1. Study examines brain activity and anxiety symptoms in youth with autism spectrum disorder

    December 14, 2017 by Ashley

    From the Wiley press release:

    The error-related negativity (ERN) is a brain signal response to errors that is thought to reflect threat sensitivity and has been implicated in anxiety disorders in individuals without autism spectrum disorder (ASD). A new Autism Research study has revealed that the ERN is related to social anxiety symptoms — specifically performance fears — in youth with ASD.

    The findings suggest that heightened threat sensitivity may be characteristic of people with ASD who exhibit social fearfulness. Those with more severe ASD symptoms and/or lower verbal abilities may have difficulty identifying or communicating their performance anxieties. Therefore, the ERN may provide important and perhaps otherwise inaccessible information on how these individuals experience internal sources of threat.

    “This study, led by my graduate student, Tamara Rosen, clarifies and focuses inconsistencies in previous research on the unique way error processing manifests and can impact anxiety symptoms in individuals with ASD,” said senior author Dr. Matthew Lerner, of Stony Brook University. “These findings can help guide and pinpoint efforts to diagnose and treat the substantial co-occurring anxiety experienced by many people with ASD.”


  2. Study suggests odors that carry social cues seem to affect volunteers on the autism spectrum differently

    December 8, 2017 by Ashley

    From the Weizmann Institute of Science press release:

    Autism typically involves the inability to read social cues. We most often associate this with visual difficulty in interpreting facial expression, but new research at the Weizmann Institute of Science suggests that the sense of smell may also play a central role in autism. As reported in Nature Neuroscience, Weizmann Institute of Science researchers show that people on the autism spectrum have different — and even opposite — reactions to odors produced by the human body. These odors are ones that we are unaware of smelling, but which are, nonetheless, a part of the nonverbal communication that takes place between people, and which have been shown to affect our moods and behavior. Their findings may provide a unique window on autism, including, possibly, on the underlying developmental malfunctions in the disorder.

    Researchers in the lab of Prof. Noam Sobel in the Institute’s Neurobiology Department investigate, among other things, the smells that announce such emotions as happiness, fear or aggression to others. Although this sense is not our primary sense, as it is in many other mammals, we still subliminally read and react to certain odors. For example “smelling fear,” even if we cannot consciously detect its odor, is something we may do without thinking. Since this is a form of social communication, Sobel and members of his lab wondered whether it might be disrupted in a social disorder like autism.

    To conduct their experiments, Sobel and lab members Yaara Endevelt-Shapira and Ofer Perl, together with other members of his lab, devised a series of experiments with a group of participants on the high functioning end of the autism spectrum who volunteered for the study. To begin with, the researchers tested the ability of both autistic and control volunteers to identify smells that can be consciously detected, including human smells like sweat. There was no significant difference between the groups at this stage, meaning the sense of smell in the autistic participants was not significantly different from that of controls.

    Two groups were then exposed to either to the “smell of fear” or to a control odor. The smell of fear was sweat collected from people taking skydiving classes, and control odor was sweat from the same people, only this time it had been collected when they were just exercising — without feeling fear.

    This is where differences emerged: Although neither group reported detecting dissimilarities between the two smells, their bodies reacted to each in a different way. In the control group, smelling the fear-induced sweat produced measurable increases in the fear response, for example in skin conductivity, while the everyday sweat did not. In the autistic men, fear-induced sweat lowered their fear responses, while the odor of “calm sweat” did the opposite: It raised their measurable anxiety levels.

    Next, the group created talking robotic mannequins that emitted different odors through their nostrils. These mannequins gave the volunteers, who were unaware of the olfactory aspect of the experiment, different tasks to conduct. Using mannequins enabled the researchers to have complete control over the social cues — odor-based or other — that the subjects received. The tasks were designed to evaluate the level of trust that the volunteers placed in the mannequins — and here, too, the behavior of autistic volunteers was the opposite of the control group: They displayed more trust in the mannequin that emitted the fear-induced odor and less in the one that smelled “calmer.”

