1
Experience dependent maturation of emotional systems
of the brain in children with autism spectrum disorder (ASD)
2
Schore (2003) outlines a model of the experience-dependent maturation of the
brain’s evaluative system, also referred to as an appraisal system. The learning and
experience that lead to this maturation take place in large part within what Schore (2003),
and others, describe as a “resonant dyad” between a mother (or primary caregiver) and
infant. In this way, the social relationship created through the attachment bond between
mother and child becomes the primary environment for the self-organization of the
infant’s affect regulation and evaluative systems in the brain. However, in the case of
autism spectrum disorder (ASD), there is accumulating evidence that the important
precursors to the establishment of this resonant dyad are impaired or abnormal. In
particular, there appears to be abnormalities in the infant’s social attention mechanisms,
such as to faces and eyes, maternal tone of voice and other socially relevant stimuli. The
effect of these impairments would be to prevent the formation of the resonant dyadic
interaction in infancy, and consequently disrupt the experience-expectant development of
evaluative and emotional regulation systems in the brain (Nelson, 2000), in particular the
frontolimbic cortex (Schore, 2003). This hypothesis will be explored in light of current
behavioural and neuroanatomical findings in ASD. Implications of this hypothesis for an
intervention treatment for ASD will also be discussed.
The resonant dyad is created through the reciprocal social attention between the
caregiver and the child. From birth, a typically developing child will demonstrate
heightened “social attention” to faces, such as prolonged visual attention to face over
non-face stimuli (Johnson, Dziurawiec, Ellis, & Morton, 1991). A visual fixation
preference for face stimuli emerges around two months of age (Maurer & Barerra, 1981),
and infants will fixate on features within photographs of faces, giving particular attention
3
to the eye region (Maurer & Salpatek, 1967). A sample of five-month-olds demonstrated
sensitivity to small horizontal or vertical deviations in eye gaze (Symons, Hains, & Muir,
1998). This attention to the face, and the eye region in particular, leads to prolonged
periods of “intense mutual gaze” (Schore, 2003, p. 38) between mother and baby,
providing the primary forum for interpersonal communication. In typical development,
these prolonged periods of mutual gaze also provide the opportunity for “mirroring
sequences”, where mother and child simultaneously and instinctively match each other’s
facial expressions over short intervals of approximately 3 seconds (Beebe & Lachmann,
1988; as cited in Schore, 2003). Over the course of these sequences, the level of
engagement and positive affect between the dyad increases, peaks, and then returns to
equilibrium as first the infant and then the mother averts their gaze temporarily. When the
relationship is well attuned, the mother will wait for the infant’s signal to reengage in the
interaction again. In this way, the mother regulates the infant’s physiological arousal
from the intense emotional interchanges, and regulates information processing by
providing the stimulation in the appropriate doses and at the appropriate times (Schore,
2003). It is also hypothesized that through this process, the mother facilitates the infant’s
ability to tolerate increasingly higher levels of arousal, promoting development of the
infant’s emotion regulation system (Schore, 2003). Shared gaze is also important for the
development of social referencing and shared visual attention (Dawson, Meltzoff,
Osterling, Rinaldi, & Brown, 1998). At around 10-12 months of age, the infant begins to
socially reference his or her mother/caregiver when exploring their environment,
“reading” her emotional expression and following her gaze to objects (Schore, 2003). At
this stage in development, the child also begins to demonstrate pointing to communicate,
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and joint attention; where the child will use shifts of gaze to look back and forth between
an object of interest and the caregiver, creating a “shared visual reality” (Schore, 2003).
This type of shared visual attention is thought to provide a foundation for later
development of theory of mind, as the child is able to understand that its own and
another’s perception of the world are distinct (and thus require sharing).
