What causes buckling of the knee in spastic paraparesis?

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Last updated: August 24, 2025View editorial policy

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Buckling of Knee in Spastic Paraparesis

Knee buckling in spastic paraparesis primarily occurs due to 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

Pathophysiological Mechanism

The mechanism involves several key components:

  1. Muscle Imbalance:

    • Excessive stretch reflex activation of antagonist muscles (hamstrings)
    • Reciprocal inhibition of agonist muscles (quadriceps) during voluntary movement
    • This creates a dynamic imbalance during gait 2
  2. Contributing Factors:

    • Hamstring spasticity - causes increased knee flexion during stance phase
    • Quadriceps weakness - reduces ability to stabilize the knee
    • Soleus weakness - affects overall lower limb stability
    • Lever-arm dysfunction - alters biomechanical efficiency 3

Clinical Manifestations

The knee buckling manifests as:

  • Increased knee flexion during stance phase
  • Reduced knee flexion during swing phase (stiff-knee gait)
  • Esthetically poor gait pattern
  • Increased energy consumption during ambulation
  • Potential knee pain over time 3

Biomechanical Analysis

Research has demonstrated that:

  • Isometric muscle strength is significantly decreased in spastic paraparesis, with over 50% reduction in ankle dorsiflexor strength
  • Passive stiffness is approximately 35% higher in the plantarflexors
  • Fast stretches induce large stretch-evoked muscle activity (>110% increase in stiffness at ankle and knee)
  • Reduced knee flexion during swing phase correlates with reduced knee flexion velocity at the end of stance phase
  • This reduced velocity is associated with plantarflexor weakness and increased passive stiffness in knee extensors 4

Natural History

Without intervention, knee flexion gait tends to deteriorate over time, leading to:

  • Progressive functional limitations
  • Increased energy expenditure
  • Development of secondary complications like joint contractures
  • Potential for chronic pain 3, 5

Clinical Implications

Understanding this pathophysiology is crucial because:

  • It explains why patients with spastic paraparesis have difficulty with ambulation
  • It guides treatment approaches targeting both the neural components (spasticity) and musculoskeletal adaptations (weakness, contractures)
  • It highlights the importance of early intervention to prevent the vicious cycle of paresis-disuse-paresis 5

This knowledge helps clinicians develop targeted interventions focusing on improving muscle balance, reducing spasticity, and enhancing functional mobility in patients with spastic paraparesis.

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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