    In continuing experiments, the researchers asked whether other subliminal “social odors” have a different impact in autism than in control groups. In one, the volunteers were exposed to sudden loud noises during their sessions while at the same time they were also exposed to a potentially calming component of body-odor named hexadecanal. Another automatic fear response — blinking — was recorded using electrodes above the muscles of the eye. Indeed, the blink response in the control group was weaker when they were exposed to hexadecanal, while for those in the autistic group this response was stronger with hexadecanal.

    In other words, the autistic volunteers in the experiment did not display an inability to read the olfactory social cues in smell, but rather they misread them. Sobel and his group think that this unconscious difference may point to a deeper connection between our sense of smell and early development. Research in recent years has turned up smell receptors like those in our nasal passages in all sorts of other places in our bodies — from our brains to our uteri. It has been suggested that these play a role in development, among other things. In other words, it is possible that the sensing of subtle chemical signals may go awry at crucial stages in the brain’s development in autism. “We are still speculating, at this point,” says Sobel, “but we are hoping that further research in our lab and others will clarify both the function of these unconscious olfactory social cues and their roots in such social disorders as autism.”

     


  3. Researchers develop video game that improves balance in youth with autism

    December 2, 2017 by Ashley

    From the University of Wisconsin-Madison press release:

    Playing a video game that rewards participants for holding various “ninja” poses could help children and youth with autism spectrum disorder (ASD) improve their balance, according to a recent study in the Journal of Autism and Developmental Disorders led by researchers at the University of Wisconsin-Madison.

    Balance challenges are more common among people with ASD compared to the broader population, says study lead author Brittany Travers, and difficulties with balance and postural stability are commonly thought to relate to more severe ASD symptoms and impaired activities in daily living.

    “We think this video game-based training could be a unique way to help individuals with ASD who have challenges with their balance address these issues,” says Travers, an investigator at UW-Madison’s Waisman Center and an assistant professor of kinesiology.

    In this pilot study — the largest ever to look at the effects of balance training on individuals with ASD — 29 participants between the ages of 7 and 17 with ASD completed a six-week training program playing a video game developed by the researchers.

    By the end of the program, study participants showed significant improvements in not only their in-game poses but also their balance and posture outside of the game environment.

    According to Travers, balance improvements outside the video game context are especially important. “Our participants are incredibly clever when it comes to finding ways to beat video games!” she says. “We wanted to make sure that the improvements we were seeing were truly balance-related and not limited to the video game.”

    Ten out of 11 study participants who completed a post-game questionnaire also said they enjoyed playing the video games.

    “We always aim to make the interventions fun,” says Travers. “We have couched a rigorous exercise (by the end of some gaming sessions, participants had been standing on one foot for 30 minutes) in a video game format, so we were delighted to hear that the participants enjoyed the game.”

    Travers developed the video game with help from Andrea Mason, professor of kinesiology at UW-Madison, Leigh Ann Mrotek, professor of kinesiology at UW-Oshkosh and Anthony Ellertson, program director of gaming and interactive technology at Boise State University.

    The gaming system uses a Microsoft Kinect camera and a Nintendo Wii balance board connected to software developed on a Windows platform using Adobe Air.

    “Players see themselves on the screen doing different ‘ninja’ poses and postures, and they are rewarded for doing those poses and postures; that’s how they advance in the game,” says Travers.

    The study also explored individual differences that might predict who would benefit most from this type of video game-based balance training.

    For example, the study showed that participants with some characteristics, such as ritualistic behaviors (like the need to follow a set routine around mealtimes or bedtime) did not benefit as much from the video game as those without these behaviors.

    On the other hand, some characteristics, such as body mass index or IQ, did not influence whether a participant benefited from balance training.

    “There is a lot of variability in the clinical profile of ASD, and it’s unlikely that there will be a one-size-fits-all approach for balance training that helps all individuals with ASD,” says Travers.