Children with ASD, in contrast to this typical pattern, show abnormalities in
attention to faces. Decreased eye contact is known as one of the hallmark features of the
disorder. Evidence comes from a number of retrospective studies of home movies, which
show decreased levels of attention to faces compared to typically developing children
(e.g., Osterling, Dawson, & Munson, 2002) and at least one prospective case study
(Dawson, Osterling, Meltzoff, & Kuhl, 2000). Furthermore, a recent study of infants who
have an older sibling with a diagnosis of autism, and are therefore at higher genetic risk
for developing the disease, showed an abnormal pattern of visual attention to the mouth
instead of the eyes on a live video image of their mother during a facial interaction
paradigm (Merin, Young, Ozonoff, & Rogers, 2007). Therefore, infants with ASD have
far fewer opportunities for the intense mutual gaze interactions with their caregiver as
described above. They also do not go on to develop reliable pointing for the purposes of
sharing interest, or joint attention. In a study of gaze shifts between objects and people,
20-month-olds with ASD performed the majority of attentional shifts between two
objects, as opposed to between an object and a person, or two people. In contrast, the
typically developing and developmentally delayed control groups shifted attention more
frequently between an object and a person than between an object and another object or
between two people. The toddlers with ASD also spent less time in general looking at
5
people and looked for longer durations at objects, compared to the two control groups
(Swettenham et al., 1998).
Typically developing infants are also sensitive to the social signal of maternal
tone of voice. This type of vocalization often accompanies the mutual gaze interactions,
along with other gestures and body language (Schore, 2003). Sometimes referred to as
“motherese”, or “infant-directed”, this type of speech is characterized by higher pitch,
slower tempo, and exaggerated intonation contours (Grieser & Kuhl, 1988). Infants as
young as seven months not only discriminate between this infant-directed and normal,
adult-directed speech, but show a strong preference for the “motherese” (Pegg, Werker &
McLeod, 1992). Furthermore, study has shown that this type of speech is important for
language learning. When compared to adult-directed speech, motherese contains clearer
phonetic exemplars and may contribute to better phonetic discrimination in infants (Kuhl
et al., 1997). Additionally, the social responsiveness seen during these dyadic
interactions, where the mother responds with social reinforcement (e.g., smiling, moving
closer, touching) when the infant vocalizes, has also been shown to result in more mature
babbling in infants around 8 months of age. When mothers were socially responsive to
their infants within a short tests session (10 minutes), babbling was had more mature
voicing, syllable structure, and faster (canonical) consonant–vowel transitions, as
compared to infants who received the same number of social responses, but which were
not linked to their own production (Goldstein, King & West, 2003).
However, children with ASD do not show the typical preference for this type of
infant directed speech. One study used an electronic toy that played short recordings of
either the child’s mother’s voice or a blend of superimposed voices (similar to speech in a
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crowded room) (Klin, 1991). Whereas typically developing children and developmentally
delayed children spent a significant majority of time listening to the mother’s voice, the
majority of the children in the ASD group spent more time listening to the superimposed
speech sounds (Klin, 1991). In a more recent study, “motherese” type speech samples
were contrasted with non-speech sounds, while matched on acoustic properties. The ASD
group showed a significant preference for the non-speech sounds, as compared to the
control group (Kuhl, Coffey-Corrina, Padden & Dawson, 2005).
Typically developing infants are also sensitive to other social stimuli, such as
responding to their name being called, or sounds produced by humans as opposed to
objects. Turning reliably to one’s name typically emerges around 5-7 months of age
(Dawson et al., 2004). When social sounds (e.g., calling infant’s name, humming a tune,
patting hands on thighs) were contrasted with nonsocial sounds (e.g., phone, whistle,
horn), children with ASD were reduced in orienting overall, but the impairment was more
pronounced for the social stimuli (Dawson et al., 2004).
The cause of these abnormalities is as yet unknown. One hypothesis is that
sharing attention with others, the downstream product of early social attention, requires
rapid shifting of attention back and forth between people and items of interest.
Courchesne, Chisum & Townsend (1995) suggest that difficulties with this rapid
switching may be the underlying cause. A second hypothesis suggests that inherent
complexity of social stimuli may be the issue, with an underlying problem in ASD being
difficulties with processing and representation of complex information (Dawson, 2004).
