The various anxiety disorders involve many different areas of the brain. These areas reflect both the uniqueness of each of these disorders and the features that they have in common.

The amygdala, for example, plays a central role in anxiety disorders. This structure in thelimbic systemwarns us when a danger is present in our environment and triggers the fear reaction and then the fight or flight reaction to get us out of it.

It is therefore no surprise that the central part of the amygdala seems to play an important role in anxiety disorders that involve specific fears, such as phobias. Researchers have also observed that a group of very anxious children had larger amygdalas, on average, than a group of normal children.

Source: J. Douglas Brenner

Left: Functional magnetic resonance image (MRI) of the hippocampus of a normal child.
Right: Functional MRI of a child who has suffered sexual abuse; the volume of the hippocampus is reduced significantly.

In addition to these differences in the size of various brain structures, abormally high or low activity in a particular region of the brain, as revealed by brain imaging, may be another kind of anomaly that results in anxiety disorders.

Though extinction may thus be a process that the cortex applies “from the top down” to soothe the fears conditioned by the amygdala, these fears may in fact never be fully erased during an individual's lifetime. There is much evidence supporting this hypothesis, some of it right in the circuits of the amygdala itself. Moreover, it is thought to be precisely these circuits that psychotherapy addresses, by increasing the repertoire of soothing messages that can be sent down to them from the cortex.

People with various anxiety disorders display abnormalities in the size or neural activity of various structures in their brains.

For instance, brain-imaging studies of combat veterans withpost-traumatic stress disorder show that when they listen to recordings that bring back their worst memories, theiramygdalae become more active than other people's. The amygdala also appears to be involves in triggering panic attacks, through itscentral nucleus. This structure maintains connections with several other brain structures, particularly in the brainstem, that control autonomic functions such as respiration and heart rate.

Source: Irwin et al., 2001 Activation of the amygdalae by a negative stimulus

The amygdala is thus ideally positioned to set off the various symptoms of a panic attack. And animal studies have in fact shown that stimulating the central nucleus of the amygdala either electrically or with drugs does in fact produce the behaviours associated with panic.

Cross-section of the pons (rostral to the motor nuclei of the trigeminal)

The locus coeruleus is one of the brainstem nuclei that maintains close communications with the amygdala. This small nucleus contains almost half of all the brain neurons that use norepinephrine as a neurotransmitter. The locus coeruleus also projects its axons to those parts of the brain that may be associated with panic disorders (the amygdala, hippocampus, septum, cortex, brainstem, reticular formation, etc). Stimulating an animal's locus coeruleus, like stimulating its amygdala, produces anxiety behaviours. As therefore follows logically, substances with tranquilizing effects, such asbenzodiazepines,alcohol, and opiates, make the locus coeruleus less active.

Other studies indicate that the central grey nuclei, subcortical areas of the brain that are involved in the involuntary component of body movements, are abnormally active in people with obsessive-compulsive disorder.

The cortex plays its own significant part in anxiety disorders. The ventromedial region of the prefrontal cortex, which is recognized for its role as a modulator of the emotions and for its involvement in depression, also seems to play a primary role in the process of extinction that is the basis for many effective therapies for anxiety disorders.

Anxiety, like fear and other emotions, reflects the activity of specific, identifiable circuits in the brain. Early on, researchers studying the brain circuits involved in anxiety realized that the amygdala was a key structure for understanding this phenomenon. The amygdala is a complex structure in the brain and is composed ofseveral interconnected nuclei.

The sensory stimuli associated with pain follow one of two pain pathways to the brain, then converge at the lateral nucleus of the amygdala. Because of its position at the "gateway" to the amygdala, this nucleus seems to play an important role in the process of fear conditioning, which underlies many anxiety disorders (follow the Experiment module link to the left). The nerve cells in the lateral nucleus of the amygdala project their axons to its other nuclei, thus forming various circuits that ultimately converge on the central nucleus. This nucleus acts as the output pathway from the amygdala, which in turns activates the hypothalamus, thelocus coeruleus,and other parts of the brain that are responsible for the characteristic symptoms of anxiety.

During the fear-conditioning process, certain internal circuits in the amygdala may be strengthened to create a memory trace of the conditioned fear. Such traces appear to be very persistent, and perhaps even permanent. If these potentiated circuits in the amygdala are strengthened enough, they could even become the source of a specific phobia.

Many researchers think that fear conditioning records memories in these strengthened circuits of the amygdala permanently. Hence these researchers believe that the efforts involved in psychotherapyachieve their positive results not by removing the fearful memories encoded in the amygdala's circuits, but rather by strengthening other neural pathways, particularly ones originating in the cortex, that calm these circuits.

This is why a phobia that seemed to have been successfully cured through therapy can re-emerge suddenly during a particularly stressful event. The calming influence of the cortex no longer suffices, and the conditioned fear in the circuits of the amygdala expresses itself once again.

Even years later, some of these same stimuli, or others associated with them, may suffice to trigger an intense fear reaction, by reactivating these strongly conditioned circuits in the amygdala.

But in our complex modern world, where change is an integral part of our daily lives and the contexts in which we operate are no longer the same, persistent fears can become a handicap instead. Thus we pay a heavy price for the formidable efficiency of the fear pathways in our nervous systems.

PHOBIAS

A phobia is a fear of a particular situation or thing, a fear so excessive that it drives the sufferer to do anything possible to avoid that situation or thing. If there is nothing the person can do to avoid it, he or she suffers from a form of anxiety whose symptoms are well known: sweating, noisy breathing, rapid heartbeat, dizziness, and even fainting.

Unlike normal fear, which is a useful reaction to avoid a real danger, the fright reactions generated by phobias are completely irrational and disproportionate to the actual risks involved. Sometimes the anxiety induced by the feared situation or thing (or sometimes even by a mere picture of it!) can become so intense that it triggers a panic attack.

In what are known as specific phobias, the object of the phobia is clearly defined. The situations or things that are the objects of specific phobias generally belong to categories that seem to have hadparticular significance in the course of human existence.

Thus, some of the most common objects of specific phobias, such as insects, snakes, or high places, represented real potential dangers forour ancestors. Other objects of specific phobias include blood, germs, thunderstorms, flying in airplanes, vomiting, or even simply arriving late someplace. In addition to specific phobias, there areother types of phobias that are, in many respects, even more disabling.