Sunday, 26 March 2017

Sensory Gating in Autism, Particularly Asperger's

Sensory gating is an issue in autism, schizophrenia and ADHD.   It is the neurological process of filtering out redundant or unnecessary stimuli in the brain; like the child who sits in his classroom and gets bothered by the noise of the clock on the wall.  He is unable to filter out and ignore this sound. He becomes preoccupied by the sound and cannot concentrate on his work.
There are also sometimes advantages to not filtering out environmental stimuli, because you would have more situational awareness and notice things that others miss.
An example of sensory gating is the fact that young children are not waken by smoke detectors that have high pitched siren, but are waken by a recorded human voice telling them there is a fire and to wake up.
There may be times when sensory overload in autism is not a case of too much volume from each of the senses, but rather too many inputs being processed by the brain, instead of some just being ignored.  It is more a case of information overload.
Note that this blog has already covered hypokalemic sensory overload in some depth, which is treatable.
Much is known about sensory gating because it has long been known to be a problem in schizophrenia.
An EEG (Electroencephalography) test measures your brain waves / neural oscillations. Many people with autism have EEGs, but mainly those in which epilepsy is a consideration.
In the world of the EEG, the P50 is an event occurring approximately 50 millisecond after the presentation of an auditory click.  The P50 response is used to measure sensory gating, or the reduced neurophysiological response to redundant stimuli.
Abnormal P50 suppression is a biomarker of schizophrenia, but is present in other disorders, including Asperger’s, post-traumatic stress disorder (PTSD) and traumatic brain injury (TBI).
In more severe autism abnormal P50 suppression was found not to be present in one study.  This might be because cognition and the senses are dimmed by the excitatory-inhibitory imbalance.
More broadly, sensory gating is seen as an issue in wider autism and ADHD.

Correcting P50 gating
It is known that α7 nicotinic acetylcholine receptor (α7 nAChR) agonists can correct the impaired P50 gating. It is also known that people with schizophrenia have less expression of this receptor in their brains than typical people.

One short term such agonist is the nicotine released from smoking.  This likely contributes to why people with schizophrenia can be heavy smokers.  The effect is thought to last for about 30 minutes.
Clinical trials using Tropisetron, a drug that is a α7 nAChR agonist and used off-label to treat fibromyalgia, have shown that it can correct defective P50 gating and improve cognitive function in schizophrenia.

An alternative α7 nAChR agonist that is widely available is varenicline, a drug approved to help people stop smoking.
So you might expect varenicline to improve P50 gating and improve cognition. You might also expect it to help people with fibromyalgia and indeed some other people with chronic inflammation, as shown by elevated inflammatory cytokines.

You may recall that the α7 nAChR is the key to stimulating the vagus nerve and this should be beneficial to many people with inflammatory conditions (from arthritis to fibromyalgia).

Abnormalities in CHRNA7, the alpha7-nicotinic receptor gene, have been reported in autism spectrum disorder. These genetic abnormalities potentially decrease the receptor’s expression and diminish its functional role. This double-blind, placebo-controlled crossover study in two adult patients investigated whether an investigational receptor-specific partial agonist drug would increase the inhibitory functions of the gene and thereby increase patients’ attention. An electrophysiological biomarker, P50 inhibition, verified the intended neurobiological effect of the agonist, and neuropsychological testing verified a primary cognitive effect. Both patients perceived increased attention in their self-ratings. Alpha7-nicotinic receptor agonists, currently the target of drug development in schizophrenia and Alzheimer Disease, may also have positive clinical effects in autism spectrum disorder.

A role for H3 and HI histamine receptors
It has also been suggested that histamine plays a role in sensory gating via the H1 and H3 receptors.

It had also been thought H3 receptors could be targeted to improve cognition in schizophrenia, but that research really did not go anywhere.

