Selective serotonin reuptake inhibitor (SSRI)-associated bruxism is an increasingly recognized medication-associated phenomenon, although its incidence, neuropharmacologic mechanisms, and optimal management remain incompletely understood. This focused narrative review examines the clinical evidence, proposed mechanisms, and therapeutic implications of SSRI-associated bruxism. Available literature demonstrates recurring temporal associations between SSRI initiation or dose escalation and the emergence of jaw clenching, tooth grinding, pain, and related orofacial symptoms across multiple agents. Proposed mechanisms are multifactorial and may involve altered monoaminergic regulation within central motor networks, including serotonergic-dopaminergic interactions, 5-hydroxytryptamine (serotonin) receptor 1A (5-HT1A) signaling, and possible noradrenergic contributions; however, these mechanisms remain unconfirmed in affected patients. Adjunctive buspirone is the most consistently described pharmacologic strategy and may permit the continuation of an otherwise effective SSRI, although evidence for benefit remains primarily case-based. The literature is limited by heterogeneous bruxism definitions, inconsistent differentiation between awake and sleep manifestations, variable antidepressant exposures, and sparse objective physiologic assessment. Prospective studies using standardized assessment methods and controlled treatment designs are needed to clarify incidence, susceptibility, pathophysiology, and treatment response.

Nationwide studies of selective mutism (SM) are scarce. This study examined the prevalence of SM in Child and Adolescent Mental Health Services (CAMHS), referral reasons, occurrence of additional mental disorders, and psychotropic medication use in a nationally representative clinical population. The sample comprised all youth referred to CAMHS and registered with a diagnosis of SM in the Norwegian Patient Registry from 2008 to 2022. In total, 1591 youth with SM were identified, with a female-to-male ratio of 2:1. The mean age at first CAMHS referral was 9.1 years (SD 4.0). Boys were referred significantly earlier than girls (8.8 years (SD 4.0) versus 9.3 years (SD 4.0, t = -2.29, df 1589, p = .02)). The main referral reasons were suspected anxiety and affective disorders. The mean age at SM diagnosis was 10.1 years (SD 4.2); boys were diagnosed slightly earlier than girls (9.8 years (SD 4.2) versus 10.2 years (SD 4.2, t = -2.12, df 1589, p = .03)). Additional mental disorders were diagnosed in 51.4% at a mean age of 13.2 years (SD 3.7), most commonly anxiety disorders (33%; ICD-10 F40-F41, F93). Learning difficulties were diagnosed in 9% at a mean age of 11.0 years (SD 4.0). Nearly one-third (31.5%) were prescribed psychotropic medication, mainly during adolescence, with selective serotonin reuptake inhibitors (SSRIs) being most common. This nationwide study demonstrates a relatively late age at SM diagnosis and frequent additional mental disorders. Though further longitudinal research is warranted, findings suggest that earlier diagnosis with earlier specialist care for anxiety may be needed to improve outcomes in SM, especially in girls.

Selective serotonin reuptake inhibitors (SSRIs) are reported to be implicated in altering glucose homeostasis and inducing hypoglycemia in diabetic patients and mice. Herein, the effects of paroxetine on glucose homeostasis, insulin secretion, and insulin sensitivity were investigated in both healthy and streptozotocin-induced-insulin deficient mouse model. Mice were administered with paroxetine (1, 10, and 50 mg/kg) and fasting insulin levels and glucose-stimulated insulin secretion were assessed in healthy mice, whereas the glycemic profile in diabetic mice was evaluated after glucose or insulin challenge. Muscle mRNA expression of insulin signaling-relevant genes was analyzed, in addition to protein kinase B (PKB/Akt) activity and glucose transporter 4 (GLUT4) plasma membrane expression assessed in C2C12 myotubes. Paroxetine modulated glucose homeostasis and reduced the spike in blood glucose in diabetic mice in a dose-dependent manner after a glucose tolerance test. On the other hand, a reverse relationship was observed in the insulin tolerance test, with no evidence of acute hypoglycemia, suggesting that paroxetine did not further exacerbate insulin-induced glucose lowering under the tested conditions. Paroxetine (50 mg/kg) significantly increased fasting insulin secretion and upregulated genes involved in insulin receptor and Akt signaling, while reducing Glut4 mRNA expression. At 10 mg/kg, paroxetine significantly elevated Akt phosphorylation (p < 0.01). Paroxetine enhanced GLUT4 translocation and Akt phosphorylation in C2C12 myotubes. These findings suggest that paroxetine influences glucose homeostasis in diabetic conditions without causing acute hypoglycemia. Nevertheless, further preclinical and clinical investigations are warranted to clarify its metabolic effects and to determine the clinical implications for glycemic management in diabetic patients receiving paroxetine.

