The spasticity paradox: movement disorder or disorder of resting limbs?

Abstract

Background: Spasticity is defined/assessed in resting limbs, where increased stretch reflex activity and mechanical joint resistance are evident. Treatment with antispastic agents assumes that these features contribute to the movement disorder, although it is unclear whether they persist during voluntary contraction. Objectives: To compare reflex amplitude and joint resistance in spastic and normal limbs over an equivalent range of background contraction. Methods: Thirteen normal and eight hemiparetic subjects with mild/moderate spasticity and without significant contracture were studied. Reflex and passive joint resistance were compared at rest and during six small increments of biceps voluntary contraction, up to 15% of normal maximum. A novel approach was used to match contraction levels between groups. Results: Reflex amplitude and joint mechanical resistance were linearly related to contraction in both groups. The slopes of these relations were not above normal in the spastic subjects on linear regression. Thus, reflex amplitude and joint resistance were not different between groups over a comparable range of contraction levels. Spastic subjects exhibited a smaller range of reflex modulation than normals because of decreased maximal contraction levels (weakness) and significant increases of resting contraction levels. Conclusions: Spasticity was most evident at rest because subjects could not reduce background contraction to normal. When background contractions were matched to normal levels, no evidence of exaggerated reflex activity or mechanical resistance was found. Instead, reduced capacity to modulate reflex activity dynamically over the normal range may contribute to the movement disorder. This finding does not support the routine use of antispastic agents to treat the movement disorder.

Disturbances of motor unit rate modulation are prevalent in muscles of spastic-paretic stroke survivors

“…The observed impaired modulation in firing rates during voluntary contractions is in contrast to the enhanced excitability of spastic-paretic motoneurons observed at rest (Mottram et al 2009(Mottram et al , 2010. These paradoxical findings are similar to previous observations for enhanced stretch or Hoffman reflexes at rest (Burne et al 2005;Chardon et al 2009;Huang et al 2006;Powers et al 1988), yet not during a background contraction (Burne et al 2005; Thompson et al 2009). We suggest that the enhanced reflex responses at rest in stroke survivors are explained by the presence of a low-level tonic depolarizing synaptic drive to the spastic-paretic motoneuron pool.…”

Spastic movement disorder: impaired reflex function and altered muscle mechanics

“…increased muscle tone 50,69 . When background contractions are matched to normal levels in spastic subjects, little evidence exists for exaggerated reflex activity 58,61,70 (for exception see 71 ). However, during isotonic leg muscle contractions modulation and inhibition of Ib afferents (innervating the force sensitive Golgi tendon organs) is reduced 72 and some co-contraction of antagonistic arm muscles can occur 73,74 .…”

“…The consequence is a reduced adaptation of muscle activity to the actual ground conditions 88 . Together with the reduced capacity to modulate reflex activity over the normal range, this might contribute to the spastic movement disorder 70,87 .…”

Clonus is explained from increased reflex gain and enlarged tissue viscoelasticity

“…Candidate mechanisms are the spinal reflex and passive muscle stiffness, both of which can potentially destabilize the joint. Both factors were found to be increased in UMND (Mirbagheri et al, 2001;Friden and Lieber, 2003;Lieber et al, 2004;Burne et al, 2005;de Vlugt et al, 2010). In a simulation study, the observed variation in clonus frequency with loading was explained from the isolated increased gain of the Ia reflex pathway (Hidler and Rymer, 2000).…”