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- Greg James, Ben Ahern, Wendy Goodwin, Ben Goss, and Paul Hodges.
- University of Queensland, Brisbane, Australia.
- Eur Spine J. 2025 Jan 15.
PurposeFibrosis of muscle spindles (sensory organs) in back muscles induced by intervertebral disc (IVD) degeneration could limit transmission of muscle stretch to the sensory receptor and explain the proprioceptive deficits common in back pain. Exercise reduces back muscles fibrosis. This study investigated whether targeted muscle activation via neurostimulation reverses or resolves muscle spindle fibrosis in a model of IVD injury.MethodsIn eighteen sheep, lumbar (L)1-2 and L3-4 IVD degeneration was induced by partial thickness anulus fibrosis incision and a neurostimulator was implanted. After IVD-degeneration developed for 3 months, neurostimulation of the L2 nerve root activated multifidus in nine randomly selected animals. Multifidus muscle adjacent to the spinous process of L2 (non-stimulated) and L4 (stimulated) was harvested 3 months after activation. Muscle spindles were identified in Van Giessen's-stained sections. Connective tissue spindle capsule thickness, and cross-sectional area (CSA) of the spindle, its periaxial fluid and sensory elements were measured. Immunofluorescence assays evaluated Collagen-I and -III.ResultsMultifidus muscle spindle capsule thickness and Collagen-1 were significantly less in the neurostimulation animals than IVD-injury animals at L4 (stimulated muscle) (P < 0.05), but not L2 (non-stimulated muscle). Spindle capsule thickness was less in lateral than medial regions. CSA of the muscle spindle and sensory elements was less in neurostimulated animals at L4.ConclusionTargeted multifidus activation reverses or prevents accumulation of connective tissue of the multifidus muscle spindle capsule caused by IVD injury. Reduced fibrosis should maintain sensory function of this important muscle mechanoreceptor and might provide an effective solution to resolve the commonly identified proprioceptive deficits in back pain and maintain healthy spine function.© 2025. The Author(s).
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