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I suppose everyone has moments where they feel something that's coming from abnormal sensory neuron activity-- an itch, a crawling sensation, a little shock, a pinprick, etc. which might happen anywhere on the body and it does not persist there. So, just for clarification, I don't regard those things as "neuropathy". The nervous system is constantly making little adjustments and you might notice some of those events. Great raw material for a hypochondriac, but I'm not in that category.

The only persistent sensory neuron symptom I've got is a hot and/or/numb sensation of variable intensity (usually not even aware of it) over my right thigh. It was originally over the quadriceps rectus (the muscle that early on was completely paralyzed), but it later spread to the right side. Note that the surface sensory neurons and underlying muscles don't map the same and that I was able to use pinprick mapping to identify the specific sensory nerves involved.

In my mid-30's I pranged my lumbar back (just an awkward movement, not lifting an engine block)resulting in sciatica and was just about flat on my back (had to crawl to the bathroom) for 2 weeks. It seemed to heal just fine and after a couple years no more back problems. It's possible that some of that damage didn't actually heal 100% and the weak part became a vulnerability for spinal motor neuron disease preceded by a sensory abnormality. ......At time of MND Dx ultrasound and X-rays were done on lumbar spine looking for abnormalities but nothing interesting showed up using those methods.


Why is sporadic ALS over 90% of ALS, and why is it sporadic? I like to ask this question because I'm a sporadic case and if you ask me why I developed motor neuron disease, nearly 10 years later the answer is "I don't know".

But there are clues. Without the stretching injury to my thigh muscles at the knee, I wouldn't have developed ALS at that particular time. It was The Trigger.

But that should have been no biggie. Why ALS? Well, there's a clue: the sensory neuropathy in the same region where the motor neuropathy later showed up. Hard to believe that's a coincidence. The stretching injury pulled the trigger, but the only reason anything interesting happened was because the gun was loaded. The smell of gunpowder was already there before the trigger was pulled.

Then there's that slipped disc" thing two decades earlier. It caused damage. And is healing ever 100%? Almost never, there's a residual weakness that healing processes couldn't restore to pristine conditions. So, if there were genetic and/or environmental biochemical susceptibilities to motor neuron and/or sensory neuron disease, the logical place for those diseases to begin would be at the spinal ganglia where the original spinal injury had occurred.

Textbook ALS is focal. It starts "someplace". It spreads from there, and usually other foci develop independently. The fact that it is so distinctively focal emphasizes the importance of prior local injury in defining those loci.

Lurking behind the textbook ALS that emerges in incipient fogeydom (i.e. when regulation & repair mechanisms start to run into things they can't fix any more) are things much earlier, especially genetic susceptibilities but not limited to such. Lots of "diseases of aging" are of that character. Alzheimer's and ALS probably share a number of susceptibility genes and environmental influences in common, but they're different omelette scrambles. There's a thousand ways to fry the eggs, different ingredients and different menu items, but still your eggs done been fried.


I was born 'way preemie under anesthesia. Back when medicine wasn't very good at those things. Luckily most of it went well (so it seemed at the time) and as a kid I didn't offer much employment for doctors. Later the Army regarded me as being sufficiently healthy to draft, but psychologically unfit for Vietnam duty. Fit, however, to run a dispensary in beautiful southeast Arizona. When I left, the dispensary flight surgeon Dr. John Cavender MD knowing my interest in medicine and especially pharmacology gave me a copy of "The Pharmacological Basis of Therapeutics." Several years later the perfect opportunity arose for me to pass on the gift to someone else, but that's another story.

60 years ago nobody knew what "autism" was. Well, some of us knew, it's just that it hadn't entered mainstream medical consciousness yet and therefore didn't even have a name. For autism to go mainstream, the medical profession needed an FDA approved drug to prescribe to make it worthwhile to do the diagnosis, and that drug was Ritalin (an amphetamine). What causes autism? The availability of money to treat it. Do vaccines cause autism? Of course-- just not very much. The primary cause of autism is having a category to check on the insurance claim form.

I'd have been Dx'd as borderline autistic. Thank God or Reality or whatever that they had no such Dx back then! I had to figure out coping mechanisms and fortunately I was growing up in a supportive environment.

There are connections between autism and motor neuron disease. One of those connections is the role of MMP-9. Another is the number of engineers on this very forum and the way you see us interacting. Yet another is the "fact" that autism is caused by inadequate synaptic pruning during development and therefore (depending on which synapses were mostly involved) either sympathomimetic or GABAergic drugs may be therapeutically useful, or both.


You know who we are. If you read the comic strip "Dilbert", there we are. We're here on these forums, too. Sometimes we're even lovable, Camille can attest to that. MDA thinks we're ugly poster children but Camille entered our world to tell us we're not nearly that ugly after all. Words fail right about now........

Of what I think I know about the biology of autism, most comes from recent research on Fragile-X on behalf of my boss's son. The things I'm about to say are broad generalities in the realm of speculative hypothesis. I'll word it as though it were fact just to make it more readable.

* * * * *

Autism is a developmental disorder that begins at conception due to genetic combinations and permutations that create the risk factors. The psychological-sociological outcome many years later is greatly influenced by environmental influences.

