A patient suffering from severe asthma, requiring multiple trips to the emergency room for epinephrine injection, and suicidal depression refractory to standard treatment, was recently admitted to our hospital. Trial of a monoamine oxidase inhibitor (MAOI) antidepressant seemed indicated, but what if the patient had an asthma attack while taking this medication? Most acute treatments for asthma are contraindicated in patients on MAOI, including epinephrine injection. We called the local pulmonary specialist who carefully outlined a plan for managing the patients asthma should an attack occur while receiving the MAOI. The psychiatric staff held its collective breath as each day on the antidepressant passed.
Yellowlees and Kalucy would probably not be surprised to learn that not only did this patients depression remit after four weeks on the antidepressant, she never again had an asthma attack (see their article, p 628, this issue). All of our elaborate plans for pharmacologic management of her asthma were unnecessary. Was the antidepressant acting specifically to relieve the respiratory pathology, perhaps by elevating levels of endogenous catecholamines and therefore serving as a bronchodilator, or was it the relief of her depression and its consequent stress that induced the remission from asthma? The excellent review article by Yellowlees and Kalucy suggests that both possibilities are probable and point to the increasing evidence that psychiatric disturbance can be intimately involved in causing or exacerbating medical illness in two ways: by specific biochemical pathways, and by the nonspecific induction of stress. kamagra soft tablets
Increasingly, our group and others have recognized in the last decade that one form of pathologic anxiety— panic disorder—prominently involves ventilatory disturbance. Hyperventilation is a common event during acute panic attacks and there is now the suggestion that at least some patients with panic disorder may have abnormally high sensitivity to inhalation of carbon dioxide. These and other data suggest that at least part of the etiology of panic disorder may be an inherited hypersensitivity of brain stem autonomic nervous system neurons. Administration of anti-panic drugs, such as imipramine, may act to block panic attacks by reducing the threshold for response of these neurons.