Anxiety disorders encompass a broad, heterogeneous group of psychiatric problems. Like depression, anxiety disorders have multiple etiologies. Some appear to be clearly related to biochemical abnormalities, while others are psychogenic in origin.
And treatments vary considerably depending on the diagnosis and presumed underlying pathophysiology.
Anxiety disorders have often been erroneously seen as mild or benign disorders. However, recent clinical and epidemiological studies indicate that anxiety disorders are quite common –more common even than depression and exact a heavy toll on individuals and society alike.
The current view sees anxiety disorders as often serious, chronic mental illnesses. Especially in severe cases, such as panic disorder, suicide rates are high, alcohol abuse rates reach 30 percent or more, medical services are inappropriately over-utilized, and the cardiac-death rate is higher than average.
Below I discuss a few of the more common anxiety disorders and their etiology.
Generalized Anxiety Disorder (GAD) and Anxiety Associated with Acute Stress
In GAD, the individual is almost continuously predicting, anticipating, or imagining (unpleasant) events. The limbic system is kept in a perpetual state of alert, on guard for a multitude of “what-ifs.” Since daily life rarely presents GAD patients with severely traumatic or life-threatening events, the level of activation does not reach the intensity of threshold of full-blown fight or flight. The result is a low-grade, but chronic, state of anxiety.
GAD is primarily believed to be a psychogenic disorder. However, there is some speculation that at least some GAD patients may suffer from a biologically mediated disorder. One hypothesis is that mentioned above: a deficiency of neurochemicals. Another model has emerged more recently. Treatment with serotonin agonists such as buspirone and 5-HT antidepressants (SSRIs and SNRIs) has been shown to reduce “what-ifing” (worry) in GAD patients.
However, the mechanism of action and underlying pathophysiology are not well understood.
In stress-induced anxiety disorders, actual psychological stressors have evoked another version of ongoing limbic alert. And in the wake of severe stress, such patients often may have occasional full-blown panic attacks. These disorders emerge in response to life-threatening stressors (natural disasters, combat, assaults, automobile accidents) and in response to a host of emotional stressors (loss of a job, serious illness in a relative, marital separation).
In many cases, the anxiety symptoms can be seen as normal responses; that is, they are not pathological. However, the symptoms can be severe enough to warrant treatment.
With GAD and stress-related anxiety, in all likelihood the basic neurobiology is not grossly abnormal. Rather, real or imagined stresses are provoking psychological reactions, which, of course, ultimately are biologically mediated.
Social phobias are certainly influenced by developmental and other life experiences (such as the quality of early attachments, the development of appropriate social skills, and adequate experience interacting with others). At the same time, there is rather compelling evidence suggesting that social phobics (and their more pervasively impaired cousins, avoidant personalities) may have a biologically based disorder.
Animal studies have shown that when baby animals are separated from their parents, they typically enter a state of high arousal and agitation, frequently producing some form of vocal distress signal. This is obviously the case with human infants as well.
Separation stresses appear to elicit extremely high levels of neuronal activity in the locus coeruleus (LC). One hypothesis holds that this brain area, in addition to its role in evoking fight-or-flight responses, may be a key brain structure designed to trigger arousal and distress behavior in infants separated from caregivers. Presumably, with psychological development and neurologic maturation, the threshold of LC activity gradually raises. Behaviorally, we see an increased capacity to tolerate separation as children and young animals mature.
What does this have to do with social phobias? One view is that the underlying fear in many social phobias is that the person will be embarrassed, humiliated, and ultimately rejected, which is equivalent to separation.
This fear of rejection is also seen in avoidant personalities, so-called hysteroid-dysphorics, and many people suffering from borderline personality disorders. Animals treated with antidepressants or MAO inhibitors (drugs shown to reduce excitation in the LC) exhibit markedly decreased distress in the face of separation stresses.
And during the past decade, clinical trials with antidepressants and MAO inhibitors have shown improvement in broad groups of patients with social phobias and rejection sensitivity. The theory contends that such patients may be chronically experiencing very low thresholds of arousal at the level of the LC accounting for their exquisite sensitivity to humiliation, separation, and rejection.
Agoraphobia Without Panic
The anxiety experienced with this disorder occurs only when the patient must go into feared situations (such as a store) or in the moments before entering the phobic situation (anticipating anxiety).
Although such experiences of anxiety ultimately do involve an activation of the limbic system, the primary disorder is felt to be largely psychogenic, a conditioned fear response. Medications are sometimes used to treat agoraphobia without panic; however, this disorder is not believed to be primarily biologically based.
*This article is based on Dr. Moore’s latest book “Handbook of Clinical Psychopharmacology for Therapists” published by New Harbinger Press and coauthored by John Preston, John O’Neal, and Mary Talaga.
Preston, J., O’Neal, J., Talaga, M., & Moore, B. A. (in press). Handbook of Clinical Psychopharmacology for Therapists-Ninth Edition. Oakland, CA: New Harbinger Press.