    Researchers are working to make the game more accessible to different individuals within the autism spectrum. “We already have some features that help — the game has very little verbal instruction, which should make it more accessible to individuals who are minimally verbal,” says Travers. “Ultimately, we would like to move this video game-based training outside the lab.”


  4. Study suggests time between pregnancies may affect autism risk

    December 1, 2017 by Ashley

    From the Wiley press release:

    Investigators have found a link between the amount of time between pregnancies and Autism Spectrum Disorder in children. The findings are published in Autism Research.

    Autism Spectrum Disorder was increased in second and later-born children who were conceived less than 18 months or 60 or more months after the mother’s previous birth. Other developmental disabilities were not associated with birth spacing.

    “These findings support existing guidelines on pregnancy spacing and further highlight the association between autism and pregnancy health,” said lead author Dr. Laura Schieve, of the Centers for Disease Control and Prevention. “Couples thinking about getting pregnant should discuss pregnancy planning with a trusted doctor or healthcare provider.”


  5. Study suggests school exacerbates feelings of being ‘different’ in pupils with Autism Spectrum Conditions

    November 28, 2017 by Ashley

    From the University of Surrey press release:

    autism_stairsNegative school experiences can have harmful long term effects on pupils with Autism Spectrum Conditions, a new study in the journal Autism reports.

    Researchers from the University of Surrey have discovered that experiences of social and emotional exclusion in mainstream schools can adversely affect how pupils with autism view themselves, increasing their risk of developing low self-esteem, a poor sense of self-worth and mental health problems.

    Examining 17 previous studies in the area, researchers discovered that how pupils with autism view themselves is closely linked to their perceptions of how other’s treat and interact with them. They found that a tendency of many pupils with the condition to internalise the negative attitudes and reactions of others toward them, combined with unfavourable social comparisons to classmates, leads to a sense of being ‘different’ and more limited than peers.

    Negative self-perception can lead to increased isolation and low self-esteem making pupils with autism more susceptible to mental health problems.

    It was discovered that the physical environment of schools can impact on children’s ability to interact with other pupils. Sensory sensitivity, which is a common characteristic of autism and can magnify sounds to an intolerable level, can lead to everyday classroom and playground noises such as shrieks and chatter being a source of anxiety and distraction. This impacts on a pupil’s ability to concentrate in the classroom and to socialise with others, further increasing isolation and a sense of being ‘different.’

    It was also found that pupils with autism who developed supportive friendships and felt accepted by classmates said this helped alleviate their social difficulties and made them feel good about themselves.

    These findings suggest it is crucial for schools to create a culture of acceptance for all pupils to ensure the long term wellbeing of pupils with autism in mainstream settings.

    Lead author of the paper Dr Emma Williams, from the University of Surrey, said: “Inclusive mainstream education settings may inadvertently accentuate the sense of being ‘different’ in a negative way to classmates.

    “We are not saying that mainstream schools are ‘bad’ for pupils with autism, as other evidence suggests they have a number of positive effects, including increasing academic performance and social skills.

    “Rather, we are suggesting that by cultivating a culture of acceptance of all and making small changes, such as creating non-distracting places to socialise, and listening to their pupils’ needs, schools can help these pupils think and feel more positively about themselves.

    “With over 100,000 children in the UK diagnosed with autism, it is important that we get this right to ensure that pupils with autism get the education they deserve and leave school feeling accepted, loved and valued, rather than with additional mental health issues.”


  6. Study suggests potential treatment for autism, intellectual disability

    November 26, 2017 by Ashley

    From the University of Nebraska Medical Center (UNMC) press release:

    A breakthrough in finding the mechanism and a possible therapeutic fix for autism and intellectual disability has been made by a University of Nebraska Medical Center researcher and his team at the Munroe-Meyer Institute (MMI).

