The following discussion is adapted from LeDoux (1996), who reported that there are two separate brain paths that link to the amygdala. When we perceive a possible threat, the brain’s switchboard (the thalamus) divides the signal in two and sends it along two different paths, both of which lead independently to the amygdala. One route goes directly to the amygdala, which immediately triggers the “fight, flight, or freeze” alarm. We become frightened and aroused, ready to defend ourselves, get out of the way, or freeze in place. This path is direct, but also fast and foggy. The amygdala gets only the gist of the signal and sounds an alarm whenever the possibility of danger exists. Better to over-react and turn off false alarms later, than to under-react and get blindsided by an actual threat.
Figure 3.1 illustrates that a signal going along the “direct” route triggers the amygdala very quickly. So quickly, in fact, that the body takes action before the brain realizes what is going on. Reactions are in the service of survival, they originate in primitive brain areas, and they are unconscious and outside of our control.
Figure 3.1 Two routes to the amygdala.
But there is also a second path, a higher route: the second part of the signal takes a longer path past the more primitive brain and up to the cortex—this is the part of the brain that controls rational thought—where it determines whether an actual danger exists. This second signal arrives at the amygdala after making rounds of the cortex— about a half second later than the first. Modified by information provided by the cortex, this slower and wiser signal has the capacity to stop the amygdala from continuing to issue alarms, although it cannot interrupt the initial alarm which has already fired before full information got there.
Here is a simple example to see the process at work: there is a loud sound, whose signal is sent on to the amygdala via two pathways. Via the quick route, the amygdala reacts to the sound by triggering an immediate rush of fear. About half a second later, the other part of the signal arrives after having been processed by the cortex. The cortex has determined that the loud sound is a pot crashing down and that no danger exists. (It could have very well been a gunshot.) Based on that information the cortex communicates that a false alarm was sounded, the amygdala stops sending out its arousal signal, and, after some
Patients become frightened before there is any conscious assessment of danger.
time passes, the physiological effects of the original alarm subside and stop. Calming happens on its own, naturally.1
Think of a friend surprising you in your home and yelling “BOO!” when you thought you were alone. You get a jolt of fear and then realize it is harmless, even though your body might need a few minutes to calm down completely. This is the process at work.
There are two essential points here. The first is that patients become frightened before there is any conscious assessment of danger. Their initial fear reaction is primitive and unconscious. It precedes their conscious mind, and is not yet connected to the part of their brain that controls conscious thoughts. That is why patients are unable to use willpower to stop this initial rush of anxious arousal. The fear develops before there is any chance to intervene and gets there before the will. This first fear cannot be intentionally suppressed. This should be repeated to patients. It speaks to differentiating what the patient can control from what is outside of his control, what is automatic and what is not, and focusing psychic energy where it is most helpful. The second point is that the cortex is capable of affecting subsequent reactions of the amygdala, depending on whether or not it determines that a danger exists. Fear continues to spiral when the cortex interprets signals as dangerous, and this is important indeed, since it frames the neurological basis of anxiety disorders. In Chapter 4 we discuss how these neurological facts affect clinical work.
The first fear is automatic and unstoppable, and goes away quickly if it is left alone.
First and Second Fear
Now let’s take this process one step further: when the cortex interprets the first fear arousal—not the original trigger, but the arousal itself—as dangerous, then the cortex tells the amygdala that danger does indeed exist, and to continue sending out alarms. This is a neurological description of anxiety sensitivity, or fear of fear. The original alarm signal arousal (first fear) is perceived as dangerous, which engenders additional arousal (second fear), and so starts the anxiety cycle.
A signal initially reaches the amygdala through the fast and foggy route, triggering a fearful whoosh. This whoosh occurs prior to any conscious awareness, and is the neurological representation of sensitization. This first fear is automatic, unstoppable, and goes away quite quickly if left alone. Up until this point there is no involvement of the cortex. Figure 3.2 illustrates the production of this first fear.
Terror caused by anxiety feels the same as terror caused by legitimately dangerous situations.
First fear has been triggered, and the patient is experiencing a whoosh of distress.
The patient must now label their terror either as “anxiety” or “danger,” because each of these is handled differently. However, terror caused by anxiety feels the same as terror caused by legitimately dangerous situations—the physiological reactions and bodily
Labeling terror as anxiety constitutes a leap of faith.
sensations are the same. To accurately label their arousal as anxiety, patients must learn to say something like, “My terror is an aspect of my anxiety, and not because I’m in danger.” Labeling terror as anxiety constitutes a leap of faith.
Figure 3.2 First fear is triggered.
Figure 3.3 The labeling decision.
Whoosh and the Decision Process
Since people with anxiety disorders are sensitized to certain triggers, they experience a characteristic whoosh of arousal. It can be represented as illustrated in Figure 3.3.
