Velocity dependent passive plantarflexor resistive torque in patients with acquired brain injury (original) (raw)
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Clinical Biomechanics, 2008
Background: Increased calf muscle stiffness is a common impairment following acquired brain injury. This study examined the immediate effects of cyclic ankle stretching at two stretch velocities on calf stiffness in individuals with hemiparesis (n=17) and control subjects (n=10). Methods: Cyclic ankle stretching was applied for three minutes at velocities of 5° sec-1 and 25° sec-1 using a purpose-built dynamometer. Surface electromyography was employed to ensure stretches were passive. Peak plantarflexor resistive torque was derived from torque-angle curves. Comparisons were made between groups, velocities and between limbs for hemiparetic subjects. Findings: At baseline, mean peak plantarflexor resistive torque was greater in the affected limbs of hemiparetic subjects than their contralateral limbs (p<0.001); however there was no significant difference between groups. Plantarflexor resistive torque was reduced in all limbs following cyclic stretching regardless of stretch velocity (p<0.005). Two distinct patterns of response were observed in hemiparetic subjects. In nine cases the affected limb responses did not differ from the contralateral limb or control data. In the remaining eight cases mean peak plantarflexor resistive torque in the affected limb was greater than the contralateral limb and control values. In this subgroup, peak plantarflexor resistive torque was significantly affected by stretch velocity and showed the greatest reduction following cyclic stretching. Interpretation: Cyclic stretching has been shown to produce a short term reduction in calf stiffness in a subgroup of individuals with hemiplegia. Further investigation is required to elaborate the characteristics of those most likely to respond optimally to this intervention.
Clinical Biomechanics, 2002
Objective. To examine changes in muscle length and resistance to passive lengthening in the triceps surae muscles in patients with recently acquired brain injury. Background. Increased passive resistance in the triceps surae muscles is common following acquired brain injury. Adaptive shortening secondary to relative immobility, and increased stiffness due to rheologic changes within the musculo-tendinous unit, may be exacerbated by plantarflexor muscle overactivity related to the brain injury itself. Design. Three variables representing resistance to passive lengthening and soleus muscle length were compared between subjects with recent brain injury and age matched normal controls. Comparison between limbs was made for subjects with unilateral neurological impairment. Methods. Slow passive dorsiflexion stretches were performed using a computer controlled dynamometer. Muscle stiffness in the initial and latter portion of the range, and the angles achieved at torques of 5 and 10 N m were determined from torque-angle curves. Maximal ankle dorsiflexion with the knee flexed was considered to reflect soleus muscle length. Results. Significant differences were demonstrated for all variables, except passive stiffness near the end of available range. The limb ipsilateral to unilateral brain injury differed from control limbs in that significantly less passive range of dorsiflexion was available and initial resistance to passive stretch was significantly less. Conclusions. The reduction in soleus muscle length evident in subjects with recent acquired brain injury, even in neurologically unaffected limbs, may reflect the influence of relative immobility. Although plantarflexor muscle overactivity was found to be associated with increased resistance to slow passive stretch, the mechanism was unable to be elucidated from these data. The limb ipsilateral to unilateral neurological impairment cannot be considered to be a 'normal' control for comparative purposes. Relevance Adaptive shortening and increased resistance to passive lengthening limit active ankle dorsiflexion, and alter ankle biomechanics. Tonic muscle overactivity has the potential to exacerbate these changes. Prophylactic management of inappropriate muscle activity and maintenance of muscle length may facilitate the achievement of rehabilitation goals and reduce subsequent disability following acquired brain injury.
Measurement of Plantarflexor Spasticity in Traumatic Brain Injury
American Journal of Physical Medicine & Rehabilitation, 2007
Annaswamy T, Mallempati S, Allison SC, Abraham LD: Measurement of plantarflexor spasticity in traumatic brain injury: correlational study of resistance torque compared with the modified Ashworth scale. Am J Phys Med Rehabil 2007;86:404 -411. Objectives: To examine the usefulness of a biomechanical measure, resistance torque (RT), in quantifying spasticity by comparing its use with a clinical scale, the modified Ashworth scale (MAS), and quantitative electrophysiological measures.
Mechanisms of disturbed motor control in ankle weakness during gait after stroke
Gait & Posture, 2002
This study investigated the role of paresis, excessive antagonist coactivation, increased muscle-tendon passive stiffness and spasticity in the reduced stance phase plantarflexor moment (Mmax) and swing phase dorsiflexion during gait (DFmax) in subjects with a recent ( B6 months post-stroke) hemiparesis (patients). The gait pattern of the paretic and non-paretic sides was evaluated in 30 patients (aged 57.8 910.8 years), whereas only one side was evaluated in 15 healthy controls (aged 59.1 9 9.8 years) while walking at natural and very slow speeds. Peak plantarflexor moment (Mmax) and peak medial gastrocnemius (MG) activation during the stance phase, as well as peak dorsiflexion angle (Dfmax) and peak tibialis anterior (TA) activation during the swing phase, were retained for analysis. In addition, a coactivation index and a plantarflexor spasticity index were calculated for both the stance and the swing phase, and plantarflexor passive stiffness was evaluated on an isokinetic dynamometer. The results showed that Mmax on the paretic and non-paretic sides were both reduced compared with control values at natural speed. This reduction was combined to a low MG activation (paresis) on the paretic side. On the non-paretic side, the reduced plantarflexor moment was related to excessive coactivation levels. The swing phase Dfmax tended to be reduced (not significantly) on the paretic side of the patients compared with control values. This reduction was neither associated with excessive antagonist coactivation nor to plantarflexor hyperactive stretch reflexes, but rather to an increased plantarflexor passive stiffness. In some of the patients, however, an increased TA activation that overcame the plantarflexor passive stiffness allowed for normal DFmax values. The functional consequences of the disturbed mechanisms of motor control observed in both the paretic and non-paretic sides are discussed.
Gait & posture, 2018
Gait and balance disorders are common among individuals who have experienced a mild to moderate traumatic brain injury (TBI). However, little is known about how the neuromuscular control of gait is altered following a TBI. Investigate the relationship between lower limb muscle activation patterns and chronic gait deficits in individuals who previously experienced a mild to moderate TBI. Lower extremity electromyographic (EMG) signals were collected bilaterally during treadmill and overground walking in 44 ambulatory individuals with a TBI >1 year prior and 20 unimpaired controls. Activation patterns of TBI muscles were cross-correlated with normative data from control subjects to assess temporal phasing of muscle recruitment. Clinical assessments of gait and balance were performed using dynamic posturography, the dynamic gait index, six-minute walk test, and preferred walking speed. TBI subjects exhibited abnormal activation patterns in the tibialis anterior, medial gastrocnemius...