Spasticity

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.

An upper motor neuron lesion, commonly caused by:

• Stroke
• Subdural or epidural hemorrhage
• Cerebral palsy
• Brain tumor
• Multiple sclerosis
• Hydrocephalus
• Amyotrophic lateral sclerosis
• Hereditary spastic paraplegia
• Spinal cord injury (e.g., trauma, tumor)

References:^[1]

• 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 the limb is moved rapidly, followed by a sudden decrease in resistance
  • 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]

• 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
    • Baclofen
    • Dantrolene
  • Oral benzodiazepines
    • Diazepam
    • Clonazepam
  • Oral alpha-2 adrenergic agonists
    • Tizanidine
    • Clonidine
  • Intramuscular injections: botulinum toxin A, lidocaine, or phenol
  • Intrathecal infusion
    • Baclofen: central acting muscle relaxant
      • Contraindications: renal failure
      • Therapeutic guidelines: should always be started at a slow dose and gradually increased to minimize potential side effects (particularly hypotension, sedation, nausea, depression).
      • Plasma half-life: 3–4 hours
      • Effect
        • Agonist of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA)
        • Stimulated presynaptic and postsynaptic GABA receptors in the spinal cord → direct inhibition of impulse transmission
        • Analgesic in addition to muscle relaxant
• 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]