A third hypothesis is that the underlying deficit is in the reward system; such that social
stimuli are not appropriately tagged with rewarding value, and therefore do not attract
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attention as they would for a typical child who finds social interactions inherently
rewarding (e.g., Dawson et al., 2005). But overall, a pattern of abnormal social attention
emerges in the children with ASD, which will consequently interfere with the typical
establishment of the resonant dyad between the infant and the primary caregiver. As a
result, the parts of the brain that require this type of input for typical maturation (i.e.,
experience expectant plasticity) will not develop typically. According to Schore (2003),
the intense visual and auditory stimulation that the infant receives during the face to face
interactions early in infancy are critical for promoting the growth of the prefrontal and
frontolimbic cortex, which are known to be important for emotion processing and
emotion regulation. One area of particular importance is the orbitofrontal cortex, (Schore,
1997, 2000, 2003). It is uniquely well positioned at the interface between cortical and
subcortical limbic structures, such as the insula, cingulate, and amygdala, but is also
afferently and efferently connected to autonomic structures, allowing it to both process
and regulate autonomic responses to environmental stimuli (Schore, 1997). According to
Schore (2003), during the process of the mother-child attachment interactions, the infant
is storing relations between the affective input from the mother’s face, voice, and body
language and its own internal emotional experiences. In this way, automatic appraisal
prototypes are formed and stored and form the basis of the infant’s own evaluative
system.
Consistent with this model, there is neuroanatomical evidence of abnormalities in
prefrontal cortex in individuals with autism spectrum disorders. One robust finding in
children with autism is significantly increased total brain volume. In a study by
Courchesne et al., (2001), 90 % of boys 2-4 years with ASD had larger than average
8
brain volumes, with an average of 18% more cerebral white matter, and 12% more
cerebral gray matter. Interestingly, these results seemed to follow a posterior to anterior
pattern, with frontal lobes most enlarged. Other studies of the white matter tracts in the
brain of individuals with ASD have also implicated the frontal cortex in particular. Using
diffusion tensor imaging (DTI), a measure of white matter tract integrity, results showed
reduced fractional anisotropy particularly in white matter adjacent to ventromedial
prefrontal cortex, anterior cingulate cortex, and the temporoparietal junction (BarneaGoraly, Kwon, Menon, Eliez, Lotspeich & Reiss, 2004). Frontal cortices have also been
implicated in studies of minicolumnar microstructure, where abnormally narrow
minicolumns were found in area 9 of the prefrontal cortex (Casanova, Buxhoeveden,
Switala, & Roy, 2002), and in a recent unpublished pilot study in the dorsal, mesial and
orbitofrontal areas of prefrontal cortex (reported in Courchesne & Pierce, 2005a).
Minicolumns in the cortex are thought to be the basic unit of information processing,
vertically integrated assemblies of pyramidal cells and interneurons which are arranged in
columns through the different lamina of cortex (Buxhoeveden & Casanova, 2002). These
minicolumns are thicker in association cortices, such as frontal areas, as compared to
primary sensory cortices. It is suggested that the thickness of minicolumns is proportional
to the amount of different information that is being integrated (Buxhoeveden &
Casanova, 2002).
Functional studies have also implicated abnormalities in frontal areas. An fMRI
study of the processing of socially familiar faces demonstrated a lack of activation in
medial frontal areas (including the anterior cingulate) in the ASD group, which was
significantly active in the typical control group (Pierce, Haist, Sedaghat, & Courchesne,
9
2004). Taken together, the evidence has led to the suggestion that the frontal cortices are
especially affected in autism (Courchesne & Pierce, 2005b).
Another area of the limbic system that is important for emotion processing and
regulation is the amygdala (LeDoux, 1996). Although Schore (2003) focuses on the role
of the orbitofrontal cortex in emotional “valence tagging”, the amygdala is thought to
play an important role in that function as well (LeDoux, 1996), and may be even more
important for associations that involve the more “basic” emotions such as fear, anger, joy,
sadness, disgust and surprise (Devinsky & D’Esposito, 2004). The amygdala has also
been shown to be abnormal in children with ASD (Acosta & Pearl, 2002). For example, a
recent study showed significantly larger volume of the left and right amygdala in children
with ASD as compared to typically developing children (Schumann et al., 2004).
