This stuff is
V. Interesting, thank you so much for posting. This is a really interesting theory, and it's great that you're thinking about it. Also, I'm sorry if I say things that you already know, I don't know what you know, all I know is the stuff *I* didn't know when I was 14. I started my neuroscience interest when I was about 13, and I remember, I was 15 when we officially learnt about neurons in school. Very basic and quick, just here's the axon, here's the dendrite, the gap in the middle is the synapse. Customers at my part time work often ask me what I study at uni, and when I say 'Behavioural Neuroscience' roughly half of them (middle aged people) don't know what the 'neuro' bit means. But here you are, pumping out words like 'mirror neuron' and 'choroid plexus', which I only learnt about last year.
I searched up "cerebrospinal fluid and autism" on PyschInfo and Medline.PychInfo gave 35 results, and medline: 21. These are databases of most of the scientific journals out there, which I can access through uni. PubMed is a free one, I think Google Scholar as well, but I don't really know how to use those

A scientific journal is what published original research reports from a specific field. There is even a journal called "Journal of Autism and Developmental Disorders". Done lab reports before? You know, the report about introduction, aims, hypothesis, method, results, discussion, etc. This is what people use to see what past research has been done in their area of research, because maybe somebody has already thought of your hypothesis. Or, looking at previous research to see what would be improved on it. (Sorry if you already know about scientific journals). Though I don't have access to a lot of the full text, so the whole report, I can get bibliographical details and the abstract, which is the summary of the research. Though, I've got access to enough, I guess, for a student. If you want me to search something on it, just ask (just guessing you don't have access to a database. Sorry if you already do!)
Here are some interesting studies I found:
"Cerebrospinal fluid insulin-like growth factors IGF-1 and IGF-2 in infantile autism"
Abstract:
There has been little exploration of major biologic regulators of cerebral development in autism. We measured insulin-like growth factors (IGF) -1 and -2 from cerebrospinal fluid (CSF) by radio immunoassay in 25 children with autism (median age 5y 5mo; range 1y 11mo-15y 10mo; 20 males, 5 females), and in 16 age-matched comparison children without disability (median age 7y 4mo; range 1y 1mo-15y 2mo; eight males, eight females). IGF-1 and -2 concentrations were further correlated with age of patients and head size. CSF IGF-1 concentration was significantly lower in patients with autism than in the comparison group. The CSF concentrations of children with autism under 5 years of age were significantly lower than their age-matched comparisons. The head circumferences correlated with CSF IGF-1 in children with autism but no such correlation was found in the comparison group. There was no difference between the two groups in CSF IGF-2 concentrations. No patients with autism had macrocephaly. We conclude that low concentrations of CSF IGF-1 at an early age might be linked with the pathogenesis in autism because IGF-1 is important for the survival of Purkinje cells of the cerebellum. The head growth might be explained by the actions of IGF-1 and -2 reflected in CSF concentrations.
I put the abstract of that on, because it sounds a little bit like what you're talking about, or you may be interested. More titles:
"Low levels of insulin-like growth factor-I in cerebrospinal fluid in children with autism."
"Characterization of the various forms of the Reelin protein in the cerebrospinal fluid of normal subjects and in neurological diseases."
"Gluten- and casein-free diets for autistic spectrum disorder. " (This one has full text access)
"Immunity, neuroglia and neuroinflammation in autism. "
"Gangliosides in cerebrospinal fluid in children with autism spectrum disorders."
"CSF monoamines in autistic syndromes and other pervasive developmental disorders of early childhood."
Okay, I think you've had enough, lol. If not, say so. I can email abstracts and articles (if I happen to score access to it, that is) over if you want more information on thing. Also, database results also depend on what terms you search. Autism and autistic disorder can be different. Or cerebrospinal fluid, or CSF.
