Currently, complete recovery is unattainable for most individuals with spinal cord injury (SCI). Instead, recovery is typically accompanied by persistent sensory and motor deficits. Restoration of preinjury function will likely depend on improving plasticity and integration of these impaired systems. Eccentric muscle actions require precise integration of sensorimotor signals and are predominant during the yield (E2) phase of locomotion. Motor neuron activation and control during eccentric contractions is impaired across a number of central nervous system (CNS) disorders, but remains unexamined after SCI. Therefore, we characterized locomotor recovery after contusive SCI using hindlimb (HL) kinematics and electromyographic (EMG) recordings with specific consideration of eccentric phases of treadmill (TM) walking. Deficits in E2 and a caudal shift of locomotor subphases persisted throughout the 3‐week recovery period. EMG records showed notable deficits in the semitendinosus (ST) during yield. Unlike other HL muscles, recruitment of ST changed with recovery. At 7 days, the typical dual‐burst pattern of ST was lost and the second burst (ST2) was indistinct. By 21 days, the dual‐burst pattern returned, but latencies remained impaired. We show that ST2 burst duration is highly predictive of open field Basso, Beattie, Bresnahan (BBB) scores. Moreover, we found that simple changes in locomotor specificity which enhance eccentric actions result in new motor patterns after SCI. Our findings identify a caudal shift in stepping kinematics, irregularities in E2, and aberrant ST2 bursting as markers of incomplete recovery. These residual impairments may provide opportunities for targeted rehabilitation.

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To identify serum biomarkers differentiating dogs with and without osteoarthritis (OA). MethodsFollowing institutional ethical approval, 24 dogs (27.2-48.5 kg, 3.6-13.6 years) previously diagnosed with OA affecting different joints with varying severity were included in the study. Sixteen dogs (16.2-36 kg, 2.0-6.7 years) without detectable orthopaedic pathology were included as clinically healthy controls. Other disorders were ruled out by thorough clinical examinations and standard hematological and biochemical analyses. Serum was stored at -80 o C until analysis of five biomarkers using commercially available enzyme-linked immunosorbent assays: hyaloronic acid (HA), matrix metalloproteinase 13 (MMP-13), procollagen type IIA (PIIANP), cartilage oligomeric matrix protein (COMP), and collagen type-2 cleavage (C2C). Medians and confidence intervals were calculated and differences between groups were tested for significance using Mann Whitney tests (p<0.05). ResultsHigher concentrations of C2C and MMP-13 were observed in dogs with OA (median, [95% CIs] C2C: 23.7 ng/ml [18.2; 45.2 ng/ml], MMP-13: 0.70 ng/ml [0.51;1.09 ng/ml]) compared to clinically healthy dogs (C2C: 12.3 ng/ml [10.1; 35.3 ng/ml], MMP 13: 0.34 ng/ml [0.27; 0.88 ng/ml]), whereas lower concentrations of PIIANP were observed in dogs with OA (11.6 ng/ml [10.7; 18.02 ng/ml] compared to clinically healthy dogs (15.8 ng/ml [11.7; 31.7 ng/ml]). Observed differences were not significant. Statement (conclusions)None of the 5 biomarkers measured in the present study could differentiate heterogeneous groups of dogs with and without OA. Further studies are recommended to investigate possible diagnostic potentials of C2C, MMP-13 or PIIANP in subgroups of dogs with OA.

A three-year-old spayed female Yorkshire terrier presented with a three-week history of lethargy and weight loss. Physical examination showed left exophthalmos with left nasal discharge. A lesion in the left brainstem was suspected based on the neurological examination. Pre/postcontrast CT images were consistent with an extensive subdural empyema in the region of the left forebrain, extending from the level of the frontal to the occipital lobe. At presentation, transcranial Doppler (TCD) ultrasound was performed in the left (LMCA) and right middle cerebral arteries (RMCA) showing marked hyperaemia (LMCA velocity: 81.9 cm/s; RMCA velocity: 90.3 cm/s; reference ranges: LMCA velocity 62.3±10.9 cm/s; RMCA velocity 62.5±10.9 cm/s). A left-sided rostrotentorial craniectomy was performed, followed by medical treatment. TCD was monitored daily postoperatively returning to within the reference range five days after surgery (LMCA velocity: 54.9 cm/s; RMCA velocity: 63.6 cm/s). Normalisation of the systolic velocity was associated with clinical improvement. TCD is a useful and non-invasive method for monitoring of cerebral blood flow in patients with intracranial empyema.