“Restricted, repetitive, and stereotyped patterns of behavior, interests, and activities”—-these are noted in one of the DSM-IV criteria for Autism Spectrum Disorder. A study published in the December 10th Neuron has found that reducing the activity of the gene FKBP12 in the brains of mice affected their synapses, and increased obsessive behavior and “fearful memory.” As noted in today’s Science Daily:

The protein FKBP12 regulates several important cell signaling pathways, and decreasing its activity enhances long-term potentiation in the hippocampus, said Dr. Susan Hamilton, chair of molecular physiology and biophysics at [Baylow College of Medicine] and a senior author of the report. (Long-term potentiation means the enhancement of the synapse or communication between neurons.)

It accomplishes this by fine-tuning a particular pathway called mTOR signaling (mammalian target of rapamycin). The mice in whose brains the activity of the gene was reduced had longer memories and were more likely to exhibit repetitive behaviors than normal mice.

Researchers suggest that their findings might lead to the develop of drugs for autism and also for obsessive compulsive disorders.

Although—-what about the use of such repetitive actions to calm and self-soothe?

Experimental drugs that are said to “correct” symptoms of Fragile X, Rett Syndrome, and tuberous sclerosis complex are now in early-stage human trials, the MIT Technology Review reports. The drugs reduce the activity of a receptor called metabotropic glutamate receptor 5, or mGluR5, and have previously been tested on mice, as reported in the June 25-29 issue of the Proceedings of the National Academy of Science. From the MIT Technology Review:

People with fragile X, the most common form of heritable mental retardation and a leading cause of autism, have a mutation in the FMRP gene, which normally inhibits protein synthesis stimulated by a receptor called metabotropic glutamate receptor 5, or mGluR5.

Last year, [lead researcher and MIT neuroscientist Mark Bear] and Gul Dolen, also at MIT, announced that they could correct abnormal brain development and faulty memory and reduce seizures in affected mice by decreasing mGluR5 activity by 50 percent. “The idea that you could reintroduce function is a sea-change event,” said Emanuel DiCicco-Bloom, a neuroscientist and physician at the University of Medicine and Dentistry of New Jersey, at the neuroscience conference.

Bear has founded a company, Seaside Therapeutics, at which human trials of one of the drugs are now underway. He also says:

“We may have our finger on a biochemical pathway that is applicable more generally in autism.”

More about the STX107, the “lead drug canditate, can be found at the Seaside Therapeutics website.

One of the main concerns that people raise in regard to giving medication to autistic children, and to children more generally, is that there’s a lack of information about the long-term effects of the medication on a child. According to a new study by researchers from the National Institutes of Health (NIH) and Duke University Medical Center, two medications commonly prescribed for treating ADHD—methylphenidate and amphetamine—do not cause chromosomal damage in children. (My son briefly—very briefly—took Ritalin; while taking it, he became so focused that he became extremely anxious, lost his appetite and looked—this is the best word—skittish; we discontinued the medication after less than a week.)

From Science Daily:

The current study included 63 children, ranging from 6-12 years of age, who met full criteria for ADHD but who had not previously been treated with stimulant medications. Children in the study were divided into two groups and treated by a board-certified child psychiatrist with either methylphenidate (commercially available as Ritalin LA and Concerta) or with mixed amphetamine salts (Adderall and Adderall XR). Blood samples were taken before the medication was started to establish baseline values for the cytogenetic [chromosomal] measures that were analyzed in the study, and a second sample was collected after three months of continuous treatment. Forty-seven children completed the full three-month treatment schedule.

The researchers found no significant differences between the two groups of children with regard to age, gender, race, body weight, height, or ADHD subtype. The groups also showed very similar ADHD symptom levels at initial screening and children in both groups responded equally well to the medication.

The researchers looked at three standard indicators of chromosomal damage: structural chromosomal aberrations (breaks in chromosomes), micronuclei (small nuclei consisting of chromosome fragments produced by breakage or whole chromosomes lost from the main nucleus after the cell divides), and sister chromatid exchanges (exchanges of genetic material between a pair of identical chromosomes)

The study, researchers noted, is not to be taken as the final word on the long-term safety of using stimulant medications for treating ADHD in children. It is published in the Journal of the American Academy of Child and Adolescent Psychiatry (JAACAP).

