|Bron bij Psychologische krachten: spiegelneuronen en autisme||
Dit artikel is een vervolg op een artikel over spiegelneuronen
. De tekst bevat verkleinde versies van de met tekst toegelichte illustraties, die
hyperlinks zijn naar de grotere leesbare, versies.
Scientific American, nov. 2006, door Vilayanur S. Ramachandran en Lindsay M.
Overview | Mirror neurons and autism
■ Because mirror neurons appear to be involved in social
interaction, dysfunctions of this neural system could explain some of the
primary symptoms of autism, including isolation and absence of empathy.
■ Studies of people with autism show
a lack of mirror neuron activity in several regions of the brain. Researchers
speculate that treatments designed to restore this activity could alleviate some
of autism's symptoms.
■ A complementary hypothesis, the
salience landscape theory, could account for secondary symptoms of autism such
Broken mirrors - a theory of autism
Studies of the mirror neuron system may reveal clues to the causes of autism and
help researchers develop new ways to diagnose and treat the disorder
Tussentitels: Mirror neurons appear to be performing precisely the same
are disrupted in autism.
These findings provide compelling evidence that people with autism have
dysfunctional mirror neuron systems.
If the child's mirror neuron functions are dormant rather than lost, it may
be possible to revive this ability.
first glance you might not notice anything odd on meeting a young boy with
autism. But if you try to talk to him, it will quickly become obvious that
something is seriously wrong. He may not make eye contact with you; instead he
may avoid your gaze and fidget, rock his body to and fro, or bang his head
against the wall. More disconcerting, he may not be able to conduct anything
remotely resembling a normal conver-sation. Even though he can experience
emotions such as fear, rage and pleasure, he may lack genuine empathy for other
people and be oblivious to subtle social cues that most children would pick up
In the 1940s two physicians - American psychiatrist Leo
Kanner and Austrian pediatrician Hans Asperger - independently discovered this
developmental disorder, which afflicts about 0.5 percent of American children.
Neither researcher had any knowledge of the other's work, and yet by an uncanny
coincidence each gave the syndrome the same name: autism, which derives from the
Greek word autos, meaning "self." The name is apt, because the most conspicuous
feature of the disorder is a withdrawal from social interaction. More recently,
doctors have adopted the term "autism spectrum disorder" to make it clear that
the illness has many related variants that range widely in severity but share
some characteristic symptoms.
Ever since autism was identified, researchers have struggled to determine what
causes it. Scientists know that susceptibility to autism is inherited, although
environmental risk factors also seem to play a role [see "The Early Origins of
Autism," by Patricia M. Rodier; SCIENTIFIC AMERICAN, February 2000]. Starting in
the late 1990s, investigators in our laboratory at the University of California,
San Diego, set out to explore whether there was a connection between autism and
a newly discovered class of nerve cells in the brain called mirror neurons.
Because these neurons appeared to be involved in abilities such as empathy and
the perception of another individual's intentions, it seemed logical to
hypothesize that a dysfunction of the mirror neuron system could result in some
of the symptoms of autism. Over the past decade, several studies have provided
evidence for this theory. Further investigations of mirror neurons may explain
how autism arises, and in the process physicians may develop better ways to
diagnose and successfully treat the disorder.
Explaining the Symptoms
Although the chief diagnostic signs of autism are social isolation, lack of eye
contact, poor language capacity and absence of empathy, other less well known
symptoms are commonly evident. Many people with autism have problems
understanding metaphors, sometimes interpreting them literally. They also have
difficulty miming other people's actions. Often they display an eccentric
preoccupation with trifles yet ignore important aspects of their environment,
especially their social surroundings. Equally puzzling is the fact that they
frequently show an extreme aversion to certain sounds that, for no obvious
reason, set off alarm bells in their minds.
The theories that have been proposed to explain autism can be
divided into two groups: anatomical and psychological. (Researchers have
rejected a third group of theories-such as the "refrigerator mother"
hypothesis-that blame the disorder on poor upbringing.) Eric Courchesne
ofU.C.S.D. and other anatomists have shown elegantly that children with autism
have characteristic abnormalities in the cerebellum, the brain structure
responsible for coordinating complex voluntary muscle movements. Although these
observations must be taken into account in any final explanation of autism, it
would be premature to conclude that damage to the cerebellum is the sole cause
of the disorder. Cerebellar damage inflicted by a stroke in a child usually
produces tremors, swaying gait and abnormal eye movements-symptoms rarely seen
in autism. Conversely, one does not see any of the symptoms typical of autism in
patients with cerebellar disease. It is possible that the cerebellar changes
observed in children with autism may be unrelated side effects of abnormal genes
whose other effects are the true causes of the disorder.
