Neurofeedback for Autism

[RobinN]

Neurofeedback May Help 'Retrain' Brainwaves In Children With Autism

“The more neurofeedback training given to a child with autism, the more often the correct brain pathways are used and the stronger they become. It’s like a ‘tune-up’ for a brain that is out of sync,” McCormack said. “The brain has a lot of plasticity and, as children continue this training, it becomes engrained and spills into other parts of their lives.”

[Bernard]

Here's the press release from the University of Missouri:

MU Researcher Studies Neurofeedback to 'Retrain' Brainwaves in Children with Autism


COLUMBIA, Mo. – Playing a video game called ‘Space Race’ that requires nothing more than brainpower to make rockets on a computer screen move forward is more than just fun and games. A University of Missouri researcher is using video games to see if the brainwaves of children with autism can be ‘retrained’ to improve focus and concentration.

“We are trying to awaken their brains. Often children with autism disconnect and we want to use neurofeedback to teach them how it feels to pay attention and be more alert. We want to teach them to regulate their own brain function,” said Guy McCormack, chair of the occupational therapy and occupational science department in the MU School of Health Professions. “The ultimate goal is to lay down new neural pathways and, hopefully, see changes in focus and attention span, social interaction, improved sleep, and appetite.”

Neurofeedback is a way of observing how the brain works from moment to moment. While the children play the video games, their concentration and focus are rewarded by movements on the screen and special sounds. If attention wanes, the rocket on the screen slows, sounds stop and the color changes until more attention is given to the image. As this occurs, researches watch another screen that monitors brainwave activity. The brainwave activity is measured by placing sensors on the scalp.

“The more neurofeedback training given to a child with autism, the more often the correct brain pathways are used and the stronger they become. It’s like a ‘tune-up’ for a brain that is out of sync,” McCormack said. “The brain has a lot of plasticity and, as children continue this training, it becomes engrained and spills into other parts of their lives.”

Neurofeedback technology was designed by NASA for flight simulations. It also is used to help high-powered executives achieve peak performance and to help athletes train their brains to ‘get into a zone.’

“The aim of neurofeedback is to enable children to consciously control their brainwave activity by being rewarded for their ability to focus,” McCormack said. “Neurofeedback can be compared to physical conditioning for the brain.”

McCormack says a body of evidence already exists that has found the use of neurofeedback training helps with other neurological disorders such as traumatic brain injuries, strokes, seizures, depression, anxiety disorders, alcoholism and premenstrual syndrome.

The Sinquefield Charitable Foundation gave $213,511 to fund McCormack’s study of neurofeedback for treatment of autism. The study is being conducted at the MU Thompson Center for Autism and Neurodevelopmental Disorders.

MU Researcher Studies Neurofeedback to 'Retrain' Brainwaves in Children with Autism

[hootie]

My son (10, autism, absence seizures) had his second session of NFB. He has 20 total sessions scheduled thru the beginning of February. He will then get another QEEG to see how things are progressing. We plan on doing at least 60 sessions over the next several months. I am praying for increased socialization, communication and faster learning. The provider we are using uses a coherence/connectivity training method (I hope I am saying this right). From what I hear, this is supposed to make the NFB more focused/effective.

I'll let you know how it goes.

[hootie]

Here is an article of what we are doing:
Connectivity-Guided Neurofeedback for Autism Spectrum Disorder
Robert Coben, PhD

You will have to search for it yourself since I am too new to post links just yet.

[epileric]

Here is an article of what we are doing:
Connectivity-Guided Neurofeedback for Autism Spectrum Disorder
Robert Coben, PhD

You will have to search for it yourself since I am too new to post links just yet.

http://www.aapb.org/tl_files/AAPB/files/biof_ASD.pdf

[RobinN]

Hootie - I wish your son positive results. I know what a commitment it is to go this route.
I can't remember if you are also controlling nutrition too. It is helpful to do them at the same time.

[Bernard]

Awesome. I look forward to hearing another success story.

[hootie]

Robin--
Yes, we are controlling nutrition to the best of our abilities. My son has many food allergies which really restrict his diet. I really wish he could eat eggs. It would make my job so much easier.

Have you ever tried to make a gluten-free, egg-free pancake on a sunny day???
For some reason (probably the barometric pressure or humidity), the pancakes burn on the outside and are uncooked on the inside when it is sunny.

[Nakamova]

How about waffles?

[hootie]

Do you have a recipe using gluten-free oat flour?
(remember...no eggs, corn, soy, nuts, peanuts, gluten, dairy, ummm...anything else???) Or do I just use the same batter and cook it in a waffle maker? Is it hard to make waffles?

Time to shop for a waffle maker...maybe. Any suggestions on brands? I would prefer one without teflon, but I wonder if this is even an option with waffle makers.

[Meetz1064]

look later today, but I bet I have one. PM me, to remind me.......

[RobinN]

You might consider that elimination of refined grains are needed for your son's GI system to heal.

[Bernard]

Research adds to evidence that autism is a brain 'connectivity' disorder

Tuberous sclerosis, commonly associated with autism, is linked to defects in axon guidance

January 10, 2010

Boston, Mass. -- Studying a rare disorder known as tuberous sclerosis complex (TSC), researchers at Children's Hospital Boston add to a growing body of evidence suggesting that autism spectrum disorders, which affect 25 to 50 percent of TSC patients, result from a miswiring of connections in the developing brain, leading to improper information flow. The finding may also help explain why many people with TSC have seizures and intellectual disabilities. Findings were published online in Nature Neuroscience on January 10.