Histamine H1 receptor systems have been shown in animal studies to have important roles in the reversal of sensorimotor gating deficits, as measured by prepulse inhibition (PPI). H1-antagonist treatment attenuates the PPI impairments caused by either blockade of NMDA glutamate receptors or facilitation of dopamine transmission. The current experiment brought the investigation of H1 effects on sensorimotor gating to human studies. The effects of the histamine H1 antagonist meclizine on the startle response and PPI were investigated in healthy male subjects with high baseline startle responses and low PPI levels. Meclizine was administered to participants (n=24) using a within-subjects design with each participant receiving 0, 12.5, and 25 mg of meclizine in a counterbalanced order. Startle response, PPI, heart rate response, galvanic skin response, and changes in self-report ratings of alertness levels and affective states (arousal and valence) were assessed. When compared with the control (placebo) condition, the two doses of meclizine analyzed (12.5 and 25 mg) produced significant increases in PPI without affecting the magnitude of the startle response or other physiological variables. Meclizine also caused a significant increase in overall self-reported arousal levels, which was not correlated with the observed increase in PPI. These results are in agreement with previous reports in the animal literature and suggest that H1 antagonists may have beneficial effects in the treatment of subjects with compromised sensorimotor gating and enhanced motor responses to sensory stimuli.

The aim of this study was to investigate an established rat model of decreased PPI induced by administration of the NMDA antagonist, dizocilpine and the reversal of this PPI impairment by the histaminergic H1-antagonist, pyrilamine. H1-antagonism is a potential mechanism of the therapeutic effects of the atypical antipsychotic, clozapine, which improves PPI following dizocilpine administration in rats as well as in patients with schizophrenia. In the present study we show that chronic pyrilamine administration prevents the PPI impairment induced by chronic dizocilpine administration, an effect that is correlated with a reduction in ligand-binding potential of H1 receptors in the anterior cingulate and an increase in nicotinic receptor α7 subunit binding in the insular cortex. In light of the functional anatomical connectivity of the anterior cingulate and insular cortex, both of which interact extensively with the core PPI network, our findings support the inclusion of both cortical areas in an expanded network capable of regulating sensorimotor gating.

The brain histamine system has been implicated in regulation of sensorimotor gating deficits and in Gilles de la Tourette syndrome. Histamine also regulates alcohol reward and consumption via H3 receptor (H3R), possibly through an interaction with the brain dopaminergic system. Here, we identified the histaminergic mechanism of sensorimotor gating and the role of histamine H3R in the regulation of dopaminergic signaling. We found that H3R knockout mice displayed impaired prepulse inhibition (PPI), indicating deficiency in sensorimotor gating. Histamine H1 receptor knockout and histidine decarboxylase knockout mice had similar PPI as their controls. Dopaminergic drugs increased PPI of H3R knockout mice to the same level as in control mice, suggesting that changes in dopamine receptors might underlie deficient PPI response when H3R is lacking. Striatal dopamine D1 receptor mRNA level was lower, and D1 and D2 receptor-mediated activation of extracellular signal-regulated kinase 1/2 was absent in the striatum of H3R knockout mice, suggesting that H3R is essential for the dopamine receptor-mediated signaling. In conclusion, these findings demonstrate that H3R is an important regulator of sensorimotor gating, and the lack of H3R significantly modifies striatal dopaminergic signaling. These data support the usefulness of H3R ligands in neuropsychiatric disorders with preattentional deficits and disturbances in dopaminergic signaling.


Other than nicotine, varenicline would seem a good potential therapy for sensory gating.  There are α7-nicotinic acetylcholine receptor agonists in development.
There are many H1 histamine antagonists.  Histamine release in the brain triggers secondary release of excitatory neurotransmitters such as glutamate and acetylcholine via stimulation of H1 receptors. Centrally acting H1 antihistamines are sedating.

H3 antagonists have stimulant and nootropic effects. Betahistine is an approved drug in this class, there are many research drugs.