Perhaps the most ingenious of the psychological theories is
that of Uta Frith of University College London and Simon Baron-Cohen of the
University of Cambridge, who posit that the main abnormality in autism is a
deficit in the ability to construct a "theory of other minds." Frith and
Baron-Cohen argue that specialized neural circuitry in the brain allows us to
create sophisticated hypotheses about the inner workings of other people's
minds. These hypotheses, in turn, enable us to make useful predictions about
others' behavior. Frith and Baron-Cohen are obviously on the right track, but
their theory does not provide a complete explanation for the constellation of
seemingly unrelated symptoms of autism. Indeed, saying that people with autism
cannot interact socially because they lack a "theory of other minds" does not go
very far beyond restating the symptoms. What researchers need to identify are
the brain mechanisms whose known functions match those that are disrupted in
One clue comes from the work of Giacomo Rizzolatti and his
colleagues at the University of Parma in Italy, who in the 1990s studied neural
activity in the brains of macaque monkeys while the animals were performing
goal-directed actions [see "Mirrors in the Mind," by Giacomo Rizzolatti,
Leonardo Fogassi and Vittorio Gallese, on page 30]. Researchers have known for
decades that certain neurons in the premotor cortex part of the brain's frontal
lobe-are involved in controlling voluntary movements. For instance, one neuron
will fire when the monkey reaches for a peanut, another will fire when the
animal pulls a lever, and so on. These brain cells are often referred to as
motor command neurons. (Bear in mind that the neuron whose activity is recorded
does not control the arm by itself; it is part of a circuit that can be
monitored by observing the signals in the constituent neurons.) What surprised
Rizzolatti and his coworkers was that a subset of the motor command neurons also
fired when the monkey watched another monkey or a researcher perform the same
action. For example, a neuron involved in controlling the reach-for-the-peanut
action fired when the monkey saw one of his fellows making that movement.
Brain-imaging techniques subsequently showed that these so-called mirror neurons
also exist in the corresponding regions of the human cortex. These observations
implied that mirror neurons-or, more accurately, the networks they are part
of-not only send motor commands but also enable both monkeys and humans to
determine the intentions of other individuals by mentally simulating their
actions. In monkeys, the role of the neurons may be limited to predicting simple
goal-directed actions, but in humans the mirror neuron system may have evolved
the ability to interpret more complex intentions.
Later research showed that mirror neurons are located in other parts of the
human brain, such as the cingulate and insular cortices, and that they may play
a role in empathetic emotional responses. While studying the anterior cingulate
cortex of awake human subjects, investigators found that certain neurons that
typically fire in response to pain also fired when the person saw someone else
in pain. Mirror neurons may also be involved in imitation, an ability that
appears to exist in rudimentary form in the great apes but is most pronounced in
humans. The propensity to imitate must be at least partly innate: Andrew
Meltzoff of the University of Washington has shown that if you stick your tongue
out at a newborn baby, the infant will do the same. Because the baby cannot see
its own tongue, it cannot use visual feedback and error correction to learn the
skill. Instead there must be a hardwired mechanism in the child's brain for
mapping the mother's visual appearance-whether it be a tongue sticking out or a
smile-onto the motor command neurons.
Language development in childhood also requires a remapping
of sorts between brain areas. To imitate the mother's or father's words, the
child's brain must transform auditory signals in the hearing centers of the
brain's temporal lobes into verbal output from the motor cortex. Whether mirror
neurons are directly involved in this skill is not known, but clearly some
analogous process must be going on. Last, mirror neurons may enable humans to
see themselves as others see them, which may be an essential ability for
self-awareness and introspection.