TSC causes benign tumors throughout the body, including the brain. But patients with TSC may have autism, epilepsy or intellectual disabilities even in the absence of these growths. Now, researchers led by Mustafa Sahin, MD, PhD, of Children's Department of Neurology, provide evidence that mutations in one of the TSC's causative genes, known as TSC2, prevent growing nerve fibers (axons) from finding their proper destinations in the developing brain.

Studying a well-characterized axon route--between the eye's retina and the visual area of the brain--Sahin and colleagues showed that when mouse neurons were deficient in TSC2, their axons failed to land in the right places. Further investigation showed that the axons' tips, known as "growth cones," did not respond to navigation cues from a group of molecules called ephrins. "Normally ephrins cause growth cones to collapse in neurons, but in tuberous sclerosis the axons don't heed these repulsive cues, so keep growing," says Sahin, the study's senior investigator.

Additional experiments indicated that the loss of responsiveness to ephrin signals resulted from activation of a molecular pathway called mTOR, whose activity increased when neurons were deficient in TSC2. Axon tracing in the mice showed that many axons originating in the retina were not mapping to the expected part of the brain.

Although the study looked only at retinal connections to the brain, the researchers believe their findings may have general relevance for the organization of the developing brain. Scientists speculate that in autism, wiring may be abnormal in the areas of the brain involved in social cognition.

"People have started to look at autism as a developmental disconnection syndrome--there are either too many connections or too few connections between different parts of the brain," says Sahin. "In the mouse models, we're seeing an exuberance of connections, consistent with the idea that autism may involve a sensory overload, and/or a lack of filtering of information."

Sahin hopes that the brain's miswiring can be corrected by drugs targeting the molecular pathways that cause it. The mTOR pathway is emerging as central to various kinds of axon abnormalities, and drugs inhibiting mTOR has already been approved by the FDA. For example, one mTOR inhibitor, rapamycin, is currently used mainly to prevent organ rejection in transplant patients, and Sahin plans to launch a clinical trial of a rapamycin-like drug in approximately 50 patients with TSC later this year, to see if the drug improves neurocognition, autism and seizures.

In 2008, Sahin and colleagues published related research in Genes & Development showing that when TSC1 and TSC2 are inactivated, brain cells grow more than one axon--an abnormal configuration that exacerbates abnormal brain connectivity. The mTOR pathway was, again, shown to be involved, and when it was inhibited with rapamycin, neurons grew normally, sprouting just one axon.

Supporting the mouse data, a study by Sahin and his colleague Simon Warfield, PhD, in the Computational Radiology Laboratory at Children's, examined the brains of 10 patients with TSC, 7 of whom also had autism or developmental delay, and 6 unaffected controls. Using an advanced kind of MRI imaging called diffusion tensor imaging, they documented disorganized and structurally abnormal tracts of axons in the TSC group, particularly in the visual and social cognition areas of the brain (see image). The axons also were poorly myelinated--their fatty coating, which helps axons conduct electrical signals, was compromised. (In other studies, done in collaboration with David Kwiatkowski at Brigham and Women's Hospital, giving rapamycin normalized myelination in mice.)

Sahin has also been studying additional genes previously found to be deleted or duplicated in patients with autism, and finding that deletion of some of them causes neurons to produce multiple axons–-an abnormality that, again, appears to be reversed with rapamycin.

"Many of the genes implicated in autism may possibly converge on a few common pathways controlling the wiring of nerve cells," says Sahin. "Rare genetic disorders like TSC are providing us with vital clues about brain mechanisms leading to autism spectrum disorders. Understanding the neurobiology of these disorders is likely to lead to new treatment options not only for TSC patients, but also for patients with other neurodevelopmental diseases caused by defective myelination and connectivity, such as autism, epilepsy and intellectual disability."

The current study, titled "Tsc2-Rheb signaling regulates EphA-mediated axon guidance," was funded by grants from the National Institutes of Health, the John Merck Scholars Fund, Tuberous Sclerosis Alliance, the Manton Foundation, the Children's Hospital Boston Translational Research Program, and the Children's Hospital Boston Mental Retardation and Developmental Disabilities Research Center.

Duyu Nie was first author on the paper. Coauthors were Duyu Nie, Alessia Di Nardo, Juliette M Han, Hasani Baharanyi, Ioannis Kramvis, and ThanhThao Huynh, all of the F.M. Kirby Neurobiology Center and Department of Neurology, Children's Hospital Boston; Sandra Dabora of Brigham and Women's Hospital; Simone Codeluppi and Elena B Pasquale of the Burnham Institute for Medical Research, and University of California San Diego; and Pier Paolo Pandolfi of Beth Israel Deaconess Cancer Center.

http://www.childrenshospital.org/new...blevel599.html

This ties in nicely with the recent research showing that at least some forms of epilepsy may also be related to the way the brain forms during development.

[hootie]

Just an update for my son that is doing NFB for seizures and autism--
he started depakote about a month before starting NFB and he has had 20 sessions since his last QEEG. His newest QEEG after 20 treatments indicates a 24% decrease in seizure activity in the area we were treating. We can not know how much of the benefit is due to the depakote and how much is due to the NFB at this point, but the next QEEG will be more telling of the benefits of QEEG itself. I the practitioner said the connectivity (how the brain communicates with itself) in the area we treated was better since the last test as well but did not give a % (I did not think to ask until just now).

He is now having the left side of his brain addressed since his connectivity is REALLY bad there (no wonder he has such problems with speech!!!). He will finish up with the next 20 treatments April 20something and have another QEEG.

I think I am seeing some minor benefits overall (using words a little differently, having more of an opinion about things that affect is life, better problem solving, going through the "terrible twos at 11...UGH!!!). He has a lot of issues to address other than just the seizures so I am thinking he will need more treatments than the "usual" person.

Take this seizures and autism!!!