The River Lethe

For some time, there has been research into off-label use of beta blockers in the treatment of anxiety disorders, specifically panic disorder. Mostly I’ve yawned at this research. *yawn* The premise is fairly simple: panic attacks involve both physiological and psychological reactions, which essentially feed into one another. By using a beta blocker, the physiological responses connected with fear – sweating, shaking, rapid heartbeat – are short-circuited by affecting neuroreceptors, thereby diminishing the effect of the hormones normally released through that mechanism into the bloodstream (basically, it cuts short your adrenaline rush). This is not really all that exciting: a drug to slow your heartbeat slows your heartbeat.

*yawn*

There has been some preliminary research into the use of beta blockers to treat other anxiety disorders, most notably posttraumatic stress disorder. This looks a bit more interesting, primarily because certain ethical dilemmas arise from their use.

Clinical trials seem to be generally focused on preventing the disorder in the first place by giving trauma survivors beta blockers during the initial period after the event, sometimes known as the ‘crisis stage.’ The goal in this case is to prevent memories of the event from being stored in the amygdala in the right hemisphere – presumably connected through the limbic system to affect response. Normally, input (sensory data) is received by the brain in the thalamus and its importance is then determined by the amygdala; the hippocampus creates a kind of ‘map’ or schema that determines the importance of various sensory input. Presumably, negative ‘triggers’ fall into the higher range of that map, meaning of course that one is keyed to their perception as well as that the attention filter of the brain will give them priority. This is all a very simplistic explanation: memories are actually stored in neural networks connecting different parts of the brain: your memories are spread out inside your head.

What happens in ptsd is twofold. In the first place, the traumatic memory is never connected to positive memories of the same or similar stimuli. In the second, damage to the hippocampus caused by the trauma seems to make learning new information related to the memory difficult. Analysis and recognition with regard to the event, processed in the prefrontal cortex, are effectively neutralized by these neurological anomalies. It is reasonable to locate the disconnect between traumatic memories and other memories (which can be modified by experience) in the nature of the strong, negative emotional response to which they are tied – an emotional response belonging to the primitive part of the brain which always seems to run the show when it comes to fear. Therefore, the theory is that by giving trauma survivors these medications, the lessening of the fear reaction in relation to the memory will separate the negative emotion from the cognitive (non emotional) content of the memory, allowing the memory to better integrate into existing networks.

I’m a little nervous about this. After all, survivors of trauma are experiencing completely normal emotional reactions; you also don’t know which of them will develop ptsd. Not enough research has been done in this area to assure me that normal fear responses to similar situations the person might face will not be extinguished. After all, fear can often save your life.

Beta blockers have also been tested as a treatment strategy for survivors who have developed ptsd (which is by no means an automatic or necessary development). This is based on the same theory. ‘Flashback’ memories are not all identical and in many cases the stereotypical representation is not what you will observe. Stereotypically, a person for a short period of time ‘relives’ the event, usually in fragments, in a complete fashion: sensory and emotional information are felt as present realities. This is frightening both for the person experiencing the memory and those who see it happen. Often flashbacks are composed entirely of a strong emotional and fearful reaction to an environmental trigger which does not include explicit remembrance of the traumatic event. You feel intense fear, and it isn’t immediately apparent why. Thinking about the trauma can trigger intense emotional reactions and panic. What has happened is what happens in all memories that involve strong emotions. When you remember your grandfather giving you a whole pile of balloons, and you remember feeling joyful and happy, you actually feel joyful and happy while having that memory: the content and the emotion have become fused. The same is true of traumatic memories. Since the acquisition of new information has little or no effect on the memory-feeling (because of the hippocampus damage we discussed earlier), the survivor will often feel that no matter what he does the psychic injury will never fade.

What the beta blockers offer is not an erasure of the memory. The theory is that by cutting off the physiological fear response to the painful memory, the two will become ‘unfused.’ The possibility of remembering the event without the debilitating emotional-fear response should then allow the survivor to process it and integrate it into a network of similar memories. New experience should also begin to affect it, including situational novelty (you don’t get stabbed by a sociopath every time you go to the local theatre) and cognitive reflection (it isn’t your fault the sociopath stabbed), alleviating many ptsd symptoms. The symptoms, of course, are normal coping mechanisms to deal with total loss of control that have become pathological by virtue of their long endurance and their uncontrollable resurgence – they are bothering the person. The reason they do not go away – or do so only with difficulty – is because by reliving the experience emotionally the same strategies to deal with it also become attached to the memory, and are then generalized to other similar instances or triggers in an attempt to protect the person from the previous outcome. These coping mechanisms become part of the global thought-processes of the person, which is part of the reason they are so difficult to challenge or change even when they are clearly maladaptive.

So: give patient beta blocker, patient processes memory, patient moves on with life at least more well adjusted if not completely ‘normal.’ This would really only work in the context of therapy.

But is it ethical? It seems absurd to say that alleviating suffering might pose an ethical dilemma. But, in the first place, we don’t know enough about how memory works to understand the possibly far-reaching consequences. In the second, it is unclear what the effect will be on neurological damage that has already been sustained.

More importantly, does this short-circuit the survivor’s genuine healing process that has the potential to result in greater self-knowledge? I mean, will you ever know what about you makes you prone to reacting to trauma in this way, why you are vulnerable to developing ptsd? What about all the hard work of plowing through it? Is this yet another instance of our need for instant gratification – a kind of drive-through clinic? But then again, will you ever thrive again without this medication? Most importantly: who decides?

There is also the question of spirituality, something often deeply affected by trauma, changed in your journey (if it survives), and deepened by the struggle to find light in the midst of darkness. Too often I think we forget about God and all He can tell us, and we do not ask God if the suffering is His Will. When does He say ‘grab hold of the rope and be pulled out,’ and when does He say ‘My grace is sufficient for you?’ In the face of such a powerful temptation as this kind of forgetfulness, will we be able to discern the difference?