We have located links that may give you full text access.
Journal Article
Review
The neurophysiology of deforming spastic paresis: A revised taxonomy.
Annals of Physical and Rehabilitation Medicine 2019 November
This paper revisits the taxonomy of the neurophysiological consequences of a persistent impairment of motor command execution in the classic environment of sensorimotor restriction and muscle hypo-mobilization in short position. Around each joint, the syndrome involves 2 disorders, muscular and neurologic. The muscular disorder is promoted by muscle hypo-mobilization in short position in the context of paresis, in the hours and days after paresis onset: this genetically mediated, evolving myopathy, is called spastic myopathy. The clinician may suspect it by feeling extensibility loss in a resting muscle, although long after the actual onset of the disease. The neurologic disorder, promoted by sensorimotor restriction in the context of paresis and by the muscle disorder itself, comprises 4 main components, mostly affecting antagonists to desired movements: the first is spastic dystonia, an unwanted, involuntary muscle activation at rest, in the absence of stretch or voluntary effort; spastic dystonia superimposes on spastic myopathy to cause visible, gradually increasing body deformities; the second is spastic cocontraction, an unwanted, involuntary antagonist muscle activation during voluntary effort directed to the agonist, aggravated by antagonist stretch; it is primarily due to misdirection of the supraspinal descending drive and contributes to reducing movement amplitude; and the third is spasticity, one form of hyperreflexia, defined by an enhancement of the velocity-dependent responses to phasic stretch, detected and measured at rest (another form of hyperreflexia is "nociceptive spasms", following flexor reflex afferent stimulation, particularly after spinal cord lesions). The 3 main forms of overactivity, spastic dystonia, spastic cocontraction and spasticity, share the same motor neuron hyperexcitability as a contributing factor, all being predominant in the muscles that are more affected by spastic myopathy. The fourth component of the neurologic disorder affects the agonist: it is stretch-sensitive paresis, which is a decreased access of the central command to the agonist, aggravated by antagonist stretch. Improved understanding of the pathophysiology of deforming spastic paresis should help clinicians select meaningful assessments and refined treatments, including the utmost need to preserve muscle tissue integrity as soon as paresis sets in.
Full text links
Related Resources
Trending Papers
Challenges in Septic Shock: From New Hemodynamics to Blood Purification Therapies.Journal of Personalized Medicine 2024 Februrary 4
Molecular Targets of Novel Therapeutics for Diabetic Kidney Disease: A New Era of Nephroprotection.International Journal of Molecular Sciences 2024 April 4
The 'Ten Commandments' for the 2023 European Society of Cardiology guidelines for the management of endocarditis.European Heart Journal 2024 April 18
A Guide to the Use of Vasopressors and Inotropes for Patients in Shock.Journal of Intensive Care Medicine 2024 April 14
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app