scholarly journals Motor Impairment–Related Alterations in Biceps and Triceps Brachii Fascicle Lengths in Chronic Hemiparetic Stroke

2018 ◽  
Vol 32 (9) ◽  
pp. 799-809 ◽  
Author(s):  
Christa M. Nelson ◽  
Wendy M. Murray ◽  
Julius P. A. Dewald

Poststroke deficits in upper extremity function occur during activities of daily living due to motor impairments of the paretic arm, including weakness and abnormal synergies, both of which result in altered use of the paretic arm. Over time, chronic disuse and a resultant flexed elbow posture may result in secondary changes in the musculoskeletal system that may limit use of the arm and impact functional mobility. This study utilized extended field-of-view ultrasound to measure fascicle lengths of the biceps (long head) and triceps (distal portion of the lateral head) brachii in order to investigate secondary alterations in muscles of the paretic elbow. Data were collected from both arms in 11 individuals with chronic hemiparetic stroke, with moderate to severe impairment as classified by the Fugl-Meyer assessment score. Across all participants, significantly shorter fascicles were observed in both biceps and triceps brachii ( P < .0005) in the paretic limb under passive conditions. The shortening in paretic fascicle length relative to the nonparetic arm measured under passive conditions remained observable during active muscle contraction for the biceps but not for the triceps brachii. Finally, average fascicle length differences between arms were significantly correlated to impairment level, with more severely impaired participants showing greater shortening of paretic biceps fascicle length relative to changes seen in the triceps across all elbow positions ( r = −0.82, P = .002). Characterization of this secondary adaptation is necessary to facilitate development of interventions designed to reduce or prevent the shortening from occurring in the acute stages of recovery poststroke.

2021 ◽  
Vol 118 (26) ◽  
pp. e2008597118
Author(s):  
Amy N. Adkins ◽  
Julius P. A. Dewald ◽  
Lindsay P. Garmirian ◽  
Christa M. Nelson ◽  
Wendy M. Murray

A muscle’s structure, or architecture, is indicative of its function and is plastic; changes in input to or use of the muscle alter its architecture. Stroke-induced neural deficits substantially alter both input to and usage of individual muscles. We combined in vivo imaging methods (second-harmonic generation microendoscopy, extended field-of-view ultrasound, and fat-suppression MRI) to quantify functionally meaningful architecture parameters in the biceps brachii of both limbs of individuals with chronic hemiparetic stroke and in age-matched, unimpaired controls. Specifically, serial sarcomere number (SSN) and physiological cross-sectional area (PCSA) were calculated from data collected at three anatomical scales: sarcomere length, fascicle length, and muscle volume. The interlimb differences in SSN and PCSA were significantly larger for stroke participants than for participants without stroke (P = 0.0126 and P = 0.0042, respectively), suggesting we observed muscle adaptations associated with stroke rather than natural interlimb variability. The paretic biceps brachii had ∼8,200 fewer serial sarcomeres and ∼2 cm2 smaller PCSA on average than the contralateral limb (both P < 0.0001). This was manifested by substantially smaller muscle volumes (112 versus 163 cm3), significantly shorter fascicles (11.0 versus 14.0 cm; P < 0.0001), and comparable sarcomere lengths (3.55 versus 3.59 μm; P = 0.6151) between limbs. Most notably, this study provides direct evidence of the loss of serial sarcomeres in human muscle observed in a population with neural impairments that lead to disuse and chronically place the affected muscle at a shortened position. This adaptation is consistent with functional consequences (increased passive resistance to elbow extension) that would amplify already problematic, neurally driven motor impairments.


2020 ◽  
Author(s):  
Amy N. Adkins ◽  
Julius P.A. Dewald ◽  
Lindsay Garmirian ◽  
Christa M. Nelson ◽  
Wendy M. Murray

