Brain’s Fear Center Shrinks in Autism’s Most Severely Socially-Impaired
Researchers Tie Size of Amygdala with Social Impairment
Researchers at the University of Wisconsin have examined the age-dependent changes in the size of brain region named the amygdala on face processing in a group of individuals both affected and not affected with autism.
As children get older, the size of their brain increases, and so does the size of the amygdala. This recent study shows that this age-related increase in amygdala size does not occur in individuals with autism. In addition, those individuals with the smallest amygdala measured in adolescence also showed the greatest deficits in recognition of facial features, as well as a reduction in time spent looking at the eyes (eye gaze). Both of these behavioral characteristics are consistent with autism-specific impairments. Social communication deficits in early childhood were also linked to smaller amygdala size in adolescence, suggesting that this atrophy may begin earlier than the first changes in amygdala size are experimentally observed.
The amygdala has been well studied as a part of the brain circuit which controls emotional response to faces as well as fear-related memories. Changes in the size of this brain region as well as the number of brain cells in different areas of the amygdala have been associated with autism, however, this study specifically investigated whether the size of the amygdala is related to specific deficits in the ability to recognize facial expressions and examine specific facial features, especially the eyes. Because the group that showed the greatest deficits on this task also exhibited the smallest amygdala, this research provides further evidence that changes in the structure and function of this brain region are related to autism-specific behaviors such as deficits in face processing.
While the cause of this deceleration in brain size is not yet known, this research group, led by Dr. Richard Davidson, reports a hypothesis on why individuals with the most severe behavioral impairments show the smallest amygdala size. One explanation for this finding states that the amygdala of severely affected individuals may be hypersensitive and hyperactive, leading to a phenomenon called “excitotoxicity”. That is, the amygdala in individuals with autism shows a maladaptive cellular response during development, leading to cell death and shrinkage of the size of the structure. Further studies are needed to determine if this hypothesis is true.
The funders of this study, the National Institutes of Health, are proud to provide a detailed summary of this study which can be found below: http://www.nih.gov/news/pr/dec2006/nimh-04b.htm
Brain’s Fear Center Shrinks in Autism’s Most Severely Socially-Impaired
Well Siblings Share Some of the Same Behavioral, Neural Features
The brain’s fear hub likely becomes abnormally small in the most severely socially impaired males with autism spectrum disorders (http://www.nimh.nih.gov/healthinformation/autismmenu.cfm), researchers funded by the National Institutes of Health’s (NIH) National Institute of Mental Health (NIMH) and National Institute on Child Health and Human Development (NICHD) have discovered.
Teens and young men who were slowest at distinguishing emotional from neutral expressions and gazed at eyes least — indicators of social impairment — had a smaller than normal amygdala, an almond-shaped danger-detector deep in the brain. The researchers also linked such amygdala shrinkage to impaired nonverbal social behavior in early childhood.
The new findings suggest that social fear in autism may initially trigger a hyperactive, abnormally enlarged amygdala, which eventually gives way to a toxic adaptation that kills amygdala cells and shrinks the structure, propose Richard Davidson, Ph.D., and colleagues at the University of Wisconsin, who report on their magnetic resonance imaging (MRI) study in the December 2006 Archives of General Psychiatry.*
In a related study, another research team led by Davidson found that well siblings of people with autism share some of the same differences in amygdala volume, and in the way they look at faces and activate social/emotional brain circuitry, particularly an area critical for face processing.“
Together, these results provide the first evidence linking objective measures of social impairment and amygdala structure and related brain function in autism,” explained Davidson.
“Finding many of the same differences, albeit more moderate, in well siblings helps to confirm that autism is likely the most severe expression of a broad spectrum of genetically-influenced characteristics.”
While SOME people with minimal expression of these traits might be perceived as aloof or loners, those at the more severe end of the spectrum are unable to engage in give-and-take interactions and fail to develop age-appropriate peer relationships. Notably, they shy away from looking at eyes. Davidson’s research team had reported last year linked such eye-gazing with hyperactivation of their fear hub.** Yet different studies have found the amygdala in autism to be variously enlarged, shrunken or even normal in size.
Davidson, Kim Dalton and colleagues suspected that these seemingly inconsistent findings resulted from the wide variability of the autism spectrum, which masked amygdala changes — that a clearer picture would emerge if the length and severity of hypersensitivity to social interactions were factored in. They brought to bear eye-tracking and other measures of facial emotion processing in combination with MRI to find out if degree of non-verbal social impairment might predict amygdala volume in 49 males, aged 8-25, including 25 with autism spectrum disorders.
Those in the autism group who had a small amygdala were significantly slower at identifying happy, angry, or sad facial expressions and spent the least time looking at eyes relative to other facial regions. Autistic subjects with the smallest amygdalae took 40 percent longer than those with the largest fear hubs to recognize such emotional facial expressions, and those with the largest amygdalae spent about four times longer looking at eyes than those with the smallest. Eye fixation did not correlate with amygdala volume among 24 control subjects. The size of the amygdala increased early in autism group subjects with normal eye fixation, while it increased little in those with low eye fixation. Moreover, autism group subjects with small amygdalae had the most non-verbal social impairment as children.
The researchers suggest that the amygdala in autism fits a model in which a brain structure adapts to chronic stress — in this case, fear of people — by first becoming hyperactive, but over time succumbing to a process of toxic cell death and atrophy, as has been proposed occurs in the hippocampus for some forms of depression.*** Children with autism who are least hypersensitive to interaction with people would thus show slower amygdala shrinkage while those who were most hypersensitive would begin to show amygdala changes early in life. Such amygdala adaptations likely affect most people with autism by adulthood, according to the researchers. However, they caution that these changes do not explain all autistic behavior, but account for slightly more than half of the variability in nonverbal social impairment.