More than 389,000 children and teenagers were treated with Risperdal—an atypical antipsychotic—last year. And, 240,000 of them were 12 years old or younger, the November 18th New York Times reports. A panel of federal drug experts stated that medications like Risperdal are ” being used far too cavalierly in children” and that “federal drug regulators must do more to warn doctors of their substantial risks.”

Risperdal has been approved for treating irritability in autistic children. The New York Times notes that “in many cases, the drug was prescribed to treat attention deficit disorders,” for which it has not been approved for:

The meeting on Tuesday was scheduled to be a routine review of the pediatric safety of Risperdal and Zyprexa, popular antipsychotic medicines made, respectively, by Johnson & Johnson and Eli Lilly & Company. Food and Drug Administration officials proposed that the committee endorse the agency’s routine monitoring of the safety of the medicines in children and support its previous efforts to highlight the drugs’ risks.

But committee members unanimously rejected the agency’s proposals, saying that far more needed to be done to discourage the medicines’ growing use in children, particularly to treat conditions for which the medicines have not been approved.

“The data show there is a substantial amount of prescribing for attention deficit disorder, and I wonder if we have given enough weight to the adverse-event profile of the drug in light of this,” Dr. Daniel Notterman, a senior health policy analyst at Princeton University and a panel member, said when speaking about Risperdal.

The side effects of Risperdal are serious and include substantial weight gain, metabolic disorders, tardive dyskinesia and dystonia.

My son’s among those 389,000 children, and among those 240,000 children aged 12 and younger, who are taking Risperdal. He’s been taking Risperdal since the spring of 2004, at a time when his self-injurious behavior—head-banging—-was severe and he was on the verge of being removed from a public school special education classroom to an out-of-district placement. This is a more detailed account of what Charlie’s experience on Risperdal has been. The most difficult side effect has been the substantial increase in his appetite and the resulting wet gain; we’ve sought to address this by watching Charlie’s diet (and minimizing junk food, in particular) and by making sure he gets a lot of exercise.

I really didn’t want to put Charlie on medication. And truly, it’s not the “answer” in and of itself for addressing aggressive or “problem behaviors.” Even as he wrote the first prescription for Risperdal for Charlie, our pediatric neurologist told us sternly that Charlie also had to have behavior therapy; that we had to keep his education in mind first.

Charlie was 7 1/2 when he started taking Risperdal — since then, mostly via this post, I’ve heard of younger and younger children being prescribed Risperdal. The federal panel’s concern seems very much justified. The New York Times notes a few more reasons why, including the rise of the diagnosis of bipolar disorder in children; however:

The leading advocate for the bipolar diagnosis is Dr. Joseph Biederman, a child psychiatrist at Harvard University whose work is under a cloud after a Congressional investigation revealed that he had failed to report to his university at least $1.4 million in outside income from the makers of antipsychotic medicines.

In the past year, Risperdal prescriptions to patients 17 and younger increased 10 percent, while prescriptions among adults declined 5 percent. Most of the pediatric prescriptions were written by psychiatrists.

From 1993 through the first three months of 2008, 1,207 children given Risperdal suffered serious problems, including 31 who died. Among the deaths was a 9-year-old with attention deficit problems who suffered a fatal stroke 12 days after starting therapy with Risperdal.

At least 11 of the deaths were children whose treatment with Risperdal was unapproved by the F.D.A. Once the agency approves a medicine for a particular condition, doctors are free to prescribe it for other problems.

Panel members said they had for years been concerned about the effects of Risperdal and similar medicines, but F.D.A. officials said no studies had been done to test the drugs’ long-term safety.

No studies done to test the drugs’ long-term safety: It’s a phrase that keeps ringing in my ears; in any parents’ ears. Charlie can’t tell us how he feels taking the medications so it’s up to us and Charlie’s teachers to watch and observe, to adjust and alter. And to know that, medications can help, but they’re just on part of the picture, and a part that needs to be kept under very careful scrutiny.

While studying drug abuse and addiction, researchers at the Ohio State University College of Medicine have found a link between nicotine addiction and autism. Neurexins are proteins that, along with neurologins, are thought to play a key role in the formation and functioning of synapses, of connections between nerve cells. In the new study, a protein made by the neurexin-1 gene was found to have a very particular role, as noted in today’s Science Daily:

The discovery identified a defining role for a protein made by the neurexin-1 gene, which is located in brain cells and assists in connecting neurons as part of the brain’s chemical communication system. The neurexin-1 beta protein’s job is to lure another protein, a specific type of nicotinic acetylcholine receptor, to the synapses, where the receptor then has a role in helping neurons communicate signals among themselves and to the rest of the body.

