No abstract

Myodural bridges have been described in various species as connective tissue structures “bridging” small cranio-cervical muscles to the dura. Myodural bridges are thought to stabilize the dural sac during head and neck movements and promote cerebrospinal fluid motion; however, their role in neurological diseases has not yet been established. We report ultrasonographic visualization, necropsy, histopathologic and ultrastructural findings of myodural bridges in horses with hereditary equine regional dermal asthenia (HERDA), an equine model of Ehlers-Danlos syndromes. Five HERDA and 5 control horses were studied. Post-mortem examination and ultrasonographic studies (3 HERDA and 4 controls) demonstrated that the atlanto-occipital and atlanto-axial myodural bridges are dynamic structures “moving” the dura. En block resection of the myodural bridges (4 HERDA and 5 controls) was accomplished and histopathology showed myofiber degeneration in 3 HERDA horses and 1 control. Ultrastructural examination revealed loosely packed collagen fibrils with abnormal orientation in all HERDA horses compared to mild abnormalities in 2 controls. Our study provides necropsy and ultrasonographic evidence of the dynamic aspect of the myodural bridges as dural sac stabilizers. Myodural bridges may be pathologically altered in connective tissue disease as evidenced by the ultrastructural morphology in the HERDA myodural bridge.

Objectives The aim of this study was to evaluate the effect of amikacin (AK) and enrofloxacin (EF) at concentrations consistent with those obtained by intra-articular and intravenous regional limb perfusion on both cytotoxicity and prostaglandin E2 (PGE2) production by equine chondrocytes. This study also determines if PGE2 production could be reduced by avocado/soybean unsaponifiables (ASU), glucosamine (GLU) and chondroitin sulphate (CS). Study Design Chondrocytes were grown in monolayer from the articular cartilage of 12 horses and treated with clinically relevant concentrations of AK and EF, with or without the combination of ASU + GLU + CS. Positive controls consisted of chondrocytes that were activated with lipopolysaccharide (LPS). Chondrocyte response was evaluated using both MTT cytotoxicity assay and immunoassay for PGE2 production. Results Amikacin and EF generated a dose-dependent cytotoxicity. Amikacin induced 90% cell death at a concentration of 25 mg/mL. Enrofloxacin induced 90% cell death at 1.0 mg/mL and 98% cell death at 10 mg/mL (p < 0.05). Amikacin failed to induce PGE2 production at any of the concentrations studied. In contrast, EF and the positive control (LPS) induced PGE2 production at all concentrations. Induction of PGE2 by EF at all concentrations was significantly reduced (p < 0.05) by pre-treatment with ASU + GLU + CS. Conclusions and Clinical Relevance Horses receiving commonly used dosages of AK and EF may benefit from administration of ASU + GLU + CS.

The objectives of this study were to describe the anatomy, histology, and ultrastructure of the equine filum terminale (FT) and to describe the FT in hereditary equine regional dermal asthenia (HERDA), a model of human Ehlers-Danlos syndromes (EDS). Those humans suffer from tethered cord syndrome (TCS) caused by an abnormally structured FT wherein its attachment at the base of the vertebral column leads to long-term stretch-induced injury to the spinal cord. The pathophysiology of TCS in EDS is poorly understood, and there is a need for an animal model of the condition. Histopathologic and ultrastructural examinations were performed on FT from HERDA ( n = 4) and control horses ( n = 5) and were compared to FT from human TCS patients with and without EDS. Adipose, fibrous tissue, and neuronal elements were assessed. CD3 and CD20 immunohistochemistry was performed to clarify cell types (HERDA n = 2; control n = 5). Collagen fibrils were assessed in cross-section for fibril diameter and shape, and in longitudinal section for fibril disorganization, swelling, and fragmentation. The equine and human FT were similar, with both containing fibrous tissue, ependyma, neuropil, and nerve twigs. Hypervascularity was observed in both HERDA horses and human EDS-TCS patients and was not observed in equine or human controls. Moderate to severe abnormalities in collagen fibril orientation and architecture were observed in all HERDA horses and were similar to those observed in human EDS-TCS patients.