What causes buckling of the knee in spastic paraparesis?

Buckling of Knee in Spastic Paraparesis: Pathophysiology and Management

Knee buckling in spastic paraparesis primarily occurs due to the 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.

Pathophysiological Mechanism

The mechanism of knee buckling in spastic paraparesis involves several interrelated factors:

1. Stretch Reflex Hyperactivity:

   • During concentric knee extension movements, the antagonist hamstring muscles undergo stretch, triggering exaggerated stretch reflexes due to spasticity 1
   • This inappropriate hamstring activation counteracts the quadriceps force needed for knee stability during weight-bearing

2. Reciprocal Inhibition Dysfunction:

   • The hyperactive stretch reflexes in antagonist muscles cause abnormal reciprocal inhibition of agonist muscles (quadriceps) 1
   • This reduces voluntary activation of quadriceps during critical phases of gait

3. Muscle Weakness and Imbalance:

   • Reduced voluntary strength and agonist EMG activity in all movements, with greatest reduction in concentric actions at high velocity 1
   • Asymmetric distribution of weakness between agonists and antagonists creates torque imbalance around the knee joint 2

4. Contracture Development:

   • Adaptive shortening of muscles left in shortened positions due to relative immobilization 3
   • Muscle contracture further contributes to excessive responsiveness to stretch, creating a vicious cycle 2

Clinical Manifestations

The buckling phenomenon typically presents as:

• Sudden knee flexion during weight-bearing phases of gait
• Inability to maintain knee extension against gravity
• Increased risk of falls and decreased mobility
• Worsening with fatigue or increased walking speed
• Exacerbation during concentric movements that stretch antagonist muscles 1

Management Approaches

Pharmacological Management

1. First-line: Baclofen

   • Recommended for generalized spasticity at 30-80 mg/day in divided doses 4
   • Acts as a GABA-B receptor agonist to reduce excitatory signals maintaining muscle tone
   • Must avoid abrupt discontinuation due to risk of withdrawal symptoms including hallucinations, anxiety, seizures

2. For Chronic Stroke Patients: Tizanidine

   • Start with 2mg once daily and gradually titrate up 4
   • Particularly effective for spasticity resulting in pain and decreased function
   • Has fewer renal clearance concerns compared to baclofen

3. For Focal Spasticity: Botulinum Toxin

   • Effective for painful spasticity that impairs function or positioning
   • Dosage of 100-300 IU based on affected muscles 4
   • Particularly useful in patients with renal impairment as it doesn't undergo renal elimination

4. Alternative Option: Dantrolene

   • Consider if cognitive side effects must be minimized
   • Start at low doses (25mg daily) and titrate slowly 4

Non-Pharmacological Interventions

1. Physical Therapy

   • Implement positioning, passive stretching, and range-of-motion exercises several times daily 5, 4
   • Focus on strengthening the weaker quadriceps muscles to improve knee stability
   • Train compensatory strategies including posture changes and heightening sensory input 5

2. Orthotic Management

   • Consider knee-ankle-foot orthoses to prevent knee buckling during ambulation
   • Splinting or serial casting if contractures are developing 4

3. Electrical Stimulation

   • Functional electrical stimulation (FES) can provide short-term increases in motor strength and motor control 5
   • May be used as an adjunct to conventional therapy, though evidence for functional improvement is limited

4. Advanced Interventions

   • For severe, refractory spasticity: intrathecal baclofen therapy 4
   • Surgical correction may be considered for contractures that interfere with function 5

Important Clinical Considerations

• Treatment should focus on improving function rather than just reducing muscle tone 4
• Identify and treat factors that can worsen spasticity, such as skin pressure sores, urinary tract infections, and pain 4
• Regular assessment of skin integrity is important as spasticity can contribute to pressure ulcer development 4
• Gait analysis may help differentiate spastic paraparesis from other conditions with similar presentations 6

Prevention of Complications

• Early intervention is key to preventing disabling contractures and learned compensatory behaviors
• Intensive motor training of less overactive muscles should disrupt the cycle of paresis-disuse-paresis 2
• Concomitant use of aggressive stretch and focal weakening agents in more overactive muscles should break the cycle of overactivity-contracture-overactivity 2

By addressing both the neural mechanisms (spasticity) and mechanical factors (muscle imbalance, contractures) contributing to knee buckling, patients with spastic paraparesis can achieve improved mobility and reduced fall risk.