However, other studies have been inconsistent, showing either enlarged or reduced
volumes of the amygdala (see Acosta & Pearl, 2002). The other important limbic
structure of the hippocampus has also been shown across studies to have abnormalities.
In particular, Kemper and Bauman (2002) found evidence of small, densely packed
neurons in amygdala, hippocampus, entorhinal cortex and mammilary bodies, upon
autopsy of nine children with autism compared to well matched controls. Thus it appears
that consistent abnormalities in well-known limbic structures, along with frontal
structures, are very commonly observed in neuroanatomical structures of ASD.
However, it is important to note that in the case of autism, that the relationship
between neural abnormalities and lack of attachment-based experiential input is likely not
unidirectional. It is more probable that the relationship for this disorder is bidirectional.
That is, certain genetically based neural abnormalities precede, and lead to, the
10
abnormalities in social orienting detailed above. However, the lack of environmental
experience normally gained from the attachment relationship is a critical factor for further
experience-dependent maturation of emotion systems within the brain. More specifically,
without the typical development of the social attachment relationship, the brain will be
left to self-organize in a relatively non-social environment. This is consistent with
common behavioural observations of children with ASD as they grow up, such as a lack
of interest in others, solitary, repetitive play, interest in objects or parts of objects.
Evidence for this comes from behavioural observations, such as the home movies
mentioned earlier, and studies such as the one conducted by Swettenham and colleagues
(1998), showing that children with ASD spent more time looking at objects that people,
and frequently looked from object to object, but very infrequently back at a person.
Objects and solitary repetitive activities become attractor states that reinforce the
withdrawal from the social world, leading to further deprivation of social interactional
experience. This will also lead to further deficits in learning in general, as studies have
also begun to show the importance of social contexts for learning, such as language
acquisition. In a study by Kuhl, Tsao, and Liu (2003), two groups of infants received
identical exposure to a second language for a brief but intensive time period. However,
one group of infants was exposed to the second language in a live social context, with an
examiner reading a story. The second group was exposed in a non-social context, using
audio-visual presentation of the same examiner reading the story. Results showed that
infants who were exposed to the language in the live, social context showed preserved
phonetic discrimination for the second language; whereas infants who were exposed to
the non-social condition could not discriminate the phonemes (Kuhl et al., 2003). Thus,
11
mere exposure to the second language was not sufficient; the exposure had to take place
in a social context. This finding is consistent with Schore’s (2002) notion of learning and
development taking place within a social relationship. As the infants grow and develop,
relationships expand out from the primary caregiver to include other members of the
family, friends, teachers, and other members of the community. However, as the neural
systems in a child with ASD continue to self-organize within non-social contexts, this
becomes more and more difficult for them to achieve. Furthermore, deficits in the neural
development of the emotional regulation system, due to deprivation of normal social
experience, will lead to difficulties regulating emotion or dealing with distress. This will
lead to abnormal coping and soothing strategies, which often focus around objects and
repetitive sensory stimulation.
More recent types of behavioural interventions for children with ASD are also
consistent with this hypothesis. One method of therapy, known as the developmental,
individual-differences, relationship-based (DIR) model, otherwise known as floortime,
reflects this goal of establishing a social relationship with the child to promote learning.
The overall goals of the floortime technique are to follow the child’s lead, and through
the therapist or family members actions and emotional expression, to “woo the child into
engaging”. The goal is to intrude on the child’s play in a way that forces t him or her to
engage socially in order to achieve goals, and gradually increase the social demands of
the interaction over time, being sensitive to the child’s developmental level and particular
sensitivities or challenges. Interestingly, aspects of the technique as described by a senior
clinician using the model are similar to Schore’s (2003) description of the resonant dyad.
