Autism Spectrum Disorder (ASD) is an umbrella term used to describe a group of complex neurological disorders characterized by socio-communicative impairments and restricted/repetitive patterns of behavior. ASD is predominantly idiopathic or of unknown origin; however, in 4-20% of ASD cases a specific cause can be identified. In previous blogs I have spoken of many conditions where a large percentage of individuals express autism-like symptoms (e.g., tuberous sclerosis, Smith-Lemli-Opitz syndrome, Dravet syndrome). Research into these secondary cases is of importance because of the availability of possible treatment avenues targeting core pathological features of the condition and the knowledge we may gain regarding our understanding into early risk factors.
One important cause of secondary autism is Ehlers Danlos syndrome. This is a connective tissue disorder usually characterized by joint hypermobility. I initially became interested in Ehlers-Danlos syndrome (EDS) after studying neuropathological reports that, for me, indicated similarities to the findings that I had reported in autism. Fortunately, my wife has been able to establish contact with a large cohort of patients and procure their cooperation in answering questions for different screening surveys. The results (unpublished) reveal a large amount of comorbidity between the conditions (Ehlers-Danlos and autism). More relevant to the subject of this blog, we have been alarmed by the large number of complaints involving different aspects of pain (e.g., menstrual cramps, irritable bowel syndrome) and autonomic instability (e.g., resting tachycardia, orthostatic hypotension, constipation) reported by those answering my wife’s survey.
In medicine it is often the case that the simplest explanation for multiple complaints is usually the correct one (Occam’s razor). It is therefore of interest to consider whether all of the strange symptoms that we have mentioned can be explained by the same phenomenon or mechanism. This appears to be the case for many of the symptoms of Ehlers Danlos and autism.
Central sensitization is a condition where the nervous system of an individual is highly reactive and exhibits a lowered threshold for pain perception. This leads to oversensitization and increased pain in response to non-painful stimuli, e.g., the texture of certain clothes as they brush the skin or the mushiness of certain types of food. Other patients may report increased sensitivity to sounds (e.g., the bell in between school classes) or to visual stimuli. The symptoms are often difficult to describe and there are no defining criteria (lab tests) to confirm the same. In the end, patients live in chronic pain and remain undiagnosed. The veracity of their symptoms is often questioned by medical professionals and even close acquaintances. In many cases the patient may be deemed to be a psychiatric case and “accused”, rather than diagnosed, of having a somatofom type of disorder.
A combination of multiple pain-related complaints, a pain-prone phenotype, should make a clinician suspect central sensitization. The may have a family history of pain or mood disorder. Postural tachycardia, temporomandibular joint dysfunction, irritable bowel syndrome, interstitial cystitis, paresthesias, headaches, arthralgia, myalgia, menstrual problems, chronic pelvic pain, restless leg syndrome are all part of this syndrome. Patients are prone to fatigue, dizziness, sleep disturbances, brain fog, and generalized weakness. Lack of sleep may be partially responsible for cognitive symptoms. Without proper diagnoses some patients call themselves “dumb”.
The underlying cause of central sensitization is unknown. However, in many cases there seems to be a trigger, in terms of a preceding infection (e.g., mononucleosis), a car accident, surgery or a psychological stressor. Sleep deprivation appears to be an important predisposition in many cases. It is important to note that in some cases medications can make the syndrome worse. Opiods may lead to a worsening symptoms (opiod induced hyperalgesia). Corticosteroids can affect immunity and, when injected, can weaken the same tendons and ligaments that are already affected in EDS. Some patients have improved with low dose antidepressants but they may also provide for side effects. Other drugs of use have been non-steroidal anti-inflammatory agents and some types of anticonvulsants. Some patients have benefited from exercise. Physical activity, in moderation, increases blood flow to the brain, releases endorphines (chemicals that trigger positive feelings in the body), and makes you sleep better. Specialized centers are available around the nation capable of providing a multidisciplinary approach to treatment.
Cortical Chauvinism 
“Autism Spectrum Disorder (ASD) is an umbrella term used to describe a group of complex neurological disorders characterized by socio-communicative impairments and restricted/repetitive patterns of behavior.”
Groan! I have already shown that there is not the slightest real evidence that autism/ASD/Asperger’s/whatever is a disorder. And that there is much compelling evidence that it is NOT a disorder – Chapter 2 at http://www.pseudoexpertise.com.
“Autism Spectrum Disorder (ASD) is….”
….a silly pseudoscientific label invented by some autism researchers to make themselves sound more important!
“I’m researching a serious disorder, please give generously!” “I’m just researching why some people behave oddly, unfriendly, troublemaking, upsetting the rest of the class….” “In that case p. off please!”
A better way of thinking of it all is that there is an (one) autistic syndrome, which includes various features including (as you mention here!) abnormal hypersensitivities among much else. And rather than something pathological per se, the level of autisticness is one of those dimensions of normal variation such as IQ or extraversion.
