From the top to the bottom
Bottom to top I stop
At the core I’ve forgotten
In the middle of my thoughts
Taken far from my safety
The picture is there
The memory won't escape me
But why should I care
Forgetting the most traumatic parts of one's past would seem to be of benefit to the lead singer of Linkin Park (as it would be to many of us). And now you can!! [according to recent reports in the press.] The first irresponsible story is old hat at this point (i.e, more than a week old), but since news cycles last for, oh, about 24 seconds these days [before collective amnesia supposedly sets in], let's review some of the most egregious headlines:
New Drug Deletes Bad MemoriesAND
By Bill Christensen
posted: 02 July 2007
Do you have a really bad memory, or past heartache, that you would prefer to forget?
Researchers at Harvard and McGill University (in Montreal) are working on an amnesia drug that blocks or deletes bad memories. The technique seems to allow psychiatrists to disrupt the biochemical pathways that allow a memory to be recalled.
In a new study, published in the Journal of Psychiatric Research, the drug propranolol is used along with therapy to "dampen" [not delete, after all?] memories of trauma victims....
Scientists find drug to banish bad memoriesBut really, propranolol does no such thing! [as discussed recently in Psych Central and Mind Hacks.] Back in March, The Neurocritic reviewed the literature on post-traumatic stress disorder and norepinephrine:
By Richard Gray, Science Correspondent
Last Updated: 12:01am BST 01 July 2007
It failed to bring Jim Carrey happiness in the award-winning film Eternal Sunshine of the Spotless Mind, but scientists have now developed a way to block and even delete unwanted memories from people's brains.
Researchers have found they can use drugs to wipe away single, specific memories while leaving other memories intact. By injecting an amnesia drug at the right time, when a subject was recalling a particular thought, neuro-scientists discovered they could disrupt the way the memory is stored and even make it disappear.
So what about propranolol for PTSD? According to Strawn & Geracioti (2007),So you might imagine that the discerning and jaded eye would be skeptical if confronted with the latest headline:The utility of these anti-adrenergics in the clinical treatment of PTSD remains to be determined, though it is possible that they may prove to have primary roles in a disorder that is only modestly responsive to antidepressant treatment.
You can forget the unhappy past: studyDude, do you really shut off the visual cortex and thalamus and hippocampus and amygdala entirely? Stay tuned...
By Ishani Ganguli
WASHINGTON (Reuters) - Researchers have confirmed what common wisdom has long held -- that people can suppress emotionally troubling memories -- and said on Thursday they have sketched out how the brain accomplishes this.
They said their findings might lead to a way to help patients with post-traumatic stress disorder or anxiety to gain control of debilitating memories.
"You're shutting down parts of the brain that are responsible for supporting memories," said Brendan Depue, a neuroscience doctoral student at the University of Colorado who worked on the study. He said his team discovered the brain's emotional center is also shut down.
Depue BE, Curran T, Banich MT. (2007). Prefrontal Regions Orchestrate Suppression of Emotional Memories via a Two-Phase Process. Science 317:215-219.
Whether memories can be suppressed has been a controversial issue in psychology and cognitive neuroscience for decades. We found evidence that emotional memories are suppressed via two time-differentiated neural mechanisms: (i) an initial suppression by the right inferior frontal gyrus over regions supporting sensory components of the memory representation (visual cortex, thalamus), followed by (ii) right medial frontal gyrus control over regions supporting multimodal and emotional components of the memory representation (hippocampus, amygdala), both of which are influenced by fronto-polar regions. These results indicate that memory suppression does occur and, at least in nonpsychiatric populations, is under the control of prefrontal regions.
And wash away
What I've done
I'll face myself
To cross out what I've become
And let go of what I've done
-- Linkin Park, What I've Done
Brunet A, Orr SP, Tremblay J, Robertson K, Nader K, Pitman RK. (2007). Effect of post-retrieval propranolol on psychophysiologic responding during subsequent script-driven traumatic imagery in post-traumatic stress disorder. J Psychiatr Res. Jun 21; [Epub ahead of print]
The β-adrenergic blocker propranolol given within hours of a psychologically traumatic event reduces physiologic responses during subsequent mental imagery of the event. Here we tested the effect of propranolol given after the retrieval of memories of past traumatic events. Subjects with chronic post-traumatic stress disorder described their traumatic event during a script preparation session and then received a one-day dose of propranolol (n = 9) or placebo (n = 10), randomized and double-blind. A week later, they engaged in script-driven mental imagery of their traumatic event while heart rate, skin conductance, and left corrugator electromyogram were measured. Physiologic responses were significantly smaller in the subjects who had received post-reactivation propranolol a week earlier. Propranolol given after reactivation of the memory of a past traumatic event reduces physiologic responding during subsequent mental imagery of the event in a similar manner to propranolol given shortly after the occurrence of a traumatic event.
Strawn JR, Geracioti TD Jr. (2007). Noradrenergic dysfunction and the psychopharmacology of posttraumatic stress disorder. Depress Anxiety Mar 12; [Epub ahead of print].
The catecholamine norepinephrine is a critical effector of the mammalian stress response and has been implicated in the pathophysiology of posttraumatic stress disorder (PTSD) -- a syndrome intrinsically related to the experience of extraordinary stress. Symptom-linked hypernoradrenergic derangements have been observed in PTSD and several studies have examined the potential therapeutic effects of agents that dampen the centrally hyperactive noradrenergic state. These agents include compounds that decrease norepinephrine release (e.g. centrally acting alpha(2) agonists such as clonidine) and those which block post-synaptic norepinephrine receptors (e.g. centrally acting alpha(1) or beta receptor antagonists such as prazosin or propranolol). In this article, we review studies of central noreadrenergic hyperactivity under both basal and challenge conditions and explore the evidence for these derangements as potential psychopharmacologic targets in patients with PTSD. Given the significant involvement of CNS norepinephrine hyperactivity in PTSD, and its link to intrusive and hyperarousal symptoms, it is not surprising that interventions directed at this system have therapeutic potential in PTSD. The utility of these anti-adrenergics in the clinical treatment of PTSD remains to be determined, though it is possible that they may prove to have primary roles in a disorder that is only modestly responsive to antidepressant treatment.
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