The aim of this study is to investigate the role of the neurotransmitter histamine in sensory and cognitive deficits as they often occur in schizophrenia patients (e.g. hearing voices, planning and memory problems). The ideal location to conduct the study and to obtain a unique learning experience is at the Institute of Psychiatry, London, United Kingdom, where staff comprises of leading experts in the field of schizophrenia and Magnetic Resonance Imaging of pharmacological effects. Current pharmacological treatment of psychotic symptoms including sensory and cognitive deficits remains partially unsuccessful due to side effects and treatment resistance. The neurotransmitter histamine seems to be a very promising target for new treatments. It has been found that histamine neurotransmission is altered in brains of schizophrenics, which may contribute to both the hallucinatory and cognitive symptoms. However, this specific role of histamine has not been investigated before. I will assess the effects of increased histaminergic activity, by administration of betahistine to healthy volunteers, on performance (sensory gating, executive functioning or planning and memory) and associated brain activity using fMRI. Altered performance and brain activity would support the importance of histamine in schizophrenia and would provide a research model and target for new treatments.


  1. Peter, Iam using histidine, don´t know if for the regulation of the sensorymotor gating of my son, you know his case, would be better to use an H3 antagonist like betahistine. Or could I use both of them? Perhaps it is a safer approach than enalapril.What do you think?

    1. Peter,sorry if I can´t be clear with this question or I am mistaken, there is a study of betahistine and its interaction in the histaminergic system. It says that betahistine upregulates histidine and also histamine turnover and release.My son´s sensorimotor processing dysfunction or sensorimotor gating deficit, was his hallmark since the 1st year of age. So, I would like to know if could use betahistine and histidine or try only with betahistine.

    2. Valentina, I think the only way to find out what works best is to do some trials. Histidine is supposed to reduce the release of histamine from mast cells. You already have experience with histidine, so it would make sense to try betahistine by itself. Depending on the results you might then try the two together.

      ACE inhibitors are put forward as being very safe.

      You just need to try things one at a time to find what is most effective. What works great for your son may be different to what helps in another person.

    3. Ok, there are many things that could be of great help and don´t want to spoil the interventions, that has happened to me in the past. In addition to BCAAs and NR that started yesterday, I will continue with enalapril 2.5 mg and will add betahistine, which dose would be ok?

    4. Valentina, first see if your ACE inhibitor does any good. Give it a couple of weeks at least.

      Betahistine affects H1 in your ears (it is used to treat vertigo)as well as H3 everywhere. It will increase the levels of histamine, acetylcholine, norepinephrine, serotonin, and GABA.

      For some readers of this blog you would expect betahistine to have a negative effect. This is like the Biogaia Gastrus product that has very positive effects in some, but immediate negative effects in others, possibly due to its effect on histamine levels.

      In the study below they used Betahistine to treat weight gain in schizophrenia. It has the dose they used. I thought this was quite a high dose.

      A Randomized, Double-Blind, Placebo-Controlled Pilot Study of Betahistine to Counteract Olanzapine-Associated Weight Gain.

  2. Might low-dose nicotine patches be useful in such cases?

    1. Nicotine is addictive, permanently rewires brain reward pathways in the brain (which are already compromised in autism), and also builds tolerance over time necessitating the need to use more nicotine. Nicotine also has negative epigenetic effects where there is evidence in mice/rats that can survive three generations (i.e your grandma's and grandpa's smoking effects your health and life expectancy today).

      If nicotine was a good drug to use as a α7 nAChR agonist, then it would be a first line treatment for Alzheimer's disease. There are alternatives though which unfortunately require a prescription (at least in the USA where the medical guilds act as the gatekeepers to safe medication, while potent and damaging drugs in the form of cigarettes, marijuana, alcohol, and even sugar are legal and don't require a doctor's visit).

    2. Roger, nicotine has negative effects. In people not going to have children, they might decide to accept those negative effects for the positive effects some people will experience. So for example people with schizophrenia already have reduced life expectancy and a high suicide risk, they might decide that a nicotine patch, e-cigarette, nicotine gum was worth it to make life more bearable.

      Selective α7 nAChR agonists probably will also have some side effects.

      Smoking tobacco is much more damaging than e-cigarettes/nicotine patches etc.

      A perfect solution does not exist.

  3. Peter, as you mention, a7 nAChR agonists will also have side effects, so for the time being we are on nicotine vaporing.
    This seems to have a positive effect and I am afraid we cannot do otherwise.
    As for fluoxetine, the main reason I am using it is that it can have a positive effect on Gaba through allopregnanolone.

