Alcohol and Panic Attacks

2015

Panic attacks with and without agoraphobia are more common among alcoholics than the rest of the population. The simplest explanation may be that certain patients with panic attacks drink alcohol to alleviate anticipatory anxiety. The relationship between panic attacks and alcoholism may, however, be complex.

Both alcohol withdrawal and panic attacks have been demonstrated to be associated with noradrenergic overactivity. Furthermore, tolerance to alcohol seems to be partly conditioned, at least in experimental animals, and it involves physiological changes compatible with sympathetic activation. Tolerance is not maintained in experimental animals with central noradrenergic lesions. Thus, noradrenergic activation may play an important role both in conditioning tolerance and panic attacks. Another phenomenon pertinent to alcohol withdrawal, with implications for panic attacks, is kindling. Repeated alcohol withdrawals may lead to kindling. This was first postulated based on a retrospective chart review of patients with alcohol dependence which showed that repeated withdrawals became progressively more severe. More recently, it was demonstrated that blunted responsiveness of noradrenergic a2-autore-ceptors was positively correlated with the number of withdrawals. This finding provides pharmacological support to the kindling hypothesis and suggests that repeated withdrawals may produce a hyperreactive noradrenergic system. Whether alcoholics do kindle their noradrenergic system to such an extent that they begin to experience spontaneous panic attacks during abstinence remains to be established. Kindling and conditioning to tolerance may act in an additive fashion to produce a hyperreactive noradrenergic system.

In general, the treatments of choice for panic disorder are probably monoamine oxidase inhabitors (MAOI) but the patients also respond well to tri-cyclic antidepressants and alprazolam. The conventional 1,4-benzodiaze-pines have been thought to be effective only in alleviating anticipatory anxiety associated with panic attacks. This concept may, however, be changing because of the recently reported efficacies of clonazepam and lorazepam in the treatment of panic attacks.°

If an alcohol-dependent patient with panic attacks is determined not to present a suicide risk then secondary amine tricyclic antidepressants are probably the treatment of choice. These drugs have only mild additive adverse effects with alcohol on psychomotor performance. Furthermore, unlike MAOIs, they do not produce catastrophic interactions with tyramine-containing foods and beverages should an alcoholic relapse to drinking during drug treatment and stop following dietary restrictions.

Stopping alprazolam abruptly is associated with an increased risk of seizures and the same may pertain to other relatively potent benzodiazepine receptor agonists. Thus, these drugs should probably be avoided in the treatment of alcoholic patients with panic attacks.

According to preliminary reports, serotonin reuptake inhibitors may be effective in the treatment of panic disorder. These drugs do not produce dependence and yet, on a short-term basis at least, they reduce drinking in heavy social drinkers and are less toxic than tricyclics in overdose. Thus, they may become the treatment of choice for panic attacks in patients with alcoholism.

Behavioral treatment strategies to alleviate symptoms of panic attacks in alcoholics have not been tested in controlled studies. If panic attacks have a strong conditioned component in a given alcoholic, as suggested, for example, by the attacks being primarily situational, manipulations aiming at facilitating extinction should theoretically be an effective treatment.

 

Selections from the book: “Recent Developments in Alcoholism. Volume 7. Treatment Research: Alcoholics Anonymous. The Family. Serotonin and Preference. Clinical Pharmacology.” Edited by Marc Galanter. An Official Publication of the American Medical Society on Alcoholism, the Research Society on Alcoholism, and the National Council on Alcoholism. 1989.