    Woo-Yang Kim, Ph.D., associate professor, developmental neuroscience, led a team of researchers from UNMC and Creighton University into a deeper exploration of a genetic mutation that reduces the function of certain neurons in the brain.

    Dr. Kim’s findings were published in this week’s online issue of Nature Neuroscience.

    “This is an exciting development because we have identified the pathological mechanism for a certain type of autism and intellectual disability,” Dr. Kim said.

    Recent studies have shown that the disorder occurs when a first-time mutation causes only one copy of the human AT-rich interactive domain 1B (ARID1B) gene to remain functional, but it was unknown how it led to abnormal cognitive and social behaviors.

    Autism spectrum disorder (ASD) impairs the ability of individuals to communicate and interact with others. About 75 percent of individuals with ASD also have intellectual disability, which is characterized by significant limitations in cognitive functions and adaptive behaviors.

    There are no drugs or genetic treatments to prevent ASD or intellectual disability; the only treatment options focus on behavioral management and educational and physical therapies.

    The team created and analyzed a genetically modified mouse and found that a mutated Arid1b gene impairs GABA neurons, the ‘downer’ neurotransmitter, leading to an imbalance of communication in the brain.

    GABA blocks impulses between nerve cells in the brain. Low levels of GABA may be linked to anxiety or mood disorders, epilepsy and chronic pain. It counters glutamate (the upper neurotransmitter), as the two mediate brain activation in a Yin and Yang manner. People take GABA supplements for anxiety.

    “In normal behavior, the brain is balanced between excitation and inhibition,” Dr. Kim said. “But when the inhibition is decreased, the balance is broken and the brain becomes more excited causing abnormal behavior.

    “We showed that cognitive and social deficits induced by an Arid1bmutation in mice are reversed by pharmacological treatment with a GABA receptor modulating drug. And, now we have a designer mouse that can be used for future studies.”

    Next steps for Dr. Kim and his team are to even further refine the specific mechanism for autism and intellectual disability and to identify which of the many GABA neurons are specifically involved.


  7. Potential new autism drug shows promise in mice

    November 24, 2017 by Ashley

    From the Scripps Research Institute press release:

    Scientists have performed a successful test of a possible new drug in a mouse model of an autism disorder. The candidate drug, called NitroSynapsin, largely corrected electrical, behavioral and brain abnormalities in the mice.

    NitroSynapsin is intended to restore an electrical signaling imbalance in the brain found in virtually all forms of autism spectrum disorder (ASD).

    “This drug candidate is poised to go into clinical trials, and we think it might be effective against multiple forms of autism,” said senior investigator Stuart Lipton, M.D., Ph.D., Professor and Hannah and Eugene Step Chair at The Scripps Research Institute (TSRI), who is also a clinical neurologist caring for patients.

    The research, published on today in the journal Nature Communications, was a collaboration involving scientists at the Scintillon Institute; the University of California, San Diego School of Medicine; Sanford Burnham Prebys Medical Discovery Institute and other institutions. Lipton’s fellow senior investigators on the project were Drs. Nobuki Nakanishi and Shichun Tu of the Scintillon Institute in San Diego.

    ASD is brain development disorder that affects 1 in 68 children in the United States alone. Because ASD has been diagnosed more often in recent years, most Americans now living with autism diagnoses are children — roughly 2.4 percent of boys and 0.5 percent of girls.

    Genetic Analysis Leads to Potential Treatment

    The new study stemmed from a 1993 study in which Lipton and his laboratory, then at Harvard Medical School, identified a gene called MEF2C as a potentially important factor in brain development.

    This breakthrough led Lipton and colleagues to the discovery that disrupting the mouse version of MEF2C in the brain, early in fetal development, causes mice to be born with severe, autism-like abnormalities. Since that discovery in mice in 2008, other researchers have reported many cases of children who have a very similar disorder, resulting from a mutation to one copy of MEF2C (human DNA normally contains two copies of every gene, one copy inherited from the father and one from the mother). The condition is now called MEF2C Haploinsufficiency Syndrome (MHS).

