The fentanyl era has produced recurrent community observations of people remaining upright or semi-upright in sustained forward flexion of the head and trunk with intermittent nodding, colloquially referred to as the "fentanyl nod" or "fentanyl fold." Yet the motor state producing this appearance has never been measured directly. We conducted a structured narrative review spanning axial postural-control and reticulospinal neurophysiology, mu-opioid pharmacology, fentanyl-associated rigidity, alpha-2 adulterants, and observations from supervised consumption settings, and integrated these literatures into a testable framework. We introduce opioid flexion phenotype as a descriptive term for the observed configuration, deliberately holding it apart from any diagnostic or mechanistic claim. We advance disproportionate impairment of axial antigravity control as the primary hypothesis, set against three alternatives the evidence does not yet exclude: generalized sedation with loss of postural support; flexor-predominant rigidity or dystonia; and a mixed or fluctuating motor state. The hypothesis predicts that axial extensor activity will be reduced beyond that expected for the level of arousal at comparable ventilation, without increased flexor co-contraction or passive resistance. The rigidity literature prevents visual flexion from being equated with hypotonia, while alpha-2 agonists such as xylazine and medetomidine are better understood as state-dependent modifiers because they may deepen sedation, alter postural support or attenuate an established rigidity state. Persistent flexion after naloxone is non-specific and does not identify either co-exposure or motor mechanism. Discrimination among the accounts requires concurrent assessment of axial muscle activity, passive tone, arousal, ventilation, kinematics, toxicological exposure and longitudinal response. The immediate clinical and harm reduction implications are mechanism-independent: forward flexion should prompt assessment for toxicity rather than dismissal as sleep or voluntary posture; ventilation, not posture, governs urgency and naloxone titration in suspected opioid overdose; and neither appearance nor naloxone response identifies the underlying motor state. The flexed presentation has been read confidently as sedation, hypotonia and rigidity; none of these interpretations is yet warranted, and the instruments needed to adjudicate among them exist, while the observational protocol does not.

Papillary thyroid carcinoma (PTC) is the most common type of well-differentiated thyroid cancer and usually has a favorable prognosis with a low risk of metastasis. However, distant metastasis significantly worsens the prognosis. Brain metastasis of papillary thyroid carcinoma is very rare, and there is currently no standardized treatment protocol for this condition. Case Presentation: A 56-year-old woman was admitted to our hospital 7 years after undergoing total thyroidectomy for primary papillary thyroid carcinoma, presenting with neurological symptoms including decreased mental responsiveness, memory impairment, and motor aphasia. Brain MRI revealed an abnormal mass in the left frontal lobe with extensive surrounding edema. The patient underwent left fronto-temporal craniotomy with complete tumor resection. Postoperatively, the patient showed significant neurological improvement and was started on oral thyroxine replacement therapy. Innovation and Significance: This case provides several noteworthy contributions: (1) It is one of the few reported cases of a single frontal lobe metastatic lesion occurring more than 7 years after primary tumor treatment; (2) It establishes a standardized approach to comprehensive pre- and postoperative neurological assessments; (3) It challenges the traditional view that brain metastases in PTC are almost always associated with extensive systemic dissemination; (4) It provides detailed immunohistochemical characterization of both the primary tumor and the metastatic site. Conclusion: PTC is the most common type of thyroid cancer, typically slow-growing with generally favorable outcomes. Metastases most commonly involve regional lymph nodes, with occasional distant metastases to the lungs and bones. Brain metastases from PTC are extremely rare. In this paper, we present a case of pathologically confirmed PTC brain metastasis in the left frontal lobe and review the available literature on its clinical significance.

Schizophrenia spectrum disorders are typically described using positive and negative symptoms, yet standard diagnostic systems may not reflect the full range of how individuals experience the disorder. We hypothesized that synthesizing first-person accounts would yield a broader, clinically useful symptom framework that better represents lived experience.

We performed a systematic review and qualitative meta-synthesis following Enhancing Transparency in Reporting the Synthesis of Qualitative Research guidelines (PROSPERO: CRD420251069446). PubMed, PsycINFO, and Scopus were searched up to January 2026. Eligible studies used qualitative or mixed methods and reported first-person accounts from individuals with schizophrenia spectrum disorders. We included 52 peer-reviewed studies (2856 participants). We conducted two thematic syntheses: (1) general illness experience and (2) symptom experience organized using the Manual for Assessment and Documentation of Psychopathology in Psychiatry framework.