    "Fluoxetine's effect on neurosteroids is primarily related to an increase in allopregnanolone, a potent GABAA receptor positive allosteric modulator;[65] a reduction in circulating brain (primarily mesocorticolimbic) allopregnanolone has been associated with both depression and anxiety disorders.[65] Improvement in depressive symptoms in medicated individuals is correlated with fluoxetine-induced increases in allopregnanolone levels.[65] Norfluoxetine, a primary active metabolite of fluoxetine, produces a similar effect on allopregnanolone levels in the brain, and has therefore also been characterized as a selective brain steroidogenic stimulant.[65]"
    People using fluoxetine for this mechanism of action are talking about low/very low dose such as 5mg or even lower for adults.
    Fluoxetine has a very long half life and it builds up over time.
    It is strange because for most people it doesn't work from the first pill and also brings anxiety in the beginning of treatment. This didn't happen with my son. I gave 20mg tablet and it worked from the same day.
    He is on this dose for three days with stable results. I read that when it seems that it doesn't work anymore, you lower the dose instead of raising it.
    Fluoxetine has been used in autism with modrate success. I suppose it can't be seen as a monotherapy but part of many other interventions.

  4. Peter, during a meltdown, my son had tetany and his hands were like obstetrician hands for quite a while.
    It was really shocking. We massaged them and he recovered.
    I called the neurologist and told me not to worry about it.
    Calling him gave me the chance to ask about P-50 test. He said that schizophrenia cannot be diagnosed through EEG.
    If you know labs in Europe that could test P-50 effectively I would really be interested in getting in touch with them.

    1. Petra, I do not think measuring P50 is a big task for those who use EEG equipment.

      This paper with an interesting video, is about P50 in infants, but it explains things very clearly.

      P50 Sensory Gating in Infants

      They just measure the response to a sound and then the response when it is repeated. The response should be much less when the sound is repeated.

  5. Here is some research that is sort of on topic that relates to opioids and another potential mechanism in how they influence mast cell degranulation (which releases histamine):

    Press Release:


    Basically, there are a bunch of opioid receptors that exist but which scientists have no idea what they actually do and this research first screened a bunch of molecules to see which molecules activated the receptors, and then once they identified which molecules activated the receptors, they then studied the effects of those relevant molecules on the receptor being studied. In this particular case, they found an opioid receptor involved in itching that is also related to mast cell degranulation.

    What caught my eye was that this receptor is activated by Dynorphin A and Dynorphin B (these are endogenous opioids) primarily activate the kappa opioid receptors while opioids like beta-endorphin primarily activate the mu-opioid receptors. Generally speaking kappa opioid receptors are sort of like the opposite of mu-opioid receptors as mu-opioid receptors promote dopamine release while kappa opioid receptors decrease dopamine release. Think of mu receptors as the gas and kappa receptors as the brakes.

    In autism, many people have histamine or histamine-like issues resulting from too much mast cell degranulation as well as problems with the endogenous opioid system in the body. Some people with autism have benefited from broad spectrum opioid antagonists like nalaxone or naltrexone (which block both kappa and mu as well as other opioid receptors), and a dysregulated opioid system could (if you take this research at face value) have a potential indirect effect on histamine issues as well which of course could potentially cause inflammation problems downstream causing even more autism related symptoms.

    I think one commenter said they were trialing Low-Dose Naltrexone (I believe there are actually a few studies of this intervention in autism, though I recall them being rather small), but it would be interesting for people here who have children with histamine-like issues if opioid antagonists would have an acute effect on improving overall symptoms.

    Now here is something extremely interesting to me. My reasoning for L-Aspartate (which is one of my top interventions) was based upon three decade old research on its use in attenuating heroin withdrawal (just to reiterate naltrexone/naloxone are the first line drugs here and have been for a long time). So I got a hunch here about your (Peter) Verapamil intervention for dealing with summertime allergy flareups in attenuating histamine/allergy related symptoms which seemed to cause your son even worse autism related symptoms and apparently there is a lot of research on Verapamil being used for opioid withdrawal and here is one of the papers I dug up:

    So this is all connect-the-dots and does not have any studies backing this idea, but it is intriguing to think that perhaps the "summertime flareups" you have alluded to in the past could really be opioid related problems (more sunshine in the summer might drive hedonic production of opioids harder) and Verapamil's effects here could really instead be the result of attenuating hyperactive Dynorphin signaling that leads to mast cell degranulation and the histamine related issues thereafter based upon the first bit of new research I cited.

