I Hate You--Don't Leave Me - Jerold J. Kreisman [88]
Neuroendocrinology
Other endocrine (hormone) neurotransmitters have been implicated in borderline pathology. NMDA (N-methyl-D-aspartate) dysregulation has been noted in BPD (as well as in some other illnesses) and implicated with dissociation, psychotic episodes, and impaired cognition.3 Disruptions in the body’s opioid (endorphin) system has been demonstrated in BPD and associated with dissociative experiences, pain insensitivity (particularly among self-mutilating individuals), and opiate abuse.4 Acetylcholine is another neurotransmitter affecting memory, attention, learning, mood, aggression, and sexual behavior, which has been linked to BPD.5
Chronic or repeated stress can also disrupt the neuroendocrine balance. Stress activates the hypothalamic-pitiutary-adrenal (HPA) axis, which secretes cortisol and activates the body’s immune system. In the usual acute stress situation, this system activates the “fight-flight” mechanisms of the body in a productive way. An internal feedback mechanism acts like a thermostat to then turn down the axis and return the body to equilibrium. However, ongoing stress dismantles the regenerative circuit and the stress alarms continue unabated, inflicting negative impact on the body, including shrinkage in characteristic areas of the brain. This pattern has been observed in several disorders, including BPD, PTSD, major depression, and certain anxiety disorders.
Neurological Dysfunction
Disturbances in brain function have been frequently associated with BPD. A significant subset of borderline patients have experienced a history of head trauma, encephalitis, epilepsy, learning disability, EEG (electroencephalogram, or brain wave) abnormalities, sleep pattern dysfunction, and abnormal, subtle neurologic “soft signs.”6,7
Sophisticated brain imaging—such as fMRI (functional magnetic resonance imaging), CT (computerized tomography), PET (positron emission tomography), and SPECT (single photon emission computed tomography)—has elucidated some of the anatomical and physiological deviations associated with BPD. As already noted (see chapter 3), these studies seem to imply overactivity of those parts of the brain involved with emotional response (the limbic system), which includes such deep brain structures as the amygdala, hippocampus, and cingulate gyrus, while demonstrating underactivity of the outer parts of the brain involved with executive thinking and control, such as the prefrontal cortex.8
Future Considerations
With these advances in genetics and neurobiology, scientists will eventually be able to subtype more discretely different presentations of pathology, and, based on this knowledge, doctors may be able to more precisely “customize” a particular drug to a particular patient. To use an analogy: Our current understanding of psychiatric illnesses is roughly similar to our understanding of infections in the early and mid-1900s, before doctors could adequately culture the infecting agent. At that time, it was generally acknowledged that all antibiotics were equally beneficial—penicillin was just as effective, among all patients with infections, as any other antibiotic. However, when scientists discovered how to culture individual strains of bacteria and establish their sensitivities to particular antibiotics, doctors could prescribe a specific drug with the greatest likelihood of success. In other words, doctors were not simply treating infection or pneumonia; they were treating the specific strain, staphylococcus aureus. Similarly, in the future, the hope is that we will be able to “culture” the psychiatric illness and determine the best treatment. We will be treating the individual’s unique biology, not simply the diagnosis. As a result, the concept of “off-label” (in which a medicine is prescribed for a condition not formally approved—see page 200) will become moot, since the