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.