Project description:BackgroundComplex regional pain syndrome (CRPS) is a multifactorial condition that may affect patients who sustain a fracture in the upper and lower extremities. Prior investigations have formed a foundation for exploring a possible association between psychiatric disorders and the development of CRPS; however, current studies are conflicted regarding the existence and temporality of a relationship between psychiatric disorders and the potential development of CRPS.Questions/purposes(1) Are patients with preexisting anxiety and mood disorders (AMDs) at increased risk of receiving a diagnosis of CRPS after upper or lower extremity fractures? (2) Are patients with preexisting AMDs at increased risk of being diagnosed with CRPS after surgical fixation of their fracture?MethodsA large, retrospective cohort study was conducted using the TriNetX electronic medical record platform, which contains data from more than 100 million patients. This platform gathers data from healthcare organizations in the United States and Europe and collects comprehensive data over time that includes temporality rather than simply the binary presence or absence of conditions. The cohort included 760,595 patients older than 18 years with upper or lower extremity fractures between 2003 and 2022. Included patients had a minimum 1-year follow-up. We defined AMDs as any diagnosis of anxiety, depressive episode or disorder, a manic episode, or bipolar disorder. Patients with polytrauma or concurrent upper and lower extremity fractures were excluded to reduce confounders. CRPS I diagnosis was identified via International Classification of Diseases, Tenth Edition codes. Propensity score matching was performed to balance cohorts based on age, gender, and race. Hazard ratios and Aalen-Johansen cumulative incidence curves for the diagnosis of CRPS were calculated for patients with and without AMD diagnoses before sustaining a fracture. A subanalysis was performed in which we examined individuals in the upper and lower extremity fracture cohorts who underwent surgical treatment.ResultsPatients with preexisting AMDs were at a higher risk of experiencing CRPS I than patients without AMDs were (upper extremity: HR 1.8 [95% CI 1.7 to 1.9]; p < 0.01, lower extremity: HR 2.2 [95% CI 2.0 to 2.3]; p < 0.01). Similarly, patients with preexisting AMDs were at higher risk of experiencing CRPS I after fracture fixation than patients without AMDs were (upper extremity: HR 1.3 [95% CI 1.2 to 1.5]; p < 0.01, lower extremity: HR 2.3 [95% CI 2.1 to 2.5]; p < 0.01).ConclusionAwareness of the relationship between AMDs and CRPS I will direct future research about the development of this condition and associated neurologic changes. Additionally, surgeons can address AMDs perioperatively and arrange for the treatment of these AMDs with psychiatrists, neurologists, or social work, as appropriate. Accordingly, patients with AMDs should also be made aware of the inherent risk of CRPS I after an upper or lower extremity fracture to comprehensively educate and care for this at-risk patient population.Level of evidenceLevel III, therapeutic study.

Project description:BackgroundNon-suicidal self-injury (NSSI) is an emerging public concern in both clinical and non-clinical settings, especially in the background of the coronavirus disease 2019 (COVID-19) pandemic. Nevertheless, knowledge of NSSI on a certain disease entity in the later stage of the pandemic was scarce.ObjectiveThis study was conducted for the purpose of exploring the current occurrence and characteristics of NSSI in patients diagnosed with mood disorders (MDs) as well as its correlated factors in the later stage of the pandemic.MethodsThree hundred and forty-nine eligible subjects (M ± SD, 21.54 ± 7.62) admitted to a mental health center in Wuhan from 11 November 2021 to 31 January 2022 were included in our study. An umbrella questionnaire comprised of demographics, COVID-19-related factors, Yale-Brown Obsessive and Compulsive Scale (Y-BOCS), Pittsburgh Sleep Quality Index-Revised (PSQI-R), Mobile Phone Addiction Index (MPAI), and Ottawa Self-injury Inventory (OSI) was extended to each subject via shared QR code.ResultsOf 349 patients with MDs included, 151 (43.27%) reported NSSI in the recent 1 month, among whom hand, lower arm/wrist, and scalp were the most hurt body parts, and cutting, hitting, and headbanging were the most adopted methods. "Own idea" was the most common origin of NSSI. In the logistic regression model, age bracket, family monthly income, occupation, level of obsessive-compulsive disorder (OCD) symptoms, sleep duration, withdrawal reaction to the mobile phone, and habits of using a mobile phone were independently associated with NSSI.ConclusionIt was revealed by our study that NSSI was quite prevalent among patients with MDs, especially among those students, adolescents, comorbid with OCD symptoms, inadequate sleeping hours, and suffering from withdrawal reaction to mobile phones. Further research on NSSI in various psychiatric disorders and even in non-clinical settings such as the community population was in urgent need since NSSI in China was not rare.

