November 13, 2012

Our everyday lives are filled with sensory information from the outside world and from our own motor behaviors. We can’t possibly remember everything we experience. Our brain helps us select new information worthy of remembering. Such information may be tagged with “attention” markers, which involve the chemical transmitter norepinephrine (adrenaline), and “reward” markers, which involve the chemical transmitter dopamine.

Memories of events (episodic memories) are stored in a brain area called the hippocampus. Memories of actions that we perform (procedural memories) are stored in a brain area called the caudate nucleus. Events and actions worthy of particular attention involve activation of the amygdala, the brain’s emotion center. Emotional episodic memories involve activation of both the amygdala and the hippocampus, and may be stored in the posterior cingulate gyrus of the cerebral cortex (PCC). The degree of amygdalar activation is regulated by the anterior cingulate gyrus of the cerebral cortex (ACC).

The anterior cingulate cortex is involved in decision making and response selection. Once we decide on a particular response (motor behavior) to make, the success or failure of that response is registered by reward centers in the caudate nucleus and nucleus accumbens.
All of the above-mentioned brain areas (hippocampus, caudate nucleus, amygdala, PCC, ACC, nucleus accumbens) are activated during dreaming, as demonstrated with brain imaging studies in sleeping human subjects. Dreaming is thought to be involved in memory formation, though the details remain to be determined. Dreaming is difficult to study scientifically because the dreamer must be awakened to report the content of their dream.

People with posttraumatic stress disorder (PTSD) suffer from an overactive amygdala and an underactive anterior cingulate cortex (ACC), as has been shown in brain imaging studies during wakefulness. A possible brain mechanism for PTSD is that trauma causes excessive amounts of norepinephrine (adrenaline) activation in the brain, which overloads the system, thereby preventing normal dreaming and normal memory formation from occurring.

The goal in PTSD treatment is to reduce activity in the amygdala and to increase activity in the ACC. Dream revision therapy may calm the amygdala by providing soothing input from the ACC. The frightening nightmare is changed so it is not so frightening or anger-provoking. The goal of dream revision is to empower the dreamer to take charge of their nightmare and make it more manageable. That is, the goal is to change the dreamer from trauma victim to trauma survivor.

The antihypertensive medication prazosin (Minipress), a blocker of norepinephrine alpha receptors (“alpha blocker”), can help in calming the amygdala. Dream revision therapy may be more successful with some prazosin to make the nightmare less frightening; too much prazosin might block the dream altogether and preclude the possibility of doing dream revision therapy. Therapy is preferable to medication in that it eliminates the nightmare permanently. With medication (i.e., prazosin) the nightmare goes away only so long as one takes the medication; stop the prazosin and the nightmare returns.

One can thus think of PTSD as a disorder of memory, and in particular, a disorder of memory formation during dreaming. If the dreaming mechanism can be fixed, then memory formation can be returned to normal, and waking life can be fixed as well.