Abstract

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:

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]

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 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]

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
  - 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]

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]