Key moments, in order
Sixty years of bench neuroscience, in every mammal studied, points to the same thing: conserved, homologous circuits are responsible for affective impulses.
When DSM-III came out, the push was to get things down to reliability and checklists, and emotions were felt to be beyond measuring.
Many patients get a label and a pill that kind of works: call it generalized anxiety disorder, give sertraline, and both sides put on blinders and pretend it is a categorical thing while the real problem goes undiscussed.
Severe personality pathology is often quiet: an internal struggle in people who are not manipulative or interpersonally problematic. Many patients have borderline-type struggles, such as trouble controlling anger, without ever overdosing or cutting, and still seek care.
The more activated the subcortical systems are during big feelings and strong arousal, the less active the cortical systems are, and the reverse is true.
The aim is not to change the primary feelings, the fear, grief or suffering. It is to build the capacity to observe them and not be forced to act on them.
A simple drawing of the brain helps: the midbrain is where affect and our ancestral emotional inheritance come from, and that information takes precedence as it moves up.
We do not plan feelings. They come and go, and there is not much control over their flow: you cannot just make yourself feel differently.
In an older patient with new depression or anxiety, the subcortical systems may be firing just as they always have (panic, grief, separation, rage, fear), but as the cortex recedes and loses neurons, the person can no longer modulate that affect properly.
Slow down and explain the process that is going on, rather than saying "you have depression" or "you have anxiety, that's why you feel bad now." It helps patients and it helps families understand.
Panic grief is the mammalian separation-distress system: being separated from a caregiver is supposed to feel bad so that you are motivated to reattach. It is one of the most important systems for psychiatry.
Humans have a great deal of capacity for reappraisal and modulation, and for acting on values held in the cortex rather than on ancient animal-brain impulses.
An otherwise highly functional person with an anger problem is better formulated as one thing causing bigger problems than it needs to, not as a whole broken personality.
One formulation: patients lack the cortical capacity to appraise and modulate intense affective arousal. People with severe BPD are pretty much fine until they are not.
Instead of "you have a personality disorder," offer it as one way to think about the problem, with the good news that calibration can change.
Mapping out your emotions, what happens when you have them and how long they last, is a useful group exercise.
There are four positive-valence systems (seeking, lust, care and play) and three negative-valence systems that animals have a strong aversion to.
Affect is the raw subcortical valence and arousal the midbrain sends up when these circuits fire. Emotion is what the rest of the brain makes of it.
For affective dysregulation, frame it as maybe 8 out of 10 anger instead of 10. If it means one less big fight with your partner a week, it might be a good medication for you.
Bring up emotional blunting early. Patients toward the borderline or more severe end feel things so intensely that they are prone to noticing and reporting it.
Make the patient the judge of the effect: you'll have to tell me whether this is helpful for you or not, and that will be different with every patient.
We are not there yet for decreasing the bottom-up drive. That seems to get set early, from early experiences.
Contacting the present moment through mindfulness is absolutely step one: without the ability to come to the present moment, you will not observe any information.
In medication visits, pair in ACT processes and skills, and be very clear that this is not therapy: the patient needs to engage in actual psychotherapy.
Change is growth, not deletion. Extinction is growing new inhibitory connections; we do not delete old memories, we grow new ones.
Most of the thoughts in your head are nonsense, 99% of them not true, almost like breathing. You have a little control to guide them in ways that calm things down.
Keep a high threshold for the label. When someone is not doing well on antidepressants, it is better to reformulate the patient and make sure the work on affect or personality is being done.
Ask: if this medication worked and everything changed, what would be different about your life, what would you do differently? If they cannot answer that well, futile prescribing has little use.
Bluntly telling someone they have a personality disorder can be the most invalidating thing you can do, and many patients will not engage with it.
One way to describe each affect is by four amounts: its level at rest, how strong it gets when activated, how long it takes to burn off, and how much stimulus sets it off.
Stimulating the cortex in awake surgery can make an arm move, but it never produces an emotional response.
TMS does not go deep enough to hit subcortical structures, but it speaks to the dynamic relationship between the cortex and the emotional systems, strengthening the top-down system.
Religion can work as a strong cortical module patients can send down to calm things. Whether it is true is irrelevant to that effect.
Research that ignores affective systems can miss the target. In the NK1 antagonist depression studies, rage was never mentioned once, nor what the animal brain science shows the NK1 system is for.
In a bucket as big as depression, a drug that works for a subgroup (say the 20 percent with major rage problems) washes out in trials. The NK1 antagonist studies in depression never once mentioned rage, or what the animal science says that system is for.
Each moment is a point made in the episode, linked to the second it was said. The topic links open everything the podcast has said on that topic.