    Just an idea, but an easy way to test this is if a child response to verapamil in these situations, if they respond to naltrexone just as well, then perhaps the problem at its core is not excess histamine or allergies but rather aberrant opioid signaling of the mast cells causing them to degranulate.

  6. Here is another alternative idea I had on Bumetanide's potential mechanism of action based upon this new research:

    Press Release:


    The main points in this paper are that they found a capillary sensing network dependent upon the function of a potassium ion channel for sending electrical current for the purposes of directing blood flow to areas with recent neural activity.

    I am not gonna beat a dead horse about circulation issues in the brain and how they relate to autism, but one conclusion of the study was that if potassium levels are too high in the brain, this capillary potassium based sensing system shuts down.

    So one side-effect of Bumetanide is that it wastes potassium in the body and the brain and one very interesting conclusion of the recent Ben-Ari study was that the best results for improving CARS scores were with the 2mg intervention, however, that intervention also led to the greatest problems with hypokalemia.

    However, just because potassium levels in the peripheral blood may be low, the question begs as to what are the potassium levels in the brain and whether potassium accumulates for some reason.

    Here is a study looking at the permeability of various potassium salts with respect to the BBB:

    Obviously, too little potassium in the brain will cause problems, but too much causes seizures and too much potassium could also cause blood flow problems to parts of the brain that need more nutrients due to recent activity (which this capillary potassium sensing system mentioned above handles and which is shut down from excess potassium).

    So in light of all this evidence, could Bumetanide be helping by clearing out excess potassium in the brain and could the type of potassium salt ingested by diet or as a supplement matter greatly in terms of providing the body and brain with enough potassium to function properly, while also allowing Bumetanide to clear out potassium salts that seem to accumulate too much in the brain's extracellular space.

    This is just another hypothesis of course, but have we considered that maybe the problem in autism too much potassium, rather than too little (which is the current conventional wisdom).

  7. Peter, do you think nAchR bulgarotoxin binding site model could tell us something practical about sensory overload/seizures in autism?

    1. They use it for research, but I don't think it tells us anything practical.

  8. Tyler, I wanted to know your opinion since you know very well the case of may son, about adding betahistine, iam now thinking that it is not a good idea, since Peter told me that it increases norepinephrine levels and this is the last that we want, increase extracellular neurotransmission of both norepinephrine and dopamine,
    that is why iam using BCAAs. Is this right? My son didn´t respond well to biogaia gastrus. Perhaps adding an H1 antagonist would be fine to regulate his sensory motor disorder. I must say, that he is very much better, but the core symptoms remain in stressful situations.

    1. The only histamine intervention I used was DAO enzymes. It was fairly expensive and it was hard to tell if it was helping or not, because it is not like an epipen where if your child is getting beat rid and going hyper, you can do something to see if there is an immediate effect or not. DAO enzymes you take half an hour before a meal. Like any parent I have to sometimes shelve interventions if their cost/benefit ratio does not seem justified. NR is expensive, but I believe it makes a big difference and is especially important if you chronically limit tryptophan/kynurenine into the brain via BCAA blockage.

      But the question is how do you know your son has a histamine issue at all? Try getting some regular niacin (the cheaper form of B3) and then see how much he can tolerate before flushing occurs.

      Here is a study (this is for schizophrenia) involving the niacin flush test (it works via prostaglandins and serotonin release from mast cells though):

      I recall the general protocol for histamine is that you basically do 50mg doses in increasing intervals. Start with 50mg of nicotinic acid (niacin) and if there is flushing, then supposedly the person doing the test has high histamine. If you don't flush, do another 50mg of niacin (total 100mg) and if you flush you have normal levels of histamine. If you don't flush, then take another 50mg of niacin (total 150mg) and if you don't flush you have low levels of histamine. I have read there is some debate about this, but that is all I can say right now.

