Orthopaedic surgery for patients with central nervous system lesions: Concepts and techniques

Genêt, F.; Denormandie, P.; Keenan, Mary Ann

doi:10.1016/j.rehab.2018.09.004

Cited by 32 publications

(27 citation statements)

References 66 publications

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“…NHO growth can also cause nerve, blood vessel compression, and irreversibly damage the affected joint further increasing patient morbidity (8). Despite knowing this pathology for 100 years, treatment is currently limited to surgical resection after NHO have matured and become symptomatic (2, 7, 9–11). The surgical procedure is challenging, particularly when ossifications entrap joints, large blood vessels and nerves.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of JAK1/2 Tyrosine Kinases Reduces Neurogenic Heterotopic Ossification After Spinal Cord Injury

et al. 2019

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Neurogenic heterotopic ossifications (NHO) are very incapacitating complications of traumatic brain and spinal cord injuries (SCI) which manifest as abnormal formation of bone tissue in periarticular muscles. NHO are debilitating as they cause pain, partial or total joint ankylosis and vascular and nerve compression. NHO pathogenesis is unknown and the only effective treatment remains surgical resection, however once resected, NHO can re-occur. To further understand NHO pathogenesis, we developed the first animal model of NHO following SCI in genetically unmodified mice, which mimics most clinical features of NHO in patients. We have previously shown that the combination of (1) a central nervous system lesion (SCI) and (2) muscular damage (via an intramuscular injection of cardiotoxin) is required for NHO development. Furthermore, macrophages within the injured muscle play a critical role in driving NHO pathogenesis. More recently we demonstrated that macrophage-derived oncostatin M (OSM) is a key mediator of both human and mouse NHO. We now report that inflammatory monocytes infiltrate the injured muscles of SCI mice developing NHO at significantly higher levels compared to mice without SCI. Muscle infiltrating monocytes and neutrophils expressed OSM whereas mouse muscle satellite and interstitial cell expressed the OSM receptor (OSMR). In vitro recombinant mouse OSM induced tyrosine phosphorylation of the transcription factor STAT3, a downstream target of OSMR:gp130 signaling in muscle progenitor cells. As STAT3 is tyrosine phosphorylated by JAK1/2 tyrosine kinases downstream of OSMR:gp130, we demonstrated that the JAK1/2 tyrosine kinase inhibitor ruxolitinib blocked OSM driven STAT3 tyrosine phosphorylation in mouse muscle progenitor cells. We further demonstrated in vivo that STAT3 tyrosine phosphorylation was not only significantly higher but persisted for a longer duration in injured muscles of SCI mice developing NHO compared to mice with muscle injury without SCI. Finally, administration of ruxolitinib for 7 days post-surgery significantly reduced STAT3 phosphorylation in injured muscles in vivo as well as NHO volume at all analyzed time-points up to 3 weeks post-surgery. Our results identify the JAK/STAT3 signaling pathway as a potential therapeutic target to reduce NHO development following SCI.

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Section: Introductionmentioning

confidence: 99%

Inhibition of JAK1/2 Tyrosine Kinases Reduces Neurogenic Heterotopic Ossification After Spinal Cord Injury

et al. 2019

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“…The Achilles tendon is a key target for the neuro-orthopedic management of spastic equinovarus/equinus [3,4]. Predictably, given that BoNT-A acts on the "neurological" components of PSS, we found no direct or indirect effects of BoNT-A injection into the spastic gastrocnemius medialis and lateralis on the Achilles tendon, which is mainly involved in the spastic "rheological" components of spastic equinovarus/equinus.…”

Section: Discussionmentioning

confidence: 65%

“…Spastic equinovarus/equinus can present with a mix of calf muscle spasticity, tricep surae/Achilles tendon shortening, ankle dorsiflexor weakness and tibialis anterior/peroneus muscle imbalance [3]. This group of conditions may require combined treatment with drugs, physical therapy, orthoses, surgery and other rehabilitation procedures [3][4][5][6].…”

Section: Introductionmentioning

confidence: 99%

Does Botulinum Toxin Treatment Affect the Ultrasonographic Characteristics of Post-Stroke Spastic Equinus? A Retrospective Pilot Study

Picelli

Filippetti

Melotti

et al. 2020

Toxins

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Equinovarus/equinus foot is a pattern most commonly treated with botulinum toxin type A in patients with post-stroke spasticity involving the lower limbs; the gastrocnemius is the muscle most frequently injected. Spastic equinovarus/equinus can present a mixture of conditions, including spasticity, muscle/tendon shortening, muscle weakness and imbalance. In this study, we wanted to determine whether botulinum toxin treatment affects the ultrasonographic characteristics of post-stroke spastic equinus. The same dose of AbobotulinumtoxinA was injected into the gastrocnemius medialis and lateralis of 21 chronic stroke patients with spastic equinus. Clinical (Ashworth scale and ankle range of motion) and ultrasound (conventional and sonoelastography) evaluation of the treated leg was carried out before and 4 weeks after injection. No significant effects of botulinum toxin treatment on the ultrasonographic characteristics of spastic equinus were observed. As expected, there were significant improvements in ankle passive dorsiflexion range of motion and calf muscle spasticity at 1 month after treatment. There was a direct association between Achilles tendon elasticity and calf muscle spasticity at baseline evaluation. Larger studies with a long-term timeline of serial evaluations are needed to further investigate the possible effects of botulinum toxin injection on spastic muscle characteristics in patients with post-stroke spasticity.

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“…Despite the recognized effectiveness of orthopedic surgery for neuro-orthopedic disorders like chronic stroke patients with spastic contractures, few studies have formally evaluated them. Hence, there is a need for research to provide evidence to support orthopedic surgery for treating such neuro-orthopedic disorders (Genet et al 2018).…”

Section: Surgical Managementmentioning

confidence: 99%

Post-Stroke Spasticity

Francisco

Wissel

Platz

et al. 2021

Clinical Pathways in Stroke Rehabilitation

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Orthopaedic surgery for patients with central nervous system lesions: Concepts and techniques

Cited by 32 publications

References 66 publications

Inhibition of JAK1/2 Tyrosine Kinases Reduces Neurogenic Heterotopic Ossification After Spinal Cord Injury

Inhibition of JAK1/2 Tyrosine Kinases Reduces Neurogenic Heterotopic Ossification After Spinal Cord Injury

Does Botulinum Toxin Treatment Affect the Ultrasonographic Characteristics of Post-Stroke Spastic Equinus? A Retrospective Pilot Study

Post-Stroke Spasticity

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