ABSTRACTA muscle’s structure, or architecture, is indicative of its function and is plastic; changes in input to or use of the muscle alter its architecture. Stroke-induced neural deficits substantially alter both input to and usage of individual muscles. Here, we combined novel in vivo imaging methods (second harmonic generation microendoscopy, extended field-of-view ultrasound, and fat-supression MRI) to quantify functionally meaningful muscle architecture parameters in the biceps brachii of both limbs of individuals with chronic hemiparetic stroke and in age-matched, unimpaired controls. Specifically, serial sarcomere number and physiological cross-sectional area were calculated from data collected at three anatomical scales: sarcomere length, fascicle length, and muscle volume. Our data indicate that the paretic biceps brachii had ~8,500 fewer serial sarcomeres compared to the contralateral limb (p=0.0044). In the single joint posture tested, the decreased serial sarcomere number was manifested by significantly shorter fascicles (10.7cm vs 13.6cm; p<0.0001) without significant differences in sarcomere lengths (3.58μm vs. 3.54μm; p=0.6787) in the paretic compared to the contralateral biceps. No interlimb differences were observed in unimpaired controls, suggesting we observed muscle adaptations associated with stroke rather than natural interlimb variability. This study provides the first direct evidence of the loss of serial sarcomeres in human muscle, observed in a population with neural impairments that lead to disuse and chronically place the affected muscle at a shortened position. This adaptation is consistent with functional consequences (increased passive resistance to elbow extension) that would amplify already problematic, neurally driven motor impairments.SIGNIFICANCE STATEMENTSerial sarcomere number determines a muscle’s length during maximum force production and its available length range for active force generation. Skeletal muscle length adapts to functional demands; for example, animal studies demonstrate that chronically shortened muscles decrease length by losing serial sarcomeres. This phenomenon has never been demonstrated in humans. Integrating multi-scale imaging techniques, including two photon microendoscopy, an innovative advance from traditional, invasive measurement methods at the sarcomere scale, we establish that chronic impairments that place a muscle in a shortened position are associated with the loss of serial sarcomeres in humans. Understanding how muscle adapts following impairment is critical to the design of more effective clinical interventions to mitigate such adaptations and to improve function following motor impairments.


2017 ◽  
Vol 31 (9) ◽  
pp. 814-826 ◽  
Author(s):  
Natalia Sánchez ◽  
Ana Maria Acosta ◽  
Roberto Lopez-Rosado ◽  
Arno H. A. Stienen ◽  
Julius P. A. Dewald

Although global movement abnormalities in the lower extremity poststroke have been studied, the expression of specific motor impairments such as weakness and abnormal muscle and joint torque coupling patterns have received less attention. We characterized changes in strength, muscle coactivation and associated joint torque couples in the paretic and nonparetic extremity of 15 participants with chronic poststroke hemiparesis (age 59.6 ± 15.2 years) compared with 8 age-matched controls. Participants performed isometric maximum torques in hip abduction, adduction, flexion and extension, knee flexion and extension, ankle dorsi- and plantarflexion and submaximal torques in hip extension and ankle plantarflexion. Surface electromyograms (EMGs) of 10 lower extremity muscles were measured. Relative weakness (paretic extremity compared with the nonparetic extremity) was measured in poststroke participants. Differences in EMGs and joint torques associated with maximum voluntary torques were tested using linear mixed effects models. Results indicate significant poststroke torque weakness in all degrees of freedom except hip extension and adduction, adductor coactivation during extensor tasks, in addition to synergistic muscle coactivation patterns. This was more pronounced in the paretic extremity compared with the nonparetic extremity and with controls. Results also indicated significant interjoint torque couples during maximum and submaximal hip extension in both extremities of poststroke participants and in controls only during maximal hip extension. Additionally, significant interjoint torque couples were identified only in the paretic extremity during ankle plantarflexion. A better understanding of these motor impairments is expected to lead to more effective interventions for poststroke gait and posture.


2001 ◽  
Vol 15 (2) ◽  
pp. 105-112 ◽  
Author(s):  
Michelle L. Harris-Love ◽  
Larry W. Forrester ◽  
Richard F. Macko ◽  
Kenneth H. C. Silver ◽  
Gerald V. Smith

Objective: Hemiparetic gait is characterized by high stride-cycle variability, di minished stance time, single-limb stance time, and stance/swing ratio in the paretic limb. Recent studies suggest treadmill (TM) training may improve the motor control underlying these variables, but supporting evidence is sparse. Methods: This study compared gait patterns of untrained chronic hemiparetic stroke patients (n = 18; mean, 39.5 months poststroke) during overground (OG) and TM walking at matched velocities. Variables included relative stance time, relative single-limb stance time, stance/swing ratio, peak force, and impulse. Within-subject variability of these meas ures (CV) was used to assess gait pattern stability. Results: OG and TM cycle dura tions were similar, but CVs differed (TM < OG, p < 0.05). In the paretic limb, dif ferences were seen in relative stance time, relative single-limb stance time, and stance/swing ratio, respectively (TM > OG, p < 0.05). These variables decreased in the nonparetic limb during TM walking (p < 0.05 for all). Improved interlimb sym metry and coordination were evidenced by decreased between-limb differences and improved relative temporal phasing, respectively, in the TM condition (p < 0.05). Conclusions: Collectively, these results demonstrate that the TM induces an imme diate alteration toward a more consistent and symmetric gait pattern. Further inves tigation is needed to determine whether TM training leads to motor relearning and neuroplasticity in chronic hemiparetic subjects. Key Words: Stroke—Rehabilitation— Hemiparetic gait-Treadmill-Gait symmetry.