Project description:BACKGROUND:Mood disorders are expressed in many heterogeneous forms, varying from anxiety to severe major clinical depression. The disorders are expressed in individual variety through manifestations governed by co-morbidities, symptom frequency, severity, and duration, and the effects of genes on phenotypes. The underlying etiologies of mood disorders consist of complex interactive operations of genetic and environmental factors. The notion of endophenotypes, which encompasses the markers of several underlying liabilities to the disorders, may facilitate efforts to detect and define, through staging, the genetic risks inherent to the extreme complexity of disease state. AIMS:This review evaluates the role of genetic biomarkers in assisting clinical diagnosis, identification of risk factors, and treatment of mood disorders. METHODS:Through a systematic assessment of studies investigating the epigenetic basis for mood disorders, the present review examines the interaction of genes and environment underlying the pathophysiology of these disorders. RESULTS:The majority of research findings suggest that the notion of endophenotypes, which encompasses the markers of several underlying liabilities to the disorders, may facilitate efforts to detect and define, through staging, the genetic risks inherent to the extreme complexity of the disease states. Several strategies under development and refinement show the propensity for derivation of essential elements in the etiopathogenesis of the disorders affecting drug-efficacy, drug metabolism, and drug adverse effects, e.g., with regard to selective serotonin reuptake inhibitors. These include: transporter gene expression and genes encoding receptor systems, hypothalamic-pituitary-adrenal axis factors, neurotrophic factors, and inflammatory factors affecting neuroimmune function. Nevertheless, procedural considerations of pharmacogenetics presume the parallel investment of policies and regulations to withstand eventual attempts at misuse, thereby ensuring patient integrity. CONCLUSIONS:Identification of genetic biomarkers facilitates choice of treatment, prediction of response, and prognosis of outcome over a wide spectrum of symptoms associated with affective states, thereby optimizing clinical practice procedures. Epigenetic regulation of primary brain signaling, e.g., serotonin and hypothalamic-pituitary-adrenal function, and factors governing their metabolism are necessary considerations. The participation of neurotrophic factors remains indispensable for neurogenesis, survival, and functional maintenance of brain systems.

Project description:Cannabis has a long history of anecdotal medicinal use and limited licensed medicinal use. Until recently, alleged clinical effects from anecdotal reports and the use of licensed cannabinoid medicines are most likely mediated by tetrahydrocannabinol by virtue of: 1) this cannabinoid being present in the most significant quantities in these preparations; and b) the proportion:potency relationship between tetrahydrocannabinol and other plant cannabinoids derived from cannabis. However, there has recently been considerable interest in the therapeutic potential for the plant cannabinoid, cannabidiol (CBD), in neurological disorders but the current evidence suggests that CBD does not directly interact with the endocannabinoid system except in vitro at supraphysiological concentrations. Thus, as further evidence for CBD's beneficial effects in neurological disease emerges, there remains an urgent need to establish the molecular targets through which it exerts its therapeutic effects. Here, we conducted a systematic search of the extant literature for original articles describing the molecular pharmacology of CBD. We critically appraised the results for the validity of the molecular targets proposed. Thereafter, we considered whether the molecular targets of CBD identified hold therapeutic potential in relevant neurological diseases. The molecular targets identified include numerous classical ion channels, receptors, transporters, and enzymes. Some CBD effects at these targets in in vitro assays only manifest at high concentrations, which may be difficult to achieve in vivo, particularly given CBD's relatively poor bioavailability. Moreover, several targets were asserted through experimental designs that demonstrate only correlation with a given target rather than a causal proof. When the molecular targets of CBD that were physiologically plausible were considered for their potential for exploitation in neurological therapeutics, the results were variable. In some cases, the targets identified had little or no established link to the diseases considered. In others, molecular targets of CBD were entirely consistent with those already actively exploited in relevant, clinically used, neurological treatments. Finally, CBD was found to act upon a number of targets that are linked to neurological therapeutics but that its actions were not consistent withmodulation of such targets that would derive a therapeutically beneficial outcome. Overall, we find that while >65 discrete molecular targets have been reported in the literature for CBD, a relatively limited number represent plausible targets for the drug's action in neurological disorders when judged by the criteria we set. We conclude that CBD is very unlikely to exert effects in neurological diseases through modulation of the endocannabinoid system. Moreover, a number of other molecular targets of CBD reported in the literature are unlikely to be of relevance owing to effects only being observed at supraphysiological concentrations. Of interest and after excluding unlikely and implausible targets, the remaining molecular targets of CBD with plausible evidence for involvement in therapeutic effects in neurological disorders (e.g., voltage-dependent anion channel 1, G protein-coupled receptor 55, CaV3.x, etc.) are associated with either the regulation of, or responses to changes in, intracellular calcium levels. While no causal proof yet exists for CBD's effects at these targets, they represent the most probable for such investigations and should be prioritized in further studies of CBD's therapeutic mechanism of action.

Dataset Information

Cannabidiol for Mood Disorders: A Call for More Research.

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Cannabidiol for Mood Disorders: A Call for More Research.

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