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Old 25-01-2017, 09:19 PM   #1
Mabo
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Default Spasticity

Has anyone an idea how spasticity is different from a normal muscle contraction?
Cannot find a neurofysiological explanation anywhere
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Old 25-01-2017, 09:46 PM   #2
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Default Pathophysiology of Spasticity: Implications for Neurorehabilitation

https://www.hindawi.com/journals/bmri/2014/354906/

Abstract

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Spasticity is the velocity-dependent increase in muscle tone due to the exaggeration of stretch reflex. It is only one of the several components of the upper motor neuron syndrome (UMNS). The central lesion causing the UMNS disrupts the balance of supraspinal inhibitory and excitatory inputs directed to the spinal cord, leading to a state of disinhibition of the stretch reflex. However, the delay between the acute neurological insult (trauma or stroke) and the appearance of spasticity argues against it simply being a release phenomenon and suggests some sort of plastic changes, occurring in the spinal cord and also in the brain. An important plastic change in the spinal cord could be the progressive reduction of postactivation depression due to limb immobilization. As well as hyperexcitable stretch reflexes, secondary soft tissue changes in the paretic limbs enhance muscle resistance to passive displacements. Therefore, in patients with UMNS, hypertonia can be divided into two components: hypertonia mediated by the stretch reflex, which corresponds to spasticity, and hypertonia due to soft tissue changes, which is often referred as nonreflex hypertonia or intrinsic hypertonia. Compelling evidences state that limb mobilisation in patients with UMNS is essential to prevent and treat both spasticity and intrinsic hypertonia.
Stretch Reflex and Muscle Tone in Healthy Subjects

Quote:
In healthy subjects, stretch reflexes are mediated by excitatory connections between Ia afferent fibers from muscle spindles and α-motoneurons innervating the same muscles from which they arise. Passive stretch of the muscle excites the muscle spindles, leading Ia fibers to discharge and send inputs to the α-motoneurons through mainly monosynaptic, but also oligosynaptic pathways. The α-motoneurons in turn send an efferent impulse to the muscle, causing it to contract.

Surface EMG recordings in a normal subject at rest clearly show that passive muscle stretches, performed at the velocities used in the clinical practice to assess muscle tone, do not produce any reflex contraction of the stretched muscle. For instance, recording the EMG of elbow flexors during imposed elbow extension, no stretch reflex appears in the biceps when the passive displacement occurs at the velocities usually used during the clinical examination of muscle tone (60°–180° per second). It is only above 200° per second that a stretch reflex can be usually seen. Therefore, stretch reflex is not the cause of the muscle tone in healthy subjects. The muscle tone in healthy subjects is completely due to biomechanical factors
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Old 25-01-2017, 11:48 PM   #3
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https://www.ncbi.nlm.nih.gov/books/NBK10898/

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Damage to Descending Motor Pathways: The Upper Motor Neuron Syndrome

Spasticity.

Spasticity is increased muscle tone, hyperactive stretch reflexes, and clonus (an oscillatory motor response to muscle stretching). Extensive upper motor neuron lesions may also be accompanied by rigidity of the extensor muscles of the leg and the flexor muscles of the arm (called decerebrate rigidity; see below). Spasticity is probably caused by the removal of inhibitory influences exerted by the cortex on the postural centers of the vestibular nuclei and reticular formation. In experimental animals, for instance, lesions of the vestibular nuclei ameliorate the spasticity that follows damage to the corticospinal tract. Spasticity is also eliminated by sectioning the dorsal roots, suggesting that it represents an abnormal increase in the gain of the spinal cord reflex due to loss of descending inhibition (see Chapter 16). This increased gain is also thought to explain clonus
For a quick basic overview of THE MOTOR CORTEX:
http://thebrain.mcgill.ca/flash/a/a_...06_cr_mou.html
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Old 26-01-2017, 09:11 PM   #4
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CONTRACTION
NICOTINIC ACETYLCHOLINE RECEPTORS


The contraction of a motor unit in a muscle is initiated by the release of acetylcholine into the neuromuscular junction.



The acetylcholine activates cholinergic nicotinic receptors in the motor end plate of the muscle fibre, triggering an excitatory potential in its post-synaptic membrane, the sarcolemma. If this potential reaches a certain threshold, a muscular action potential is generated by the potential-dependent sodium channels in this membrane.

This action potential travels first over the surface of the sarcolemma and then over that of the T tubules, causing calcium stored in the sarcoplasmic reticulum to be released. This calcium diffuses into the myofibrils, which are divided by Z stripes into segments called sarcomeres. In each sarcomere, thick and thin filaments then slide past each other, thus drawing the Z stripes closer together, reducing the length of the sarcomere, and causing the muscle to contract.


To understand how the calcium causes these thick and thin filaments to slide past each other, we must consider the proteins of which they are composed. The thick filaments consist mostly of myosin, while the thin filaments consist mostly of actin. Each myosin molecule has a "head" at either end, including a site that can bind with actin.

