@paulhanke,
Thanks for staying tuned, folks . . .
paulhanke;104908 wrote:... what this last post makes clear is that it is the "normal build" of the sensorimotor loops in the brain that participates in the control of body movement ... the role of "brain" here seems to be of a more general and remote nature, . . .
I'm not 100% sure that I see the follow up of your concern, yet I'd like to make note that the quoted portion in the post (
my #174), while summarizing not only that post and
#172, though not mentioned, is very secure. Of course there is a specific, and most empirically sound reason why we have these cortical areas called
M1,
PMA,
SMA(1), and in that same manner of application of the terms, there is a most empirically sound reason why I use the word form brain (as opposed to non-brain things) here.
paulhanke;104908 wrote:... in addition, it seems that to make the claim "brain controls body movement" based upon a detailed analysis of the operation of the brain (as opposed to a detailed analysis of the operation of the organism) could be an overstatement. . .
I am presently of the position that the statement is not an overstatement. I think this will come out, as I go--
to a clear enough degree--and will probably bring that up later.
jeeprs;106051 wrote:So am I correct in thinking that a neurological, or biological, explanation of consciousness is the attempt to explain the act of thinking in terms of the activities of neurons?
As far as I have seen, this is not the so precisely-just-as-worded case. There is a fair enough effort to simply come to testable, workable understandings, interpretations, and models, for more pragmatic application. In the process of investigation, however, it has become quite clear that thinking, as commonly used in English, is especially a brain thing, and thus, largely enough (but not only-other cell types evidence being involved too) a neuron thing.
jeeprs;106051 wrote:If so, it would seem to me that any transaction which causes physical changes to occur (for example, the 'piano exercise' example, or the 'placebo' example) are clear cases of downward causation. And as a matter of principle, there is no reason why this ought not to have been occuring ever since anything had consciousness.
There is probably no really justifiable (in the practical sense) reason for thinking of 'causations' in terms as seem to nuanced in your presentation--
as Paulhanke has brought out, earlier. The study you again mentioned, about motor action being learned by picturing motor action, is just a brain thing (as I have been, and will continue to emphasize, what makes consciousness is very little of what brain does; and that may be confusing for some.
The placebo effect is very interesting--though not 100% effective either--and doesn't cover such a broad area of brain/mental problems (for example,
frontal-lobe dementia,
Alzheimer's,
Parkinson's [and related types],
Huntington's,
aphasia, apraxia and dyslexia [of various forms], among others). I'll touch on that, and these, in more detail down the road (although I'll have to do some extra search, I tend to believe, on the placebo effect...meaning I don't recall having read any papers on it at the moment).
In the continuation of
#172, and
#174, looking at deficits in the normal build/state, will be useful. (this is repeat) With the removal of dopamine function from the basal ganglia we have Parkinson's Disease.
Parkinson's Disease (PD) is best to be thought of as a highly heterogeneous group of diseases, generally grouped as idiopathic parkinsonism, symptomatic parkinsonism, P-plus syndromes, and heterodegenerative disorders, and would include, therefore both genetically based forms (autosomal recessive juvenile parkinsonism (AR-JP), and familia parkinsonism (FPD)), and non-genetic based ones.
By a tragic 'underground' drug accident, it was further evidenced that MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydrapyridine) attacks the DA neurons of the substantia nigra (SN), and results in PD symptoms. This is because the primary projector of PD symptom is the death of L-DOPA (dopamine (DA) precursor) cells in especially the SN area. Therefore in non-genetical cases--that is, from toxins in the enviornment, or cases caused by faulty metabolism, or (possibly) unrecognized infectious disorders--we find what appear to be possible upstream causes of PD, or PD-like disorders.
Evident causes of cell death in the genetic-based cases, give rise to the likelihood of missense and nonsense mutations in the gene encoding a-synuclein (a protein) which has a similar effect with the build-up of Lewy bodies (LBs) and Lewy neutries (LNs), and appears to work with molecular chaperone Hsp70. The bodies are filamentious inclusions, and result in a placque-like build up; as is often seen in Alzheimer's disease. PARK2, SNCA, UCHILI, and DJ-1 are seen to be genes involved in one way or another, with PARK2 (parkin) being most widespread. Parkin operates in the ubiquitin-proteasome (Ub-Pr) pathway, giving rise to a faulty protein degradation, and thus a collection of Poly-Ub substrates, which in turn, lead to cell apoptosis.
It has been seen that efforts to make up for DA system losses by estrogen increase (as a kind of repair function), and tyrosine hydroxylase (TH) upregulation occur naturally. There are likely other pathway events which also occur due to the loss of basal ganglion projection, but futher study will have to draw those out. These efforts to compensate are, of course, things that happen internal due to the natural tendency for homeostasis.
The effects are seen in a resting tremor (shaking head, hands, and so on) and 'cog' motion--a slow, rigid point-by-point motion as if a move depends on the turn of a cogwheel. There is also a degree of cognitive deficiency
(2) in many cases, and dementia in later age ranges. In a number of cases, sexual disfunction or hypersexuality or aberrent sexual behavior (probably due to DA replacement therapy) is also seen. The main pharmacological is L-DOPA, a medication which replenishes the loss of the DA precursor. It is often taken in combination with some other chemicals which back up the desired result. L-DOPA will often result in sensitization, and dosage will have to be increased, and some patients do not seem to respond to it.
Another treatment is to replace damaged cells with fetal tissue. This has resulted in positive results. Recently, embroynic stem (ES) cells have been shown to be able to electrophysiologically and behaviorally lead to recovery of PD symptoms in mouse models of the disease. Another way which is still under study and testing, is gene therapy with glial cell line-derived neurotrophic factor (GDNF) injection. Then there is deep brain stimulation (DBS) which is proving to have a fair enough degree of efficacy, but which can cause (a least when first switched on) mood changes towards the depressive state. In the past, pallidotomies (surgical destruction of the GPi) was used for severe cases, and resulted in a degree of recovered movement, but in some cases made symptoms worse, or caused partial blindness (due to damage to the optic tract that lies right next door).
What is seen in PD, is a non-normal brain-build where (among some other possible, minor elements) a required level of neurons which project with DA in the basal ganglion system, resulting in the normal command controls for movement, is lost. This is all in an area of brain that has projections to and from areas which participate in cognitive decision making as well as thought--what we usually consider when we think of mind--and a degree of deficit can be found, to various degrees cognition, as well. As has been made very clear, in very many case histories, PD (especially earlier stages) can be alleviated from a very high degree at first, to almost nothing (in later stages and after habituation), and is the fullness of that particular biologically based brain build . . . in action and cognition.
1. M1=primary motor cortex (Brodmann's 4), PMA=premotor cortex (Brodmann's 6), and SMA=supplementary motor cortex (Brodmann's 7).
2. This often may mean simply a re-routing of cognitive funtions from a normal route used by non-PD brains, and thus an only slightly measurable reduction of accuracy in learning skills.