      Also, here is the study suggesting histamine is not reduced from flushing from a researcher who has done some autism specific research himself:

      This is one study and I have yet to see any replications, but hopefully this information is useful to you nonetheless. Prostaglandins are intimately related to histamine which is why I am not totally convinced the "niacin flush test" is bunk. I would try it anyways.

    2. Tyler, I almost didn´t see any flush with niacin, in spite of the fact that he taked 250 mg, only one day I saw a flush in all of his body. I think he has been protected by histidine. So, I will keep histidine and enalapril and NR that I have recently started.Stopped niacin. I don´t know if L serine would be of any help.

    3. Hello Tyler,

      Though I too am concerned, in fact, confused about my sons histamine status, I would not try a niacin flush test on son since I read that for some it can have serious consequences, requiring emergency measures. Also, it seems that histamine tolerance status is not fixed but variable depending on ones changing body chemistry in response to diet, infections, stress...the list goes on. I have started feeding my son legume sprouts frequently (though I can see him reaching the end of his tether as far as savouring the stuff is concerned) as a natural source of DAO. I am aware those quantities might be miniscule against the formidable histamine intolerance giant, if present, but something is better than nothing and sprouts have other benefits as well.

      I also read that ultimately histamine issues are linked to methylation issues..too much confusion for one lifetime!

    4. You either use DAO enzymes, or don't bother (natural sources won't do it). DAO enzymes are basically purified pig kidney and you won't find that in plants.

      The product I used was from Swanson's which was much cheaper than the one I came across first called "Histame", which at the time was way more expensive. For all I know there are many other options now.

      Also, DAO enzymes only soak up the extra histamine in the gut so the idea is to use them on a low histamine diet or at the very least not a high histamine diet. But mast cell activation can occur from many vectors so simply lowering histamine/histidine ingestion is not necessarily going to prevent mast cell degranulation issues. I also supplemented Perilla Oil (high in rosmarinic acid) which seemed to help at the time, but at the moment I do not do any of those interventions because he never seems to get histamine symptoms (red cheeks and ears and hyperactivity) anymore. My guess is the interventions related to supplemental fiber and probiotics in the form of Biogaia Gastrus may be what has made my previous histamine intervention unnecessary anymore. This is of course all speculation as I have no tests to prove this one way or another, but this is simply what I have observed. Perilla oil tastes pretty good (kind of a sweet nutty taste) so you can easily mix it into just about anything (I would not cook/bake with it though if you want to use it therapeutically).

    5. Tyler,

      Thanks for the perilla oil suggestion...rosmarinic acid has multiple benefits. I will surely try it, in low dose. Actually its not really a question of natural versus synthetic or nutraceutical versus pharmaceutical for me. Its the concentrated form of certain compounds with unknown effects that I am uncomfortable with....I tried withania and bacopa tablets on my son..did not make me/him happy. So I am not jumping on any of the chemical bandwagons anytime soon. A conservative approach works better for my son. God, I have still not got over the catastrophic biogaia gastrus, carnosine, liverlife combo disaster.

      And, its good gastrus works for you but do not be too casual about it.

  9. Peter, would memantine also be a candidate drug of choice?

    1. Yes there are sound reasons why both memantine and galantamine might improve sensory gating. It is the same mechanism as the nicotine.

    2. We have found that memantine (from ceretropic liquid) combined with galantamine definately help in this regard. The combined effect is greater than either by themselves.

    3. To correct my comment above. Galantamine (as a positive allosteric modulator of α7 receptors) should be similar in effect to nicotine, as an agonist of α7.

      Even though both Memantine and Galantamine are used for Alzheimer's, Memantine is an antagonist of α7. It has the opposite effect to nicotine.

    4. That´s why perhaps my son had a bad reaction to memantine,even at very low doses, like he was under the effect of a psychodelic drug.I didn´t try Galantamine.

    5. combination therapy with galantamine and memantine in Alzheimer's disease

      Geerts H, Grossberg GT. Pharmacology of acetylcholinesterase inhibitors and N-methyl-D-aspartate receptors for combination therapy in the treatment of Alzheimer’s disease. J Clin Pharmacol 2006;46:8S-16S.