Pharmacogenomics is the study of how genetic differences influence drug responses, offering a safer and more effective prescribing model. While pharmacogenomics is well-established in specialties such as oncology and psychiatry, its application in sports medicine remains limited. Athletes frequently use medications such as nonsteroidal anti-inflammatory drugs, opioids, and selective serotonin reuptake inhibitors, and these medications have well-documented gene-drug interactions. This review explores pharmacogenomics considerations for these commonly used substances in athletic populations, emphasizing how genetic variability in drug-metabolizing enzymes, including CYP2C9, CYP2D6, and CYP2C19, can impact medication efficacy and side effect risks. We summarize current evidence, highlight clinical guidelines, and outline how pharmacogenomics-guided prescribing could improve athlete care. By integrating pharmacogenomics into sports medicine, clinicians can tailor medication strategies to each athlete's genetic profile, supporting both health and performance. Broader adoption will require increased clinician education, interdisciplinary collaboration, and research specific to athletic populations, but pharmacogenomics offers a promising tool for advancing individualized, precision-based athlete healthcare.

Beta-adrenoreceptor blockers (beta-blockers) and selective serotonin reuptake inhibitors (SSRIs) are commonly used medications and often used together, such as for the treatment of anxiety. However, there is no recent review of any potential adverse events related to concomitant use of medicines from each group. This scoping review therefore aimed to provide this narrative synthesis. Key databases were searched for articles published in English from 1 January 1990 to 24 November 2025 reporting any adverse event due to the concomitant use of beta-blockers and SSRIs in people aged 18 or over. Any study design was permitted. From 2211 distinct records, 117 articles were eligible for full-text screening, and 48 articles were included. Eight of these were review articles referring to otherwise-included empirical studies. Most were interventional (n = 19, 36.9%) or case reports (n = 14, 29.2%). Bradycardia was the most frequently reported adverse event (n = 11) mostly in case reports involving metoprolol-fluoxetine, metoprolol-paroxetine, metoprolol-sertraline or propranolol-fluoxetine. Blood pressure changes (including hypotension) were observed in half of studies which explored them. Neurocognitive-related symptoms were heterogeneous and there were four case reports/series of self-poisoning suicide or self-harm. The adverse events discussed in this review could be signals for drug-drug interactions. Where mechanism was postulated, authors mostly proposed pharmacokinetically mediated effects via Cytochrome P450 2D6. Signals described in this review of potential adverse events should be examined in robust observational studies of specific beta-blocker-SSRI combinations. This will enable precise estimation of the magnitude of any associated risks and provide insight into the potential mechanism.

Depression is a major and under-recognized comorbidity in Sjögren's disease, contributing to disease burden and impaired quality of life. This narrative review summarizes current evidence regarding the prevalence, pathophysiological mechanisms, clinical impact, assessment, and treatment of depression in patients with Sjögren's disease. Reported prevalence rates range widely from 3.2% to 78.6%, largely owing to methodological heterogeneity, although meta-analytic data demonstrate a significantly increased risk of depression in patients with Sjögren's disease than in healthy controls. Etiology is multifactorial, involving chronic pain, fatigue, dryness, psychosocial stressors, and immune-mediated mechanisms. Elevated inflammatory cytokines, altered serotonergic pathways, antibodies, gut dysbiosis, and neuroimaging abnormalities are the potential underlying links to depression. Furthermore, depression is associated with greater symptom burden, autonomic dysfunction, sleep disturbances, fatigue, reduced health-related quality of life, and impaired functional status. Patient-reported outcomes often correlate more closely with depression than with systemic disease activity. Although several screening instruments are available, their validation in patients with Sjögren's disease remains limited. Management requires a multidisciplinary approach integrating psychological interventions, lifestyle modification, and pharmacologic treatment. Selective serotonin reuptake inhibitors and other agents with low anticholinergic burden are preferred. Optimization of systemic disease control may provide additional benefits. Early recognition and comprehensive management of depression are essential to improve outcomes in patients with Sjögren's disease.

The American College of Physicians (ACP) developed this clinical guideline on pharmacologic treatments for internal medicine physicians and other clinicians caring in outpatient settings for females with menopausal vasomotor symptoms.