[Adta] Fw: BRAIN'S FEAR CENTER SHRINKS IN AUTISM'S MOST SEVERELY
SOCIALLY-IMPAIRED
Barbara A Busse
busse002 at mc.duke.edu
Tue Dec 5 10:55:36 EST 2006
Hello!
Thougth this looked really interesting. Have not had time to read it
all myself. I would love to hear any reactions from you all.
TAKE CARE! Barbara
----- Forwarded by Barbara A Busse/MCLibrary/mc/Duke on 12/05/2006 10:46 AM
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H.GOV> BRAIN'S FEAR CENTER SHRINKS IN
AUTISM'S MOST SEVERELY
SOCIALLY-IMPAIRED
12/05/2006 10:35
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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.
Also participating in the Biological Psychiatry study were: Brendon
Nacewicz, Andrew Alexander, Ph.D., University of Wisconsin.
The Archives study was also funded by NARSAD. The Biological Psychiatry
study was also funded by NARSAD and NAAR.
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]
###
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