@odenskrigare,
In the normal brain build/state, one may turn their head upon hearing the phone ring, put down the magazine they've been reading, uncross their legs, stand up, cross the room going through the door into the hallway, walk down the hallway, and answer the phone--as they kind of twist around on one leg to lean up against the wall, answering in a fairly clear and loud enough voice.
If you remove dopamine function from the basal ganglia of their brain build/state, they'd not be able to do so in time to reach the phone before the other party (unless knowing of and allowing time for the case) hangs up. This is
Parkinson's Disease in a general nutshell. To fill it out a bit, please do see below, and visualize (based on our foundation now in hand) the whole of the state (including cause and result):
[indent]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, toxins--in the enviornment, or caused by faulty metabolism, or (possibly) unrecognized infectious disorders--appear to be possible upstream causes.
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, conscious [
note: new sense used here] brain acts--brain does it--but are not recorded in the usual (at least) ways, so that none represent an act within consciousness.
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
(1) 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). [/indent]
What is seen in PD, is a brain-build which undershoots a normal brain-build in that--among a few other possible factors--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 just like those other areas, have no choice but to work with and within (through 'push' and 'pull') the systems (to applicable genetic function, even) that make brain, which in turn give brain-build, thus providing the brain.
When we are presented with and study these cases, and see that normal brain build/state is lost (it once was, we must acknowlege), do we find any evidence at all that any contact (reception) with
something out there, external to brain, has been lost by the structures of brain responsible for body movement control? No, we do not. In fact, we find just exactly the opposite; viz. that it is the very performance of the biological systems (brain build/state) that act on the biological system that the H. sapien
is which are projected (thus interpreted [so to speak]) as the movements of the biological body that we are (on the pragmatic level here) ! Does the '
brain function as a TV' imagery work here (jeeper's
#98 [and note flow up to my
#299])? No, it does not (unless, perhaps, we'd like to include
all [/i][/u](especially animal)
life forms as recievers of '
something out there.'
Huntington's disease (HD) is purely genetic in cause, and also shows the fallacy of refusing to understand brain build/state as a biological source. I'll do that next, then summarize and apply these two before moving on.
Additionally, to answer to Pathfinder's possible (not sure, but it just might be, you see) charge of my simply 'cutting' from somewhere and 'pasting' (see his number
279, third paragraph), I'll site some of my source material below...for those not interested, please just skip it (but do see the footnote just below). [
No, Pathfinder, it is not cut and paste material which I present . . . not at all, so please do keep that in mind. Thanks.] KJ
1. 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.
SOURCES (most, but not all)
Science Vol 304, 21 May '04; pp 1158-1160
[indent]Vol 247, 2 Feb '90; pp ?
Vol 295, 1 Feb '02; pp 865-868
Vol 209, 27 Oct '00; pp 721-724
Vol 302, 31 Oct '03; pp 819-822[/indent]
Brain and Cognition Vol 68, '08; pp 134-143
[indent]Vol 67, '08; pp 340-350
Vol 53, '03; pp 190-192
Vol 52, '03; pp 343-352[/indent]
Journal of Neurological Sciences Vol 284, issues 1-2, Sept '09; pp 177,178
Archives of CLINICAL NEUROPSYCHOLOGY Vol 23, '08, pp 399-408
Neuroscience vol 156, '08, pp 830-840
Parkinsonsim and Related Disorders Vol 14, '08; pp 451-456
[indent]Vol 14, '08; pp 553-557[/indent]
Behavioural Brain Research Vol 190, '08; pp 224-232
Trends in Neuroscience Vol 30, No 5, '07; pp 194-202
Encyclopedia of Cognitive Science Vol 1, editor-in-chief Lynn Nadel, '03; pp 328-333
ibid Vol 3; p 458
Encyclopedia of the Human Genome Vol 4, '03; pp 492-497
and the other reference works, texts, and journals (with my mainstay being
Journal of Neuroscience).