What is the pathophysiology of knee buckling in spastic paraparesis?

Pathophysiology of Knee Buckling in Spastic Paraparesis

The primary mechanism of knee buckling in spastic paraparesis involves an imbalance between antagonist muscle activation during movement, specifically excessive stretch reflex activation of antagonist muscles combined with reciprocal inhibition of agonist muscles during voluntary movement. 1

Neuromuscular Mechanisms

The pathophysiological process involves several interconnected mechanisms:

1. Muscle Imbalance

   • Excessive activation of knee flexors (hamstrings) with inadequate activation of knee extensors (quadriceps)
   • This creates torque imbalance around the knee joint leading to instability 2

2. Spastic Overactivity Components

   • Spastic dystonia: Involuntary muscle activation at rest without stretch or voluntary effort
   • Spastic cocontraction: Unwanted antagonist muscle activation during voluntary agonist effort
   • Spasticity: Enhanced velocity-dependent responses to phasic stretch 3

3. Stretch-Sensitive Paresis

   • Decreased access of central command to the agonist muscles (quadriceps)
   • This weakness is aggravated by antagonist stretch 3

Biomechanical Factors

• Peak knee flexion during swing phase is frequently reduced, affecting gait stability 4
• The quadriceps weakness combined with hamstring overactivity creates a mechanical disadvantage
• This leads to sudden knee collapse during weight-bearing activities

Pathological Cycle

The pathophysiology follows a self-perpetuating cycle:

• Initial paresis → reduced voluntary motor unit recruitment
• Relative immobilization → adaptive shortening of muscles and joint contracture
• Chronic disuse → further plastic rearrangements in higher centers
• Worsening paresis → more disuse 5

Sensory Contributions

• Altered proprioception contributes to the problem
• In patients with spastic paraparesis, sural nerve stimulation can increase innervation of tibialis anterior muscle
• This suggests that sensory input significantly modulates motor control in these patients 6

Tissue Changes

Spastic myopathy develops in the affected muscles:

• Genetically mediated, evolving myopathy promoted by muscle hypo-mobilization in short position
• Clinically manifests as extensibility loss in resting muscle
• Contributes to the overall deformity and dysfunction 3

Clinical Implications

Understanding this pathophysiology has important treatment implications:

• Physical therapy should focus on strengthening weaker quadriceps muscles
• Orthotic management can prevent knee buckling during ambulation
• Pharmacological interventions (baclofen, botulinum toxin) can address spasticity
• Functional electrical stimulation may improve motor control 1

The imbalance between flexor and extensor muscle groups, combined with altered neural control and tissue changes, creates the perfect storm for knee buckling in spastic paraparesis. This understanding guides targeted therapeutic approaches to improve stability and function.