Suppressing Mu Waves
What has all this to do with autism? In the late 1990s our group at U.C.S.D.
noted that mirror neurons appear to be performing precisely the same functions
that seem to be disrupted in autism. If the mirror neuron system is indeed
involved in the interpretation of complex intentions, then a breakdown of this
neural circuitry could explain the most striking deficit in people with autism,
their lack of social skills. The other cardinal signs of the disorder-absence of
empathy, language deficits, poor imitation, and so on-are also the kinds of
things you would expect to see if mirror neurons were dysfunctional. Andrew
Whitten's group at the University of St. Andrews in Scotland made this proposal
at about the same time we did, but the first experimental evidence for the
hypothesis came from our lab, working in collaboration with Eric L. Altschuler
and Jaime A. Pineda of U.C.S.D.
To demonstrate mirror neuron dysfunction in children with autism, we needed to
find a way to monitor the activity of their nerve cells without putting
electrodes in their brains (as Rizzolatti and his colleagues did with their
monkeys). We realized that we could do so using an electroencephalogram (EEG)
measurement of the children's brain waves. For more than half a century,
scientists have known that an EEG component called the mu wave is blocked
anytime a person makes a voluntary muscle movement, such as opening and closing
one's hands. Interestingly, this component is also blocked when a person watches
someone else perform the same action. One of us (Ramachandran) and Altschuler
suggested that mu-wave suppression might provide a simple, noninvasive probe for
monitoring mirror neuron activity.
We decided to focus our first experiments on a
high-functioning child with autism-that is, a child without severe cognitive
impairments. (Very young, low-functioning children did not participate in this
study because we wanted to confirm that any differences we found were not a
result of problems in attention, understanding instructions or the general
effects of mental retardation.) The EEG showed that the child had an observable
mu wave that was suppressed when he made a simple, voluntary movement, just as
in normal children. But when the child watched someone else perform the action,
the suppression did not occur. We concluded that the child's motor command
system was intact but that his mirror neuron system was deficient. This
observation, which we presented at the annual meeting of the Society for
Neuroscience in 2000, provided a striking vindication of our hypothesis.
One has to be careful, however, of generalizing from a single
case, so our lab group later conducted a more systematic series of experiments
in 10 highfunctioning individuals with autism spectrum disorder and 10 age- and
gendermatched control subjects. We saw the expected suppression of mu waves when
the control subjects moved their hands and watched videos of a moving hand, but
the EEGs of the subjects with autism showed mu suppression only when they moved
their own hands.
Other researchers have confirmed our results using different
techniques for monitoring neural activity. A group led by Riitta Hari of the
Helsinki University of Technology found mirror neuron deficits in children with
autism by employing magnetoencephalography, which measures the magnetic fields
produced by electric currents in the brain.
More recently, Mirella Dapretto of the University of California, Los Angeles,
and her colleagues used functional magnetic resonance imaging to show a
reduction in mirror neuron activity in the prefrontal cortices of individuals
with autism. And Hugo Theoret of the University of Montreal and his co-workers
used transcranial magnetic stimulation, a technique that induces electric
currents in the motor cortex to generate muscle movements, to study mirror
neuron activity in subjects with autism. In the control subjects, induced hand
movements became more pronounced when the subjects watched videos of the same
movements; this effect was much weaker in the subjects with autism. Taken
together, these findings provide compelling evidence that people with autism
have dysfunctional mirror neuron systems. Scientists do not yet know which
genetic and environmental risk factors can prevent the development of mirror
neurons or alter their function, but many research groups are now actively
pursuing the hypothesis because it predicts symptoms that are unique to autism.
In addition to explaining the primary signs of autism, deficiencies in the
mirror neuron system can also account for some of the less well known symptoms.
For instance, researchers have long known that children with autism often have
problems interpreting proverbs and metaphors.
When we told one of our subjects to "get a grip on yourself," he took the
message literally and started grabbing his own body. Though seen in only a
subset of children with autism, this difficulty with metaphors cries out for an
Understanding metaphors requires the ability to extract a
common denominator from superficially dissimilar entities. Consider the bouba/kiki
effect, which was discovered by German-American psychologist Wolfgang K6hler
more than 60 years ago. In this test, a researcher displays two crudely drawn
shapes, one jagged and one curvy, to an audience and asks, "Which of these
shapes is bouba and which is kiki?" No matter what languages the respondents
speak, 98 percent will pick the curvy shape as bouba and the jagged one as kiki.
