Borderline personality disorder (BPD) is defined by a persistent pattern of instability in interpersonal relationships, identity, impulsivity, and affect, according to the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV). BPD is a serious psychiatric condition that affects 0.5% to 5.9% of people in the US. Impulsivity, non-suicidal self-injury, anxiety, substance abuse, significant functional impairment, and other personality disorders are among the high-risk behaviors it is linked to. Although there isn't one identifiable cause, there are known risk factors related to the environment, anatomy, function, genetics, and epigenetics. With direct visualization of brain structures and function using neuroimaging, it is possible to investigate the multidimensional structure of BPD that consists of disturbed relatedness, behavioral dysregulation, and affective dysregulation.
Borderline personality disorder is associated with an impaired and hyperactive limbic system, the emotional center where trauma, mental illness, and neural circuitry converge. It pertains to the amygdala, insula, posterior cingulate cortex, hippocampus, anterior cingulate cortex, and prefrontal regulatory regions of the brain, which are involved in emotional processing. The orbital frontal cortex, the dorsolateral prefrontal cortex, and the ventral lateral prefrontal cortex are also included. The amygdala is the primitive part of the brain regulating fear and aggression and in the general population, it is a vital tool for survival. The amygdala is considerably smaller in people with BPD, which causes overactivity and emotionally intense experiences. The hippocampus, the body's data processor, is linked to emotional responses. In BPD, it’s in a constant state of hyperarousal, with observable dysfunction and incoordination. The hippocampus consistently misinterprets threats and sends false signals to the amygdala, creating the impression that the world is threatening. The prefrontal cortex, which controls reason, rationality, and decision-making, is inactive and ineffective in BPD, which explains symptoms like impulsivity.
When employing cognitive strategy to regulate reactions to unpleasant stimuli, patients with BPD do not engage the cognitive control areas to the same degree that healthy individuals do. In comparison to controls, patients' superior temporal sulcus and superior frontal gyri showed more activation and fewer blood-oxygen-level dependent signal alterations.
Changes in frontal glucose metabolism in BPD and reported hypometabolism supports the concept of a frontolimbic dysfunction and anomalies in those networks. The default mode, the salience network, and the medial temporal lobe network are the most prominent in BPD. When the brain is at rest and not engaged in goal-directed activity, the default network is activated. It controls self-referential thought and is controlled by the medial prefrontal cortex and posterior cingulate cortex. The orbital frontal insula and dorsal anterior cingulate cortex are parts of the salience network, and the medial temporal lobe network is in charge of processing unpleasant emotions. The intensity of symptoms like affective instability, avoidance of abandonment, and anger is related to frontolimbic connection deficits. In BPD, changes to these networks result in problematic connectivity between salience detection and self-referential encoding, leading to misidentification with neutral stimuli and a failure to integrate salience information.
Another crucial network is the hypothalamic-pituitary-adrenal axis, which is made up of the interconnected glands of the pituitary, the adrenal, and the hypothalamus. These glands are all in charge of producing the hormone cortisol, which is released naturally in response to stress. Patients with BPD have excessive cortisol levels in their blood, which makes daily life constantly overwhelming.
Symptoms of BPD are categorized into 4 phenotypes or sectors, each with varied degrees of severity: affective, interpersonal, cognitive, and behavioral. The affective or emotional sector comprises difficult emotions such as emptiness, loneliness, inappropriate and excessive anger, and quick fluctuations in mood. The interpersonal sector encompasses a patient's propensity for intense and volatile relationships or to be both reliant, idealizing, and afraid of abandonment as well as manipulative, entitled, and devaluing. The cognitive sector includes distressing perceptual distortions like dissociation and paranoia whereas dangerous, impulsive behaviors such as self-harm are behavioral sector symptoms. Each sector's phenotypic manifestation is a reflection of possible genetic predisposition
Anxiety, sadness, and suicidal thoughts have been linked to a gene that encodes a particular tryptophan hydroxylase 2 (TPH2) isoform, according to studies on molecular genetics. Aggressive outbursts and suicidal thoughts were more frequent in those at TPH2 risk. This neuron-specific enzyme generates 5-hydroxytryptamine (5-HT), a rate-limiting enzyme in serotonin production. Variants of the serotonin receptor genes 5HT2A and 5HTR2C, which are associated with borderline symptoms and BPD, are correlated with suicide, affective lability, and impuslive control. Patients might be more susceptible to 5HTR2C, which might contribute to the pathogenesis of BPD.
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