Mirka Lisbeth Alchundia Solís

Borderline Personality Disorder (BPD) is a complex psychiatric condition characterized by emotional dysregulation, impulsivity, and heightened sensitivity to stress. In recent years, growing attention has been directed toward the role of neuroinflammation as a biological process potentially contributing to the pathophysiology of BPD. This narrative review synthesizes current evidence on immune and inflammatory mechanisms associated with BPD, with particular emphasis on their conceptual and biological overlap with neuroinflammatory pathways described in Alzheimer’s disease. Findings from empirical studies, systematic reviews, and neuroimaging research indicate that cytokine dysregulation, microglial activation, and central–peripheral immune interactions are recurrent features across psychiatric disorders and are also evident in BPD. The integration of Alzheimer’s disease as a reference model provides a framework for understanding how sustained neuroinflammation may influence neural connectivity, stress responsivity, and potential cognitive vulnerability without implying neurodegenerative progression. The review further discusses the implications of immune modulation as a complementary perspective within current treatment models, while emphasizing the continued centrality of psychotherapeutic interventions. By situating BPD within a broader neuroimmune framework, this work contributes to an integrative understanding of psychiatric disorders and supports future research and educational approaches that bridge psychiatry, neuroscience, and immunology.

Acute catatonic compromise in individuals with borderline personality disorder (BPD) represents an underrecognized clinical intersection with significant diagnostic and therapeutic implications. This review integrates neurobiological, trauma-related, clinical, and treatment evidence to clarify the mechanisms through which catatonia may emerge within the BPD spectrum. Across neuroimaging and molecular studies, consistent findings highlight fronto-limbic dysregulation, altered GABAergic and glutamatergic signaling, and motor network inhibition as core vulnerabilities. Trauma-related autonomic collapse and affective overload frequently act as precipitants, particularly in individuals with chronic emotional instability or dissociative tendencies. Clinical reports describe abrupt psychomotor shutdown, stupor, mutism, and behavioral freezing triggered by interpersonal crises or trauma reminders, suggesting that catatonia may represent an extreme endpoint of dysregulation in BPD. Therapeutically, benzodiazepines—especially lorazepam—remain first-line interventions, with rapid response serving as a critical diagnostic indicator. Electroconvulsive therapy is consistently effective for refractory or malignant presentations, while long-term management relies on evidence-based psychotherapies that target emotional regulation, interpersonal functioning, and trauma processing. The conceptual framework proposed in this review synthesizes predisposing factors (neurobiological instability, trauma history), precipitating factors (affective surges, autonomic collapse), and maintaining factors (motor inhibition, unresolved emotional overload). This model underscores the need for integrated care strategies that address acute catatonia while simultaneously targeting the longstanding vulnerabilities that define BPD. Improved diagnostic training, broader trauma-informed evaluations, and systematic implementation of catatonia assessments may enhance outcomes, particularly in clinical settings within Mexico, Colombia, and Ecuador. This review aims to support clinicians and researchers in recognizing and managing catatonic compromise in BPD as a multidimensional neuropsychiatric phenomenon requiring comprehensive intervention.

Postpartum depression (PPD) is a major global health concern that affects a substantial proportion of women during the first year after childbirth. Despite advances in screening and intervention, important gaps persist in early detection and access to integrative care—particularly in middle-income regions such as Mexico, Colombia, and Ecuador. This review synthesizes recent international evidence to examine the effectiveness of early identification strategies and therapeutic interventions designed to improve maternal mental-health outcomes. Findings show that PPD prevalence remains consistently high worldwide, but rates are significantly elevated in Latin America, reflecting contextual stressors, socioeconomic disparities, and limited availability of specialized perinatal mental-health services. Screening tools such as the Edinburgh Postnatal Depression Scale (EPDS) and PHQ-9 continue to demonstrate robust psychometric performance, yet emerging models—especially repeated web-based assessments and digital phenotyping—offer enhanced sensitivity for identifying women at risk. Therapeutically, multidisciplinary collaborative care models consistently achieve the strongest clinical outcomes, followed by cognitive behavioral therapy (CBT) and blended in-person/digital approaches. Digital interventions, while highly scalable, show variable adherence depending on the level of clinician guidance. Analysis of risk factors underscores that psychosocial determinants—including prior depression or anxiety, low social support, economic stress, and sleep disturbance—are more influential in predicting PPD than obstetric complications alone. Overall, the review emphasizes the importance of comprehensive, culturally responsive, and system-integrated strategies that combine validated screening tools, psychological therapies, digital resources, and social-support interventions. Strengthening PPD care in Latin America will require expanding screening programs, improving continuity between obstetric and mental-health services, and investing in community-based and technological supports. These measures are essential to improve maternal well-being and long-term family health.

Sensorineural hearing loss remains a major global health challenge due to the limited regenerative capacity of the mammalian cochlea and the predominantly compensatory nature of current therapeutic options. In recent years, gene therapy has emerged as a promising strategy aimed at restoring auditory function by directly targeting the molecular and cellular mechanisms underlying cochlear dysfunction. This review analyzes and synthesizes contemporary advances in cochlear regeneration through gene-based interventions, including gene replacement, gene editing, transcription factor–mediated reprogramming, and RNA-based therapies. The evidence highlights that gene replacement approaches, particularly for monogenic forms of hearing loss with preserved cochlear architecture, currently demonstrate the most direct translational potential. Regenerative strategies focused on reactivating developmental pathways show encouraging structural and functional outcomes, although their long-term integration and stability remain critical challenges. Across all modalities, delivery platforms and administration routes emerge as decisive factors influencing efficacy, safety, and clinical feasibility. Functional auditory outcomes and translational readiness are increasingly emphasized as essential benchmarks for therapeutic relevance. This review also underscores the importance of international collaboration and the inclusion of research and healthcare contexts from Mexico, Colombia, and Ecuador to support equitable translation and implementation. Collectively, the findings position cochlear gene therapy as a rapidly evolving and clinically relevant field, with realistic prospects for biological hearing restoration contingent upon continued interdisciplinary and global efforts.

El trastorno del espectro autista (TEA) es una condición neurodesarrollamental compleja que presenta desafíos significativos en la comunicación, la interacción social y los comportamientos repetitivos. Este artículo de revisión narrativa aborda las intervenciones terapéuticas actuales y emergentes para el manejo del TEA, proporcionando un análisis integral de los enfoques más relevantes. Entre las terapias tradicionales, se destacan las intervenciones conductuales, como el Análisis Conductual Aplicado (ACA), y los enfoques educativos estructurados, como el modelo TEACCH. Estas intervenciones han demostrado eficacia en mejorar habilidades sociales, comunicativas y adaptativas en personas con TEA. En los últimos años, han surgido estrategias innovadoras que buscan complementar los métodos convencionales. Entre ellas, se encuentran la terapia asistida por tecnología, como el uso de aplicaciones móviles y robots sociales, y terapias basadas en la neurociencia, como la estimulación transcraneal. Asimismo, se exploran enfoques centrados en la intervención temprana y personalizada, que consideran la heterogeneidad del TEA. Si bien estas intervenciones muestran resultados prometedores, el artículo subraya la necesidad de investigaciones adicionales para evaluar su eficacia a largo plazo y su aplicabilidad en diferentes contextos culturales. Finalmente, se enfatiza la importancia de un abordaje multidisciplinario que integre las necesidades específicas de cada individuo y su entorno familiar.