Quantification of atrophy and activation failure in the plantarflexors post-stroke 1 Brian A. Knarr, 1 John Ramsay, 1 Thomas S. Buchanan, 1 Stuart A. Binder-Macleod, 1 Jill S. Higginson 1 Biomechanics and Movement Science, University of Delaware, Newark, DE, USA email: bknarr@udel.edu INTRODUCTION Muscle weakness is a common impairment for chronic stroke survivors, and is characterized by lower forces during maximal volitional contraction on the affected side. Weakness in the plantarflexor muscle group is associated with decreased walking speed in stroke subjects (1). Post-stroke muscle weakness is commonly thought to be a result of a combination of central nervous system impairments and muscular atrophy due to disuse. Recent studies have attempted to parse the causes of weakness post-stroke, examining a combination of volitional force, muscle volumes from MRI, and agonist and antagonist EMG (2). While results indicate that activation failure is a primary cause of muscle weakness in persons post-stroke, its contribution to weakness has not been quantified. Muscle atrophy, as well as changes in muscle properties such as specific tension (3) and architecture (4), may also contribute to muscle weakness. The goal of this study is to assess the loss in force generating ability of the plantarflexor muscle group related to activation failure. We hypothesize that activation failure will account for a large portion, but not all, of muscle weakness. METHODS 13 subjects post-stroke (Age 60 ± 8 yrs., 2 Female, 4.2 ± 3.2 yrs. post-stroke) were recruited to participate in this study. All subjects were at least 6 months post-stroke and signed informed consent forms approved by the Human Subjects Review Board at the University of Delaware. Muscle strength was tested using the burst superimposition test. Subjects lay supine on a KIN- COM III dynamometer (Chattecx Corp, Chattanooga, Tennessee) with their knee in extension and ankle at neutral. Velcro straps were used to hold the foot and shank in position. Restraints were placed on the shoulders of the subject to ensure that all forces were directed into the transducer and not lost to body displacement. A maximal electrical stimulation burst (600 μs pulse duration, 100 ms train duration, 135 V, 100 Hz train) (Grass Technologies, Warwick, RI) was delivered while subjects produced their maximum volitional force. Predicted maximum force generating ability (MFGA) using the burst superimposition test (MFGAburst) was calculated using the following equation: (1) F F MFGA stim vol burst where Fvol is the volitional force produced by the subject and Fstim is the additional force produced by the stimulation. A cubic adjustment, similar to methods previously used for the quadriceps (5; 6), was applied to the MFGA prediction to account for the incomplete activation of the muscle with the burst. MFGA was converted to torque (Tmax) for comparison to previous studies. Axial MRI Images were acquired for both legs using a 1.5 T Signa LX scanner (GE Medical, Milwaukee, WI). Two overlapping images were taken for the lower leg using a repetition time of 450 ms, echo time of 10 ms, slice thickness of 10 mm and a space between slices of 11.5 mm. IMOD software was used to manually trace the boundaries of the soleus (SOL), medial gastrocnemius (MG), and lateral gastrocnemius (LG) muscles over the entire muscle length. After adjusting the pixel threshold for fat suppression, volume was calculated by summing the cross-sectional areas multiplied by the slice thickness over the length of the muscle. Difference between interlimb Tmax and muscle volume were evaluated using a t-test. RESULTS AND DISCUSSION Average paretic limb MVC plantarflexion torque (34.4 ± 21.3 Nm) was 41 ±17% of the non-paretic MVC (89 ± 41.5 Nm) (Figure 1). Predicted max torque of the paretic plantarflexors (82.4 ± 20.2 Nm) was 66.5 ± 9.6% of the non-paretic limb (124.9 ± 30.4 Nm). The average paretic plantarflexor volume was 79.8 ± 9.1 % of the non-