Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Thursday, August 28, 2014

Vasa concept - Is there a connection between increased degrees of freedom from flaccidity following stroke, and development of passive tissue contracture and spasticity?

I noticed a lot of hits on my blog for this. Rajul Vasa has a 66 page paper on this if you want to wade thru it.  She totally lost me in the clinically drawn conclusion section. I don't know whom this is written for but I'd be willing to bet not a single stroke survivor is going to be able to understand this and apply it to their recovery. And probably few therapists.
Great word salad though. Maybe the whole point is to increase your cognitive abilities of reading comprehension.
My earlier post on it here including pros and cons.
Vasa concept

Is there a connection between increased degrees of freedom from flaccidity following stroke, and development of passive tissue contracture and spasticity?

I'm kinda smart and I have absolutely no clue what the following gibberish is supposed to mean.


Clinically Drawn Conclusion:
1. Increased degrees of freedom of paretic flail MSS (Musculoskeletal system) of one side of the body from a small lesion in CNS make self-organizing dynamic system unstable from within. (And what the hell does this mean?)
2. For safety reasons brain switches off the control on Centre of Mass [COM] from affected hemisphere and solves the problem of safety of COM by steering the control on COM exclusively to good side of MSS that is to non-lesioned hemisphere. This is positive instant plasticity that facilitates good side to control COM but is functionally negative plasticity on a long run with adaptation of good side of the body to control COM exclusively making it hard for the stroke subject to use affected side despite natural recovery of brain tissue.  (Wow, just Wow?)
3. Action plans of self-organizing stroke CNS and MSS to re-stabilize the system and to combat external invariant forces like gravity to control and defend COM [a priority of all living organisms] becomes the added constraint to restoration of lost control besides the presence of lesion.
a. Self-organizing stroke CNS exploits anticipatory postural activity and Spino-Spinal interlimb sensory motor neuronal connectivity [left side of the spine to right side of the spine and from cranial to caudal and caudal to cranial connections] to induce muscle contraction in a chain of paretic muscles during functional acts with slightest movement of COM to restrict increased degrees of freedom from paresis that poses threat to safety of COM.
b. Synergic activity in chain of paretic muscles in paretic limbs is considered as pathological abnormal movement and associated reaction, when in fact it is uninterrupted extended anticipatory activity in chain of paretic muscles with slightest movement of COM. This extended anticipatory activity is the result of uninterrupted control on COM by good side of body that renders paretic side as an automatic follower of good side with interlimb Spino-Spinal connectivity.
(Wow, just Wow?)
c. Self-organizing brain exploits anticipatory postural control to induce uninterrupted continuous contraction in Paretic weak muscles to turn them stiff and spastic in order to reduce degrees of freedom in paretic limbs to reduce threat to the safety of global COM by inducing so called abnormal pathological synergic movement that remain constant in one direction only towards the central axis to remain within narrow base of support [BOS] and do not allow any variability in direction for safety reasons.
d. Spasticity, synergic grouping and contracture act optimally not only to reduce increased degrees of freedom from flaccidity but act as a “BRAKE” on the fluid movement of COM for safety a priority.
e. In my view, Spasticity in stroke patients is in fact the resultant effect of uninterrupted muscle activity from anticipatory postural control with slightest movement of COM whereas muscle’s velocity dependent spastic behavior well described by neurophysiologists in laboratory set up in unloaded condition when the limb segment is moved passively by examiner is a reflex action.
f. Self organizing stroke CNS promotes automatic central postural control of global COM with synergic grouping of chain of muscles in priority over the development of voluntary selective control on segmental COM.
g. Automatic postural gravicentric muscle activities allow segmental COM to move only in the direction towards the central axis and do not yield in any other direction for safety of COM and for COM to remain within the narrow Base of Support [BOS].
4. Microscopic morphological changes like contracture, loss of viscosity, stiffness in paretic muscles, in connective tissue and in basic fabric (the fascia) that binds the entire skeleton together at the central axis, ‘the spine’ enable the paretic side MSS anatomically connected to non paretic MSS to get mechanically bound together for a macroscopic change in behavior of paretic MSS for, “The whole is bigger than sum total of its individual parts”. Meaning that the system as a whole determines in an important way how the parts behave.  (Wow, just Wow?)
o Macroscopic change in behavior of paretic MSS can be compared with passive ‘Towing’ by non-paretic MSS when muscle motors of paretic MSS fail.
(what the hell is this?)
o Towing the huge mass of paretic MSS by non-paretic MSS becomes easy with contracture in widely spread Thoraco-lumbar fascia that spans both sides of the central axis and houses large trunk muscles bilaterally with bilateral innervation helping to bind both paretic and non-paretic MSS together at the central axis with contracture and contraction.  (Wow, just Wow?)
5. Contracture in muscles of limbs that has an origin on the central axis the trunk [Lattissimus, Pectoral and Iliopsoas] enable the limbs to get bound to the trunk with microscopic morphological changes like stiffness, loss of viscosity, loss of sarcomere, thus binding entire paretic MSS with non paretic MSS.