Now, your hypothesis. Is this 'inefficiency in the circulation' happening during embryonic development (therefore caused changes to parts of the brain), or is it always like that? Same with the irregular cells. A hypothesis like that, I think, is simple to test. Take a brain scan, compare autistic with neurotypical. Or perhaps some other tests, such as looking at cell structure post mortem. Also, we have to think about what the actual fluid does, and what consequences a change is it has. If we took it away, what would happen? Does activity stop? Can neurons send action potentials without it?
I think I understand it that you're saying that flow is fast around the cortex, which explains hypersensitivity. So, in a way, the faster the flow rate of the CSF, the more brain activity in that area. I don't know too much about this, or whether or not it's true. And since the CSF contains a number of proteins, and an oxygen supply, it's possible. Oxygen is a requirement of brain activity. BUT on the other hand, the CSF does not come into contact with most of the brain, and there is a covering over the the cortex anyway. The meninges has three layers, dura mater, arachnoid mater and pia mater. The arachnoid mater, in the middle has a space called the sub arachnoid area, which is where the CSF flows. There is still the pia mater, which is directly attached to the cortex, following the convolutions of the sulci and gyri, so no direct contact between the CSF and the brain. BUT the pia mater is probably permeable to oxygen, maybe other things in the CSF. I don't know. And the CSF doesn't need to be in direct contact with something to put pressure on it.And then you have to define what 'faster processing' means. Are the neurons sending action potentials faster? Or is there a lower threshold for action potential (more sensitive). Or maybe more efficient/specific pathways are formed?
I personally think a general change, such as flow rate (I'm not even sure how the stuff flows, actively or passively), it would probably cause something more drastic than autism, as it would effect the entire cortex. If flow rate has an effect on processing speed in the first place. BUT on the other hand, flow rate itself might not do anything, but flow rate of a protein (maybe a nerve growth factor) within the CFS might do something. Or, the immune cells in the CFS.
Now, about cell differences. A LOT of research already shows a variety of cell differences in various parts of the brain, as well as different activity rates (which is usually concluded from rate of oxygen and glucose consumption in the brain) and anatomical sizes and cell numbers. I am not up to speed on all this research though, and how valid and reliable each study is. What the question is what cells and why? how? If autism is genetic, it must mean there are some proteins somewhere in the body that are different (one gene codes for one protein, a change in the gene changes the protein normally, though not always). One protein has the potential to do a lot, or perhaps nothing at all. I have looked up to see if anyone has connected ependymal cells with autism, and I didn't find anything. That might be an interesting area to look at.
The 'pruning' theory is a good one too(since there is evidence to support it). For an interesting fact, when you weight train, and get stronger, it's not the increase in muscle mass that does it, but having a more specific neural pathway worked out. Practice does this. (of course, later on, it's muscle mass as well). But again, why? Why would cells growing like this be good of 'analytical' stuff, but not social stuff? I don't know how those two types of information is represented in the brain in the first place exactly. And are these cell changes specific to just parts of the brain? (I suppose I could read about this!) And what annoys me most, what is this 'juice' they are talking about!?! I guess that's what you get when reading about this stuff from newspaper type articles, targeted at the general public. I picture orange juice flowing around in the brain

By what they said about 'long conections' in the brain, they might mean the action potentials gets weaker as it goes a long, and eventually it can't reach threshold in the next neuron. Or maybe oxygen and glucose resorces are limited, or the neurotransmitters are limited? Article's fault (Gah, and six brains per group? Those results couldn't be statistically significant. I sure hope they did more studies, and that was just a pilot.)
Also a cause for autism may not mean a cure for autism. Though, even worse, if the gene is found, it may lead to autism testing and termination in pregnant women (which has been discussed on these forms somewhere). The changes may be irreversible. But the changes in brain structure caused by autism may be treated. So this way, perhaps language problems or communication problems may be treated without changing the 'autistic personality'. Finding a cause is more knowledge, and I can't say no to that. It may help us further understand how the brain works. How language is processed, and how non verbal communication is processed.