      Grossberg GT, Edwards KR, Zhao Q. Rationale for combination therapy with galantamine and memantine in Alzheimer’s disease. J Clin Pharmacol 2006;46:17S-26S.

    6. Valentina, some autism and most schizophrenia is characterized by NMDA hypo function (too little activity). Memantine blocks NMDA receptors and so will make any hypo function even worse. Some people have NMDA hyper function, and they would benefit from this effect of Memantine. The problem with drugs is that they have multiple effects and it is not clear which one will dominate, and it may even vary person to person.

    7. On the subject of treating sensory gating with Alzheimer's therapies, Donepezil is the one I mixed up with Memantine.

      Donepezil stimulates α7 nAChR and this then down-regulates of NMDA receptors. This is neuroprotective in those at risk of glutamate excitotoxicity.

      So if you have sensory gating (P50) and NMDA hyperfunction, Donepezil could help.

      Both Galantamine and Donepezil have been trialed in autism and schizophrenia.

  10. Peter, what you say makes sense to me and clarifies the kind of autism my son has, may be explains why of the best Tyler´s interventions for his sons is aspartic acid.I can´t deny that he suggested me more than once to try it.

  11. My son's sensory processing is imbalanced. Its really related to his epilepsy which has caused autism. While the ketogenic diet seems to help I still don't understand why we have breakthrough seizures. I was hoping to go seizure free for a week, well hit the three week mark and then today he had a seizure at therapy. I did notice red ears and red cheeks. The therapy students had him up against a brick building with intense sunlight on him as they were interacting with him. I was inside speaking to their instructor. There has to be many underlying mechanisms that cause seizures. The diet seems to control the excitatory type seizures. But it never works when his body temp exceeds 99 degrees. Our son gets red ears that hurt to touch kind of random and sometimes not random (heat). I wonder if the red ears are a symptom of a pathological process---or could it be that the red ears are the result of a hyper-responsive capillary reaction? Could it be that my son's entire neurological and biological responses are hypersensitive, hyper-alert, and hyper-aware? How do I help him to regulate this? I have brought it up numerous times with different doctors but it is dismissed. It seems to happen randomly but their has to be a reason that it occurs. Today I noticed it when I arrived at the scene. I am also noticing severe bruxism. It used to be at night only and now it occurs during the day on a pretty consistent basis to the point I am getting notes home from school. The dentist seems to think it is ok to let him grind his teeth to the gumline as long as they are not adult teeth. I don't see that as being a very good idea for chewing and infection reasons. Anyone have this happen?

    1. There are some papers on "red ear syndrome" and several reasons were proposed.

      Red ear is one of many strange symptoms I used to see in my son - along with abnormal upgaze spells, minor angioedema of the lips at night and periodic headaches at full moon for example. In my child I think that red ear is a kind of flushing related to mast cell activation. Drugs targeting mast cell (antihistamines, sodium cromoglicate, verapamil) helped with that.

      Actually, I recall some reports of seizures controlled only when mast cell stabilizing treatments were used.

    2. This article has good references you can look at:-

      I would first rule out bruxism being his version of stereotypy. Use NAC 600mg, 3 or 4 times a day. If it is going to help, it will only take a day or two.

      If that did not work, I would consider anxiety, unless he has ADHD in which case consider hyperactivity.

  12. Maybe this sounds out there to some but I am concerned about the epigenetic gene expression and regulation when metals such as aluminum have become so abundant in our everyday use. I wonder about certain forms of aluminum and the impact it has in the developing brain. I wonder just how many areas the circulating aluminum interferes in epigenetic expression and regulation. How does all of this effect how the genetic information is read? C. Exely speaks a great deal about Aluminium and ridding the body of its burden using Silicon rich mineral water. The Silica has to be in the proper form to bind and eliminate the Aluminium and the mineral water seems to be the best way to rid the body of the burden.

  13. Peter what are your thoughts on this article, a PDE4 inhibitor that enhances sensory gating (im assuming this is improvement of prepulse inhibition?).

