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Subject: BRAIN'S FEAR CENTER SHRINKS IN AUTISM'S MOST SEVERELY SOCIALLY-IMPAIRED

U.S. Department of Health and Human Services NATIONAL INSTITUTES OF HEALTH NIH
News National Institute of Mental Health (NIMH) <http://www.nimh.nih.gov/>
National Institute of Child Health and Human Development (NICHD)
<http://www.nichd.nih.gov/>
 
EMBARGOED FOR RELEASE: Monday, December 4, 2006, 4:00 p.m. ET
 
CONTACT: Jules Asher, NIMH Press Office
<e-mail: [log in to unmask]>
301-443-4536
 
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]
 
###
 
This NIH News Release is available online at:
http://www.nih.gov/news/pr/dec2006/nimh-04b.htm.
 
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