Across illness experience, five themes emerged: pervasive effects on physical, psychological, social, and relational life; stigma and isolation; interactions with medication, clinicians, and services; disruption and fragmentation of self, reality, and meaning; and coping strategies, including the protective role of social support. Across symptom experience, fear recurred across psychotic and non-psychotic domains, and participants often described psychosis as a transformed experience of reality rather than discrete symptoms. Accounts spanned disturbances in consciousness, perception, thinking, cognition, affect, and behavior.

Lived experience highlights marked heterogeneity that extends beyond traditional symptom dichotomies and is only partly captured by current diagnostic frameworks. Incorporating patient-reported perspectives may support more nuanced, person-centered assessment and evaluation of treatment response.

Juvenile idiopathic arthritis (JIA) impacts children and their families, often increasing caregiver burden and diminishing quality of life. This study assessed the care-related quality of life of parent-caregivers of children with JIA using the Care-Related Quality of Life instrument (CarerQol), identified the most affected caregiving dimensions, and explored associations with sociodemographic and clinical factors.

We analyzed baseline data from the Canada-Netherlands Personalized Medicine Network in Childhood Arthritis and Rheumatic Diseases (UCAN CAN-DU) study. Clinical data including symptoms, disease activity, and caregiver-reported data were collected. Caregivers of children under 18 completed the CarerQol, a preference-weighted caregiver quality-of-life instrument from which a utility score (0-100, worst to better caregiving situation) can be calculated, as well as a well-being visual analog scale (VAS; 0-10, completely unhappy to happy). Stepwise linear regression examined associations between CarerQol utility and VAS; and sociodemographic and clinical variables, with model selection based on goodness of fit.

Among 439 caregivers, 86% were mothers, the mean age was 41 years, and 44% of children had oligoarticular JIA. The mean CarerQol scores were utility of 81.5 (SD 10.8); VAS of 7.3 (SD 1.7). Most caregivers reported fulfillment and caregiving support. Over 40% reported problems in physical health, mental health, and combining caregiving with daily activities. Lower utilities were associated with receiving extra help, having physical health conditions, caring for children using injectable medication, and caring for male children. Higher utilities were associated with living with a partner, caring for children aged 10 to 15, and residing in the Netherlands (P < 0.05).

Many caregivers experience substantial burden, particularly in physical and mental health, and managing caregiving alongside daily responsibilities. Child- and family-related factors are key variables associated with caregiving quality of life. Results emphasize the need for tailored interventions and support systems to improve JIA caregivers' well-being.

Antithrombotic-associated intracranial hemorrhage (ICH) is a life-threatening condition, and rapid treatment in the setting of antithrombotic agents may limit hematoma expansion and improve outcomes. This focused update evaluated the available evidence after publication of the 2016 guidelines.

The Neurocritical Care Society, in conjunction with the Society of Critical Care Medicine, generated five questions to guide a systematic review and meta-analysis. Three of these questions update prior recommendations, while two are newly introduced. Each question followed a Population, Intervention, Comparator, Outcome (PICO) framework and focused on the management of acute ICH including spontaneous intraparenchymal hemorrhage (IPH) and traumatic ICH. The topics addressed were: (1) andexanet alfa versus 4-factor prothrombin complex concentrate (4F-PCC) for treatment of oral factor Xa inhibitor effects; (2) platelet transfusion versus no transfusion for treatment in the setting of antiplatelet agent use; (3) desmopressin versus no desmopressin for treatment in the setting of antiplatelet agent use; (4) treatment of anticoagulant effects versus no treatment in the setting of small IPH; and (5) use of viscoelastic hemostatic assays (VHAs) to treat coagulopathy in traumatic ICH. Recommendations were developed using the Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) methodology.

The panel generated eight recommendations. For patients with acute ICH, the panel issued the following conditional recommendations: use 4F-PCC rather than andexanet alfa for the treatment of the anticoagulant effects of factor Xa inhibitors, avoid platelet transfusion in non-neurosurgical patients with spontaneous IPH on antiplatelet agents, administer platelet transfusion in patients with spontaneous IPH on aspirin who are undergoing surgery, and use VHAs to guide treatment of coagulopathy in traumatic ICH. The panel was unable to issue recommendations regarding platelet transfusion for treatment of antiplatelet effects in traumatic ICH, use of desmopressin for treatment of antiplatelet effects, or treatment of anticoagulant effects in small IPH.