This function is important in autism because previous research has shown that people with autism have a shortage of these nicotinic receptors in their brains. Meanwhile, scientists also know that people who are addicted to nicotine have too many of these receptors in their brains.

“If we were to use drugs that mimic the actions of nicotine at an early time in human brain development, would we begin to help those and other circuits develop properly and thus significantly mitigate the deficits in autism? This is a novel way of thinking about how we might be able to use drugs to approach autism treatment,” said Rene Anand, associate professor of pharmacology in Ohio State University’s College of Medicine and principal investigator of the research.

“It would not be a complete cure, but right now we know very little and have no drugs that tackle the primary causes of autism.”

Cholinergic agents are drugs which play a role in countering nicotine addiction in the brain. It’s speculated that these medications, after “retailor[ing],” might help autistic individuals by increasing the level of neurexin-1 beta protein in their brains. How this might specifically help autistic individuals is only alluded to—-perhaps it might be more helpful to think about how medications can, in some cases and in discrete ways, help some autistic individuals, over and above focusing on the notion of a drug that would “cure autism“?

The research was presented today at the Society for Neuroscience meeting in Washington, D.C.

A letter abstract in the June 22nd Nature Medicine is entitled Reversal of learning deficits in a Tsc2+/- mouse model of tuberous sclerosis. Tuberous sclerosis is a rare genetic disease that affects the central nervous system and causes benign tumors to grow on the brain, kidneys, heart, eyes, lungs, and skin. Those with TSC can also have seizures, mental retardation, behavior problems, and skin abnormalities as well as developmental delays and autism: In fact, half of those with TSC have autism and epilepsy. Mutations in one of two genes, TSC1 and TSC2, been have identified as causes of TSC. The Nature Medicine abstract also notes that “even individuals with tuberous sclerosis and a normal intelligence quotient (approximately 50%) are commonly affected with specific neuropsychological problems, including long-term and working memory deficits.”

In the study, which was carried out by researchers from UCLA, mice were bred to have TSC; they specifically had deficits in learning and memory. By giving the mice rapamycin, a drug that has been approved by the FDA to fight tissue rejection following organ transplants, their learning and memory deficits were reversed. From a press release containing interviews with the study’s researchers:

Rapamycin is well-known for targeting an enzyme involved in making proteins needed for memory. The UCLA team chose it because the same enzyme is also regulated by TSC proteins.

“This is the first study to demonstrate that the drug rapamycin can repair learning deficits related to a genetic mutation that causes autism in humans. The same mutation in animals produces learning disorders, which we were able to eliminate in adult mice,” explained principal investigator Dr. Alcino Silva, professor of neurobiology and psychiatry at the David Geffen School of Medicine at UCLA. “Our work and other recent studies suggest that some forms of mental retardation can be reversed, even in the adult brain.”

“These findings challenge the theory that abnormal brain development is to blame for mental impairment in tuberous sclerosis,” added first author Dan Ehninger, postgraduate researcher in neurobiology. “Our research shows that the disease’s learning problems are caused by reversible changes in brain function — not by permanent damage to the developing brain.”

………

“Memory is as much about discarding trivial details as it is about storing useful information,” said Silva, a member of the UCLA Department of Psychology and UCLA Brain Research Institute. “Our findings suggest that mice with the mutation cannot distinguish between important and unimportant data. We suspect that their brains are filled with meaningless noise that interferes with learning.”

“After only three days of treatment, the TSC mice learned as quickly as the healthy mice,” said Ehninger. “The rapamycin corrected the biochemistry, reversed the learning deficits and restored normal hippocampal function, allowing the mice’s brains to store memories properly.”

Regan commented about the study on an earlier post; the researchers’ association of intelligence with learning and memory is particularly interesting to me, and also Dr. Silva’s definition of memory as being “‘as much about discarding trivial details as it is about storing useful information.’” My son Charlie has a great and powerful memory: He never seems to forget a therapist or teacher, a place we’ve been and the route to it, a toy or food or activity that he’s liked a lot. He tends to get stuck—fixate—on those first, earlier things he’s learned and to have trouble learning new things (getting used to new teachers and therapists, going to new places along new routes, playing with new toys and trying new foods and activities). Often it seems that the first of many things is what “something is” for Charlie and teaching him otherwise evokes cognitive dissonance,” as if he’s pushing against something in his brain to accommodate for something new.