Creation of Second Fear
For someone with panic disorder, the whoosh of first fear is usually a sensitized reaction to a feared sensation. This reaction is followed by the person thinking, “Oh no! What if I am starting to faint?” Then this thought—originating in the cortex—sends a signal to the amygdala to continue sounding the arousal alarm, creating more intense arousal. And when the person with panic disorder experiences additional fear symptoms, he might say to himself, “Oh no! Something terrible is really happening, my heart is starting to race, maybe I am having a heart attack?” Or, “Oh, No! What if I’m starting to freak out?” Or, “Oh, no! What if something dangerous is happening? What if I’m going to hurt myself? What if I’m going to hurt someone else? What if I am dying? What if I make a fool of myself? What if these feelings destroy me?” A panic attack is well on its way.
This process is illustrated in Figure 3.4.
Figure 3.4 Second fear labeled danger.
In the case where intrusive scary thoughts or images begin the process, (for example in OCD) there is a similar whoosh of first fear. In this case, however, it is the sensitized reaction to the feared thought that sets off the alarm system of the amygdala, triggering the fearful reaction, which then is interpreted by the cortex as evidence of danger. This begins the same frightening self-reinforcing feedback cycle. The pathway from scary thought to arousal by the amygdala is a lightning-fast well-conditioned pathway. This is why OCD and GAD thoughts are experienced differently from regular thoughts. They have a distinctive “jolt” or “spike” or whoosh that is attached to them. Typical second fears in OCD and GAD are “What if I am about to do something terrible?”, “What if this means I am a bad person?”, “What if this is a warning that someone is in danger?”, “Why can’t I be certain about this important thing?” Patients can readily identify such experiences when pointed out. This is explored more fully in Chapter 10 (Unwanted intrusive thoughts).
The patient with SAD might have an initial whoosh of fear quite similar to the person with panic disorder, although the thoughts and images that escalate the process (the second fear) usually focus on the possibilities of looking foolish, do
ing something embarrassing, appearing anxious, and that others will think negatively of him. Sensitivity to the emotions of shame and embarrassment keep these patients trying to suppress or avoid these feelings, which intensifies them and results in additional “What if I make a fool of myself?” messages from the cortex. At the same time, the physiological aspects of arousal might cloud their thinking, redden their faces, and make their limbs and voices tremble.
Frightening memories frequently add to second fear, since fear memories are stored in the amygdala, are retrieved quickly, and don’t require conscious thoughts to be triggered (Clark, 2011). This is one reason why exposure is essential to help the amygdala learn through direct experience that no danger exists.
Management of Second Fear
In contrast to first fear, second fear is amenable to conscious and intentional intervention; it can be reduced or eliminated by retraining the cortex to stop retriggering the amygdala. Figure 3.5 shows what happens when anxious arousal is correctly labeled as anxiety.
Neurologists say that circuits that fire together wire together. The brains of highly anxious patients have become wired to keep them anxious; the goal is to help them “rewire” their brain to reduce this connection. The goal is to allow realistic information from the cortex to stop the continual arousal of the amygdala, allowing the natural calming process to become ingrained.
Second fear is amenable to intentional interventions. It can be reduced or eliminated by retraining the cortex.
The Value of Exposure
The active ingredient for making these changes is exposure to anxious feelings. But this exposure must be done the right way. The right way means exposure that creates a manageable level of anxiety, but is not overwhelming; it allows for very little avoidance, and encourages the patient to practice new methods of managing the anxiety that arises. And, the right way means staying with these feelings long enough for new pathways to form that overlay the old. Two important changes occur: first, the brain learns new responses to formerly fearful triggers, so there is less reactivity to anxious arousal, and, second, it becomes used to accessing these newly learned patterns, so that the new reaction becomes the default one. A more comprehensive explanation of how this happens is discussed in Chapter 8.
However, it is worthwhile to note that fear circuitry is never really “unlearned,” and the modern conception of recovery is learning a new set of non-fearful experiences that can inhibit and override older fearful reactions. This means that old reactions can be retriggered under certain circumstances, and anxiety can return. Proper relapse prevention addresses this phenomenon.
Figure 3.5 Second fear labeled anxiety.
The Fear-maintaining Cycle
The fear-maintaining cycle (Figure 3.6) demonstrates how the misinterpretations of sensations, thoughts, or memories create a vicious cycle that maintains overwhelming anxiety. Highly anxious people have consistent tendencies, including a tendency to catastrophize and focus on worst-case outcomes. Among a thousand possible outcomes in a situation—the vast majority of them benign—they will spend an extraordinarily high percentage of their time and mental energy imagining an encounter with the one or two outcomes that are disastrous. So, for example, a sore throat brings up thoughts of cancer, light-headedness indicates a brain tumor. If prescribed a medication, the focus is on the possibility of getting one of the worst and most serious side effects. It is more the tendency to focus on what can go wrong (even if highly unlikely) than to consider any of the many possibilities of things going right. Anxious people are also sensitized to these “what if” catastrophic thoughts. There is a real, measurable, physiological arousal to them and these thoughts crowd out others as well. They feel sticky and are difficult to chase away.
