Treating PTSD With Beta-Blockers

People reading this weblog probably already know about Postraumatic Stress Disorder, a fairly severe anxiety and arousal problem that occurs in the wake of trauma when the trauma experience is so overloading and overpowering as to become “undigestable”. PTSD patients do their best to avoid those memories, but still fall victim to debilitating nightmares and other unwanted trauma-memory intrusions, and concurrent intense body fear arousal. Time usually heals wounds, but PTSD wounds do not heal with time. Trauma memories may remain fresh and unfaceable 20 and 40 years after the fact.

PTSD is treated with a variety of techniques, including anti-anxiety and other psychiatric medications, and various forms of psychotherapy including behaviorally informed graduated exposure and eye movement desensitization and reprocessing therapy (EMDR). The theory has been that trauma memories need to become tolerated so that they can be revisited and ‘reprocessed’ so that it can finally become clear to the patient that the memories are firmly in the past. Drugs and the therapeutic environment help to contain and blunt the patient’s fear arousal, and exposure and EMDR techniques help to reprocess the memories. These therapies are useful for many patients, but they are not curative and there is clear room for improvement.

Psychologist Alain Brunet of McGill University in Montreal (Canada) is looking for ways to make those improvements happen, through the use of an old-fashioned ‘beta-blocker’ drug called Propranolol (see articles here). Primarily intended as heart medicine, beta blocker drugs like Propranolol have long been used “off label” to treat anxiety patients because they block or lessen “peripheral autonomic activation” (e.g., symptoms of anxiety occurring in the periphery of the body such as might be noticeable in the limbs e.g., clammy skin, sweating, shaking, etc.). A socially phobic patient who normally would freak out during a speech can take Propranolol and not notice their palms getting sweaty, etc. Because they are not distracted by arousal symptoms that do not occur (or occur with less force), they are better able to remain focused on their speaking task and to execute it without incident.

This last paragraph has been reworded based on feedback from Jed Struckus, Ph.D. who noted a prior error. Dr. Struckus writes, “Beta blockers , suppress sympathetic (not parasympathetic) activity, and actually lessen the production of the physical symptoms themselves (such a sweaty palms), not simply the awareness of these symptoms”. Thank you for the clarification, Jed.

Propranolol may have another useful effect as well – in that it may suppress the long term storage of emotional memories. A Psychiatrist at Harvard, Dr. Roger Pitman, has shown that trauma patients treated with Propranolol immediately after traumas (accidents, rapes) show somewhat fewer PTSD-like symptoms than patients who did not receive Propranolol. The explanation for this is that Propranolol interferes with the formation of the strong emotional memories that might otherwise crystallize into true trauma memories.

Brunet has taken this secondary line of reasoning and applied it to PTSD. He encourages his patients to talk about their traumas after he has dosed them with Propranolol. The idea is that the Propranolol will prevent re-storage of trauma memories, resulting in a less intense trauma memory after the treatment. Apparently, his early findings with this technique are encouraging, some patients have been helped, and more trials of the approach are underway. We can only hope that test results continue to be encouraging. This Propranolol treatment would surely be a wonderful, cheap and relatively easy way to help long-term sufferers of PTSD if it pans out.

The articles I’ve read about the Brunet and Pitman research suggest these researchers are thinking that the mechanism for the Propranolol effect lays in its ability to block the storage or re-storage of trauma memories. However, another explanation is also possible. It might be enough that the drug simply blunts the PNS arousal and activation that would normally occur when trauma memories are discussed. The result would be that the patient would have an experience of talking about trauma without feeling as overwhelmed and this would translate into new learning which would potentially intermingle with prior trauma learning and lessen the overall intensity of the trauma memory.

Ultimately, it don’t much matter how it works, if it works. I’m glad to see progress being made so that people will maybe suffer less.