    “This syndrome was discovered in people only because it was first discovered in mice — it’s a good example of why basic science is so important,” Lipton said.

    MEF2C encodes a protein that works as a transcription factor, like a switch that turns on the expression of many genes. Although MHS accounts for only a small proportion of autism disorder cases, large-scale genomic studies in recent years have found that mutations underlying various autism disorders frequently involve genes whose activity is switched on by MEF2C.

    “Because MEF2C is important in driving so many autism-linked genes, we’re hopeful that a treatment that works for this MEF2C-haploinsufficiency syndrome will also be effective against other forms of autism,” Lipton said, “and in fact we already have preliminary evidence for this.”

    For the study, the researchers created a laboratory model of MHS by engineering mice to have — like human children with MHS — just one functioning copy of the mouse version of MEF2C, rather than the usual two copies. The mice showed impairments in spatial memory, abnormal anxiety and abnormal repetitive movements, plus other signs consistent with human MHS. Analyses of mouse brains revealed a host of problems, including an excess in key brain regions of excitatory signaling (which causes neurons to fire) over inhibitory signaling (which suppresses neuronal activity).

    In short, these two important kinds of brain signals were out of balance. A similar excitatory/inhibitory (E/I) imbalance is seen in most forms of ASD and is thought to explain many of the core features of these disorders, including cognitive and behavioral problems and an increased chance of epileptic seizures.

    The researchers treated the MHS-mice for three months with NitroSynapsin, an aminoadamantane nitrate compound related to the Alzheimer’s FDA-approved drug memantine, which was previously developed by Lipton’s group. NitroSynapsin is known to help reduce excess excitatory signaling in the brain, and the team found that the compound did reduce the E/I imbalance and also reduced abnormal behaviors in the mice and boosted their performance on cognitive/behavioral tests — in some cases restoring performance essentially to normal.

    Lipton and colleagues are currently testing the drug in mouse models of other autism disorders, and they hope to move NitroSynapsin into clinical trials with a biotechnology partner.

    The work also has support from parents of children with MHS. “We are all hanging on to the hope that one day our children will be able to speak, to understand and to live more independent lives,” said Michelle Dunlavy, who has a son with MHS.

    In fact, Lipton’s group is also now using stem cell technology to create cell-based models of MHS with skin cells from children who have the syndrome — and NitroSynapsin appears to work in this ‘human context’ as well. Dunlavy and other parents of children with MHS recently organized an international, Facebook-based support group, which is coordinating to assist in Lipton’s research going forward.

    In an amazing twist, the scientific team also found in Alzheimer’s disease models that the new NitroSynapsin compound improves synapse function, the specialized areas for communication between nerve cells. Thus, the ability of the drug to improve ‘network’ communication in the brain may eventually lead to its use in several neurological diseases.


  8. Study uses stem cells to explore the causes of autism

    November 17, 2017 by Ashley

    From the Elsevier press release:

    Using human induced pluripotent stem cells (iPSCs) to model autism spectrum disorder (ASD), researchers at the University of São Paulo, Brazil and University of California, San Diego have revealed for the first time that abnormalities in the supporting cells of the brain, called astrocytes, may contribute to the cause of the disorder. The findings, published in Biological Psychiatry, help explain what happens at a biological level to produce ASD behavior, and may help researchers identify new treatments for patients with the disorder.

    Astrocytes play an important role in the development and function of the nervous system. But until now, iPSC models of autism have neglected their contribution. The new study, led by Dr. Patricia Beltrão-Braga and Dr. Alysson Muotri, used iPSCs to generate neurons and astrocytes to model the interaction between these brain cells and better understand how the brain forms in the disorder.

    “This new use of pluripotent stem cells suggests that neurobiological approaches to autism based solely on abnormal neuronal development may fail to account for complex interplay of neurons and astrocytes that may be an underappreciated component of the biology of this disorder,” said Dr. John Krystal, Editor of Biological Psychiatry.

