Treatment: First try at pharmacologic treatment
When Mr. A’s worries reached the toxic level of fear of imminent death, he sought a psychiatrist’s help. Previous pharmacologic treatment had been limited to brief trials of low dosages of benzodiazepines, typically after emergency room evaluations of some somatic symptom. The benzodiazepines resulted in only minimal improvement and significant daytime sedation. At age 44, at his first appointment with a psychiatrist, Mr. A described not only severe anxiety but also a wide range of physical symptoms. These included tension, dizziness, tingling sensations, migrating pains, disrupted sleep, and low energy.
Mr. A had developed considerable insight about the link between his anxiety and these symptoms, not from psychotherapy but indirectly through extensive medical evaluations. Prior evaluations had included countless emergency room visits, multiple head CT scans and MRIs, and a series of ECGs. None of these led to either a diagnosis or a plan for systematic follow-up until Mr. A independently sought psychiatric treatment.
The psychiatrist prescribed buspirone, titrated up to 10 mg tid, which resulted in minimal improvement of Mr. A’s myriad symptoms. But side effects—including generally disrupted sleep and “crazy dreams”—by far offset any gains, and Mr. A in fact developed symptoms diagnostic of major depression. Over the next several weeks, buspirone was discontinued.
In your view, would you now treat Mr. A for depression? If so, with which agent and for how long?
Dr. Carter’s observations
The salient part of the initial treatment history is the setting. Typical of GAD and panic disorder, much of the early evaluation is done in nonpsychiatric settings. Many patients with anxiety disorders receive no consistent health care. With peak anxiety symptoms manifesting as frightening physical symptoms, such patients present to the emergency room to physicians who are unfamiliar with their longitudinal course. Catastrophic illness is “ruled out,” and with the acute anxiety resolved, no fundamental diagnosis is reached.
With Mr. A’s medical evaluations, we see a typical example: multiple emergency room visits, repeated brain imaging, and emergency ECGs in a man who exercises vigorously without cardiovascular symptoms. The indirect costs to the patient and to society are staggering, with panic disorder and GAD each ranking above lung problems, hypertension, asthma, and back problems in causing lost productivity at work.1
Mr. A is typical of anxiety disorder patients who do not pursue psychiatric treatment initially. Only one-fourth seek treatment,2 and several variables at the outset of his illness predict an even lower rate for patients such as Mr. A. He is male, had an early onset of illness, and did not have a prominent, comorbid mood disorder. His severe symptoms also predict poor compliance once treatment is initiated.3
Understandably, treatment for anxiety disorders often starts with anxiolytics. The common use of benzodiazepines to treat GAD may account for some early studies showing lower sustained remission with GAD compared with other anxiety disorders. Without treating the whole syndrome, sustained response was impossible. In contast, when patients do receive antidepressant medication and stay on it, the literature offers encouragement to those with even severe symptoms: although they do not fare as well as their healthier counterparts early on, patients with severe GAD catch up around the 3-month mark.4
Further treatment: The move to antidepressants
Mr. A was next started on sertraline, titrated up to 50 mg/d. At this dosage, he complained of significant sexual side effects and early morning awakening that did not respond to trazodone. Sertraline was stopped and the sexual side effects resolved. He began taking nortriptyline titrated up to 75 mg/d without side effects. He reported considerable improvement, with diminished anxiety, resolution of depressed mood, and less dizziness. As Mr. A stated, he was “not such a hypochondriac anymore.” Some somatic symptoms persisted, and nortriptyline was increased to 100 mg/d, resulting in further improvement (at a nortriptyline level of 114 ug/L).
After 1 month of being nearly symptom-free, Mr. A experienced a recurrence of his anxiety and an associated increase in depression symptoms, which responded to an increase in nortriptyline to 125 mg/d.
His characteristic health concerns persisted, however. Mr. A was unable to contain his worries about having Huntington’s chorea, based on a tremor that he had noted. This particular worry vanished after consultation with a Huntington’s disease expert, but from day to day he relied on his wife for constant reassurance about his physical health. Various treatment interventions were discussed, and Mr. A agreed to increase his nortriptyline further. He never did so, however, as the recurrence of his anxiety symptoms proved to be transient.