I’ve noted Charlie’s longstanding struggles to learn the alphabet and language (both understanding and speaking it). Regarding the alphabet: We started to teach it to him when he was about 3 1/2; he’d had no trouble learning numbers. It has taken years for Charlie to recognize the letters and sometimes he seems to be focusing on certain details of the letters—certain shapes and the fact that to many letters rhyme with “ee”—and not to know what aspects he should focus on.

The further results of this study will be of interest to us.  But if there were a medicine to help “reverse” memory and learning deficits, I think that Charlie’s thinking and being would be in many ways the same. He takes in so much of the world around him and I truly think his emotional intelligence is the same as other children his age: As I wrote, my husband Jim has injured his back very seriously and, consequently, has not be able to be at all as active as he is used to and as he loves to be. Jim can barely walk right now (this is my husband who easily runs a mile and a half to train station and through Manhattan streets instead of taking the subway, with a bag stuffed with books and papers). I’ve been explaining to Charlie that his dad injured his back and that Charlie has to do more for himself—-and Charlie has been getting out of bed on his own when I ask (instead of getting tugged and semi-carried; he’s always had trouble getting up in the mornings); he’s pulled on his clothes and grabbed his backpack and run down the stairs for the bus with minimal asking. What is this thing called intelligence, I sometimes wonder?

Professor Stanley Fish of Florida International University, in Miami and dean emeritus of the College of Liberal Arts and Sciences at the University of Illinois at Chicago, opens a post about “norms and deviations” on his New York Times blog by citing a letter published in Time magazine:

A letter published in the May 26 issue of Time magazine protests the inclusion, in Time’s list of the world’s 100 most influential people, of two researchers allied with the organization Cure Autism Now (a name that speaks for itself). The letter writer declares himself to be “outraged” because, in his view, “Autistic spectrum disorders are not diseases, but rather markers of ‘genetic difference’ in the same vein as skin color [and] gender.” He equates the search for a cure with genocide — it’s “part of a campaign to wipe out ASDs” [autism spectrum disorder] — and he wants the world to know that those to whom the cure would be offered neither need it nor desire it: “I speak for many when I say we are happy the way we are.”

A genetic difference is often adaptive and can be regarded as an advance in the evolutionary process; it is well-known that autism sometimes brings with it remarkable powers in the areas of music, art and mathematics. In the 2006 movie “X-Men: The Last Stand,” the augmented powers of those known as “mutants” are even more remarkable and include the ability to walk through walls, to move metal objects as large as California’s Golden Gate Bridge, to auto-generate fire or ice, to be in seven places at the same time, to read minds, to assume any identity, to kill with a touch, to fly like Icarus, to change the weather. These abilities are seen by many “normal” human beings, and a few mutants, as disabilities, as an indication that the person who possesses one of them is a freak.

Fish’s post is entitled Norms and Deviations: Who’s to Say?: Are those mutants in X-Men disabled, or differently abled, or more abled in some respects, and under-abled in others? These questions are relevant to discussions about autism. Whether you see autism as a disability and a difference, or as a disease and a disorder and, indeed, a deficiency, can profoundly influence your view of autism and of autistic individuals.

Fish is not critiquing the notion of “neurodiversity” in particular. The main business of his article is to note a pervasive similarity in how all (as he says) arguments for “difference” are constructed:

In the case of blacks and gays, the answer has already been given in the mantras “black is beautiful” and “we’re queer; we’re here; get used to it.” In the years since these battle cries were first heard, African-Americans and gay Americans have secured rights, gained in influence and earned respect, however grudging and superficial.