    Induced pluripotent stem cell technology allows researchers to reprogram human cells into any cell in the body. In the study, first authors Dr. Fabiele Russo and Beatriz Freitas and colleagues used cells from three patients diagnosed with ASD and three healthy individuals to generate neurons and astrocytes. Neurons derived from ASD patients had less complex structure than healthy neurons, but adding healthy astrocytes to the ASD neurons improved their poorly developed structure. In reverse, pairing ASD astrocytes with healthy neurons interfered with their development, making them look more like the neurons from ASD patients.

    “The article highlights for the first time the influence of astrocytes in ASD, revealing that astrocytes play a fundamental role in neuronal structure and function,” said Beltrão-Braga.

    The researchers further investigated how the astrocytes exert their influence, and pegged a substance that astrocytes produce called IL-6, already suggested as a player in ASD, as the culprit for the defects. Astrocytes from the patients with ASD appeared to be producing too much of the substance, and the findings suggest that reducing IL-6 could be a beneficial treatment for neurons in ASD.

    Importantly, ASD has been a challenging disease to model using iPSCs because of its complexity. Several genes have been linked to ASD, but their contributions remain unknown, and genetic differences between patients have made it difficult to understand the cause and develop treatments for the disorder. But in this study, the ASD subjects were selected because they shared similar behaviors, rather than similar genes. According to Beltrão-Braga, this means the findings could provide a new alternative strategy for treating ASD symptoms, independent of the patient’s genotype.


  9. Study suggests malfunctions in communication between brain cells could be at root of autism

    November 11, 2017 by Ashley

    From the Washington University School of Medicine press release:

    A defective gene linked to autism influences how neurons connect and communicate with each other in the brain, according to a study from Washington University School of Medicine in St. Louis. Rodents that lack the gene form too many connections between brain neurons and have difficulty learning.

    The findings, published Nov. 2 in Nature Communications, suggest that some of the diverse symptoms of autism may stem from a malfunction in communication among cells in the brain.

    “This study raises the possibility that there may be too many synapses in the brains of patients with autism,” said senior author Azad Bonni, MD, PhD, the Edison Professor of Neuroscience and head of the Department of Neuroscience at Washington University School of Medicine in St. Louis. “You might think that having more synapses would make the brain work better, but that doesn’t seem to be the case. An increased number of synapses creates miscommunication among neurons in the developing brain that correlates with impairments in learning, although we don’t know how.”

    Autism is a neurodevelopmental disorder affecting about one out of every 68 children. It is characterized by social and communication challenges.

    Among the many genes linked to autism in people are six genes that attach a molecular tag, called ubiquitin, to proteins. These genes, called ubiquitin ligases, function like a work order, telling the rest of the cell how to deal with the tagged proteins: This one should be discarded, that one should be rerouted to another part of the cell, a third needs to have its activity dialed up or down.

    Patients with autism may carry a mutation that prevents one of their ubiquitin genes from working properly. But how problems with tagging proteins affect how the brain is hardwired and operates, and why such problems may lead to autism, has remained poorly understood.

    To understand the role of ubiquitin genes in brain development, Bonni, first author Pamela Valnegri, PhD, and colleagues removed the ubiquitin gene RNF8 in neurons in the cerebellum of young mice. The cerebellum is one of the key brain regions affected by autism.

    The researchers found that neurons that lacked the RNF8 protein formed about 50 percent more synapses — the connections that allow neurons to send signals from one to another — than those with the gene. And the extra synapses worked. By measuring the electrical signal in the receiving cells, the researchers found that the strength of the signal was doubled in the mice that lacked the protein.

    The cerebellum is indispensable for movement and learning motor skills such as how to ride a bicycle. Some of the recognizable symptoms of autism — such as motor incoordination and a tendency to walk tippy-toed — involve control of movement.

