Anxiety, depression and PTSD in children and adolescents following the Beirut port explosion.

BACKGROUND: On August 4, 2020, Beirut's port experienced one of the strongest non-nuclear explosions in history, killing approximately 200 people, displacing 300,000 persons, and injuring more than 1000 children. METHODS: An online anonymous survey assessed the prevalence of probable mental health disorders (MHDs) and impact of blast-related and other factors controlling for sociodemographics in 801 children aged 8 to 17 years old. RESULTS: About two thirds (64%) were screened positive for probable anxiety using the Screen for Childhood Anxiety Related Disorder, 52% for probable PTSD using CRIES-13, and 33% for probable depression using the Mood and Feelings Questionnaire (MFQ). Children who resided farthest way from the explosion site or were not in Beirut during blast had a significantly lower odds of anxiety and PTSD. Children who sustained any physical injury (vs. none) or witnessed casualties (vs. not) were at higher odds for PTSD. Children of parents who reported that their homes sustained minor damages (vs. no damages at all) were at higher odds for anxiety and PTSD, and temporary displacement (vs. none) increased odds of PTSD only. Poorer perceived economic status, poorer academic performance, having a family member injured in the blast, and prior mental health care seeking were associated with higher odds for all MHDs. CONCLUSION: Our study, the only one to document the mental health impact of the Beirut Port explosion on children, highlights the critical need for an emergency mental health response, prioritizing disadvantaged communities and children with prior mental health problems.

Validity of Categories Related to Gender Identity in ICD-11 and DSM-5 Among Transgender Individuals who Seek Gender-Affirming Medical Procedures.

BACKGROUND/OBJECTIVE: The most recent versions of the two main mental disorders classifications-the World Health Organization's ICD-11 and the American Psychiatric Association's DSM-5-differ substantially in their diagnostic categories related to transgender identity. ICD-11 gender incongruence (GI), in contrast to DSM-5 gender dysphoria (GD), is explicitly not a mental disorder; neither distress nor dysfunction is a required feature. The objective was compared ICD-11 and DSM-5 diagnostic requirements in terms of their sensitivity, specificity, discriminability and ability to predict the use of gender-affirming medical procedures. METHOD: A total of 649 of transgender adults in six countries completed a retrospective structured interview. RESULTS: Using ROC analysis, sensitivity of the diagnostic requirements was equivalent for both systems, but ICD-11 showed greater specificity than DSM-5. Regression analyses indicated that history of hormones and/or surgery was predicted by variables that are an intrinsic aspect of GI/GD more than by distress and dysfunction. IRT analyses showed that the ICD-11 diagnostic formulation was more parsimonious and contained more information about caseness than the DSM-5 model. CONCLUSIONS: This study supports the ICD-11 position that GI/GD is not a mental disorder; additional diagnostic requirements of distress and/or dysfunction in DSM-5 reduce the predictive power of the diagnostic model.

ANTECEDENTES/OBJETIVO: Las versiones más recientes de las clasificaciones de trastornos mentales ­CIE-11 de la Organización Mundial de la Salud y DSM­5 de la Asociación Psiquiátrica Americana­ difieren en sus categorías diagnósticas relacionadas con la identidad transgénero. La discordancia de género (DiscG) de la CIE-11, en contraste con la disforia de género (DisfG) del DSM-5, no es considerada un trastorno mental; el distrés y la disfunción no son características requeridas para el diagnóstico. El objetivo fue comparar los requisitos diagnósticos de la CIE-11 y el DSM-5 en términos de sensibilidad, especificidad y capacidad para discriminar casos y predecir el uso de procedimientos médicos de afirmación de género. MÉTODO: 649 adultos transgénero de seis países completaron una entrevista estructurada retrospectiva. RESULTADOS: De acuerdo con el análisis ROC, la sensibilidad de ambos sistemas fue equivalente, aunque la CIE-11 mostró mayor especificidad que el DSM-5. Los análisis de regresión indicaron que la historia de uso de hormonas o cirugía se predijo por variables intrínsecas a la DiscG/DisfG y no por el distrés o disfunción. Según los análisis de respuesta al ítem (TRi) la formación CIE-11 resulta más parsimoniosa y contiene mayor información sobre los casos. CONCLUSIONES: Se aporta evidencia a favor de que la DiscG/DisfG no es un trastorno mental; los criterios diagnósticos adicionales de distrés y/o disfunción del DSM-5 reducen su poder predictivo.

Non-invasively triggered spreading depolarizations induce a rapid pro-inflammatory response in cerebral cortex.

Cortical spreading depolarization (CSD) induces pro-inflammatory gene expression in brain tissue. However, previous studies assessing the relationship between CSD and inflammation have used invasive methods that directly trigger inflammation. To eliminate the injury confounder, we induced CSDs non-invasively through intact skull using optogenetics in Thy1-channelrhodopsin-2 transgenic mice. We corroborated our findings by minimally invasive KCl-induced CSDs through thinned skull. Six CSDs induced over 1 h dramatically increased cortical interleukin-1ß (IL-1ß), chemokine (C-C motif) ligand 2 (CCL2), and tumor necrosis factor-α (TNF-α) mRNA expression peaking around 1, 2 and 4 h, respectively. Interleukin-6 (IL-6) and intercellular adhesion molecule-1 (ICAM-1) were only modestly elevated. A single CSD also increased IL-1ß, CCL2, and TNF-α, and revealed an ultra-early IL-1ß response within 10 min. The response was blunted in IL-1 receptor-1 knockout mice, implicating IL-1ß as an upstream mediator, and suppressed by dexamethasone, but not ibuprofen. CSD did not alter systemic inflammatory indices. In summary, this is the first report of pro-inflammatory gene expression after non-invasively induced CSDs. Altogether, our data provide novel insights into the role of CSD-induced neuroinflammation in migraine headache pathogenesis and have implications for the inflammatory processes in acute brain injury where numerous CSDs occur for days.

Repetitive head injury in adolescent mice: A role for vascular inflammation.

Repetitive mild traumatic brain injury during adolescence can induce neurological dysfunction through undefined mechanisms. Interleukin-1 (IL-1) contributes to experimental adult diffuse and contusion TBI models, and IL-1 antagonists have entered clinical trials for severe TBI in adults; however, no such data exist for adolescent TBI. We developed an adolescent mouse repetitive closed head injury (rCHI) model to test the role of IL-1 family members in post-injury neurological outcome. Compared to one CHI, three daily injuries (3HD) produced acute and chronic learning deficits and emergence of hyperactivity, without detectable gliosis, neurodegeneration, brain atrophy, and white matter loss at one year. Mature IL-1ß and IL-18 were induced in brain endothelium in 3HD but not 1HD, three hit weekly, or sham animals. IL-1ß processing was induced cell-autonomously in three-dimensional human endothelial cell cultures subjected to in vitro concussive trauma. Mice deficient in IL-1 receptor-1 or caspase-1 had improved post-injury Morris water maze performance. Repetitive mild CHI in adolescent mice may induce behavioral deficits in the absence of significant histopathology. The endothelium is a potential source of IL-1ß and IL-18 in rCHI, and IL-1 family members may be therapeutic targets to reduce or prevent neurological dysfunction after repetitive mild TBI in adolescents.