Psychological Defenses and Coping Styles in Patients Following a Life-Threatening Attack of Asthma: Discussion

Psychological Defenses and Coping Styles in Patients Following a Life-Threatening Attack of Asthma: DiscussionThe major finding of this study is that the psychiatric and psychological profiles of the group of patients who have suffered a NMAD are most unusual. The prediction that they would not have particularly high levels of denial because of the consequences of their NMAD has not been upheld. Instead, what has been found is that while the patients as a whole have very high levels of denial anyway, they seem to respond psychologically to the NMAD by either decompensating psychiatrically and developing symptoms of anxiety, or by increasing their levels of denial even further.

Denial is a normal coping mechanism in response to adversity and is usually adaptive. Increased levels of denial are likely to be helpful in allowing patients to cope with chronic illnesses yet retain a normal social facade, and in our culture where abnormal physical appearance or function is heavily stigmatized, an increased amount of denial is probably essential to allow patients with asthma to cope and feel relatively normal. Denial is also increased in situations of constant loss, and clearly asthma is associated with losses particularly in health and self-esteem, and is also commonly used as a defense against fear, anxiety, and depression. The NMAD patients confirm this latter point quite clearly with the non-psychiatrically diagnosed patients having much higher levels of denial than the patients with psychiatric disorders.
The psychiatric disorders seen in the NMAD patients were primarily anxiety disorders.

This is something that has been seen in previous studies of patients with chronic respiratory disease where a variety of mechanisms were proposed that would tend to lead to the evolution of symptoms of anxiety. The high prevalence of anxiety disorders is important clinically because, as has previously been discussed, hyperventilation and panic may be misconstrued as being indicative of a worsening of the patients respiratory disorder. The dosages of asthma medications may then be increased, which in the case of methylxanthines and B2 adrenergic agonists, is actually likely to physiologically make patients more agitated and anxious. A recent discussion has postulated a physiologic link between depression and death from asthma via cholinergic pathways. It is possible that these pathways may be similarly involved in the etiology of the anxiety disorders seen in the patients described in this study, as it is well known that there are significant physiologic and psychological interactions and overlaps between anxiety and depression.