What is alpha spasticity?

Alpha Spasticity: Definition and Management

Alpha spasticity is a velocity-dependent increase in muscle tone caused by hyperexcitability of the alpha motor neurons, resulting in resistance to passive stretch and characterized by exaggerated tendon reflexes as part of the upper motor neuron syndrome. 1, 2

Pathophysiology

Alpha spasticity occurs due to:

• Disruption of the balance between supraspinal inhibitory and excitatory inputs to spinal reflexes
• Hyperexcitability of the tonic stretch reflexes at the segmental level
• Disinhibition of proprioceptive (stretch) and nociceptive reflexes
• Delayed onset after upper motor neuron lesions, suggesting neuroplastic changes 3

Alpha spasticity differs from other forms of hypertonia by its:

• Velocity-dependent nature (faster stretch produces greater resistance)
• Association with other upper motor neuron signs (hyperreflexia, clonus, Babinski sign)
• Potential to cause involuntary muscle activity and abnormal limb positioning 1

Clinical Presentation

Spasticity manifests differently based on the lesion location:

• Spinal cord lesions: Slow increase in excitation with over-activity of both flexors and extensors
• Cerebral lesions: Rapid build-up of excitation with predominant involvement of antigravity muscles 2

Common clinical features include:

• Resistance to passive movement that increases with speed
• Exaggerated deep tendon reflexes
• Clonus (rhythmic contractions with sustained stretch)
• Clasp-knife phenomenon (initial resistance followed by sudden relaxation)
• Flexor and extensor spasms 3, 2

Assessment

The Modified Ashworth Scale is the most commonly used clinical measure for spasticity, assessing resistance during passive movement 4.

Management Approaches

Pharmacological Interventions

1. Focal spasticity:

   • Botulinum toxin injections are recommended as first-line treatment for localized spasticity in upper and lower limbs (Class I, Level A evidence) 1
   • Dosing: 100-300 IU based on predetermined diagrams for specific muscles 1, 5

2. Generalized spasticity:

   • Oral antispasticity agents (Class IIa, Level A evidence) 1:
     • Baclofen (30-80 mg/day in divided doses)
     • Tizanidine (particularly effective for spasticity with pain)
     • Dantrolene (useful when cognitive side effects must be avoided)
   • Warning: Oral medications may cause dose-limiting sedation 1, 5

3. Severe refractory spasticity:

   • Intrathecal baclofen therapy for severe spastic hypertonia unresponsive to other interventions (Class IIb, Level A evidence) 1
   • Can be considered as early as 3-6 months after stroke for refractory cases 1

Physical Interventions

• Neuromuscular electrical stimulation (NMES) or vibration applied to spastic muscles can temporarily improve spasticity as an adjunct to rehabilitation (Class IIb, Level A evidence) 1
• Physical therapy is essential and should always be included in the management plan 4
• Splints and taping are not recommended for prevention of wrist and finger spasticity after stroke (Class III, Level B evidence) 1

Important Clinical Considerations

• Spasticity treatment should only be initiated when it causes functional limitations, pain, or interferes with care 6
• Overtreatment can worsen function if the patient is using spasticity for mobility or posture 5
• Inadequate treatment can lead to contractures, pain, and increased care burden 5
• Abrupt discontinuation of baclofen can cause life-threatening withdrawal 5
• The cost of care is 4 times higher when spasticity is present after stroke 1

Treatment Algorithm

1. Assess if spasticity is causing functional impairment, pain, or care difficulties
2. Determine if spasticity is focal or generalized
3. For focal spasticity: Botulinum toxin injections + physical therapy
4. For generalized spasticity: Oral medications (baclofen, tizanidine, or dantrolene) + physical therapy
5. For refractory cases: Consider intrathecal baclofen or neurosurgical interventions
6. Regular reassessment to adjust treatment based on functional outcomes

The goal of treatment should always be functional improvement rather than simply reducing muscle tone 4.