scholarly journals Effects of Altered Neural Input and Botulinum Toxin on Finger and Wrist Passive Properties in Chronic Hemiparetic Stroke

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.

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.


2019 ◽  
Author(s):  
Kevin B. Wilkins ◽  
Jun Yao ◽  
Meriel Owen ◽  
Haleh Karbasforoushan ◽  
Carolina Carmona ◽  
...  

AbstractRecent findings have shown connections of ipsilateral cortico-reticulospinal tract (CRST), predominantly originating from secondary motor areas, to not only proximal but also distal portions of the arm. In unilateral stroke, CRST from the ipsilateral side is intact and thus has been proposed as a possible backup system for post-stroke rehabilitation even for the hand. We argue that although CRST from ipsilateral secondary motor areas can provide control for proximal joints, it is insufficient to control either hand or coordinated shoulder and hand movements due to its extensive branching compared to contralateral corticospinal tract. To address this issue, we combined MRI, high-density EEG, and robotics in 17 individuals with severe chronic hemiparetic stroke and 12 age-matched controls. We tested for changes in structural morphometry of the sensorimotor cortex and found that individuals with stroke demonstrated higher gray matter density in secondary motor areas ipsilateral to the paretic arm compared to controls. We then measured cortical activity while participants attempted to generate hand opening either supported on a table or while lifting against a shoulder abduction load. The addition of shoulder abduction during hand opening increased reliance on ipsilateral secondary motor areas in stroke, but not controls. Crucially, increased use of ipsilateral secondary motor areas was associated with decreased hand opening ability while lifting the arm due to involuntary coupling between the shoulder and wrist/finger flexors. Together, this evidence implicates a compensatory role for ipsilateral (i.e., contralesional) secondary motor areas post-stroke, but with limited capacity to support hand function.


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.


2021 ◽  
Vol 12 ◽  
Author(s):  
Benjamin I. Binder-Markey ◽  
Wendy M. Murray ◽  
Julius P. A. Dewald

Background: Neural impairments that follow hemiparetic stroke may negatively affect passive muscle properties, further limiting recovery. However, factors such as hypertonia, spasticity, and botulinum neurotoxin (BoNT), a common clinical intervention, confound our understanding of muscle properties in chronic stroke.Objective: To determine if muscle passive biomechanical properties are different following prolonged, stroke-induced, altered muscle activation and disuse.Methods: Torques about the metacarpophalangeal and wrist joints were measured in different joint postures in both limbs of participants with hemiparetic stroke. First, we evaluated 27 participants with no history of BoNT; hand impairments ranged from mild to severe. Subsequently, seven participants with a history of BoNT injections were evaluated. To mitigate muscle hypertonia, torques were quantified after an extensive stretching protocol and under conditions that encouraged participants to sleep. EMGs were monitored throughout data collection.Results: Among participants who never received BoNT, no significant differences in passive torques between limbs were observed. Among participants who previously received BoNT injections, passive flexion torques about their paretic wrist and finger joints were larger than their non-paretic limb (average interlimb differences = +42.0 ± 7.6SEM Ncm, +26.9 ± 3.9SEM Ncm, respectively), and the range of motion for passive finger extension was significantly smaller (average interlimb difference = −36.3° ± 4.5°SEM; degrees).Conclusion: Our results suggest that neural impairments that follow chronic, hemiparetic stroke do not lead to passive mechanical changes within the wrist and finger muscles. Rather, consistent with animal studies, the data points to potential adverse effects of BoNT on passive muscle properties post-stroke, which warrant further consideration.


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.


2009 ◽  
Vol 106 (3) ◽  
pp. 843-849 ◽  
Author(s):  
Heng Zhao ◽  
Yupeng Ren ◽  
Yi-Ning Wu ◽  
Shu Q. Liu ◽  
Li-Qun Zhang

Spasticity, contracture, and muscle weakness are commonly observed poststroke in muscles crossing the ankle. However, it is not clear how biomechanical properties of the Achilles tendon change poststroke, which may affect functions of the impaired muscles directly. Biomechanical properties of the Achilles tendon, including the length and cross-sectional area, in the impaired and unimpaired sides of 10 hemiparetic stroke survivors were evaluated using ultrasonography. Elongation of the Achilles tendon during controlled isometric ramp-and-hold and ramping up then down contractions was determined using a block-matching method. Biomechanical changes in stiffness, Young's modulus, and hysteresis of the Achilles tendon poststroke were investigated by comparing the impaired and unimpaired sides of the 10 patients. The impaired side showed increased tendon length (6%; P = 0.04), decreased stiffness (43%; P < 0.001), decreased Young's modulus (38%; P = 0.005), and increased mechanical hysteresis (1.9 times higher; P < 0.001) compared with the unimpaired side, suggesting Achilles tendon adaptations to muscle spasticity, contracture, and/or disuse poststroke. In vivo quantitative characterizations of the tendon biomechanical properties may help us better understand changes of the calf muscle-tendon unit as a whole and facilitate development of more effective treatments.


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.


Sign in / Sign up

Export Citation Format

Share Document