This result suggests that the human brain is somehow able to extract abstract
properties from the shapes and sounds-for example, the property o~ jaggedness
embodied in both the pointy drawing and the harsh sound of kiki. We conjectured
that this type of cross-domain mapping is analogous to metaphors and must surely
involve neural circuits similar to those in the mirror neuron system. Consistent
with this speculation, we discovered that children with autism perform poorly at
the bouba/kiki test, pairing the shapes and sounds incorrectly.
But which part of the human brain is involved in this skill?
The angular gyrus, which sits at the crossroads of the brain's vision, hearing
and touch centers, seemed to be a likely candidate-not only because of its
strategic location but because nerve cells with mirror neuronlike properties
have been identified there.
When we studied nonautistic subjects with damage to this area of the brain, we
found that many of them fail the bouba/ kiki test and have a disproportionate
difficulty understanding metaphors, just like people with autism. These results
suggest that cross-domain mapping may have originally developed to aid primates
in complex motor tasks such as grasping tree branches (which requires the rapid
assimilation of visual, auditory and touch information) but eventually evolved
into an ability to create metaphors. Mirror neurons allowed humans to reach for
the stars, instead of mere peanuts.
Can the Mirrors Be Repaired?
The discovery of mirror neuron deficiencies in people with autism opens up new
approaches to diagnosing and treating the disorder. For example, physicians
could use the lack of mu-wave suppression (or perhaps the failure to mimic a
mother sticking out her tongue) as a diagnostic tool to identify children with
autism in early infancy, so that the currently available behavioral therapies
can be started as quickly as possible. Timely intervention is critical; the
behavioral therapies are much less effective if begun after autism's main
symptoms appear (typically between ages two and four).
An even more intriguing possibility would be to use
biofeedback to treat autism or at least alleviate its symptoms. Doctors could
monitor the mu waves of a child with autism and display them on a screen in
front of the patient. If the child's mirror neuron functions are dormant rather
than completely lost, it may be possible for him or her to revive this ability
by learning- through trial and error and visual feedback-how to suppress the mu
waves on the screen. Our colleague Pineda is pursuing this approach, and his
preliminary results look promising. Such therapies, though, should supplement
rather than replace the traditional behavioral-training techniques.
Another novel therapeutic approach might rely on correcting
chemical imbalances that disable the mirror neurons in individuals with autism.
Our group (including students Mikhi Horvath and Mary Vertinsky) has suggested
that specialized neuromodulators may enhance the activity of mirror neurons
involved in emotional responses. According to this hypothesis, the partial
depletion of such chemicals could explain the lack of emotional empathy seen in
autism, and therefore researchers should look for compounds that stimulate the
release of the neuromodulators or mimic their effects on mirror neurons. One
candidate for investigation is MDMA, better known as ecstasy, which has been
shown to foster emotional closeness and communication. It is possible that
researchers may be able to modify the compound to develop a safe, effective
treatment that could alleviate at least some of autism's symptoms.
Such treatments, however, may offer only partial relief,
because other symptoms of autism cannot be explained by the mirror neuron
hypothesis-for example, repetitive motions such as rocking to and fro, avoidance
of eye contact, hypersensitivity, and aversion to certain sounds. In an attempt
to determine how these secondary symptoms might arise, our lab group (in
collaboration with William Hirstein of Elmhurst College and Portia Iversen of
Cure Autism Now, a nonprofit foundation based in Los Angeles) has developed what
we call the salience landscape theory.
When a person looks at the world, he or she is confronted
with an overwhelming amount of sensory information - sights, sounds, smells, and
so on. After being processed in the brain's sensory areas, the information is
relayed to the amygdala, which acts as a portal to the emotion-regulating limbic
system. Using input from the individual's stored knowledge, the amygdala
determines how the person should respond emotionally - for example, with fear
(at the sight of a burglar), lust (on seeing a lover) or indifference (when
facing something trivial).
Messages cascade from the amygdala to the rest of the limbic system and
eventually reach the autonomic nervous system, which prepares the body for
If the person is confronting a burglar, for example, his heart rate will rise
and his body will sweat to dissipate the heat from muscular exertion. The
autonomic arousal, in turn, feeds back into the brain, amplifying the emotional
response. Over time, the amygdala creates a salience landscape, a map that
details the emotional significance of everything in the individual's
Our group decided to explore the possibility that children with autism have a
distorted salience landscape, perhaps because of altered connections between the
cortical areas that process sensory input and the amygdala or between the limbic
structures and the frontal lobes that regulate the resulting behavior. As a
result of these abnormal connections, any trivial event or object could set off
an extreme emotional response - an autonomic storm - in the child's mind. This
hypothesis would explain why children with autism tend to avoid eye contact and
any other novel sensation that might trigger an upheaval. The distorted
perceptions of emotional significance might also explain why many children with
autism become intensely preoccupied with trifles such as train schedules while
expressing no interest at all in things that most children find fascinating.