In the related study, published online in Biological Psychiatry, October 24, 2006,**** Davidson, Kim Dalton, Ph.D. and colleagues at the University of Wisconsin employed functional magnetic resonance imaging (fMRI) as well as many of the same measures used in the above study in 21 subjects with autism, 12 siblings and 19 healthy controls. Notably, they found that unaffected siblings of people with autism showed a similar pattern of smaller amygdalae, and decreased eye fixation as their autistic siblings when looking at faces.
However, while the autism group showed reduced activation of a face-processing area, the fusiform gyrus, on both sides of their brains while performing a face-processing task, the well siblings showed this difference only on the right side. This suggested an “intermediate pattern” — that the well siblings were using circuitry similar to healthy controls, but with some slight changes reminiscent of their autistic siblings, but not as pervasive.
Similarly, eye fixation time did not predict amygdala activation in the well siblings as it did in their autistic relatives. This suggested that looking at faces did not boost activation of emotion-related circuitry in the well siblings. Looking at eyes may not be a negative experience for them, again suggesting an intermediate pattern. Nonetheless, their amygdalae were about the same size as those in the autism group.
The findings of both studies, taken together, suggest that measures such as eye gazing time may prove useful in clarifying the relationship between genes, brain and behavior in the autism spectrum, say the researchers.
Also participating in the Archives of General Psychiatry study were: Kim Dalton, Ph.D., Tom Johnstone, Ph.D., Micah Long, Emelia McAuliff, Terrence Oakes, Ph.D., Andrew Alexander, Ph.D., University of Wisconsin.
The National Institute of Mental Health (NIMH) mission is to reduce the burden of mental and behavioral disorders through research on mind, brain, and behavior.
More information is available at the NIMH website, http://www.nimh.nih.gov .The NICHD sponsors research on development, before and after birth; maternal, child, and family health; reproductive biology and population issues; and medical rehabilitation. For more information, visit the Web site at http://www.nichd.nih.gov/.
The National Institutes of Health (NIH) — The Nation’s Medical Research Agency — includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.
* Nacewicz BM, Dalton KM, Johnstone T, Long MT, McAuliff EM, Oakes TR, Alexander AL, Davidson RJ. Amygdala volume and nonverbal social impairment in adolescent and adult males with autism. Arch Gen Psychiatry. 2006 Dec;63(12).
** Dalton KM, Nacewicz BM, Johnstone T, Schaefer HS, Gernsbacher MA, Goldsmith HH, Alexander AL, Davidson RJ. Gaze fixation and the neural circuitry of face processing in autism. Nat Neurosci. 2005 Apr;8(4):519-26. Epub 2005 Mar 6.
***McEwen BS. Mood disorders and allostatic load. Biol Psychiatry. 2003 Aug 1;54(3):200-7. Review.
****Dalton KM, Nacewicz BM, Alexander AL, Davidson RJ. Dalton KM, Nacewicz BM, Alexander AL, Davidson RJ. Gaze-Fixation, Brain Activation, and Amygdala Volume in Unaffected Siblings of Individuals with Autism. Biol Psychiatry. 2006 Oct 24; [Epub ahead of print]
Autistic people have fought the inclusion of ABA in therapy for us since before Autism Speaks, and other non-Autistic-led autism organizations, started lobbying legislation to get it covered by insurances and Medicaid.
ABA is a myth originally sold to parents that it would keep their Autistic child out of an institution. Today, parents are told that with early intervention therapy their child will either be less Autistic or no longer Autistic by elementary school, and can be mainstreamed in typical education classes. ABA is very expensive to pay out of pocket. Essentially, Autism Speaks has justified the big price tag up front will offset the overall burden on resources for an Autistic’s lifetime. The recommendation for this therapy is 40 hours a week for children and toddlers.
The original study that showed the success rate of ABA to be at 50% has never been replicated. In fact, the study of ABA by United States Department of Defense was denounced as a failure. Not just once, but multiple times. Simply stated: ABA doesn’t work. In study after repeated study: ABA (conversion therapy) doesn’t work.
What more recent studies do show: Autistics who experienced ABA therapy are at high risk to develop PTSD and other lifelong trauma-related conditions. Historically, the autism organizations promoting ABA as a cure or solution have silenced Autistic advocates’ opposition. ABA is also known as gay conversion therapy.
The ‘cure’ for Autistics not born yet is the prevention of birth.
The ‘cure’ is a choice to terminate a pregnancy based on ‘autism risk.’ The cure is abortion. This is the same ‘cure’ society has for Down Syndrome.
This is eugenics 2021. Instead of killing Autistics and disabled children in gas chambers or ‘mercy killings’ like in Aktion T4, it’ll happen at the doctor’s office, quietly, one Autistic baby at a time. Different approaches yes, but still eugenics and the extinction of an entire minority group of people.
Fact: You can’t cure Autistics from being Autistic.
Fact: You can’t recover an Autistic from being Autistic.
Fact: You can groom an Autistic to mask and hide their traits. Somewhat. … however, this comes at the expense of the Autistic child, promotes Autistic Burnout (this should not be confused with typical burnout, Autistic Burnout can kill Autistics), and places the Autistic child at high risk for PTSD and other lifelong trauma-related conditions.
[Note: Autism is NOT a disease, but a neurodevelopmental difference and disability.]
Fact: Vaccines Do Not Cause Autism.