2019 ◽  
Author(s):  
Lindsay R. P. Garmirian ◽  
Ana Maria Acosta ◽  
Ryan Schmid ◽  
Jules P. A. Dewald

AbstractStroke survivors often experience upper extremity deficits that make activities of daily living (ADLs) like dressing, cooking and bathing difficult or impossible. Survivors experience paresis, the inability to efficiently and fully activate muscles, which combined with decreased use of the upper extremity, will lead to muscle atrophy and potentially an increase in intramuscular fat. Muscle atrophy has been linked to weakness post stroke and is an important contributor to upper extremity deficits. However, the extent of upper extremity atrophy post hemiparetic stroke is unknown and a better understanding of these changes is needed to inform the direction of intervention-based research. In this study, the volume of contractile tissue and intramuscular fat in the elbow and wrist flexors and extensors were quantified in the paretic and non-paretic upper limb using MRI and the Dixon technique for the first time. Total muscle volume (p≤0.0005) and contractile element volume (p≤0.0005) were significantly smaller in the paretic upper extremity, for all muscle groups studied. The average percent difference between limbs and across participants was 21.3% for muscle volume and 22.9% for contractile element volume. We also found that while the percent intramuscular fat was greater in the paretic limb compared to the non-paretic (p≤0.0005), however, the volume of intramuscular fat was not significantly different between upper limbs (p=0.231). The average volumes of intramuscular fat for the elbow flexors/extensors and wrist flexors/extensors were 28.1, 28.8 and 19.9, 8.8 cm3 in the paretic limb and 29.6, 27.7 and 19.7, 8.8 cm3 in the non-paretic limb. In short, these findings indicate a decrease in muscle volume and not an increase in intramuscular fat, which will contribute to the reduction in strength in the paretic upper limb.


2019 ◽  
Author(s):  
Lindsay R. P. Garmirian ◽  
Julius P. A. Dewald ◽  
Ana Maria Acosta

AbstractAfter a stroke, descending drive is impaired due to the loss of corticospinal and corticobulbar projections which causes a reduction in voluntary activation or an inability of the nervous system to activate muscles to their full capacity, which in turn contributes to weakness of the upper extremity. Voluntary activation has not been quantified at specific joints in the upper extremity, in part because directly assessing changes descending drive is difficult. In this study, voluntary activation of elbow and wrist flexors and extensors was assessed in participants with chronic hemiparetic stroke using twitch interpolation. Twitch interpolation uses electrical stimulation to estimate voluntary activation and relies on the principle that there is an inverse relationship between the amplitude of a twitch evoked by a stimulus and the voluntary force output during stimulation (Taylor, 2009). We measured voluntary activation using twitch interpolation as well as maximum voluntary torque (MVT) of the elbow and wrist flexors and extensors in the paretic and non-paretic limb of ten participants post stroke and the dominant and non-dominant limb of 2 control participants. Results show, MVT interlimb differences were significantly greater for stroke participants compared to control, across muscle groups (p≤0.005). For stroke participants, MVT interlimb differences were significantly greater at the wrist compared to the elbow (P=0.003). Voluntary activation was significantly less in the paretic limb compared to the non-paretic, dominant and non-dominant limbs, across participants and muscle groups (p<0.005 for all four muscle groups). For the stroke participants, the voluntary activation interlimb difference was significantly greater for the wrist muscles compared to the elbow muscles (p<0.005). There was a significant positive correlation (r = 0.39, P = .022) between each participant’s impairment level, as measured by a hand specific subscore of the Fugl-Meyer Assessment, and the wrist extensor voluntary activation in the paretic limb but the relationship was not significant for the other muscle groups.


2000 ◽  
Vol 14 (1) ◽  
pp. 65-71 ◽  
Author(s):  
Kenneth H.C. Silver ◽  
Richard F. Macko ◽  
Larry W. Forrester ◽  
Andrew P. Goldberg ◽  
Gerald V. Smith

