Let’s use the scenario of giving a presentation in front of a large audience in order to observe our anxiety circuit in action. This is a very common source of “normal” anxiety and most of us can identify with this experience.
Imagine you are standing backstage and hear the rumble of your audience or see them taking their seats. This sensory information is relayed to your amygdala/Emoter, which triggers your heart to race courtesy of the brainstem. The sensory feedback from your now racing heart is then sent to your insula/Internal Sensor.
The amygdala/Emoter and insula/Internal Sensor merge into an anxious harmony, projecting their information forward to your mPFC/Emotional Sensor and ACC/Attender.
Your mPFC/Emotional Sensory and ACC/Attender act as a gate to conscious awareness, determining whether the information about your anxious state makes its way from your subconscious to your conscious mind.
The combined signals from the amygdala/Emoter and insula/Internal Sensor coupled with the severity of your anxiety force their way past the gate into your conscious awareness. If we were to look at an fMRI (imaging technique that shows active parts of the brain) at this point in our discussion we would see your mPFC/Emotional Sensor and ACC/Attender light up like a Christmas tree.
Now you have the full anxious experience. You are entertaining conscious thoughts of forgetting your speech, embarrassing yourself, or being unable to speak. Your mind spins itself into an incoherent storm of worry as your heart thunders within your chest.
But wait! Maybe instead of getting lost in your swirling thoughts, you are able to step back and view them more objectively. You may even take a couple deep mindful breaths and engage your Task-Positive Network. As your heart slows, you are able to challenge your maladaptive thoughts with evidence from past events.
“I have given successful presentations in the past and there is no reason to think this one will be different.”
“So what if I forget part of my presentation. I’ll just look at my notes and get back on track.”
The thoughts and supervisory control over your runaway anxious brain are made possibly by the lPFC/Director. The lPFC/Director uses detached cognitive appraisal to reassess the emotional brain’s anxious state. And once the situation is reframed in a more logical formulation, the lPFC/Director sends signals to the mPFC/Emotional Sensor and ACC/Attender to quiet the circuit.
The mPFC/Emotional Sensor and ACC/Attender acknowledge this order from the lPFC/Director and utilize their inhibitory connections to the amygdala/Emoter to decrease its activation. In essence the mPFC/Emotional Sensor and ACC/Attender tell the amygdala/Emoter that the higher brain structures have deemed the situation nonthreatening despite the primary signals the amygdala is receiving. And luckily for you, the amygdala/Emoter generally listens to the mPFC/Emotional Sensor and ACC/Attender.
Your heart slows, your worry subsides, and you step out onto the stage and give an excellent presentation.
This sequence of events had a happy ending, but what happens in the case of someone suffering from an anxiety disorder?
Patients suffering from a wide array of anxiety disorders demonstrate increased grey matter in the amygdala/Emoter. Grey matter refers to the neuronal cells that are responsible for electrical and chemical informational transmission in the brain. And if we remember from previous discussions the brain is like a muscle; the regions that are more active hypertrophy (grow bigger). The brain-muscle analogy is not quite perfect because the association between size and activity is relational and not necessarily causal. This means that a large amygdala/Emoter is not necessarily the result of bench-pressing anxiety in a stressful environment. It is more likely that certain individuals may just be predisposed to developing a larger and thus overactive amygdala/Emoter.
Interestingly, amygdala/Emoter size in childhood has been demonstrated to predict trait anxiety levels. And childhood anxiety has a demonstrable link to adult anxiety and mood disorders.
Another important insight for the purposes of our discussion is the fact that patients with anxiety disorders also show a consistent hyperactivation of the insula/Internal Sensor.
And finally, patients with anxiety disorders have decreased grey matter in the mPFC/Emotional Sensor and ACC/Attender.
So what does this all mean?
In your hypothetical presentation you were able to overcome your anxiety by engaging the lPFC/Director and using some basic mindfulness skills. However, in a patient with an anxiety disorder this may not be possible for a variety of reasons.
First, the anxiety alarm is quite a bit louder in patients with anxiety disorders. The amygdala/Emoter and insula/Internal Sensor are hyper-reactive to the sights and sounds of the audience, so our mPFC/Emotional Sensor and ACC/Attender get a much larger anxious jolt.
This increased dose of anxious substrate is delivered to a smaller than average mPFC/Emotional Sensor and ACC/Attender. And if we recall the inhibitory role of the mPFC/Emotional Sensor and ACC/Attender in tamping down amygdala/Emoter hyperactivation, we will realize the perfect storm that results from the neuroanatomy of patients with anxiety disorders. Not only is there more oomph to the anxiety, but also our neuroanatomy is less capable of getting the proverbial genie back in the bottle.
Interestingly, there has never been any evidence for decreased activity in the lPFC/Director in patients with anxiety disorders. This fact reminds us that even though the magnitude of our anxiety may be definitively larger, there is still hope of developing control over it.
I imagine the lPFC/Director as the levee that protects the rest of the brain from the storm surge of emotional content. The lPFC/Director is able to direct the wash of emotion downstream and avoid a breach that would flood our consciousness with panic. This analogy reveals that no matter how well constructed our lPFC/Director-levee is, a storm of a large enough magnitude is still capable of overrunning its embankment. It’s all a matter of magnitude.
Thus, an anxiety disorder can be conceptualized as a hyper-reactivity to the normal stresses inherent to our world. It is not a personal weakness or defect but more accurately resembles an overrun levee.
Cognitive behavioral therapy (CBT), mindfulness, medications, and many other treatments can help build up our emotional levee and allow us to deal with the inevitable surges of life.
CBT has been demonstrated to increase the ability of the lPFC/Director, mPFC/Emotional Sensor, and ACC/Attender to exert feedback inhibition on the hyperactive amygdala/Emoter and insula/Internal Sensor circuit.
Selective serotonin reuptake inhibitors (SSRIs) are a first line treatment in anxiety disorders. Their use has been shown to decrease activation of the amygdala/Emoter during anxiety producing situations (9).
And finally, mindfulness meditation activates the Task-Positive Network (TPN). The TPN includes the ACC/Attender and lPFC/Director and is engaged during present-moment awareness tasks. The positive effects of mindfulness meditation are hypothesized to be a result of increased control over amygdala/Emoter and insula/Internal Sensor hyper-reactivity. The cognitive control over these anxiety-generating regions of the brain is believed to be from an increased collaboration between the lPFC/Director, mPFC/Emotional Sensor, and ACC/Attender.
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