The guideline writing panel provided new conditional recommendations for the treatment of antithrombotic-associated acute ICH. These recommendations are intended for consideration along with the patient's clinical status and patient-specific factors.

Catatonia in autistic individuals may resemble worsening autism yet represent a potentially treatable departure from baseline functioning. We compared item-level catatonic signs in autistic and non-autistic patients and evaluated treatment-associated change during electroconvulsive therapy (ECT). This single-center observational cohort included patients with catatonia who received ECT from May 2022 through April 2026. The 23-item Bush-Francis Catatonia Rating Scale (BFCRS) was assessed longitudinally. Pretreatment BFCRS data were available for 104 patients, including 41 autistic and 63 non-autistic patients, with 993 near-complete repeated assessments available. Pretreatment item presence was modeled using a three-level clinical-group variable with adjustment for age, biologic sex, and calendar year. Compared with non-autistic patients, patients with autism and intellectual disability had higher adjusted odds of eight activated, repetitive, or behaviorally dysregulated signs and lower odds of immobility/stupor. Among 96 patients with paired first and last eligible BFCRS assessments, multiple items improved in both cohorts. Generalized estimating equations demonstrated longitudinal declines in total BFCRS scores and multiple psychomotor-domain scores, with no clinical-group-by-time interaction surviving false-discovery rate correction in unrestricted or 30-, 60-, 90-, and 180-day models. Autism-specific Kanner analyses identified significant fixed-endpoint improvement in seven severity items after false-discovery rate correction, six of which were reproduced longitudinally. Catatonia in autistic patients with intellectual disability was characterized by a phenotype that may resemble worsening autism during later regression, and many constituent signs demonstrated treatment-associated improvement during ECT.

Chronic inflammation and mitochondrial dysfunction are hallmarks of neurodegeneration and aging, yet how mitochondrial damage contributes to inflammatory and aging-like cellular programs remains poorly understood. Gaucher disease (GD) is a lysosomal storage disorder caused by GBA1 mutations, which also represent a major genetic risk factor for Parkinson's disease. In a GD mouse model, we identified marked mitochondrial cristae disorganization accompanied by mitochondrial DNA release, activation of the cGAS-STING and NLRP3 inflammasome pathways, and subsequent inflammatory microglial activation. Circulating galectin-3 was also elevated in both model mice and patients with GD, supporting its potential relevance as a systemic marker of disease-associated inflammation. Mitochonic acid-5 (MA-5) is a mitochondria-targeting compound that interacts with mitofilin/MIC60 in the mitochondrial inner membrane and enhances ATP production. In a GD mouse model and patient-derived iPSC microglia, MA-5 increased ATP levels, preserved mitochondrial cristae integrity, limited mtDNA release, and suppressed cGAS-STING and NLRP3 inflammasome signaling, thereby attenuating microglial innate immune activation and galectin-3 expression. MA-5 also prolonged survival and reversed accelerated transcriptomic aging across multiple brain cell types, with particularly prominent effects in microglia. In the liver, GD was similarly associated with inflammatory, stress-related, and aging-associated transcriptional changes, whereas MA-5 improved liver function, restored mitochondrial morphology, suppressed inflammatory and stress responses, restored metabolic programs, and reduced transcriptomic age. Overall, MA-5 suppresses neuroinflammation and reverses accelerated transcriptomic aging, supporting its potential as a therapeutic strategy for GD and other lysosomal storage disorders, as well as for diseases characterized by mitochondrial dysfunction, chronic inflammation, and pathological accumulation.

Nomophobia (fear of being without a mobile phone) has emerged as a growing psychological concern in the digital era, negatively affecting the mental well-being and academic functioning of university students. Drawing on the Stimulus-Organism-Response (S-O-R) and Interaction of Person-Affect-Cognition-Execution (I-PACE) frameworks, this study examined the relationship between rumination and nomophobia, tested the sequential mediating roles of emotion dysregulation and interaction anxiousness, and explored the moderating effects of health literacy (HL) and digital health literacy (DHL).

