Physiological deep model

[Diane]

Hi,
I was looking at that monstrous online book site at Pubmed, and found this: (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Search&db=books&doptcmdl=GenBookHL&term=neuromodulator+AND+bnchm%5Bbook%5D+AND+161437%5Buid%5D&rid=bnchm.section.3197#3201) "Biochemical Anatomy of the Basal Ganglia and Associated Neural Systems."

The bit that jumped out at me, that I think probably has something to do with simple contact/ideomotor movement, etc., is this:
Excitatory amino acids provide afferent input to the basal ganglia
Glutamate and aspartate are excitatory amino acid neurotransmitters present in many neurons throughout the brain (Chap. 15). They are involved in basal ganglia afferent, connecting and efferent pathways, which together with thalamic and subthalamic nuclei constitute feedback circuits that modulate cerebral cortical function. The major afferent neuronal pathways to the striatum are from the sensorimotor and other cortical areas and from the thalamus; these fibers release excitatory amino acids, mostly glutamate, in synapses with dendrites on striatal neurons. Glutamate is also the excitatory neurotransmitter released from terminals of the subthalamic neurons projecting to the pallidum, particularly to the internal layer of the globus pallidus, and from the axon terminals of thalamic neurons that send fibers mainly to the cortex.

In the striatum, release of the excitatory transmitters is modulated by presynaptic receptors for acetylcholine (ACh), DA, GABA, opioids and adenosine. Also present are many peptides and other neuromodulators (Table 45-1), which may have modulatory effects similar to those of the cotransmitters. Nitric oxide (NO) is a prime example of a neuromodulator (see Chap. 10). It is a small, gaseous, lipophilic molecular mediator, which readily diffuses across cellular membranes. Thus, it can elicit both anterograde and retrograde signaling at the synapses. In addition, it plays a vital role in N-methyl-d-aspartate (NMDA)-mediated transmission. NO is synthesized from l-arginine by a family of NO synthases (NOS). NOS is found in both glia and neurons, particularly in the medium aspiny neurons of the striatum and other brain regions.

Not sure what to make of it yet, but intend to ponder it.

An aside: I wouldn't have found it if I hadn't been searching the word "neuromodulation" over there. I also searched the word "fascia" and was led straight into a dense Cartesian forest that linked to surgery and to alternative practices, and didn't tell me anything about what goes on in the brain with input or output.

I think this is the main barrier to communication, the habitual wearing of cognitive goggles that either reveal greater focal lengths of information, or don't. One wouldn't use an electron microscope to try to better see a distant shoreline, or use binoculars to look at microbes. To choose the correct vision enhancer it is first of all important to understand
1. that different focal lengths exist
2. that different cognitive goggles exist
3. that anyone who can read and think at the same time, can develop and has the right to use different cognitive goggles of differing focal lengths and strengths.

Just because we are physiotherapists/manual practitoners doesn't mean we can't learn to think and fathom. Just because we think and fathom doesn't mean we'll weaken the team.

[Diane]

Here is a snippet of text from Sagan/Skoyles Up From Dragons, the famous Chapter 12, from the section titled "Inner Maestro", on p.174:A person senses the conscious decision to move his or her little finger about a third of a second after the onset of the motion’s readiness potential (Libet 1985). It is a negative potential linked to the preparation made by our supplementary and other motor cortices before an action. It is hardly a major act of will, but it is an act of will nonetheless. But if the consciousness of making an act arises with the act itself, what of the other brain preparations? Do not the other potentials tied to our prefrontal cortex also give rise to a sense of consciousness as we think ahead and prepare – intend? After all, this part of us is focused on making and supervising the inner cues organizing our actions and thoughts. Scientists can see this on PET scans: Blood surges into part of the dorsolateral prefrontal cortex (Frith, Friston, Liddle, Frackowiak 1991; Jahanshahi, Jenkins, Brown et al., 1995) when people will actions- and only when they will them. This does not happen when our actions are guided from outside, such as when we copy movements. We do not “will” such actions. I'll be looking to see any obvious linkages between this and the info in the post above.

Here are the takeaway points for me, in this moment, and in no particular order;
1. Blood surges into "part of the dorsolateral prefrontal cortex" when we "will" an act but not when we copy one. (So, does that mean more neural activity is taking place when a movement is generated from the "idea" of moving a part than when movement results from mirror neuronal copying of a movement?)
2. The conscious decision to move comes after the brain has already "decided" on a movement plan at a deeper level, and has instituted a "readiness potential." Hmmnn....

