• Clinical science

Spasticity

Summary

Spasticity is defined as a velocity-dependent increase in muscle tone that manifests with resistance to movement and involuntary muscle spasms and contractions. It is caused by a lesion in the descending motor pathways. Common etiologies of spasticity include multiple sclerosis, stroke, tumor, cerebral palsy, and spinal or peripheral nerve injury. Nerve conduction studies and imaging of the brain and/or spinal cord may be requested to determine the underlying etiology. The management of spasticity is broad and may include physical and occupational therapy, pharmacotherapy (i.e., muscle relaxants such as diazepam, tizanidine, baclofen, or dantrolene; paralytics such as botulinum toxin), or surgery.

Etiology

An upper motor neuron lesion, commonly caused by:

References:[1]

Pathophysiology

  • The mechanism of spasticity is not completely understood.
  • It is thought that upper motor neuron damage leads to loss of descending inhibitory inputs → increased muscle stretch reflex → increased muscle tone

References:[1][2]

Clinical features

  • Increased muscle tone and velocity-dependent resistance to movement
    • Elicited by flexion and extension of various muscles with alternating speed
    • Clasp knife phenomenon: initial resistance (“catch”) when a limb is moved rapidly, followed by a sudden decrease in resistance; observed in patients with upper motor neuron lesions
    • Upper extremity flexors and lower extremity extensors are usually more affected.
    • Must be distinguished from rigidity
  • Involuntary muscle spasms or contractions

References:[3][1][2]

Diagnostics

  • Clinical diagnosis
  • Further tests (e.g., nerve conduction studies or brain imaging) depend on the suspected underlying etiology.

References:[1]

Treatment

  • Physiotherapy: including splinting of the affected extremity
  • Medical therapy: The most commonly used medication is baclofen; however, a variety of treatments (single and/or in combination) may be used and depend on patient-specific factors and patient response.
Oral muscle relaxants
Drug Mechanism of action Indication Side effects
Baclofen
  • Agonism at GABAB receptor in the spinal cord
  • Can also be intrathecally administered
  • Hypotonia
  • Nausea
  • Sedation
Dantrolene
  • Inhibition of ryanodine receptors → ↓ release of Ca2+ from sarcoplasmic reticulum of the skeletal muscle
Cyclobenzaprine
  • Agonism at central (mainly the brain stem) 5-HT2 receptor [4]
  • Muscle spasticity

Oral α2 adrenergic agonists

(e.g., tizanidine, clonidine)

Oral benzodiazepines

(e.g., diazepam, clonazepam)

  • Indirect GABAA agonism by increasing the opening frequency of Cl- channels → ↑ GABAAaction
  • Muscle spasticity
  • Psychiatric conditions (anxiety, panic disorder)
  • Detoxification
  • Anesthesia
  • Local therapy: intramuscular injections with botulinum toxin A, lidocaine, or phenol
  • Surgical therapy: for severe spasticity refractory to medical treatment
    • Selective dorsal rhizotomy: surgical destruction of nerves in the lower spinal cord in order to reduce muscle tone to the lower extremities
    • Orthopedic surgery
      • Lengthening of muscles and tendons
      • Transfer of tendons to attachment points where they cannot contract the joint into a deformed position
      • Osteotomy if muscle contracture has led to joint deformity

References:[1]

Complications

  • Musculoskeletal deformity
  • Impaired mobility
  • Reduced functional independence
  • Pain

References:[1]

We list the most important complications. The selection is not exhaustive.

Prognosis

The prognosis of spasticity depends on the underlying condition.

References:[1]

  • 1. Vanek ZF, Berman SA. Spasticity. In: Spasticity. New York, NY: WebMD. http://emedicine.medscape.com/article/2207448-overview. Updated February 4, 2016. Accessed May 22, 2017.
  • 2. Ropper A, Klein J, Samuels M. Adams and Victor's Principles of Neurology 10th Edition. McGraw-Hill Education / Medical; 2014.
  • 3. Gelb D, Aminoff MJ, Wilterdink JL. The Detailed Neurologic Examination in Adults. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/the-detailed-neurologic-examination-in-adults. Last updated September 7, 2012. Accessed March 2, 2017.
  • 4. Kobayashi H, Hasegawa Y, Ono H. Cyclobenzaprine, a centrally acting muscle relaxant, acts on descending serotonergic systems. Eur J Pharmacol. 1996; 311(1): pp. 29–35. doi: 10.1016/0014-2999(96)00402-5.
  • Brioschi TM de LS, Schramm SG, Kano EK, et al. Pharmacokinetics and Bioequivalence Evaluation of Cyclobenzaprine Tablets. BioMed Research International. 2013; 2013: pp. 1–6. doi: 10.1155/2013/281392.
last updated 06/08/2020
{{uncollapseSections(['ufXpLx', 'wfXhox', 'CfXqox', 'FncgE10', 'AfXRKx', '-fXDKx', 'uncpE10', '8ncOE10'])}}