A cross-sectional survey using multistage stratified cluster sampling recruited 22,582 participants from five higher education institutions in Jilin Province, China, between June and December 2025. Participants completed the Ruminative Responses Scale (RRS), Difficulties in Emotion Regulation Scale (DERS-16), Interaction Anxiousness Scale (IAS), Nomophobia Questionnaire (NMP-Q), and measures of HL and DHL. An observed-variable path model and separate regression-based moderation analyses were used to examine the hypothesized associations.

Rumination was positively associated with nomophobia (β = 0.133, p < 0.001). Emotion dysregulation and interaction anxiousness showed statistically significant independent and sequential indirect associations. HL moderated the association between rumination and interaction anxiousness, and DHL moderated the association between emotion dysregulation and nomophobia; however, the interactions explained only 0.05% and 0.23% additional variance, respectively.

The findings identify cross-sectional direct, indirect, and conditional associations consistent with the proposed theoretical framework. The small moderation effects should not be interpreted as evidence of substantial practical importance, and longitudinal studies are needed to evaluate temporal ordering and causality.

Emotional reactivity and emotion regulation play key roles in adolescent mental health. Positive parenting behavior has been shown to facilitate positive adolescent emotional development; however, relationships between parenting and adolescent neural emotion reactivity have not been thoroughly examined. The present study employed whole-brain analysis of fMRI data to examine associations between observed parental warmth (one type of positive parenting) and adolescent neural reactivity to negative and positive emotional stimuli among a suburban, mostly upper middle-class (53% birth-assigned girls, Mage = 12.73) sample. Given previous evidence that relationships between parenting processes and adolescent neural emotion reactivity vary by youth's assigned sex, interactions between parental warmth and assigned sex were also examined. A main effect was found in which lower parental warmth was linked to blunted neural reactivity to negative emotional stimuli in the vACC, an emotion-processing region. Further, there was a significant interaction by assigned sex, such that lower parental warmth was linked to blunted negative emotion-related neural reactivity was more so for assigned boys than assigned girls in the emotion processing, executive functioning, and sensory processing regions. Findings suggest that in parenting environments with low warmth, youth, and especially assigned boys, may be more prone to blunted neural emotion reactivity. This research suggests the importance of parental warmth in youth emotional development and negative emotion-related neural reactivity.

To investigate disparities in the management of cardiogenic shock complicating acute myocardial infarction (AMI-CS) across different hospital levels in Beijing.

A standardized questionnaire was electronically distributed to 61 hospitals through the Beijing Cardiovascular Internal Medicine Quality Control and Improvement Center and the Beijing Extracorporeal Life Support Quality Control and Improvement Center. A multistage sampling method was also used to survey hospitals in eight Beijing districts that were not included in these quality control networks. Hospitals were categorized as Level 1 hospitals, Level 2 hospitals, or Level 3 hospitals according to international standards and the domestic context.

A total of 142 hospitals were analyzed. All participating hospitals were capable of managing cardiovascular diseases. 33.1% of hospitals did not have percutaneous coronary intervention (PCI) capability; 40.8% provided only intra-aortic balloon pump and PCI, whereas 26.0% offered temporary or durable mechanical circulatory support. Level 3 hospitals often lacked established protocols for AMI-CS management. Level 1 hospitals (59.4%) and Level 2 hospitals (56.5%) were more likely to maintain a minimum mean arterial pressure target of 65 mmHg, whereas Level 3 hospitals more commonly accepted a lower target (45.5%). Pulmonary artery catheter monitoring was infrequently used across all hospital levels. Continuous lactate monitoring also differed significantly (Level 3, 39.1% vs. Level 2, 74.6% vs. Level 1, 84.4%; overall p < 0.001). Among the 61 hospitals participating in the quality control network, only 3.6% adopted the Society for Cardiovascular Angiography and Interventions shock stage classification. Shock teams were available in 71.9% of Level 1 hospitals and 44.4% of Level 2 hospitals. Furthermore, only 31.9% of Level 3 hospitals had established referral networks.

Significant disparities exist in the diagnosis and management of AMI-CS across different hospital levels in Beijing. There is an urgent need to enhance the understanding and management of AMI-CS, especially in Level 2 and Level 3 hospitals.