The diagram is a circle because the anxiety-producing process repeats itself, maintains itself, and reinforces itself as attempts are made to evade, avoid, suppress, and push back against the feelings of anxious arousal. Let’s start with the example of someone who has panic disorder: A patient feels sensations in his chest. If he misinterprets these sensations as indications that something is wrong, as opposed to automatic and uncontrollable— but harmless—arousal from his amygdala, he understandably becomes frightened. His attempt to avoid the arousal makes him focus even more on it. The fear and the arousal associated with it creates a new set of even more intense sensations. If once again these sensations are misinterpreted as verification that something is, indeed, very wrong, he would feel even greater fear. The cycle continues, his sensations and fear levels increase, and the result is often a full-blown panic attack.
Figure 3.6 Fear maintaining cycle.
A similar process goes on for people with other anxiety disorders. For a person with OCD, we can start with a thought that triggers anxious arousal, such as “what if I touched something contaminated?” The arousal that follows the thought makes the thought feel like it might very well be true, as opposed to the automatic, unconscious, and terrifying—but harmless—arousal from the amygdala. So the patient tries to reassure himself that this hasn’t happened, perhaps by playing back his memories of what he touched, or deciding that his hands need to be washed ASAP. But this attempt at reassurance brings the triggering thought squarely back into focus.
Notice the box labeled “Misinterpretation as Dangerous” because it includes the “what if” thinking that triggers the second fear. This is where we say to ourselves things like, “What if I am having a heart attack?”, “What if I lose control?”, “What if I sent obscene emails to my coworker?”, “What if I act on my ‘bad’ thoughts?”, “What if I start blushing when I speak to the girl and everyone thinks I’m weird and a loser?”, “What if I lose my mind and go crazy forever?”, “What if I caught AIDS when I touched that red spot?”, “What if I embarrass myself?”, “What if I begin to panic in the middle of the bridge?” There is a huge range of “what if” catastrophic thoughts that our patients are capable of creating, the range of catastrophes limited only by the creativity of their imagination.
Avoidance, Resistance, Neutralization
Avoidance plays an essential role in maintaining, reinforcing, and empowering the full spectrum of anxiety symptoms, from anxious arousal, to abhorred and frightening thoughts, to terrifying memories. The best definition of avoidance is a very general one, and includes whatever patients do to flee the experience of anxiety. It includes actively avoiding experiences that might cause anxiety and cognitive attempts to avoid the experience of anxiety while in the situation. We therefore include outright avoidance and a variety of mini-avoidances, rituals, superstitions, and mental reassurances—even as subtle as telling oneself that it won’t be that bad (which are sometimes called neutralizations)—or imagining who can help if things get out of hand, or having an escape plan for a social situation. In short, anything other than allowing anxious thoughts and feelings to continue unabated while focusing on the task on hand is considered an avoidance, and ultimately counter-therapeutic.
Avoidance plays an essential role in maintaining, reinforcing, and empowering the full spectrum of anxiety symptoms.
The Phenomenology of Anxiety: Anxiety Alters Consciousness
Anxiety produces an altered state of consciousness that tells patients they are in danger when they are safe. Usually, thinking is a safe way to imagine possible scenarios and their consequences. But as anxiety increases, thoughts become increasingly frightening. They don’t feel so much as trying things out—they feel more like living them out. Sensitization makes merely thinking about something feel frightening and dangerous. Trying to avoid thinking these frightening thoughts makes them more persistent, and the distinction between thoughts and actions starts to blur. When very anxious, thinking about something can feel as scary as it happening. Approaching panic, thoughts feel outright dangerous. They feel like facts. This is anxious thinking, and it is the altered state of consciousness that many patients will experience. Let’s take a look at these alterations in some detail, and point o
ut how they make exposure to anxiety-producing triggers more difficult.
It is important to note that overwhelming anxiety can make a person appear—and feel—like they are quite crazy. It is the altered state of consciousness that is the culprit. As clinicians, our job is to differentiate truly psychotic people from those who might appear temporarily psychotic because of intense anxiety. But the major characteristic of people with an anxiety disorder is the rapid reversibility of their symptoms, and the return to the non-altered state of consciousness when the anxiety-producing triggers are removed.
Thought–Action Fusion
Ordinarily, the differences between thoughts and actions are clear. Anxious thinking creates an altered state of consciousness where scary thoughts can feel as frightening as scary behaviors. It is as if thoughts and actions feel fused together.
Thought–action fusion makes it seem that there is little difference between thinking about something and it actually happening. If a patient with a fear of flying worries about losing control while on the flight, then the anxious thinking will make that thought feel like it might really happen. Thoughts no longer feel like a safe way to rehearse actions without consequences. If a patient worries about an elevator crashing, anxious thinking makes it feel like the worries actually increase the probability—or might even be a cause—of a crash
What Every Therapist Needs to Know About Anxiety Disorders Page 6