Benjamin I Binder-Markey1, Julius P A Dewald2, Wendy M Murray3. 1. Department of Biomedical Engineering, Northwestern University, Evanston, IL; Department of Physical Therapy and Human Movement Sciences, Chicago, IL; Department of Physical Medicine and Rehabilitation Science, Northwestern University, Chicago, IL; Shirley Ryan AbilityLab, Chicago, IL. 2. Department of Biomedical Engineering, Northwestern University, Evanston, IL; Department of Physical Therapy and Human Movement Sciences, Chicago, IL; Department of Physical Medicine and Rehabilitation Science, Northwestern University, Chicago, IL. 3. Department of Biomedical Engineering, Northwestern University, Evanston, IL; Department of Physical Therapy and Human Movement Sciences, Chicago, IL; Department of Physical Medicine and Rehabilitation Science, Northwestern University, Chicago, IL; Shirley Ryan AbilityLab, Chicago, IL; Research Service, Edward Hines Jr., VA Hospital, Hines, IL. Electronic address: w-murray@northwestern.edu.
Abstract
PURPOSE: Claw finger deformity occurs during attempted finger extension in patients whose intrinsic finger muscles are weakened or paralyzed by neural impairments. The deformity is generally not acutely present after intrinsic muscle palsy. The delayed onset, with severity progressing over time, suggests soft tissue changes that affect the passive biomechanics of the hand exacerbate and advance the deformity. Clinical interventions may be more effective if such secondary biomechanical changes are effectively addressed. Using a computational model, we simulated these altered soft tissue biomechanical properties to quantify their effects on coordinated finger extension. METHODS: To evaluate the effects of maladaptive changes in soft tissue biomechanical properties on the development and progression of the claw finger deformity after intrinsic muscle palsy, we completed 45 biomechanical simulations of cyclic index finger flexion and extension, varying the muscle excitation level, clinically relevant biomechanical factors, and wrist position. We evaluated to what extent (1) increased joint laxity, (2) decreased mechanical advantage of the extensors about the proximal interphalangeal joint, and (3) shortening of the flexor muscles contributed to the development of claw finger deformity in an intrinsic-minus hand model. RESULTS: Of the mechanisms studied, shortening (or contracture) of the extrinsic finger flexors was the factor most associated with the development of claw finger deformity in simulation. CONCLUSIONS: These simulations suggest that adaptive shortening of the extrinsic finger flexors is required for the development of claw finger deformity. Increased joint laxity and decreased extensor mechanical advantage only contributed to the severity of the deformity in simulations when shortening of the flexor muscles was present. CLINICAL RELEVANCE: In both the acute and chronic stages of intrinsic finger paralysis, maintaining extrinsic finger flexor length should be an area of focus in rehabilitation to prevent formation of the claw finger deformity and achieve optimal outcomes after surgical interventions.
PURPOSE:Claw finger deformity occurs during attempted finger extension in patients whose intrinsic finger muscles are weakened or paralyzed by neural impairments. The deformity is generally not acutely present after intrinsic muscle palsy. The delayed onset, with severity progressing over time, suggests soft tissue changes that affect the passive biomechanics of the hand exacerbate and advance the deformity. Clinical interventions may be more effective if such secondary biomechanical changes are effectively addressed. Using a computational model, we simulated these altered soft tissue biomechanical properties to quantify their effects on coordinated finger extension. METHODS: To evaluate the effects of maladaptive changes in soft tissue biomechanical properties on the development and progression of the claw finger deformity after intrinsic muscle palsy, we completed 45 biomechanical simulations of cyclic index finger flexion and extension, varying the muscle excitation level, clinically relevant biomechanical factors, and wrist position. We evaluated to what extent (1) increased joint laxity, (2) decreased mechanical advantage of the extensors about the proximal interphalangeal joint, and (3) shortening of the flexor muscles contributed to the development of claw finger deformity in an intrinsic-minus hand model. RESULTS: Of the mechanisms studied, shortening (or contracture) of the extrinsic finger flexors was the factor most associated with the development of claw finger deformity in simulation. CONCLUSIONS: These simulations suggest that adaptive shortening of the extrinsic finger flexors is required for the development of claw finger deformity. Increased joint laxity and decreased extensor mechanical advantage only contributed to the severity of the deformity in simulations when shortening of the flexor muscles was present. CLINICAL RELEVANCE: In both the acute and chronic stages of intrinsic finger paralysis, maintaining extrinsic finger flexor length should be an area of focus in rehabilitation to prevent formation of the claw finger deformity and achieve optimal outcomes after surgical interventions.
Authors: Jennifer A Zellers; Michael J Mueller; Paul K Commean; Ling Chen; Hyo-Jung Jeong; Mary K Hastings Journal: J Clin Med Date: 2020-04-03 Impact factor: 4.241