Borderline Personality Disorder (BPD) is often associated with impulsive behavior including substance abuse and suicide. There is little research, however, investigating the neurological mechanisms which define the behavior. The functioning of the Orbital Pre-frontal Cortex (OFC) has been shown to play a role in regulating impulsive behavior. This literature review looks in depth into the role that the OFC could possibly play in regulating impulsivity within BPD.
Of the many symptoms that accompany people afflicted with Borderline Personality Disorder (BPD), impulsive behavior is often thought to have to most serious implications. Behaviors such as binge spending, reckless driving, suicide, self-injuries, and substance abuse are often seen in people diagnosed with the disorder and can lead to severe consequences such as societal punitive restrictions or even death. Impulsivity in general, however, has not been widely researched in relation to its underlying neurological mechanisms. The Orbital Pre-frontal Cortex (OFC) has been shown to be linked to impulsive behavior and there is evidence which suggests that the OFC plays a vital role in moderating impulsive behavior in the context of BPD.
In a study done by Grafman, Schwab, Warden, & Pridegen (1996), 279 Vietnam War veterans who had suffered only frontal lobe damage were compared to a control group of men with no brain damage on measures of aggression and violence. The results reported that men with damage to the frontal lobe were much more likely to engage in aggression and/or violence than men who had suffered no brain damage. Men who scored higher on aggression and violence also had a high correlation of family problems which indicates the presence of interpersonal dysfunction and could be a consequence of their reactive aggression, or impulsivity, as seen in BPD. This would suggest that the pre-frontal cortex might be singularly responsible for moderating impulsive behavior.
Another study was conducted in 2007 also emphasized the singular role of the prefrontal cortex in regulating impulsive behavior but within the context of BPD (Chanen, Velakoulis, Carison, Gaunson, Wood, Pan Yuen, Yucel, Jackson, McGorry, & Pantelis). Twenty Australian teenagers who had been recently diagnosed with BPD were brought into a hospital and scanned with Magnetic Resonance Imaging (MRI). All the BPD patients were clinically diagnosed and eleven were also were diagnosed with conduct disorder or some sort of drug dependence. The volumetric size of the OFC, hippocampus, and amygdala were then analyzed using tracing techniques. It was found that, when compared to a group of normal controls, the size of the hippocampus and the amygdala were relatively the same. The size of the OFC, however, varied greatly. The borderline patients had much less gray matter in the left hemisphere than the normal controls. It is suggested that due to this finding, the disorder originates in the prefrontal cortex and therefore is mainly manipulated by the OFC and not the amygdala or the hippocampus. The dysfunction of the latter, the authors suggest, could possibly occur as a result of prolonged malfunction of the OFC. These results suggest that the OFC is the primary moderator of impulsivity in people with BPD.
In fact, there is also medicinal evidence to support the claim that the OFC could be singularly regulating impulsive behavior in BPD patients. In a study conducted by New, Buchsbaum, Hazlett, Goodman, Koenigsberg, Lo, Iskander, Newmark, Brand, O’Flynn, & Siever (2004), Fluoxetine was administered to patients diagnosed with impulsive aggressive BPD. The patients were then given anatomical MRIs and PET scans to analyze metabolic rate. Since frontal cortex hypometabolism had been shown in impulsive aggressive BPD patients, Fluoxetine, which blocks reuptake of serotonin and creates a higher metabolism rate, was administered to see if raising the metabolic rate would have an effect on the level of impulsive aggression. Results showed that areas in the OFC showed significant increases in their metabolic rate and resulted in reduced aggression in the participants. These findings suggest that, along with the effectiveness of Fluoxetine in reducing impulsive aggression, the orbital pre-frontal cortex primarily moderates BPD impulsive behavior.
Some evidence suggests, however, that the amygdala, along with the OFC, is responsible for impulsive behavior. Baxter, Parker, Lindner, Izquierdo, & Murray (2000) conducted a study of Rhesus monkeys which investigated the possible relationship between the OFC and the amygdala. The monkeys had the contralesional connection between the amygdala and the OFC disconnected. They then trained the monkeys on a food selection device which required the monkeys to choose between cues for two foods; one of which had been intrinsically devalued by prior satiation. Results indicated that monkeys who had had their amygdala-OFC connections fully cut were not able to avoid cues for foods which no longer had intrinsic value. They still selected cues for foods at random as opposed to the control monkeys who actively avoided the cues for food which had been devalued. This argues a perspective that states that it was not the OFC or the amygdala by itself which regulates impulsivity but the connection between the two that determines informed decision-making.
In a 2007 article New, Hazlett, Buchsbaum, Goodman, Mitelman, Newmark, Trisdorfer, Haznedar, Koenigsberg, Flory, & Siever conducted another study examining the neurological functioning of impulsive aggressive BPD patients. Results from MRIs and PET scans suggested that there is a high rate of metabolic activity between the OFC and the amygdala in normal patients. However, patients with BPD showed weak connections between the amygdala and the OFC. This would suggest that the disconnection is responsible for the alterations in impulsive behavior in those with BPD and provide evidence toward the amygdala-OFC connection as its ultimate moderator.
To conclude, given the results of these studies, it would be safe to assume that the OFC plays a major part in moderating impulsive behavior which remains an area of big concern to those afflicted with BPD. It remains unclear, however, whether or not the OFC is working by itself or in conjunction with other areas of the brain, specifically the amygdala. Further research could examine the relation between the OFC and the amygdala and possibly the role of the amygdala on its own with regards to impulsivity and possibly compare BPD patients to people with brain damage causing impulsivity. In addition, while some form of long term treatment for BPD may be preferential to reduce impulsive behavior, a short term medication arising from a further neurological understanding of impulsivity within BPD might be a great help in alleviating the immediate consequences.
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