Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

The pathophysiology of spasticity.

G Sheean1

  • 1Department of Neurosciences, Medical School, University of California - San Diego, CA, USA. gsheean@ucsd.edu

European Journal of Neurology
|March 29, 2002
PubMed
Summary

Spasticity, a muscle overactivity symptom of upper motor neurone (UMN) syndrome, results from hyperexcitable spinal reflexes. Central nervous system plasticity influences its development and progression.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

The external anal sphincter operates at short sarcomere length in humans.

Neurogastroenterology and motility·2011
Same author

International consensus statement for the use of botulinum toxin treatment in adults and children with neurological impairments--introduction.

European journal of neurology·2010
Same author

Botulinum toxin assessment, intervention and after-care for upper limb hypertonicity in adults: international consensus statement.

European journal of neurology·2010
Same author

Botulinum toxin assessment, intervention and aftercare for paediatric and adult niche indications including pain: international consensus statement.

European journal of neurology·2010
Same author

Nerve conduction changes in patients with mitochondrial diseases treated with dichloroacetate.

Muscle & nerve·2001
Same author

Evaluating the role of botulinum toxin in the management of focal hypertonia in adults.

Journal of neurology, neurosurgery, and psychiatry·2000

Area of Science:

  • Neuroscience
  • Neurology
  • Physiology

Background:

  • Spasticity is a key component of the upper motor neurone (UMN) syndrome, characterized by muscle overactivity.
  • It is a form of hypertonia caused by hyperexcitable tonic stretch reflexes, distinct from rigidity.
  • Other UMN syndrome components include hyper-reflexia, clonus, spasms, and Babinski sign.

Purpose of the Study:

  • To elucidate the pathophysiology of spasticity and related UMN syndrome phenomena.
  • To understand the role of spinal reflexes and supraspinal control in spasticity.
  • To explore the contribution of central nervous system plasticity to spasticity development.

Main Methods:

  • Review of electrophysiology and neurochemistry of spinal reflexes.
  • Analysis of the effects of antispasticity drugs.
  • Examination of supraspinal inhibitory and excitatory influences on spinal reflexes.

Main Results:

  • UMN lesions disrupt supraspinal control, leading to disinhibition of spinal reflexes.
  • Hyperactive spinal reflexes mediate many positive UMN signs, including spasticity.
  • Delayed onset and temporal changes in reflex excitability suggest central nervous system plasticity.

Conclusions:

  • Spasticity pathophysiology involves hyperexcitable spinal reflexes due to altered supraspinal control.
  • Central nervous system plasticity plays a significant role in the evolving clinical presentation of spasticity.
  • Understanding reflex mechanisms and drug actions is crucial for managing spasticity.

Related Experiment Videos