Brain region controlling
sociability identified
9 February 2009
A combination of functional magnetic resonance imaging (fMRI) and
measurement of brain electrical activity in a study of brain function
has enabled researchers to trace sociability to the amygdala region of
the brain.
People with a genetic condition called Williams syndrome are famously
gregarious. Researchers at the Stanford University School of Medicine
showed that parts of a particular brain region known as the amygdala
react more powerfully in Williams syndrome patients than in
developmentally normal subjects — or in subjects with delays in
development not caused by Williams syndrome — when exposed to facial
expressions conveying positive emotions.
The study was published in the Journal of Neuroscience.
Biopsychologist Brian Haas, PhD, a postdoctoral researcher at Stanford,
shares first authorship of the study, with Debra Mills, PhD, of Bangor
University in Gwynned, Wales. Haas conducts research in the laboratory
of Allan Reiss, MD, the Howard C. Robbins Professor of Psychiatry and
Behavioral Sciences at Stanford, who is the paper’s senior author. The
work is part of an ongoing multicenter collaboration.
Williams syndrome, a rare genetic disorder affecting perhaps one in
10,000 individuals in whom a specific and well-defined chunk of DNA in
one chromosome is missing, manifests in a distinctive pattern of
physical and behavioural abnormalities including greatly reduced spatial
and mathematical reasoning, but relatively less loss of certain verbal
abilities or capacity to read others’ emotions.
“If you give people with Williams syndrome a picture of a bicycle to
copy, they are able to draw the individual components of the bike — the
wheels, the handlebars and so forth — but these components will be all
over the page. It wouldn’t look like a bike,” said Haas. “But if you
give them pictures of faces and ask them to describe the expressions, or
ask them to talk about a story they’ve heard, they not only show just as
much skill as you or I, but in some cases use even more socially and
emotionally descriptive language. It’s been speculated that they may
even be better than the rest of us at picking up social information from
facial expressions. We aimed to study the neurological underpinnings of
social functioning in these people.”
Sociability is one trait emphatically not lacking in people with
Williams syndrome. On the contrary, they are invariably sociable — so
much so that they will not uncommonly approach and strike up
conversations with total strangers. Indeed, these individuals’ famous
gregariousness can be so pronounced as to occasionally place them in
harm’s way.
The investigators reasoned that the link between stereotypical
sociability associated with Williams syndrome and the characteristic
genetic deletion causing the condition might be mediated by a region
deep within the brain called the amygdala. This almond-shaped,
peanut-sized structure is known to be key to social and emotional
processing — reading facial expressions or voices, for example. Lesions
of the amygdala can cause a person to lose the ability to make quick
“friend or foe” assessments, which have undoubtedly had life-or-death
implications in human evolution.
Using two different techniques for objectively measuring brain
response, the team showed that when 14 individuals with Williams
syndrome looked at photos of faces judged by an independent team of
normal reviewers to be especially reflective of a positive emotional
state — like happiness — their amygdalas responded much more forcefully
than did those of 13 age-matched normally developing subjects.
One of those techniques, functional magnetic resonance imaging, was
able to localize the increased activity to specific nerve clusters in
the amygdala, while another technique, involving monitoring the brain’s
electrical signals with a device placed on subjects’ heads, charted the
course of this activity over time.
Earlier work by others had already shown that Williams syndrome
patients’ amygdalas respond less vigorously to negatively charged
stimuli (such as a face exhibiting fear) than do those of
developmentally normal subjects. The new study both confirmed that
finding and showed, for the first time, that exposure to a positive
facial expression triggers a jump in signaling within the amygdala in
these individuals, but not in healthy control subjects.
To rule out the possibility that the different response merely
reflected IQ differences between normal and Williams syndrome subjects,
the researchers also compared the latter with 15 other developmentally
challenged subjects whose IQs matched those of the Williams syndrome
group. They saw the same result here, as well.
Their reduced amygdala response to negatively charged facial
expressions may provide a physiological basis for Williams syndrome
patients’ relative lack of reticence about approaching and engaging
strangers, said Haas. Likewise, he said, the heightened response to
positively charged facial expressions suggests that exposure to these
smiling faces may be profoundly rewarding to these patients and,
therefore, enhance their sociability. It may also mean that social
rather than, say, monetary rewards may prove to be better incentives for
training persons with the syndrome to compensate for their deficits,
Haas speculated.
This differential processing in the amygdala appears to have its
roots in Williams syndrome’s defining DNA deletion, implying a genetic
basis for the difference — and, perhaps, for individual differences
among normal people.
In some ways, both the deficits and strengths of the syndrome are the
polar opposites of those that typify the far more common syndrome called
autism, in which mathematical and visuospatial skills may be not only
unimpaired but sometimes pronouncedly enhanced, while functions such as
eye contact or gregarious behaviour are markedly diminished.
But in contrast to Williams syndrome, which is always attributable to
the same distinct genetic lesion, “autism is an umbrella covering many
different conditions with similar symptoms but a wide range of causes,”
said Reiss, complicating brain-function analysis of the sort his lab is
doing. However, he said, another genetic disorder, called Fragile X
syndrome, stems from a genetic abnormality as distinctive and
well-characterized as Williams syndrome but often produces the symptoms
of autism.
Reiss has applied for funding to study and compare brain function in
very young children with these two conditions, in the hope of
determining how the loss of specific genes results in specific
behavioral changes, how and where these changes are mediated in the
brain and what role the environment plays in modifying outcome.
This research holds implications for neurologically normal individuals,
too. Studies have shown that more-extroverted people’s amygdalas are
more responsive to happy faces than less-extroverted people’s are,
suggesting the involvement of physiological hardwiring in shaping
personality traits. “The more we understand about what makes us more or
less social beings,” said Reiss, “the better we may be able to tolerate
one another’s differences.”
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