Some are suggesting that this study is some sort of groundbreaking work in understanding borderline personality disorder. While an interesting brain study, I’d suggest it tells us a lot less than the authors purport.
First, this is a classic laboratory study. And while laboratory studies of this nature are the foundation for later clinically-relevant studies, they are, by their very nature, limited in what they can test and how they test it. With limited testing ability (and re-test ability, accounting for different moods on different days, which this study did not do), results are not generalizable to a clinical population — e.g., people with this actual disorder.
Why is this a laboratory test? Because borderline personality disorder is first and foremost characterized by emotional lability, especially in interpersonal relationships. So would a word test with a computer be the best way to test such symptoms? Umm, I would humbly suggest, “No.”
Behavioral response was based on orthographically based cues: participants were instructed to perform a right-index-finger button-press immediately after (silently) reading a word appearing in normal font (go trial) and to inhibit this response after reading a word in italicized font (no-go trial). Button-press responses and reaction times were recorded. A total of 192 distinct linguistic stimuli were used (64 negative, 64 positive, 64 neutral). Words were balanced across all valence conditions for frequency, word length, part of speech, and imageability.
As far as I can figure, that’s not a test based upon any kind of real-world stimuli or interactions. It’s a behavioral word test. And while some of the words may have been designed to elicit an emotional response, a single word really can’t be seriously used as a stand-in for one’s emotional response to a situation with someone you care about.
Sample size? Paltry: 16 patients with borderline personality disorder and 14 “normal” people who had no borderline diagnosis. 11 of the 16 were on medications at the time of the trial, suggesting they should already be receiving some sort of therapeutic benefits from the medications (and therefore the researchers results may be hopelessly confounded; alternatively, the medications they were receiving had no effect on their borderline personality disorder — neither hypothesis strikes me as boding particularly well).
But the study is a good one for what it shows: while performing a simple cognitive task, people with borderline personality disorder had less activation of the subgenual anterior cingulate cortex (a specific area of the brain which is theorized to help modulate our emotions). Surprise, surprise — the brain area thought to regulate emotions shows “less activation” in someone who has problems regulating his or her emotions.
The real challenge in terms of overstating this study’s results comes with the accompanying editorial by Siegle, which is just glowing in its admiration for the study. It also nicely illustrates what’s wrong with a peer-review process that publishes self-congratulatory editorials, too.
These future directions notwithstanding, with the data from just this study, we can begin to infer that when individuals with borderline personality disorder display decreased impulse control, this loss of impulse control may reflect a deficit in recruitment of brain mechanisms of emotion regulation, and this process may be potentiated by context. Particularly stressful or negative contexts could lead to more impaired impulse control.
An implication for psychotherapy process might be that it is important to address contextual factors when considering impulse control in borderline personality disorder.
Anybody who has spent any significant amount of time helping to treat people with borderline personality disorder already knows that context and stress are important factors when it comes to understanding emotional lability. Nobody needed an fMRI study to confirm this fact. In fact, we have very successful treatment paradigms and therapies for borderline personality disorder, fMRIs notwithstanding (e.g., DBT, which has a significant research base). Heck, any first-year student in psychology knows that “context” and “stress” are likely to lead to greater flare-ups of a person’s disorder, whether it be borderline, depression or bipolar disorder.
But this is the closing zinger in the editorial that we enjoyed most:
In the past, basic neuroimaging findings have often remained separate from clinical practice. But with designs such as that used by Silbersweig et al., which so closely reflects the observed clinical phenomena, and results that appear so closely aligned with clinical studies, it is increasingly easy to recommend that clinicians read this study carefully and begin to apply its lessons, ideally to better design and monitor cognitive and pharmacological treatments by addressing the underlying neurobiology of borderline personality disorder.
Well, let’s see (trying my best to ignore the tortuous grammar)… This design had virtually nothing to do with someone who experiences this disorder’s reality (button pressing in response to a computer word versus emotional lability in relationships). We already have a well-established psychotherapy that has significant and strong research to prove its effectiveness for borderline personality disorder (DBT). We have no FDA-approved medications for borderline. You’ve got to wonder which direction he was suggesting we go there, no?
Perhaps we would do well to first really understand the “underlying neurobiology” of the brain itself before we start tackling the disorders associated with it, too, while we’re at it.
Silbersweig, D. et. al . (2007). Failure of Frontolimbic Inhibitory Function in the Context of Negative Emotion in Borderline Personality Disorder. Am J Psychiatry 164:1832-1841.
Siegle, G.J. (2007). Brain Mechanisms of Borderline Personality Disorder at the Intersection of Cognition, Emotion, and the Clinic. Am J Psychiatry 164:1776-1779.