When no calcium is present, the myosin in the thick filaments cannot bind with the actin in the thin ones, because the binding sites on the actin molecules are occupied by another protein, troponin. But when calcium is released by a muscular action potential, it binds to the troponin, thereby accomplishing two things: 1) exposing the actin-binding sites on the myosin molecule heads; and 2) altering the form of another protein, tropomyosin, so that it exposes the myosin-binding sites on the actin molecules.

The myosin heads can then bind to the sites on the actin molecules. In this process, these heads undergo a change in conformation that makes them rotate. It is this rotation that pulls the thin actin filaments past the thick myosin filaments, one notch at a time, like a ratchet mechanism, causing the muscle to contract.

The contraction will continue as long as calcium and ATP are available. One of the functions of the ATP is to break the bond between the myosin and the actin. (This explains why the muscles of a dead body become rigid as the supply of ATP begins to run short.)

The amount of calcium released by the sarcoplasmic reticulum depends on the frequency of the action potentials in the muscle fibre. (If this frequency reaches or exceeds 50 stimuli per second, it is high enough to cause a sustained muscle contraction, known as a tetanus.)

The muscle contraction ends when the action potentials cease and the concentration of calcium in the myofibrils diminishes. This reduction in calcium is due to its being recaptured by the sarcoplasmic reticulum, an active process that requires
This is what happens in a normal muscle. How is it in a spastic muscle?
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Old 27-01-2017, 12:17 AM   #5
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Fibre type-specific increase in passive muscle tension in spinal cord-injured subjects with spasticity
M Charlotte Olsson et al 2006

Patients with spasticity typically present with an increased muscle tone that is at least partly caused by an exaggerated stretch reflex. However, intrinsic changes in the skeletal muscles, such as altered mechanical properties of the extracellular matrix or the cytoskeleton, have been reported in response to spasticity and could contribute to hypertonia, although the underlying mechanisms are poorly understood. Here we examined the vastus lateralis muscles from spinal cord-injured patients with spasticity (n = 7) for their passive mechanical properties at three different levels of structural organization, in comparison to healthy controls (n = 7). We also assessed spasticity-related alterations in muscle protein expression and muscle ultrastructure. At the whole-muscle level in vivo, we observed increased passive tension (PT) in some spasticity patients particularly at long muscle lengths, unrelated to stretch reflex activation. At the single-fibre level, elevated PT was found in cells expressing fast myosin heavy chain (MyHC) isoforms, especially MyHC-IIx, but not in those expressing slow MyHC. Type IIx fibres were present in higher than normal proportions in spastic muscles, whereas type I fibres were proportionately reduced. At the level of the isolated myofibril, however, there were no differences in PT between patients and controls. The molecular size of the giant protein titin, a main contributor to PT, was unchanged in spasticity, as was the titin:MyHC ratio and the relative desmin content. Electron microscopy revealed extensive ultrastructural changes in spastic muscles, especially expanded connective tissue, but also decreased mitochondrial volume fraction and appearance of intracellular amorphous material. Results strongly suggest that the global passive muscle stiffening in spasticity patients is caused to some degree by elevated PT of the skeletal muscles themselves. We conclude that this increased PT component arises not only from extracellular matrix remodelling, but also from structural and functional adaptations inside the muscle cells, which alter their passive mechanical properties in response to spasticity in a fibre type-dependent manner.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2000690/

Probably obvious but: "don't forget the patient" ie our "fellow human being"


Quote:
Clinical Understanding of Spasticity: Implications for Practice
Rozina Bhimani and Lisa Anderson 2014

,....There is plenty of research available on spasticity; however, patients' feedback on their understanding of spasticity is missing from the literature. Spasticity symptom experiences can be devastating and patients' spasticity interpretation may differ. Ethical clinical practices require clinicians to incorporate patients' understanding of this phenomenon in their plan of care. Bhimani et al.'s [6] original study reports on the patient understanding of spasticity and their results indicate that there is a discrepancy between patients and clinicians understanding of spasticity. Therefore, omitting patient reports from clinical decision making can have grave and serious consequences on their lives manifesting as side-effects of spasticity therapy, administration of invasive and inappropriate therapies, unnecessary pain, and suffering.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4168242/
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Last edited by marcel; 27-01-2017 at 01:34 AM.
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Old 10-04-2017, 09:09 AM   #6
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Default Spasticity in stroke patients IN MY EXPERIENCE

SPASTICITY in my experience

please pardon me, i am not tech savvy.
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Old 12-04-2017, 05:41 PM   #7
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Default HELSINKI 27th April 2017

would you like o join my chain to end dependency from life of brain injured?
join me on 27th April at Helsinki seminar on Vasa Concept
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Old 13-04-2017, 08:45 AM   #8
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Would like to join but family business ....
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