Sensor analysis and initial assessment of detectable first hoof contacts and last break-overs as unique signal fluctuations for equine gait analysis

The objective of the control study was to assess 2 prominent fluctuations in a single optical signal as being either a true first hoof contact or a last break-over based on descriptive measures. The study builds on initial findings from a preliminary investigation of the embedded-optical-base system’s (EOBS) capabilities in signal capturing and feasibility as potential alternative to existing gait technologies, such as piezoelectric (e.g., load cell) systems. Hoof contacts and break-overs were measured (0 to 1 au; arbitrary units) using a 2.4-m (length) × 0.9-m (width) platform containing 1 EOBS. Three mixed-breed horses (n = 3) were injected with saline or either 100 IU or 200 IU Botox (i.e., onabotulinumtoxinA) with a 2.5-mL final volume. Injections were made into the deep digital flexor muscle at the motor end plates, with electromyography and ultrasound guidance. Horses were observed for 3 time points (pre-, post-, and recovery test days) over the span of a 4-mo period. Signal fluctuations [i.e., amplitude of hoof impacts based on true first hoof contacts (ΔSTS) and true last break-overs (ΔSTL)] and kinematics [i.e., complete gait pass (CGP) time duration (T)] were recorded from each horse. Visual observations and video analysis were used for determining gait pattern categories. Individual horse measurements were analyzed for each trial, compared with video data and classified. Comparison of primary signal fluctuations (i.e., ΔSTS vs. ΔSTL; forelimb vs. hindlimb) exhibited significant differences between hoof contacts and break-overs (P < 0.05). Right and left forelimb hoof contacts and hindlimb break-overs were not significantly different (P = 0.966; 0.063 ± 0.135; Estimate ± SE; P = 0.606; 0.176 ± 0.142; Estimate ± SE, respectively). Additionally, treatment vs. saline forelimbs did not exhibit significant difference (P = 0.7407; −0.098 ± 0.279; Estimate ± SE). Overall, data showed that the EOBS can collect repeatable and unique primary signal fluctuations as prominent and different gait measurements providing evidence to further development and research of the sensing system.

Facial Nerve Trauma: Evaluation and Considerations in Management

The management of facial paralysis continues to evolve. Understanding the facial nerve anatomy and the different methods of evaluating the degree of facial nerve injury are crucial for successful management. When the facial nerve is transected, direct coaptation leads to the best outcome, followed by interpositional nerve grafting. In cases where motor end plates are still intact but a primary repair or graft is not feasible, a nerve transfer should be employed. When complete muscle atrophy has occurred, regional muscle transfer or free flap reconstruction is an option. When dynamic reanimation cannot be undertaken, static procedures offer some benefit. Adjunctive tools such as botulinum toxin injection and biofeedback can be helpful. Several new treatment modalities lie on the horizon which hold potential to alter the current treatment algorithm.

A new paradigm in facial reanimation for long-standing palsies?

ABSTRACT Background: A chance observation of return of excellent facial movement, after 18 months following the first stage of cross-face nerve grafting, without free functional muscle transfer, in a case of long-standing facial palsy, lead the senior author (RBA) to further investigate clinically. Patients and Methods: This procedure, now christened as cross-face nerve extension and neurotization, was carried out in 12 patients of very long-standing facial palsy (mean 21 years) in years 1996-2011. The mean patient age and duration of palsy were 30.58 years and 21.08 years, respectively. In patients, 1-5 a single buccal or zygomatic branch served as a donor nerve, but subsequently, we used two donor nerves. The mean follow-up period was 20.75 months. Results: Successive patients had excellent to good return of facial expression with two fair results. Besides improved smile, patients could largely retain air in the mouth without any escape and had improved mastication. No complications were encountered except synkinesis in 1 patient. No additional surgical procedures were performed. Conclusion: There is experimental evidence to suggest that neurotization of a completely denervated muscle can occur by the formation of new ectopic motor end plates. Long-standing denervated muscle fibres eventually atrophy severely but are capable of re-innervation and regeneration, as validated by electron microscopic studies. In spite of several suggestions in the literature to clinically validate functional recovery by direct neurotization, the concept remains anecdotal. Our results substantiate this procedure, and it has the potential to simplify reanimation in longstanding facial palsy. Our work now needs validation by other investigators in the field of restoring facial animation.

TrkB kinase activity maintains synaptic function and structural integrity at adult neuromuscular junctions

Activation of the tropomyosin-related kinase receptor B (TrkB) by brain-derived neurotrophic factor acutely regulates synaptic transmission at adult neuromuscular junctions (NMJs). The role of TrkB kinase activity in the maintenance of NMJ function and structure at diaphragm muscle NMJs was explored using a chemical-genetic approach that permits reversible inactivation of TrkB kinase activity in TrkB F616A mice by 1NMPP1. Inhibiting TrkB kinase activity for 7 days resulted in significant, yet reversible, impairments in neuromuscular transmission at diaphragm NMJs. Neuromuscular transmission failure following 2 min of repetitive phrenic nerve stimulation increased from 42% in control to 59% in 1NMPP1-treated TrkB F616A mice ( P = 0.010). Recovery of TrkB kinase activity following withdrawal of 1NMPP1 treatment improved neuromuscular transmission ( P = 0.006). Electrophysiological measurements at individual diaphragm NMJs documented lack of differences in quantal content in control and 1NMPP1-treated mice ( P = 0.845). Morphological changes at diaphragm NMJs were modest following inhibition and recovery of TrkB kinase activity. Three-dimensional reconstructions of diaphragm NMJs revealed no differences in volume at motor end plates (labeled by α-bungarotoxin; P = 0.982) or presynaptic terminals (labeled by synaptophysin; P = 0.515). Inhibition of TrkB kinase activity by 1NMPP1 resulted in more compact NMJs, with increased apposition of presynaptic terminals and motor end plates ( P = 0.017) and reduced fragmentation of motor end plates ( P = 0.005). Recovery of TrkB kinase activity following withdrawal of 1NMPP1 treatment resulted in postsynaptic remodeling likely reflecting increased gutter depth ( P = 0.007), without significant presynaptic changes. These results support an essential role for TrkB kinase activity in maintaining synaptic function and structural integrity at NMJs in the adult mouse diaphragm muscle.