It is widely assumed that only limited improvement in functional mobility is pos sible beyond the subacute period following ischemic stroke. Contrary to this notion, we studied "neurologically plateaued" stroke patients with chronic hemiparesis to as sess whether a "task-oriented" treadmill-training regimen would improve walking speed, cadence, and gait cycle symmetry on a modified "Get-Up and Go" task. Five male patients with a mean age of 60.4 ± 2.7 years (mean ± S.D.) status post ischemic stroke (> 6 months prior) participated in this nonrandomized low-intensity tread mill exercise pilot study three times/week for 3 months. All patients had mild to mod erate gait asymmetries due to residual hemiparesis. Patients were videotaped before and after 3 months of treadmill aerobic exercise (AEX) while performing a functional task consisting of arising from a chair, walking 3.1 m without an assistive device as fast as safely possible, and returning to sit. Gait events were timed using a 2-D Peak Motus™ video analysis system. After 3 months AEX training, times for the overall "get-up and return-to-sit" (GURS) task and the "straight-away walk" (SAW) segment decreased from 8.2 ± 1.4 sec to 6.5 ± 0.8 sec (mean ± SEM) (p < 0.05), and from 3.7 ± 1 sec to 2.8 ± 0.7 sec (p < 0.05), respectively. These data represent improve ments of 21% and 24% for the GURS and 'SAW segments, respectively. Mean veloc ity increased from 0.9 ± 0.2 to 1.2 ± 0.21 m/sec, a 33% improvement (p < 0.01). Mean cadence (steps/min) increased from 89 ± 9 to 97 ± 8, a 9% increase (p < 0.05). Mean stance and swing duration diminished for both paretic (P) and nonparetic (NP) limbs, and the intralimb stance/swing ratio values moved toward normal for both the paretic and nonparetic limbs. However, these latter changes reached significance only for the P limb. Interlimb stance symmetry was unchanged. The more impaired subjects experienced the greatest gains in gait velocity and temporal measures. Collectively, these findings indicate that treadmill exercise improves functional overground mo bility in individuals with chronic, stable hemiparesis. Key Words: Cerebrovascular disease—Hemiplegia—Exercise—Gait.


2008 ◽  
Vol 23 (2) ◽  
pp. 125-132 ◽  
Author(s):  
Toshiyuki Fujiwara ◽  
Yuko Kasashima ◽  
Kaoru Honaga ◽  
Yoshihiro Muraoka ◽  
Tetsuya Tsuji ◽  
...  

Background and objective . We devised a therapeutic approach to facilitate the use of the hemiparetic upper extremity (UE) in daily life by combining integrated volitional control electrical stimulation with a wrist splint, called hybrid assistive neuromuscular dynamic stimulation (HANDS). Methods. Twenty patients with chronic hemiparetic stroke (median 17.5 months) had moderate to severe UE weakness. Before and immediately after completing 3 weeks of training in 40-minute sessions, 5 days per week over 3 weeks and wearing the system for 8 hours each day, clinical measures of motor impairment, spasticity, and UE functional scores, as well as neurophysiological measures including electromyography activity, reciprocal inhibition, and intracortical inhibition were assessed. A follow-up clinical assessment was performed 3 months later. Results. UE motor function, spasticity, and functional scores improved after the intervention. Neurophysiologically, the intervention induced restoration of presynaptic and long loop inhibitory connections as well as disynaptic reciprocal inhibition. Paired pulse transcranial magnetic stimulation study indicated disinhibition of the short intracortical inhibition in the affected hemisphere. The follow-up assessment showed that improved UE functions were maintained at 3 months. Conclusion. The combination of hand splint and volitional and electrically induced muscle contraction can induce corticospinal plasticity and may offer a promising option for the management of the paretic UE in patients with stroke. A larger sample size with randomized controls is needed to demonstrate effectiveness.


2019 ◽  
Author(s):  
Benjamin I Binder-Markey ◽  
Wendy M Murray ◽  
Julius P.A. Dewald

ABSTRACTBackground and PurposeFollowing a hemiparetic stroke, prolonged altered motor neuron inputs may drive passive mechanical changes within muscle that further amplify brain injury induced motor impairments, reducing optimal recovery. However, due to confounding factors, i.e. muscle hypertonicity and spasticity, and the use of botulinum neurotoxin (BoNT), chemical denervation to reduce their expression, there is no consensus on how altered neural inputs following a stroke affect muscle passive mechanical properties or the extent to which these properties ultimately limit functional recovery. Therefore, the objective of this study is to quantify muscle passive biomechanical properties following chronic hemiparetic stroke and BoNT.MethodsPassive torques about the wrist and metacarpophalangeal (MCP) joints were quantified in both hands of 34 individuals with chronic hemiparetic stroke. Participants’ hand impairments ranged from severe to mild with a subset who previously received BoNT injections. Torques were quantified with subjects in a sleep or near-sleep state, mitigating muscle hyperactivity. EMGs were continuously monitored to ensure no muscle activity during data collection.ResultsParticipants who previously received BoNT injections demonstrated significantly greater passive flexion torques about their paretic wrist and fingers as compared to those who never received BoNT. As a result, only the group who received BoNT demonstrated significant decreases in passive MCP extension.ConclusionsThe results of our thorough investigation of in vivo passive elastic torques at the wrist and fingers in chronic hemiparetic stroke contrast with the increased stiffness and decreased passive ROM observed clinically and in many previous studies. We highlight the need to effective address both stroke-induced muscle hyperactivity and BoNT treatment history as confounds. We conclude that loss of hand function post-stroke is predominantly due to motor impairments post stroke. Adverse effects of BoNT warrant consideration in future studies and rehabilitation interventions.


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