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Robin–Asperger’s and autism aren’t the same condition. Asperger’s isn’t a disorder. Please don’t try to tell me that there’s nothing disordered about head banging, pants pooping and being unable to communicate with speech–that’s autism–and that’s what has been an incredibly disabling condition for me to live with. My spouse has Asperger’s and doesn’t need any treatment or modification. I, on the other hand, am healing myself of this horrifically debilitating mast cell mediated state.
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“Robin–Asperger’s and autism aren’t the same condition.”
Sorry but I am not impressed by supposed revelations of knowledge which are unsupported by evidence. Even Tony Attwood who wrote a famous book about “Asperger’s” agreed with me that there is not a proper distinction identified. An elephant is an animal. Just because a snake is very different from an elephant does not mean it can’t also be an animal. As with “animals”, so “autistic persons” can span a huge variety with a lot not in common.
“Asperger’s isn’t a disorder.”
I agree, but I also have cited here conclusive evidence that none of the autistic syndrome is a disorder per se, though a significant number of cases are arguably CAUSED BY disorders such as MeCP gene or mercury poisoning.
“Please don’t try to tell me that there’s nothing disordered about head banging, pants pooping and being unable to communicate with speech”
Yes I will tell you exactly that. Just because something is severely disabling it does not follow that it must be a disorder. I have already carefully explained all this in FREE Chapter 2 already linked above of the Experts Catastrophe book. Until you’ve read that, please don’t waste everyone’s time reinventing square wheels here.
“that’s autism”
On the contrary, it is only examples of the more extreme manifestation of the autistic syndrome, which entirely sensibly is understood to also include the much milder “Aspie” cases and even single-feature conditions such as some dyslexia. Just because some obese people have to use two seats on a plane or train, it does not follow that a person with a waist “only” 2 inches oversize is not affected by exactly the same condition, just NOT AS MUCH (and with different consequences but the same causes).
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How will it help to put heterogeneous conditions into one basket, or (to continue your analogy) – all the animals (including humans) under the umbrella of ‘animals’?
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Good question. I think that is the crux of precision or personalized medicine at present.
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Bad question! Sure, your pet snake will not need a hip operation. But even the most varied of animals need feeding and protecting from pathogens and a preferred environment.
Likewise, mercury poisoning causes a wide diversity, some autistic, some psychotic, or neurotic, or cognitive, or endrocrine, or cancer. But they all have best treatment being removal of the mercury and supplementing of selenium.
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Re the hypermobility, I wonder if something about it is that “hypomobility” (due to the ligaments being too short and tight rather than too long and loose) would be a far more serious problem. Thus genes erring on the side of too long would be more evolutionarily advantageous than genes erring on the side of too short – and hence antiinnatia would tend to favour hypermobility genes over hypomobility genes (for reasons explained in the antiinnatia theory at pages 208-211 of Chapter 7 at http://www.pseudoexpertise.com).
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“The underlying cause of central sensitization is unknown.”
Try getting yourself into a state of deficiency of magnesium or B6. You won’t want to continue with it….
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I’ve thought for a long time that the cause of central sensitization is inappropriate mast cell activation. Mast cell degranulation can be triggered by infection, trauma–both physical and psychological–(look into how corticotropin-releasing factor affects mast cells in the diencephalon), drugs, (as well as the binders and excipients in drugs), and much, much more. The answer already exists, as do treatments to reverse these maladaptive processes in the body and brain.
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Wow, you must have been talking to my wife. That is the central thesis of her work at present- with which I agree.
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Haha! Great minds think alike. I’m just an autistic savant with an interest in logic, medicine and curing autism from the comfort of my home.
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You may like my wife’s blog scienceoveracuppa. She is very interested in the whole hypermobility spectrum and on mast cell activation.
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“Haha! Great minds think alike.”
Alternatively this is proof of Formative Causation and that Rupert Sheldrake is the unrecognised greatest genius ever.
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Very interesting stuff. However, would like to know where you got you 4-20% known cause of Autism figure from? I am genuinely intrigued, as I did not think we knew the cause (although there are many theories!)
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The wide range probably reflects an uncertainty and variability among studies. I have heard such figures in presentations. I just did a small search on the internet, Joseph Buxbaum cites 5-10% (https://www.medscape.com/viewarticle/520013) AN article on syndromic autism states, “Genetic syndromes, defined mutations, and metabolic diseases account for less than 20% of autistic patients” https://www.researchgate.net/publication/26754067_Syndromic_autism_Causes_and_pathogenetic_pathways There are many other that you could find. I have strongly advocated throughout the years to study secondary autism as a way of understanding the mechanisms underlying the pathogenesis of idiopathic autism. I made some attempts on my own that led to believe that the commonality among these causes was a migrational abnormality.
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Migration abnormality can lead to other disorders besides autism, and some with migration abnormalities only have seizures but no psychiatric symptoms of the same significance. There is still much work to be done, but asking why cannot take up all our time. Working on ways to help right now for real also is important.
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