillance describes the epidemiology and clinical characteristics of PIMS-TS in the United Kingdom and Ireland.

Acute myocarditis is commonly caused by viral infections resulting from viruses such as adenovirus, enteroviruses, and, rarely, coronavirus. It presents with nonspecific symptoms like chest pain, dyspnea, palpitation, or arrhythmias and can progress to dilated cardiomyopathy or heart failure. Fulminant myocarditis is a potentially life-threatening form of the condition and presents as acute, severe heart failure with cardiogenic shock. In this report, we discuss a case of a 41-year-old female who presented with cough and chest pain of two days' duration. The patient had a new-onset atrial flutter. Her chest auscultation revealed bilateral crackles. Laboratory workup revealed elevated troponin levels, and the patient tested positive for coronavirus disease 2019 (COVID-19) by nasopharyngeal swab polymerase chain reaction (PCR). Transthoracic echocardiogram revealed a low left ventricular (LV) ejection fraction of 35-40% compared to 55% one year prior, as well as a granular appearance of LV myocardium. The patient's condition subsequently improved clinically and she was discharged home. Due to cardiac involvement and characteristic myocardial appearance on the echocardiogram, cardiac magnetic resonance (CMR) imaging was performed for further evaluation about two months from the date of admission. CMR showed extensive myocardial inflammation with a typical pattern of sub-epicardial and mid-wall delayed enhancement, confirming the diagnosis of myocarditis. This case highlights myocarditis as a potential complication of COVID-19 that requires early diagnosis and proper management to improve patients' quality of life. Additionally, we highlight the features of myocarditis on CMR in the acute phase and two months after clinical recovery.

Mitochondrial dysfunction results in a series of defective cellular events, including decreased adenosine triphosphate (ATP) production, enhanced reactive oxygen species (ROS) output, and altered proteastasis and cellular quality control. An enhanced output of ROS may damage mitochondrial components, such as mitochondrial DNA and elements of the electron transport chain, resulting in the loss of proper electrochemical gradient across the mitochondrial inner membrane and an ensuing shutdown of mitochondrial energy production. Neurons have an increased demand for ATP and oxygen, and thus are more prone to damage induced by mitochondrial dysfunction. Mitochondrial dysfunction, damaged electron transport chains, altered membrane permeability and Ca homeostasis, and impaired mitochondrial defense systems induced by oxidative stress, are pathological changes involved in neurodegenerative disorders. A growing body of evidence suggests that the use of antioxidants could stabilize mitochondria and thus may be suitable for preventing neuronal loss. Numerous natural products exhibit the potential to counter oxidative stress and mitochondrial dysfunction; however, science is still looking for a breakthrough in the treatment of neurodegenerative disorders. -caryophyllene is a bicyclic sesquiterpene, and an active principle of essential oils derived from a large number of spices and food plants. As a selective cannabinoid receptor 2 (CB2) agonist, several studies have reported it as possessing numerous pharmacological activities such as antibacterial (e.g., ), antioxidant, anti-inflammatory, analgesic (e.g., neuropathic pain), anti-neurodegenerative and anticancer properties. The present review mainly focuses on the potential of -caryophyllene in reducing oxidative stress and mitochondrial dysfunction, and its possible links with neuroprotection.

In 2017, the legislator created a special regulation for medical cannabis in Germany. Medical cannabis can also be prescribed without marketing authorization at the expense of the statutory health insurance, if other forms of therapy are not sufficiently effective. Before starting therapy with a cannabis medicine outside of approved indications, an application for reimbursement must be submitted to the health insurance company. Cannabis medicines are mainly prescribed for the treatment of chronic pain. There are some rules to be observed when prescribing cannabis medicines: The information according to Section 9 of the Narcotic Drugs Prescription Ordinance must be complete and clear. Data on the therapeutic success and the safe use of the cannabis medicines are collected in a five-year follow-up survey. According to first interim results of this survey, many side effects have an influence on the vigilance of patients. The risk of falling is increased, especially in older patients. In the medium term, the special regulation described above should become dispensable due to the approval of cannabis-based finished medicinal products.

The Rule of 7's classifies children as low-risk for Lyme meningitis with the absence of the following: ≥7 days of headache, any cranial neuritis or ≥70% cerebrospinal fluid mononuclear cells. We sought to broadly validate this clinical prediction rule in children with meningitis undergoing evaluation for Lyme disease.

