ArticleJournal of neuroengineering and rehabilitation2023
Dysfunctional neuro-muscular mechanisms explain gradual gait changes in prodromal spastic paraplegia.
Article in Journal of neuroengineering and rehabilitation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.
- Outcome measures of instrumented gait analysis in hereditary spastic paraplegia: a systematic review.Journal of neuroengineering and rehabilitation · 2025Pooled it
- Reduced-order analysis for gait kinematics of paraplegic patients based on spatiotemporal mode decomposition.Medical & biological engineering & computing · 2026Article
- Synergy Feedback Control Predicts Walking Across Multiple Cycles.bioRxiv : the preprint server for biology · 2026Article
- Synergy-based feedforward with minimal feedback control predicts walking over multiple cycles.Frontiers in bioengineering and biotechnology · 2026Article
- A model of the cerebellum generates gait adaptations in a reflex-based neuromusculoskeletal model during split-belt walking.Journal of neuroengineering and rehabilitation · 2025Article
- A model of the cerebellum generates gait adaptations in a reflex-based neuromusculoskeletal model during split-belt walking.bioRxiv : the preprint server for biology · 2025Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIn Hereditary Spastic Paraplegia (HSP) type 4 (SPG4) a length-dependent axonal degeneration in the cortico-spinal tract leads to progressing symptoms of hyperreflexia, muscle weakness, and spasticity of lower extremities. Even before the manifestation of spastic gait, in the prodromal phase, axonal degeneration leads to subtle gait changes. These gait changes - depicted by digital gait recording - are related to disease severity in prodromal and early-to-moderate manifest SPG4 participants.
methodsWe hypothesize that dysfunctional neuro-muscular mechanisms such as hyperreflexia and muscle weakness explain these disease severity-related gait changes of prodromal and early-to-moderate manifest SPG4 participants. We test our hypothesis in computer simulation with a neuro-muscular model of human walking. We introduce neuro-muscular dysfunction by gradually increasing sensory-motor reflex sensitivity based on increased velocity feedback and gradually increasing muscle weakness by reducing maximum isometric force.
resultsBy increasing hyperreflexia of plantarflexor and dorsiflexor muscles, we found gradual muscular and kinematic changes in neuro-musculoskeletal simulations that are comparable to subtle gait changes found in prodromal SPG4 participants.
conclusionsPredicting kinematic changes of prodromal and early-to-moderate manifest SPG4 participants by gradual alterations of sensory-motor reflex sensitivity allows us to link gait as a directly accessible performance marker to emerging neuro-muscular changes for early therapeutic interventions.
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