    The animals missing the RNF8 gene in the neurons of their cerebellum did not have any obvious problems with movement: They walked normally and appeared coordinated. When the researchers tested their ability to learn motor skills, however, the mice without RNF8 failed miserably.

    The researchers trained the mice to associate a quick puff of air to the eye with the blinking of a light. Most mice learn to shut their eyes when they see the light blink, to avoid the irritation of the coming air puff. After a week of training, mice with a functioning copy of the gene closed their eyes in anticipation more than three quarters of the time, while mice without the gene shut their eyes just a third of the time.

    While it is best known for its role in movement, the cerebellum is also important in higher cognitive functions such as language and attention, both of which are affected in autism. People with autism often have language delays and pay unusually intense attention to objects or topics that interest them. The cerebellum may be involved not only in motor learning but in other features of autism as well, the researchers said.

    Of course, there is a world of difference between a mouse that can’t learn to shut its eyes and a person with autism who struggles to communicate. But the researchers said the findings suggest that changing how many connections neurons make with each other can have important implications for behavior.

    Since this paper was written, Bonni and colleagues have tested the other autism-associated ubiquitin genes. Inhibition of all genes tested cause an increase in the number of synapses in the cerebellum.

    “It’s possible that excessive connections between neurons contribute to autism,” Bonni said. “More work needs to be done to verify this hypothesis in people, but if that turns out to be true, then you can start looking at ways of controlling the number of synapses. It could potentially benefit not just people who have these rare mutations in ubiquitin genes but other patients with autism.”


  10. Autism study examines relational factors in music therapy

    November 5, 2017 by Ashley

    From the Uni Research press release:

    Relational factors in music therapy can contribute to a positive outcome of therapy for children with autism.

    It might not surprise that good relationships create good outcomes, as meaningful relational experiences are crucial to all of us in our everyday life. However, the development of a relationship with a child with autism may be disrupted due to the level of symptoms interfering with the typical development of emotional and social abilities.

    In a new study, researchers from GAMUT, Uni Research Health and University of Bergen, could show that the quality of the therapeutic relationship predicts generalized changes in social skills in children diagnosed with an autism spectrum condition (ASC).

    This predictor study included 48 children between 4 and 7 years who received improvisational music therapy weekly over a period of 5 months. Outcomes related to the child’s social skills were measured before and after treatment. Based on session videos the researchers assessed the relationship between the child and the therapist.

    Findings of this study show a significant symptom reduction, if a relationship was developed in which the therapist was emotionally and musically attuned to the child’s expressions. Especially an improvement of communication and language skills was associated with the quality of the therapeutic relationship.

    Attunement as mechanism of change

    Attunement processes between humans are particularly described for early interactions between infants and their caregivers. It has been suggested that the caregiver’s capability to attune and synchronize to the infant’s movements, rhythms, and affects influences attachment and the development of social understanding. Within these attuned musical exchanges, the infant experiences being experienced and understood emotionally.

    – In music therapy with children with autism, therapists try to transfer principles from early interaction processes by making music that is specifically tailored to the child’s sounds, movements, postures, and affect. This should allow for moments of synchronization and attunement, Karin Mössler at Uni Research explains. Mössler is the principal investigator of the study.

    Children with childhood autism

    Focusing on musical and emotional attunement might be especially important for children with low functioning childhood autism as it might be specifically powerful when working with sensory processing, affect regulation, or deviations related to the child’s movements all of which can be crucially affected in these children. Even though the primary results of a related study investigating the effects of music therapy with children with autism, do not show that music therapy works better than other therapies, subgroup analysis identified that children with childhood autism or coexisting intellectual disability improve to a greater extend from music therapy than children with another autism diagnosis.

    Stereotypical behavior as resource

    In this sense, special focus should be given to intervention strategies fostering relationship through musical and emotional attunement. These strategies should help therapists but also parents of children with ASC to cope with the child’s symptom level by, for example, using its repetitive or stereotype movements and affective expressions as a resource and starting point for attunement.