The ability to monitor the physiological effect of the analgesic agent is of interest in clinical practice. Nonstationary changes would appear in photoplethysmography (PPG) during the analgesics-driven transition to analgesia. The present work studied the properties of nonlinear methods including approximate entropy (ApEn) and sample entropy (SampEn) derived from PPG responding to a nociceptive stimulus under various opioid concentrations. Forty patients with ASA I or II were randomized to receive one of the four possible remifentanil effect-compartment target concentrations (Ce) of 0, 1, 3, and 5 ng·ml and a propofol effect-compartment target-controlled infusion to maintain the state entropy (SE) at 50 ± 10. Laryngeal mask airway (LMA) insertion was applied as a standard noxious stimulation. To optimize the performance of ApEn and SampEn, different coefficients were carefully evaluated. The monotonicity of ApEn and SampEn changing from low Ce to high Ce was assessed with prediction probabilities (P). The result showed that low Ce (0 and 1 ng·ml) could be differentiated from high Ce (3 and 5 ng·ml) by ApEn and SampEn. Depending on the coefficient employed in algorithm: ApEn with k = 0.15 yielded the largest P value (0.875) whereas SampEn gained its largest P of 0.867 with k = 0.2. Thus, PPG-based ApEn and SampEn with appropriate k values have the potential to offer good quantification of analgesia depth under general anesthesia.

A 54-year-old man sought treatment at the ED for a productive cough with green phlegm of approximately 6 months' duration that was accompanied by a 10-pound weight loss, night sweats, and occasional subjective fevers. He had made several prior visits to the ED for the cough and was hospitalized 4 months earlier for similar symptoms, at which time he underwent a bronchoscopy with BAL and was discharged with antibiotics for presumed pneumonia. He did not report any itching, rashes, sinus infections, joint swelling, joint pain, or GI symptoms. His long-term medications included omeprazole and amlodipine. The patient had a past medical history of grade III follicular lymphoma for which he completed six cycles of bendamustine 4 years before presentation and had been in remission since. He was a never smoker, had a recent travel history to the Dominican Republic 8 months before admission, and had no recent sick contacts.

We define a migraine trigger to be an endogenous agent or agency such as the menses or an exogenous agent or agency such as red wine or a drop in barometric pressure, and their ability to reduce the threshold of a migraine attack in those predisposed to migraine. This definition excludes agents with idiosyncratic mechanisms that may trigger a migrainous (migraine-like) headache in non-migraineurs such as benign cough headaches or headaches due to altitude-sickness. We also assume as axiomatic that migraine has as its basis the activation of the trigeminovascular pathway (TVP) and the key role of serotonin and the calcitonin gene-related peptide (CGRP). The network activation of the visual/auditory association cortices and the rostrodorsal pons (locus ceruleus and raphe nucleus) are also accepted as key features of activation of the TVP. In addition, we outline the role of the superior salivatory nucleus-sphenopalatine ganglion-greater superficial petrosal nerve (SSN-SPG-GSPN) arc in migraine activation. We also explore how olfactory afferents intermingle with trigeminal nerve collaterals in the glomeruli of the olfactory bulb thus allowing volatile molecules to activate the TVP and induce a migraine. The classification of migraine triggers is complex, as there is a wide panorama of inciting agents, including atmospheric conditions, a wide-ranging variety of foods and beverages, endogenous hormonal influences, synthetic alkaloids and dyes, and volatile molecules (odorants). We will explore the high-frequency migraine-provoking agents in each category. There are exciting and intriguing hypotheses regarding the role of atmospheric chemistry when the barometric pressure drops; the role of hot, dry desert winds and lightning discharges in the generation of cations and the turnover of serotonin in the nervous system. We will explore the effects of a drop in barometric pressure on the vestibular nuclei and the modulation of sympathetically mediated pain. The role of volatile odorants and their activation of the transient receptor potential ankyrin-1 (TRPA-1) receptor will be outlined. We will streamline the highly complex role of estrogen fluctuation in the precipitation of migraine headaches, its pharmacodynamic effects, and the role of the sexually dimorphic nucleus of the preoptic area (SDN-POA) of the hypothalamus. We will also adumbrate the protean effects of alcohol and its congeners and the role of stress and sleep disturbances in the allostatic load model of salience network-pain perception.

Osteoarthritis (OA) is a chronic joint disease characterized by inflammation, gradual destruction of articular cartilage, joint pain, and functional limitations that eventually lead to disability. Join tissues, including synovium and articular cartilage, release extracellular vesicles (EVs) that have been proposed to sustain joint homeostasis as well as to contribute to OA pathogenesis. EVs transport biologically active molecules, and OA can be characterized by altered EV counts and composition in synovial fluid. Of EV cargo, specific non-coding RNAs could have future potential as diagnostic biomarkers for early OA. EVs may contribute to the propagation of inflammation and cartilage destruction by transporting and enhancing the production of inflammatory mediators and cartilage-degrading proteinases. In addition to inducing OA-related gene expression patterns in synoviocytes and articular chondrocytes, EVs can induce anti-OA effects, including increased extracellular matrix deposition and cartilage protection. Especially mesenchymal stem cell-derived EVs can alleviate intra-articular inflammation and relieve OA pain. In addition, surgically- or chemically-induced cartilage defects have been repaired with EV therapies in animal models. While human clinical trials are still in the future, the potential of actual cures to OA by EV products is very promising.