Two years later, Mr. J complained of gradual worsening daytime sleepiness. Polysomnography revealed that Mr. J had severe OSA and periodic limb movement disorder. After he began nighttime CPAP and pramipexole, 0.25 to 0.5 mg/d, and continued modafinil, 200 mg/d, his anxiety symptoms completely resolved. Several months later Mr. J’s physician discontinued paroxetine because Mr. J reported it caused mildly decreased concentration.
The authors’ observations
The etiology of Mr. J’s anxiety is unclear; however, he does not meet criteria for:
- panic disorder, because he denies persistent concern about having more attacks or the implications or consequences of panic attacks, or significant change in behavior related to panic attacks (Table 2)8
- generalized anxiety disorder, because between panic attacks Mr. J’s baseline anxiety related to “real-world” stressors is mild, intermittent, and easily controllable8
- substance-induced anxiety disorder, because Mr. J denies using caffeine, tobacco, alcohol, or illicit drugs. Also, for many years he worked for a company that performed random drug screening.
Table 2
Diagnostic criteria for panic disorder without agoraphobia
| A. Both 1 and 2: 1. Recurrent unexpected panic attacks 2. At least one of the attacks has been followed by 1 month (or more) of 1 (or more) of the following: a. Persistent concern about having additional attacks b. Worry about the implications of the attack or its consequences (eg, losing control, having a heart attack, ‘going crazy’) c. A significant change in behavior related to the attacks |
| B. Absence of agoraphobia |
| C. The panic attacks are not due to the direct physiologic effects of a substance (eg, a drug of abuse, a medication) or a general medical condition (eg, hyperthyroidism). |
| D. The panic attacks are not better accounted for by another mental disorder, such as social phobia (eg, occurring on exposure to feared social situations), specific phobia (eg, on exposure to a specific phobic situation), obsessive-compulsive disorder (eg, on exposure to dirt in someone with an obsession about contamination), posttraumatic stress disorder (eg, in response to stimuli associated with a severe stressor), or separation anxiety disorder (eg, in response to being away from home or close relatives). |
| Source: Diagnostic and statistical manual of mental disorders, 4th ed, text rev. Washington, DC: American Psychiatric Association; 2000 |
Although it is difficult to draw a conclusion from a single case, Mr. J’s dramatic improvement with CPAP warrants speculation about possible etiologic relationships among daytime panic attacks, nighttime panic attacks, and OSA.
According to DSM-IV-TR, a panic attack has a distinct period of intense fear or discomfort (Table 3).8 Recurrent panic attacks can lead to anticipatory anxiety, which is an intense fear and/or dread of having another panic attack.9 According to Steven Reiss’ expectancy theory, anxiety sensitivity—ie, the fear of anxiety or fear of fear—may be a risk factor for panic disorder.10 Therefore, past panic attacks may increase the likelihood of future panic attacks.
Table 3
Diagnostic criteria for panic attack*
A discrete period of intense fear or discomfort, in which 4 (or more) of the following symptoms developed abruptly and reached a peak within 10 minutes:
|
| *Panic attacks occur in the context of several anxiety disorders and cannot be diagnosed as a separate entity |
| Source: Diagnostic and statistical manual of mental disorders, 4th ed, text rev. Washington, DC: American Psychiatric Association; 2000 |
Mr. J’s panic symptoms may be caused by multiple OSA-induced nocturnal panic attacks. These nighttime panic attacks may predispose him to daytime attacks. It is possible that Mr. J had subclinical panic disorder before developing OSA. In this scenario, his OSA-induced nocturnal panic attacks may have worsened his panic disorder. Unfortunately, we do not know precisely how long Mr. J has had OSA—only that he was diagnosed with the condition 4 years before presenting to our clinic.
Mr. J responded moderately to paroxetine monotherapy but experienced rapid resolution of his panic attacks with a combination of paroxetine and CPAP. CPAP monotherapy sufficiently prevented panic attacks for 4 years. Finally, when Mr. J experienced a single panic attack several months before presenting to our clinic—at the end of a very stressful year—reintroducing paroxetine prevented subsequent attacks. This supports our hypothesis that OSA may predispose or indirectly cause patients to develop daytime panic attacks. Alternately, this case suggests that OSA may cause subclinical panic disorder to present as an acute condition.