And why couldn’t the same thing happen to autism and mutancy or to any other mode of being that refuses the judgment of those who scorn, marginalize and seek to destroy it? For it is a question, [X-Men's director Brett] Ratner observes, of “the use and misuse of power.” Do those labeled deviant, he asks, acquiesce and “conform” to a “prejudice,” or do they “maintain their uniqueness … and embrace what makes them different?” [my emphasis]

“Difference” is the key concept in these socio-political dramas, and difference is an inherently unstable measure. In order to mark it — in order to say where difference resides — you must first identify a baseline, a center; but any such identification will appear to those exiled to the periphery as arbitrary, a function of prejudice and an illegitimate exercise of power: it’s only because there are more of you that you can consign us to the margins and refuse us respect. Armed with this argument (which flourishes in some versions of multiculturalist and deconstructive thought), there is no form of behavior that cannot make a case for its legitimacy and for its right to be free of external coercion, whether it takes the form of legal sanctions or a forced “cure.”

All right, yes. Fish states that he is looking specifically at the structure of the arguments used to justify “different”—not “normal”—-behaviors and practice. He discusses deaf culture as an example of a “minority community” that has to some extent defined and therefore empowered itself by “celebrating” how and why it is different. But where does “difference” blur into “deviance”? At what point, Fish writes, does allowing for different behaviors lead to potentially harmful acts?

I think this is a relevant question to ask in view of recent examples of excluding autistic children: A restraining order was filed against the parents of 13-year-old Adam Race because of his “dangerous” behaviors in church. 5-year-old Alex Barton was “voted out” of his kindergarten class by his fellow students in the wake of numerous behavior issues (which might have been addressed had Alex been receiving more services—perhaps a 1:1 aide to help him focus). Both Adam and Alex have (Alex more recently) diagnoses that put them on the autism spectrum. And the question was asked more than once: Where is the line to be drawn, between the “rights” of an autistic individual, and other people’s sense of what is “appropriate” and “accepted”? I don’t think the answer is as simple as saying “200 pound non-verbal severely autistic individuals” are potentially “dangerous,” while younger autistic children — still little enough to be carried — are allowed “so long as” they act in nearly normal ways.

Fish, however, goes from discussing diversity in terms of race, sexual orientation, and disability, to considering “polygamy, drug use, pedophilia or murder” and makes too vast a generalization about the politics of difference and self-empowerment. By mentioning all of the following in one sentence as various types of “difference”—”autism, deafness, blackness, gayness, polygamy, drug use, pedophilia or murder”—Fish’s argument becomes no more than an observation about a kind of rhetorical strategy that says little about the real, lived experience of real people. I was frankly troubled to see “autism” in a sentence with “pedophilia,” especially in regard to stories like this and this, and to the very real fears and worries that parents have to take to protect disabled children. There are huge differences here.

If Fish cannot see the difference about autism and disability— speaking up for the rights of autistic persons and the need for more societal understanding about disability, then his argument is only an academic one without a basis in understanding that difference is something very real and lived for an autistic individual.

Jennifer Buettner, who has three young children, has created a new company called Efficacy Brands which makes placebos for children. The company will see cherry-flavored dextrose tablets (”Obecalp”—-guess what word that is, spelled backwards?); $5.95 for a bottle of 50. Buettner came up with the idea while taking care of a niece with a “raging case of hypochondria,” the May 27th New York Times notes:

“This is designed to have the texture and taste of actual medicine so it will trick kids into thinking that they’re taking something,” Ms. Buettner said. “Then their brain takes over, and they say, ‘Oh, I feel better.’ ”

The NY Times quotes a number of doctors who note that the placebo effect can be “‘unpredictable’” and who wonder if “giving children ‘medicine for every ache and pain teaches that every ailment has a cure in a bottle.” Buettner notes that she is prepared for controversy. The overprescription of antibiotics (in some cases, to parents who just want to give their child “something”) is cited; Buettner call this “‘a serious problem” and thinks that “‘there needs to be an alternative.’”

The premise behind “Obecalp” has got me reflecting about the various supplements and medications we’ve given Charlie. When he was younger, we tried SuperNuthera, DMG, TMG, Culturelle, cod liver oil, magnesium, vitamin E, BrainChild vitamins, and probably some others and I know that I looked for results and I liked to think I saw them. With something like DMG, the effect of “more attention” or “clearer speech” often seemed immediate, and soon faded. Charlie doesn’t take any supplements (aside from regular vitamins and calcium) any more; he does take medications and attempts to have him not take these have had immediate (and not desired) results.