Neurological development happens on a spectrum of variability. The evolutionary reasons why this is so, and why so many genetic influences are located on the X-chromosome, are essays for some other time if I live long enough. Meanwhile please accept that there is no such thing as "normal", and that variability is absolutely essential to the survival of life even if not of the species.

In early (embryonic and childhood)development, the nervous system is very busy establishing synapses-- the connections between neurons that determine how they work together. In structured embedded C programming, synapses are equivalent to the layer that describes how hardware-related code constructs interact with applications code constructs.

Neurotransmitters and parameters, receptors and flag files, RAM and short-term memory vs. flash EEPROM and PROM longer-term memory, this is the world where human and artificial intelligence intersects. Grasp of the correspondences has been impaired by obsession with the technologies involved and not with the underlying principles which are about information itself and not about the technologies used to do something with information.

Establishing synapses is how learning is done. The neurotransmitter most involved in that, is......DRUM ROLL!.....[b]glutamate[/b].

In embryonic development and in childhood and to some extent as an adult, we're subjected to a thousand conflicting sensory perceptions that are both opportunities for learning and opportunities to wind up totally confused about everything. Therefore the nervous system needs mechanisms to sort through the information pile. This means that many synapses that developed in response to stimuli will have to be pruned. Ever watch a prune shrivel? Synapses are faster to form and also to shrivel, they have to be. Motor neurons are long suckers that offer nearly zero opportunity for learning by the time the body is half a meter long stretched out. Learning is the job of synapses.

Please enter now the world of an autistic kid. The basic "abnormality" is that synapses tend to form more quickly than can be pruned by adverse information. Perceptually in the moment, it's information overload. Glutamate is busy.

First step toward a solution, is to develop coping mechanisms to throttle back the information overload. The inhibitory mechanisms kick in. At first they "work" but over the longer haul they influence the continued development of the nervous system. [u]HOW THE NERVOUS SYSTEM DEVELOPS DEPENDS ON WHAT YOU'RE LEARNING.[/u] The world we're living in now is governed by the brains that developed 20-80 years ago trying to solve its problems.

Autistic brain. It starts with the learning neurotransmitter glutamate, and over the long haul the GABA inhibitory system decides the outcome. I haven't said much about outright apoptosis but please take note that glutamate is the neurotransmitter that the inflammatory system uses to kill off neurons suspected of being infected with disease organisms. It does that because glutamate overload depletes energy stores and also causes oxidative damage.

What are the "drug abuse" (perhaps better said 'self-medication') patterns we see among autism-spectrum patients? Well, kids treated with sympathomimetic stimulants grow up to prefer those same stimulants. Is it brain damage from the childhood treatment or a basic continuation of a beneficial protocol? I DON'T KNOW and the drug industry doesn't want anyone to know either.

Why do the amphetamine sympathomimetics get so much traction in treatment of childhood autism? Well, apart from the FDA approval thing recited earlier, the school system is designed around "average" students. It has to be designed around "average" to work efficiently. They're really big on "participation". From the perspective of the ed system, amphetamines drag the student out of the stupor. From the perspective of the student, the amphetamines enable classroom learning but impair the compensation mechanisms that allow reflection and organization of the learning experience. The drugs downregulate brain development in certain critical areas leading to the adult need to take sympathomimetics to substitute for coping mechanisms that were never allowed to develop.

The idea that a student who doesn't seem to be participating might be learning more than the rest of the class isn't promoted in the "one method works for all" politician-inspired dogma. ......Back in the bad old days, there was the "retarded kids class" ("special education") and in some school systems the other, smartypants curriculum. For two years in elementary school we had access to both the upper and lower grades playgrounds and I usually preferred to hang out with the "retards" who used the lower grades playground. They had really serious problems and I admired the insight and flexibility that they applied to dealing with those problems. I didn't view them as incompetents, I viewed them as problem-solvers. I was there to learn from them the things I couldn't learn from my own classmates.

I almost didn't graduate from high school because I flunked English, I was too busy studying other languages. I flunked chemistry because I didn't submit a term paper, I found out that my "negative tetrode resistance" hypothesis had already been proven so what was the point of continuing any further? Was I a genius or an idiot? Take your pick. My older relatives thought I was destined to become a nuclear physicist (that being a lucrative career choice in the 1960's) but I had absolutely zero interest in college and as they say in Japan, I "went my own way". The only college credits I ever earned that were beyond high school repeat were a 5 unit mail-order course in physical geography that took me 2 years to complete.

Anyone here ever heard of "writer's block"? What do writers do to fix it? That notorious GABA agonist "booze". In order to write, you have to see what's going on between your ears, and shut out the rest of the world's distractions meanwhile.

How do "shy people" overcome social inhibitions at parties? Some drink and loosen up, some know they can't go that route and either take it easy or abstain. Wallflowers aren't necessarily having a bad time, they may be taking in as much as they can without wrecking the experience for themselves and their host.

Considering all this, I submit that there is an autism-spectrum ALS phenotype and that it is driven by abnormal synaptic processes both between the ears and in the spinal neurons, both sensory and motor.