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Painted Brain | Neuroscience Of Borderline Personality Disorder
We're bridging communities and changing the conversation about mental illness using arts and media.
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  • April 19, 2015

Neuroscience of Borderline Personality Disorder

Lately I’ve been hearing that BPD isn’t a real mental illness because nothing is actually wrong with our brains and so, naturally, that means we’re using BPD as an excuse for our mood instability and impulsive behavior.

Guess what, naysayers? You were COMPLETELY right and totally called us out on our nefarious scheme! We all convened at a super-secret BPD convention and plotted to infiltrate the psychiatric field.

Just joking. Afraid not.

With the help of @alix660 and @porcelaindissonance I’ve learned a lot about the neuroscience behind BPD. And, while much more needs to be done in terms of BPD research, I did find strong evidence that BPD has biological causes. You know, just like a real mental illness.

So here’s what we found, sorted by brain structure:

Amygdala: This brain structure is very heavily involved in emotional regulation and responses, particularly negative emotions. An fMRI study of BPD patients while being subjected to distressing visual stimuli found that the amydala is significantly more reactive in BPD patients than in control patients. This means that either the signals in our amgydala is more intense, or the neurons in ours continue to fire, preventing us from shutting down our emotional responses.

Let’s call it both, that’s more fun.

Another thing to note is that the amygdala receives tons of visual information, sent by the thalamus. The thalamus circumvents emotional processing in the prefrontal cortex (where we would consciously process how to regulate our emotions) and thus is involved in automatic, subconscious emotional processing. This is probably why our mood swings are so fast, unpredictable, and uncontrollable. It’s a knee-jerk reaction to even the tiniest triggers we come across. (Herpetz, et al.)

Amygdala volume is significantly reduced in BPD patients as well. (van Elst, et al.)

Hippocampus: This structure is involved in formation and retention of long-term memories, as well as autobiographical memories. Not only is hippocampal volume reduced in PTSD and MDD, but also in patients with BPD. (van Elst, et al.)

I know from my studies that the reason for hippocampal volume reduction in PTSD and MDD comes from prolonged activation of the stress response. When we go into “fight or flight” mode, several physiological changes take place: our immune system shuts down, digestion stops, etc., but most importantly, when we enter “fight or flight,” glucose, which is necessary for cell metabolism, is redirected from the hippocampus to the muscles. If you’re faced by a life-challenging event, like a pack of velociraptors, you don’t want to think about it. You want to run, and you want to run fast. This is biologically adaptive in the short-term and in prey species, but not so with humans, because we can have this same reaction to long-term, non-threatening stressors. So in long-term distress—like MDD, PTSD, and BPD—our hippocampus is starved for energy and starts to atrophy. Result? We have absolutely terrible memory.

Prefrontal cortex: This is where we do our conscious thinking. More specifically, the medial prefrontal cortex, which is involved in processing emotional memories, is more active in the BPD brain. Essentially, this means we have difficulty mediating our conscious emotional responses.

In the ventrolateral prefrontal cortex, BPD brains show abnormally high reactivity to aversive stimuli. This part of the cortex is directly-connected to our good friend, the amygdala, and thus has some level of control over emotion-driven responses. (Herpetz, et al.)

In the anterior cingulate cortex, which is involved in feelings of apathy and emptiness, we see a significant reduction in volume in the BPD brain. The ACC is linked to self-harm and pain sensation (van Elst, et al.).
In the orbitofrontal cortex, we also see volume reduction in BPD. The OFC is responsible for irritability, impulsivity, and instability, which are our favorite things.

Fusiform gyrus: Found in the temporal lobe, the fusiform gyrus is the facial recognition center of the brain. And—you guessed it—it’s also shown to be hyperactive in the BPD brain. Which makes sense when you think about it: we are EXTREMELY sensitive to even the slightest changes in the facial expressions of other people. If you appear disinterested, annoyed, angry, or otherwise upset, that’s an immediate trigger. (Herpetz, et al.)

Taken together, this means that the limbic circuits (emotional regulation) and the prefrontal cortex (executive control) are uniquely involved in BPD, resulting in a hyperarousal-dyscontrol syndrome. As of right now, no other psychiatric illness has this combination of reduced brain structure volumes and hyperactivity in certain regions. (van Elst, et al.)


Serotonin: Most of us know serotonin as a crucial neurotransmitter involved in major depressive disorder. But in BPD, studies show that reduced serotonin activity is found in several locations in the brain, including the cingulate cortex, which is critical in processing incoming emotional cues. Reduced serotonin impairs inhibition of aggressive behaviors, both directed at others (like outbursts) and directed at the self (like self-harm and self-hatred). Genes involved in serotonin can easily be studied. (Skodol, et al.)


Skodol, et al. “The Borderline Diagnosis II: Biology, Genetics, and Clinical Course”

Herpetz, et al. “Evidence of Abnormal Amygdala Functioning in Borderline Personality Disorder: A Functional MRI Study”

van Elst, et al. “Frontolimbic Brain Abnormalities in Patients with Borderline Personality Disorder: A Volumetric Magnetic Resonance Imaging Study”
Tequila Mockingbird is an undercover correspondent for Painted Brain News and a member of UCLA’s Active Minds program.

for more information about UCLA’s Active Minds program, here’s the link to their Facebook page:

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