    I have alot of problems with auditory sensitivity and I noticed im able to process emotions way way better in a quiet environment, would you say I could benefit from meds that improve PPI?

    Also Ive tried to look online for a list that could help improve PPI, but I couldnt really find any :(.

    Acute administration of roflumilast enhances sensory gating in healthy young humans in a randomized trial.

    1. Aspie1983, very interesting because roflumilast shows a beneficial effect on gating at a dose that had no adverse effects. This is one fifth of the regular dosage.

      It only worked at this dosage, high doses lost the good effect.

      Ibudilast is a PDE4 inhibitor people buy online, but you would have to work out what dose equals 100-μg roflumilast.

  14. Today I have crossed the theme "nicotinic acetylcholine receptors containing the subunit a7" several times. I do not know much about this, but it looks interesting in the general context of this blog. A couple of quotes from different papers, mixed:

    α7-nAChRs unexpectedly promote formation of glutamatergic synapses during development.
    α7 nAChR null mice had decreased cortical NMDAR expression and glutamatergic synapse formation during postnatal development.
    Interestingly, synaptic, but not extrasynaptic, NMDAR currents were specifically diminished in cultured cortical pyramidal neurons. Synaptic NMDARs play crucial roles in many forms of synaptic plasticity, such as LTP and LTD. Synaptic NMDARs are preferentially gated by the endogenous coagonist, D-serine

    (..) nicotinic activation of α7-nAChRs in WT organotypic culture, as well as cell culture, increases the number of glutamatergic synapses.

    Our findings indicate that lovastatin up-regulates expression of α7 nAChR via a mechanism involving activation of the mitogen-activated protein kinase/ERK pathway, which may result in diminished production of amyloid β.

    These findings suggest that PPAR-α plays a key role in a putative antinociceptive α7 nicotinic signaling pathway.


  15. Regarding scents/aroma therapy. It seems as they can have fast and sometimes profound influence on mood and brain waves.

    Has anyone extensively used/experimentend with them yet?

    I cant help but look at some of the common overlaps that I find in this study:

    Influence of Fragrances on Human Psychophysiological Activity: With Special Reference to Human Electroencephalographic Response

    "Valeriana officinalis, Lavandula off., Passiflora incarnata, Piper methysticum, Melissa off., Eschscbolzia californica, Hypericum perforatum and Ginkgo biloba. Among the different plant extracts, valerian extract significantly increased delta and theta activities and also decreased beta activity. "

    "Jasmine oil Beta wave increased in the anterior center and left posterior regions. Increased—feeling of well-being, active, fresh and romantic."

    "Terpinolene—reducing the tension and increasing the relaxation and stabilization states of brain function"

    An intranasal herbal medicine improves executive functions and activates the underlying neural network in children with autism

    "This formula, using natural borneol as one of the active ingredients, was recently patented as a formula for improving brain function and an intervention for brain disorders (patent number ZL 2008 1 0176088.7). In Traditional Chinese Medicine, borneol is a well-known substance for improving the mind and thoughts because of its capacities to direct drugs upward to the head, targeting the brain (Liu, Liang, Chen, Feng, & Zhao, 1994), to facilitate the permeation of drugs across the blood–brain barrier, and to enhance drug distribution in brain tissue (Chen et al., 2010, Yu et al., 2011, Yu et al., 2013). In our patent application, we reported that mice receiving seven days of the herbal formula had higher levels (p < 0.001) of norepinephrine in the brain (mean: 46.10 pg/mg of tissue) compared to those receiving saline solution (mean: 22.03 pg/mg of tissue); the mice that received three days of the herbal formula also had higher levels of norepinephrine in the brain (mean: approximately 33 pg/mg of tissue) than did those receiving saline solution (p < 0.001). In sum, the preliminary data suggests that borneol may be an effective agent to improve brain activities."

    Shows how powerfull scent can be, borneol opened up the brain-blood-barrier. Not sure if this is a good thing though? admittedly I have not read the full study but it could be that it only allowed some signal/chemicals to pass the BBB?

    Intranasal Borneol Improves the Behavioral Problems and Enhances the Immunologic Function in Children with Autism


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