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 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]

• 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	Muscle spasticity Dystonia Multiple sclerosis	Hypotonia Nausea Sedation
Dantrolene	Inhibition of ryanodine receptors → ↓ release of Ca2+ from sarcoplasmic reticulum of the skeletal muscle	Malignant hyperthermia Neuroleptic malignant syndrome	CNS: headache, dizziness, seizures GI upset Muscle weakness
Cyclobenzaprine	Agonism at central (mainly the brain stem) 5-HT2 receptor [4]	Muscle spasticity	Anticholinergic (chemical structure is very similar to TCAs) Dry mouth Constipation Sedation, drowsiness, fatigue
Oral α2 adrenergic agonists (e.g., tizanidine, clonidine)	Agonism at central α2 receptors	Muscle spasticity Cerebral palsy Multiple sclerosis ALS	Orthostatic hypotension, bradycardia Sedation Dry mouth
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	Drowsiness, sleepiness, or dizziness, next-day hangover effect Anterograde amnesia Addictive potential, development of drug tolerance Paradoxical excitability

• 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]