Taking Damasio's nice "deconstruction" of consciousness into consideration, he puts the nonconscious in first place as an operator (goal: survival, always), and extended consciousness as the more lately evolved responder, a recorder of internal imagery that is related, and a source of possible information that the nonconscious can use to base its (e-)motor/emotive decisions upon. (Emotions are what if not motor events?) This is all consistent with Skoyles'/Sagan's info that the conscious sense of self part responds after the fact, after movement potential has been generated further back/down in the less selfconscious cortical brain.

I will have to go compost this for awhile. Any efforts to help me clarify will be most appreciated.

[nari]

The 'readiness' potential and 'action potential' and the whole topic of our supposed 'free will' is also talked about in Ramachandran's A Brief Tour of Human Consciousness...last chapter. Will try to post some sections later.

Nari

[Diane]

On this topic here is a bit from Butler's SNS, p 28:
Motor Control Areas as Part of the Distributed Pain Experience One of the more surprising findings of the last decade of brain imaging was that areas of the brain which were always considered to be the domains of motor control showed activity during pain state investigations. This includes areas such as the motor and premotor cortices and subcortical sites such as the cerebellum, basal ganglia and putamen. Coupled with this is the fact that there are about a million fibres in the corticospinal tract, compared to a few thousand in the spinothalamic tract (Blinkov and Glezer 1968). (Hmmnn.. more output than there is input.)

Motor control and its relationship with pain management is clearly a topic for further study. Hmmnn... yes.

As Coghill (1999) reports, subjects for brain scanning experiments have to remain still and silent to minimize movement artifacts. Thus the normal motor responses of avoidance and articulation are suppressed and a motor control process is engaged. Note that the premotor cortex, cerebellum and basal ganglia are concerned with motor planning, not necessarily movement. The cerebellum and basal ganglia receive input from almost all areas of the cerebral cortex. The basal ganglia have been proposed as structures supporting attentional mechanisms in the prefrontal region, facilitating motor program recall and movement based thoughts (Brown and Marsden 1998) Sounds like this has something to do with the previous post above. All of this has to do with ideomotor movement.

It is likely that the anterior cingulate cortex plays a role in motor control in addition and related to its role in attention. A recent functional MRI study (Lotze et al. 1999) showed that motor imagery and motor performance possess similar neural substrates in the cortex and cerebellum.

Wall (1999a) proposes that the brain analyzes sensory input in termms of what it might be able to do about it. .. Consummatory act.

Bilaterally distributed processing in the existing neuronal architecture would allow this. The proposal gives new meaning to the analysis of motor function. It also encourages novel management strategies. If motor activation is a contributor to pain processing, then can the motor areas be disengaged from the pain experience? :) Hmmnnn... probably not.

After all, disengaging the anterior cingulate by distraction will alter pain perception. Motor inputs, either novel, new, trick, meaningful or otherwise which can be accepted by the nervous system as non-painful or nonstressful may have a role in retraining the brain processing which constructs the pain experience. Sounds like simple contact/ideomotor movement fits right in here to me...

(Weiller et al. 1996; Mima et al. 1999). Passive movements activate the contralateral primary and secondary somatosensory cortex whereas other areas including the basal ganglia, cerebellum and the premotor cortex are engaged in active movements. These experiments use passive movements via machinery. I expect that the cognitive and emotional aspects of having another human perform movements would activate other brain areas and the activation would be dependent on subject/therapist interaction. Simple contact is performed in a way that doesn't interfere with patient-generated movement. But by contacting, more than just the movement producing areas must be lighting up. And lots of times the patient will think the therapist is producing the movement. Which might be why staying on the lengthening side assists to a greater extent. The feedback is clearer?

Still wool-gathering,

[Diane]

Found this (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Search&db=books&doptcmdl=GenBookHL&term=brainstem+movement+AND+neurosci%5Bbook%5D+AND+231480%5Buid%5D&rid=neurosci.figgrp.1089) at online books. I quite like the little movement flow chart. If you take away the cortical control (first chunk upper left) by voluntary suspension (the "idea" in ideomotor as per Barrett's application) there is still a lot of brain left to move the body about less inhibitedly.