o Lattissimus muscle is anatomically well placed in terms of connecting scapula and the pelvic girdle together and is attached on to Humerus bone and is in continuity with the gluteus maximus on the opposite side (Vleming & Wingerden, 1996). It is interesting to see that self organizing brain exploits anatomical advantage of Lattissimus to bind two girdles together like a log by turning it spastic to restrict dissociation between two girdles for safety of COM, a priority for all living organism.
2. To make the lattissimus muscle spastic or to induce extended continuous contraction with anticipatory activity in lattissimus muscle, brain exploits anatomical continuity of left paretic lattissimus with the right normal gluteus maximus on the opposite side. With every step of walking and standing up using good leg hip extensor muscles, paretic lattissimus gets stretched with its own inertial mass and anticipatory extended continuous contraction becomes inevitable in paretic Lattissimus turning it spastic.
3. Self-organizing stroke brain exploits un-opposing pull of normal trunk muscles pulling the torso away from paretic leg to sustain the head, arm and trunk mass (HAT) onto the normal hip thereby off-loading / reducing weight bearing on paretic limb for safety of COM. This steering of good torso away from paretic hip by selforganizing brain fails therapeutic efforts to permanently shift weight on paretic LL.
4. Reduced weight bearing on paretic leg is a huge problem in therapeutics. Forced feedback / verbal commands / visual feedback / weight training / treadmill training / force plate sensory training etc. does not get permanent shift of weight on paretic leg unless paretic LL relearns to gain control on COM in all 3 Cartesian coordinates with paretic muscles in many different basic postures and selforganizing brain feels secure and trusts paretic leg’s ability to control and restore COM.
5. In my experience, Restoration of sensory motor control of the paretic UL is dependent on the restoration of control on COM by paretic Lower Limb. With poor loading of paretic limb, stroke subject is almost hopping on single good leg making spino-spinal neuronal connections to make paretic upper limb to go in flexion posture as is seen when you and me hop on single leg.
Anatomical Coupling of paretic Lattissimus muscle with opposite normal gluteus and inertial mass of paretic lattissimus helps it get stretched with each step of walking standing up and in sitting down.
6. New functional behavior; “Towing” of paretic MSS by non-paretic MSS makes exchange of dominance between two MSS impossible. This makes “Normally Abnormal, to be Normal”.
7. “Towing” wherein one side MSS leads and the other side MSS follows automatically, it disturbs spatiotemporal efficiency, coplanar economy of hip knee actions important for energy savings.
8. Towing of paretic MSS makes it dependent on non-paretic MSS for geocentric reference. This allows non paretic MSS to lead uninterruptedly with paretic MSS turning supportive by trailing behind and acting optimally as a “brake” on COM movement to ensure further safety.
9. New functional integration between two MSS, one leading and controlling the COM all the time and the other trailing behind and following all the time ensure safety of COM, always a priority during postural and supra postural tasks.
10. Added safety to COM is provided by passive inertia of paretic mass.
11. Impedance to movement from spasticity, rigidity and stiffness in muscle and contracture in passive tissue and muscle is a defensive strategy of the self-organizing CNS in prioritizing safety of COM when it cannot control and restore COM to safety.
12. Associated reactions apparently seem to be helping to tow paretic MSS.
13. Paretic UL can be abused (with sub-cortical postural reorganization, spino-spinal reorganization and physiological constraint inter limb coupling) at every step taken by paretic LL ( that moves like a prop without coplanar movement economy at hip and knee, with poor loading and without its ability to control COM in all 3 Cartesian coordinates.
14. Poor loading on paretic leg reduces sensory input from under the paretic foot and ankle foot geography gets influenced by adjoining segments like knee joint, femur and trunk posture etc. making self-organizing brain to depend on vision with sensory reweighting.
15. Depending on vision for balance is, an automatic solution by self-organizing brain at a heavy cost of making “Normally Abnormal, to be Normal” wherein cortical vision is used for balance instead of sub-cortical proprioceptive sensation.
16. This makes the availability of vision to gauge the threat and obstacle in space only if, balance is taken care of by stopping to walk to look or by holding the wall or holding onto people around.
This makes multi-tasking a problem for stroke subject that could cause frustration / depression /
and self-image problems.
17. Power of self-organizing brain is mightier compared to any therapeutic efforts made by rehabilitation team unless therapeutics are designed to Reorganize the self-organized brain by exploiting the priority of self-organizing brain, to control and restore COM using paretic MSS.(Holy cow!)
18. Human body is the direct window to the brain. Paretic MSS itself can be therapeutically exploited to channelize the dialogue between brain, body and the external environment; ‘the gravity’ to re-organize self-organized brain to restore lost sensory-motor control on paretic side.

Amy, help please!
 

2 comments:

  1. I read the "laymans" explanation on the site and it seems like a repackaged neuroplasticity concept from SoS, like calling for active use of paretic side and let it control CoM which is Center of Mass so it can become dominant. also talks about massively focused active practice with paretic side and that functional recovery (compensation with good side) is bad. Only weird pat is it seems to discourage unnatural movement which is encouraged in SoS. It says unlearn unnatural(which includesspasticity) and learn new ones. In any case a very vague therapy and it makes no sense to me unless the goal is to make money by complicating the simple principles from SoS. and if it works thats probably the reason why.

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  2. Theres more like it. like the Anat Baniel method. attach your name to neuroplasticity and you make money?

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