I’m reminded again of how parents yearn so totally to help their child. I used to worry about what if Charlie never talks and anything that said “helps with language” or “enhances communication” got several looks from me. But I know that it’s been years of teaching, speech therapy, physical exercise, and just plain old growing up that have helped Charlie learn to talk: When he’s frowning as he tries to imitate how we hold our mouths to say words, I can see how he’s working at getting his mind and muscles to coordinate and produce—language.

And then there’s no guessing, if it was the pill—the placebo—or not.

Over at Help My Hurt, Marijke Durning has a poll up about what you think about giving a child a placebo.

The decision to put an autistic child on medication is never easy for a parent to think about. When the medications in question are antipsychotics (like Risperdal) and antidepressants (like Zoloft), and when the child is disabled and has little or no language to explain how he feels while on the meds, a parent has to proceed with caution. Weight gain is a frequently reported side effect of taking Risperdal and a new study on the use of antipsychotic medications in children indicates that taking these drugs results in an almost immediate increases in body mass index (BMI) and triglyceride levels, as reported in the May 7th WedMD. John Newcomer, MD, the Washington University School of Medicine in St. Louis, presented preliminary research from a study of children taking Zyprexa, Risperdal, or Abilify at the annual meeting of the American Psychiatric Association:

So far, 50 children ages 7 to 18 have completed the 12-week study. The children suffer from a wide range of ailments, including autism and pervasive developmental disorder. They were prescribed one of three medications: Zyprexa, Risperdal, or Abilify.

“Virtually 100% of the kids exposed to the medications had some degree of increase in body fat,” Newcomer tells WebMD.

Specifically, the kids were in the 64th percentile of BMI for their age at the start of the study. By 12 weeks later, they were in the 77th percentile on the growth curve, he says. And their triglyceride levels shot up 20 points.

Preliminary results suggest Zyprexa causes the greatest changes in body fat and lipids, and Abilify the least.

Charlie started taking Zoloft for anxiety a few years ago, after we noted to his pediatric neurologist that he sometimes head-banged because he was anxious and fretful. A year later, Charlie started taking Risperdal, as his self-injurious and aggressive behaviors were increasing, and to the point that he was becoming dangerous to others, and to himself. Almost immediately after starting the Risperdal, Charlie’s appetite increased significantly and he gained a significant amount of weight, to the point that he was not able to swim as well and seemed sometimes to be physically uncomfortable from being heavier.

We went out of our way to make sure that Charlie got some physical exercise every day, such as swimming and biking, and made sure there were lots of fruits and vegetables around the house (Charlie developed his love of watermelon and frozen edamame around this time). We have been able to keep Charlie on low doses of both medications thanks to finding him a good school program, which has taught him to deal with his anxiety and worries in other ways besides self-aggression. An attempt to take Charlie off Zoloft resulted in an almost immediate increase in aggression and anxiety.

There really is no magic pill and things still happen out of the blue. For instance, yesterday morning, Jim was getting Charlie ready to catch the bus; Jim said something like “let’s put on this cool new sweatshirt” and it was bang bang bang, and I was running to get ice out of the freezer. Jim got Charlie down the stairs crying very loudly; I held the ice on his forehead and he knocked it out of my hand. We stowed the new, lightweight hooded sweatshirt from my mom in Charlie’s backpack and the bus pulled up.

“Transitioning out of the winter coat,” I said to the bus driver, who nodded (she’s noted that, despite the rising temperatures, Charlie has been insistent on wearing his heavy blue fleece coat with the hood pulled all the way over his head.)

When I got to work, I had an email from Charlie’s teacher: Red mark, crying crying. I wrote back about what had happened and another email came around 11.30: Rough day, Charlie would not seem to get something out of his mind.

As I drove home, I remembered: The night before, I had washed Charlie’s blue fleece coat. I had hung it over a kitchen chair to finish drying, which meant that the coat was not in its usual (reassuring) spot in the living room. Which meant that Charlie concluded, he no longer had his coat. I called Jim who immediately said, “Wow, I felt odd when I didn’t see the coat this morning!”

Charlie came off the bus wearing his new, lighter blue sweatshirt. I had placed his fleece coat on a chair and he went over to it and dropped it on the floor, just so. He quietly agreed to put on the new sweatshirt when we went for a walk. It has a kangaroo style pocket in the front and he walked with both hands in it, pulling down the sweatshirt so that the hood was right over his head, and his smiling face.

Here’s another one, with a reference to an article from the Autism Research Institute.

Don’t think we’ll be trying it.