Rhee, Peter

Background: Spasticity after upper motor neuron injury (stroke, spinal cord injury, etc.) alters muscle activity and induces long-term structural remodeling of skeletal muscle [1]. Elbow flexors, including the biceps brachii, are frequently affected, leading to abnormal tone, involuntary co-contraction, and impaired elbow function. Hyper-selective neurectomy (HSN) is a well-established surgical technique that has gained renewed clinical adoption with advances in anatomic understanding and intraoperative nerve mapping [2], yet its effects on muscle properties are poorly defined. Objective: The purpose of this study was to define pre- vs. post-HSN differences in muscle gene expression, sarcomere length, and clinical outcomes of the spastic human biceps. Methods: Individuals with elbow flexor spasticity undergoing a planned two-stage HSN were prospectively enrolled (n=10). Stage 1 released the elbow flexors and provided a pre-biopsy; Stage 2, performed ~3 months later to treat the forearm flexors, provided a second exposure to the biceps and a second biopsy. In both stages, biceps biopsies were obtained with customized clamps [3] at predefined elbow angles (50°, 90°, 135°), fixed, and analyzed for sarcomere length [4]. Total RNA was extracted from pre- and post-HSN biceps samples to characterize transcriptional changes. Clinical spasticity was assessed before Stage 1 and again before Stage 2 using the Modified Ashworth Scale (MAS). Data were compared using repeated-measures models, and single-cell transcriptional changes were analyzed using established analytical pipelines. Results: Sarcomere length (SL) increased significantly after HSN at all joint angles. At 50°, SL increased from 2.45 ± 0.18 µm pre-HSN to 3.05 ± 0.28 µm post-HSN; at 90°, from 2.70 ± 0.29 µm to 2.91 ± 0.16 µm; and at 135°, from 2.72 ± 0.36 µm to 3.24 ± 0.32 µm (all p < 0.05). Clinical spasticity assessment improved significantly as well (p < 0.05), with MAS scores decreasing from 1.89± 0.93 to 0.35 ± 0.53. RNA sequencing revealed changes in key pathways and overall gene expression patterns such as enhanced inflammatory response through increased cytokine production and fibroblast proliferation, leading to elevated collagen synthesis and subsequent fibrosis. We also observed upregulated immune modulation and chemotaxis, while pathways involved in mitochondrial respiration, muscle development, and cellular homeostasis were downregulated. At the transcript level, HSN led to decreased inflammation and adipogenesis, while promoting increased extracellular matrix assembly, and vascular formation. Conclusion: HSN produced coordinated improvements across structural, clinical, and transcriptional levels in the spastic human biceps muscle. Sarcomere lengths increased toward longer resting lengths at all joint angles, clinical spasticity decreased significantly, and RNA sequencing revealed distinct post-operative transcriptional remodeling. The longer sarcomere length and decreased spasticity should contribute to improved patient function after HSN. References: 1. Lieber RL et al. Muscle Nerve. 2002;26:98–105. 2. Leclercq C et al. Hand Clin. 2018;34:537–545. 3. Lieber RL et al. J Neurophysiol. 1994;71:874–881. 4. Ward SR et al. J Biomech. 2009;42:193–196. This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.

Introduction: Upper limb spasticity can result from a variety of insults to the central nervous system. Disruption of the closely regulated spinal reflex arc, owing to loss of brain inhibition, results in an imbalance between antagonist and agonist muscle groups, leading to a loss of fluid coordination of motion across joints. Management strategies: A detailed, individualized assessment of each patient is mandatory in a multidisciplinary setting. Although there are objective parameters which guide treatment, variation and customization of strategies are needed for each patient, including defining a functional vs. a non-functional hand, and whether mobility or stability is the primary goal for surgery. Challenging areas in spasticity management: Surgical options include bony, tendon and nerve procedures. These aim to reduce tone, release contractures or reanimate paralysed muscles. This article examines four challenging areas in decision making for choosing these options: lengthening vs. hyperselective neurectomy for tone management, stability vs. mobility in wrist spasticity, grasp and release recovery through finger flexion and extension, and dystonia. Evidence-based treatments are discussed where available, along with key unresolved issues and future research directions. Conclusion: Restoring balance in the spastic upper limb, especially when voluntary control is lost, remains one of the most complex challenges in hand surgery. A thorough understanding of biomechanical principles and neurological pathways is necessary for the hand surgeon. Furthermore, working within a multidisciplinary team is essential to utilize a comprehensive array of assessment tools, ensuring accurate diagnosis and individualized patient care.

Arthrofibrosis is an inevitable consequence of elbow trauma that oftentimes requires surgical release to restore range of motion and function. Although the surgical procedure for elbow osteocapsular release can result in marked improvement in elbow motion, postrelease rehabilitation is paramount to maintaining and even improving the gains achieved in surgery. There are a variety of rehabilitation protocols and modalities that can be implemented that can be divided into an early versus late stage of rehabilitation after surgery. Irrespectively, patient ownership in the rehabilitative process and effective communication between surgeon and therapist are integral in achieving successful outcomes.