We found some support for our hypothesis when we monitored
autonomic responses in a group of 37 children with autism by measuring the
increase in their skin conductance caused by sweating. In contrast with the
control subjects, the children with autism had a higher overall level of
autonomic arousal. Although they became agitated when exposed to trivial objects
and events, they often ignored stimuli that triggered expected responses in the
But how could a child's salience landscape become so
distorted? Investigators have found that nearly one third of children with
autism have had temporal lobe epilepsy in infancy, and the proportion may be
much higher given that many epileptic seizures go undetected. Caused by repeated
random volleys of nerve impulses traversing the limbic system, these seizures
could eventually scramble the connections between the visual cortex and the
amygdala, indiscrimin-ately enhancing some links and diminishing others. In
adults, temporal lobe epilepsy results in florid emotional disturbances but does
not radically affect cognition; in infants, however, the seizures may lead to a
more profound disability. And, like autism, the risk of temporal lobe epilepsy
in infancy appears to be influenced by both genetic and environmental factors.
Some genes, for example, could make a child more susceptible to viral
infections, which could in turn predispose the child to seizures.
Our findings on autonomic responses may help explain the old
clinical observation that high fever sometimes temporarily alleviates the
symptoms of autism. The autonomic nervous system is involved in controlling body
temperature; because fever and the emotional upheavals of autism appear to be
regulated by the same neural pathways, perhaps the former can mitigate the
The salience landscape theory could also provide an
explanation for the repetitive motions and head banging seen in children with
autism: this behavior, called self-stimulation, may somehow damp the child's
autonomic storms. Our studies found that self-stimulation not only had a calming
effect but also led to a measurable reduction in skin conductance. This result
suggests a possible symptomatic therapy for autism. Hirstein is now developing a
portable device that could monitor an autistic child's skin conductance; when
the device detects autonomic arousal, it could turn on another device, called a
squeeze vest, that provides a comforting pressure by gently tightening around
the child's body.
Our two candidate theories for explaining the symptoms of
autism - mirror neuron dysfunction and distorted salience landscape - are not
necessarily contradictory. It is possible that the same event that distorts a
child's salience landscape - the scrambled connections between the limbic system
and the rest of the brain - also damages the mirror neurons. Alternatively, the
altered limbic connections could be a side effect of the same genes that trigger
the dysfunctions in the mirror neuron system. Further experiments are needed to
rigorously test these conjectures. The ultimate cause of autism remains to be
discovered. In the meantime, our speculations may provide a useful framework for
VILAYANUR S. RAMACHANDRAN and LINDSAY M. OBERMAN have investigated the links
between autism and the mirror neuron system at the Center for Brain and
Cognition at the University of California, San Diego. Ramachandran, director of
the center, earned his Ph.D. in neuroscience from the University of Cambridge. A
renowned expert on brain abnormalities, he has also studied the phenomena of
phantom limbs and synesthesia, for which he won the 2D05 Henry Dale Prize and a
lifetime fellowship from the Royal Institution of Great Britain. Oberman is a
graduate student in Ramachandran's laboratory at U.C.S.D., joining the group in
More to explore
Autonomic Responses of Autistic Children to People and Objects. William
Hirstein, Portia Iversen and Vilayanur S. Ramachandran in Proceedings of the
Royal Society of London B, Vol. 268, pages 1883-1888; 2001.
EEG Evidence for Mirror Neuron Oysfunction in Autism Spectrum Disorders.
Lindsay M. Oberman, Edward M. Hubbard, Joseph P. McCleery, Eric L. Altschuler,
Jaime A. Pineda and Vilayanur S. Ramachandran in Cognitive Brain Research,
Vol. 24, pages 190-198; 2005.
A Brief Tour of Human Consciousness. New edition. Vilayanur S.
Ramachandran. Pi Press, 2005.
Terug naar Psychologie lijst
, Psychologie overzicht
, of naar