For example, following the child’s lead, creation of circles of communication that open,
12
build, and close (Greenspan, 2000; as cited in Hess, 2004). However, the technique also
requires intrusion and intentional shaping of the child’s behaviour, as opposed to the
completely natural and instinctive interactions with a typically developing infant. The
approach has been criticized because as yet there have not been any systematic,
randomized, controlled studies of outcome. However, the technique has won support with
parents and professionals who have anecdotal evidence of its positive effects. Although
further study is required before the mechanisms underlying success of the floortime
technique will be elucidated, based on Schore’s description we can infer that this type of
therapy attempts to create a social relationship within which learning can occur. It is
possible that for some children with ASD, this type of intervention is able to establish a
resonant dyad. The duration of this dyadic interaction starts off extremely brief, but if
successful can increase in duration and eventually have impact on the child’s engagement
and response to the social world. Presumably this is happening at a neural level and may
be able to reverse some of the abnormal development that has occurred. Studies of neural
structure and function before and after this type of intervention would be extremely
interesting and beneficial.
Children with an autism spectrum disorder exhibit abnormal social orienting in a
number of different domains early on in life. These deficits, likely attributable to
genetically based neural abnormalities, result in difficulty establishing a resonant dyadic
relationship between the infant and caregiver, and it is hypothesized that this lack of
social experience in turn results in further abnormal neural development in the areas of
the brain involved in emotion regulation and appraisal; namely the prefrontal cortex and
limbic system. Consistent with this hypothesis, these areas are the major areas where
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structural abnormalities have been observed in ASD. Without intervention, the infant’s
brain will continue on a self-organizing trajectory in a relatively nonsocial world, as
compared to a typically developing child. This hypothesis is consistent with some
observed symptoms in autism, such as social avoidance and focus on objects and solitary
repetitive behaviours. Furthermore, the lack of social contexts may put children at a
disadavantage for learning in general, such as in the domain of language acquisition.
However, interventions are being explored which contain elements of the dyadic social
relationship described by Schore (2003). These interventions may be able to slow or
reverse the abnormal neural development in children with ASD, and provide mechanisms
for creation of social contexts to promote learning. Further research is needed to explore
the outcomes and mechanisms of these types of interventions.
Comments:
Nice job! The stylish and polished quality of your writing and argumentation
is excellent. You are very clear, the writing is almost transparent in its clarity, and
you integrate your claims with evidence smoothly and seamlessly throughout. Your
discussion of neural systems and their interrelations is generally spot-on. Excellent
precision in your individual points and good development of your arguments from
point to point.
I’m glad you recognized the potential confounds and circularity of proposing
the dyadic relationship as a causal factor. You dealt with this problem quite well,
and the image of an ongoing self-organizing trajectory, free of the parental
constraint, was quite persuasive and effective. Still, I think this was where you could
14
have built a stronger essay. You could have differentiated, based on what you know
of the brain and development, between the kind of anomalies likely to lead to the
breakdown of dyadic resonance and the kind likely to follow. This watershed notion
should be really strong, should even be the backbone of the model. Otherwise, it
seems a bit arbitrary that the attachment relationship suddenly steps up to the plate
(of causation) at some point along the way. Also, to say that the interaction between
the neural anomalies and the breakdown of the dyad is bidirectional is a critical
point. Again, good that you made it, but better to make more of it. Bidirectional
causation of this sort has all kinds of cool qualities—such as the likelihood of
positive feedback, phase transitions (sudden switches) in the trajectory over time,
etc. In fact, S-O can only result in systems where there is bidirectional causation (viz
positive feedback). Finally, since you make Schore’s model so central, why not argue
that the OFC is specially poised to be an effect rather than a cause in the ongoing
trajectory. This would be most powerful. I got a great paper from a student a few
years ago, arguing that lower brain anomalies (brainstem issues, and maybe those
amygdala differences you mention) are prespecified neural anomalies, but cortical
differences then manifest themselves, as a developmental cascade, completing the
picture of how autistic brains differ. I think that kind of argument is most powerful,
and you could link it with the role of the attachment relationship to make a very
tight case.
Paper: A/A+
15
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