The science behind The Linden Method
Below are references to research carried out by international research institutions with regard to the Amygdala, anxiety disorders and operant conditioning. These research findings confirm our own research into the way the amygdala works and clearly identify that anxiety is caused 100% by 'memories of fear'.
The following press release, from the National Institute of Mental Health (NIMH), also identifies a claer link between the amygdala and the anxiety response and that through simple training, a group of laboratory rats were 'taught' to be less anxious.
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Mimicking Brain's "All Clear" Quell's Fear in Rats
Researchers funded by the National Institute of Mental Health (NIMH) have discovered a high-tech way to quell panic in rats. They have detected the brain's equivalent of an "all clear" signal that, when simulated, turns off fear.
Rats normally freeze with fear when they hear a tone they have been conditioned to associate with an electric shock. Dr. Gregory Quirk and Mohammed Milad (Ponce School of Medicine, Puerto Rico) have now demonstrated that stimulating a site in the front part of the brain, the prefrontal cortex, extinguishes this fear response by mimicking the brain's own "safety signal." They report on their findings in the November 7, 2002 Nature.
"Repeated exposure to traumatic reminders without any adverse consequences causes fear responses to gradually disappear," explained Quirk. "Such reduction of fear appears to be an active rather than passive process. It doesn't erase the fear association from memory, but generates a new memory for safety."
The researchers recorded electrical activity of neurons in the prefrontal cortex as rats were fear-conditioned - taught to fear a tone by repeatedly pairing it with a shock. Then they abolished this conditioned fear by presenting the tone without the shock; the animals no longer froze when they heard the tone.
Although inactive during both procedures, neurons near the middle of the prefrontal cortex, the infra-limbic area, fired conspicuously when the tone was sounded on the following day. This activity proved to be the brain's way of signaling that the tone no longer presaged a shock. The more the cells fired, i.e. The louder this safety signal, the less the rats froze. Animals that showed the most infra-limbic activity behaved as if they had never been fear conditioned at all.
The researchers then electrically stimulated the infra-limbic area in rats that had been fear conditioned but not extinguished - in effect, simulating the safety signal, while pairing it with the tone. Remarkably, the rats showed little freezing. Later, the rats continued to be unafraid of the tone even without the stimulation, suggesting that memory for extinction was strengthened by experimentally mimicking the safety signal.
Since the prefrontal cortex is known to project to the amygdala, a hub of fear memory deep in the brain, the researchers propose that increased activity of infra-limbic neurons in the prefrontal cortex strengthens memory of safety by inhibiting the amygdala's memory of fear.
NIMH is part of the National Institutes of Health (NIH), the Federal Government's primary agency for biomedical and behavioral research. NIH is a component of the U.S. Department of Health and Human Services.
This report is taken from Nature, an international journal of science.
"The amygdala, a large structure deep within each cerebral hemisphere, is the place where the brain stores memories of fear," said University of Southern California neuroscientist Richard F. Thompson, co-author of the Nature article.
"In the presence of threatening stimuli, the amygdala signals to the prefrontal cortex, triggering the expression of fearful behavior."
Researchers at USC and the Université de Bordeaux (France) trained laboratory mice by sounding a tone and then administering a small electric shock. The mice soon learned to associate the tone with the impending shock and froze in fear as soon as they heard it. Simultaneously, the researchers detected changes in the electrical impulses measured by electrodes implanted in the subjects' prefrontal cortex. When the amygdala was then surgically removed, both the freezing behavior and the altered neuronal activity disappeared.
Lead author René Garcia, of Bordeaux's Laboratoire de Neurosciences Cognitives, designed and completed the experiment in Thompson's USC laboratory during the summer of 1999. "While a mouse's brain is far smaller than a human's, it has essentially the same structures and operates in analogous ways," Thompson explained.
"The prefrontal cortex acts as a kind of 'executive office,' controlling other parts of the brain. It makes decisions that determine how you will react. Memories of fear are stored in the amygdala, which codes them into signals and transmits those signals to the frontal cortex for action."
"Why are you afraid when you're walking alone in the dark and hear footsteps behind you? You have learned to be afraid. Nearly all of our fears are learned fears." Anxiety disorders, such as panic attacks and phobias, are expressions of your memories of fear", said Thompson.
Thompson, director of the USC Program in Neural, Informational and Behavioral Sciences, holds the William M. Keck Chair in Biological Sciences and Psychology in the USC College of Letters, Arts and Sciences.
In addition to Garcia and Thompson, USC neurobiologist Michel Baudry and Université de Bordeaux neuroscientist Rose Marie Vouimba were co-authors of the Nature article.
The study was funded by grants from the National Science Foundation, NATO and Fondation Fyssen.
Further research on Post-Traumatic Stress Disorder (one of the five main anxiety disorders) announced by Psychology Today, concluded that:
"It has been found that the fear response is coordinated by a small structure deep inside the brain, called the Amygdala. The Amygdala, although relatively small, is a very complicated structure, and recent research suggests that post-traumatic stress disorder may be associated with abnormal activation of the amygdala."
Originally published by Psychology Today: 2002-10-10
References: Bremner, J.D., Randall, P.R., Scott, T.M., Bronen, R.A., Delaney, R.C., Seibyl, J.P., Southwick, S.M., McCarthy, G., Charney, D.S., & Innis, R.B. (1995). MRI-based measurement of hippocampal volume in posttraumatic stress disorder. American Journal of Psychiatry, 152, 973-981. Narrow WE, Rae DS, Regier DA. NIMH epidemiology note: prevalence of anxiety disorders. One-year prevalence best estimates calculated from ECA and NCS data. Population estimates based on U.S. Census estimated residential population age 18 to 54 on July 1, 1998. Unpublished. Stein, M.B., Koverola, C., Hanna, C., Torchia, M.G., & McClarty, B. (1997). Hippocampal volume in women victimized by childhood sexual abuse. Psychological Medicine, 27, 951-959. LeDoux J. 'Fear and the brain: where have we been, and where are we going?' Biological Psychiatry, 1998; 44(12): 1229-38.
