6th Edition of Neurology World Conference 2026

Speakers - NWC 2026

Ana Júlia Melo Safe, Neurology World Conference,Miami,USA

Ana Julia Melo Safe

Ana Julia Melo Safe

  • Designation: Centro Universitário do Planalto Central Apparecido dos Santos
  • Country: Brazil
  • Title: Frontolimbic Circuit Dysregulation and Psychiatric Manifestations in Borderline Personality Disorder

Abstract

Borderline Personality Disorder (BPD) is a severe and complex psychiatric condition characterized by emotional instability, impulsivity, disturbed interpersonal relationships, and identity diffusion. Increasing evidence suggests that these clinical features are strongly associated with dysfunctions in frontolimbic neural circuits, which are critical for emotional regulation, impulse control, and social cognition. This abstract reviews and synthesizes current neurobiological findings linking frontolimbic circuit dysregulation to the psychiatric manifestations observed in BPD, highlighting implications for diagnosis and treatment.

Neuroimaging studies consistently demonstrate structural and functional abnormalities within key components of the frontolimbic network, including the prefrontal cortex (PFC), anterior cingulate cortex (ACC), amygdala, hippocampus, and insula. Patients with BPD frequently exhibit reduced gray matter volume and altered activation patterns in the ventromedial and dorsolateral PFC, regions essential for top-down modulation of emotional responses. Concurrently, hyperreactivity of the amygdala in response to emotional and interpersonal stimuli has been repeatedly observed, suggesting impaired inhibitory control by prefrontal regions over limbic structures.

Functional connectivity analyses further reveal disrupted communication between frontal regulatory regions and limbic areas, contributing to heightened emotional sensitivity, affective lability, and maladaptive behavioral responses. Dysregulation within the ACC and insula appears to play a central role in altered salience processing and impaired integration of emotional and cognitive information, potentially explaining the rapid shifts in mood and perception commonly reported in BPD. Additionally, hippocampal abnormalities, possibly related to early life stress and trauma, may underlie memory disturbances and heightened stress reactivity.

From a neurochemical perspective, alterations in serotonergic, dopaminergic, and glutamatergic systems within frontolimbic circuits have been implicated in impulsivity, aggression, and affective instability. These neurobiological findings align with observed

clinical symptoms and support dimensional models of psychopathology that conceptualize BPD as a disorder of neural circuit dysfunction rather than a purely behavioral syndrome.

In conclusion, converging evidence supports the central role of frontolimbic circuit dysfunction in the pathophysiology of BPD. Integrating neurobiological insights with clinical practice may improve our understanding of symptom heterogeneity and advance personalized treatment strategies for this challenging disorder.