Objective—To determine analgesic effects of intraneural injection of ethyl alcohol or formaldehyde in the palmar digital nerves of horses. Animals—6 horses. Procedures—Ethyl alcohol was injected in the medial palmar digital nerve of 1 forelimb, and formaldehyde was injected in the contralateral nerve. The lateral palmar digital nerve in 1 forelimb was surgically exposed, but not injected, and the contralateral lateral palmar digital nerve was not treated. For each heel, severity of lameness in response to experimentally induced heel pain (lameness score and peak vertical force), thermal reaction time, and heel skin sensitivity scores were recorded. Heel pain was experimentally induced by advancing a threaded bolt through a custom-made horseshoe to apply pressure to the palmar horned aspect of the hoof. Horses were followed up for 112 days, when a subset of nerves was sampled for histologic analysis. Results—Alcohol and formaldehyde significantly reduced all measures of heel pain, and analgesia was evident over the 112 days of the study. Pastern circumference was significantly greater for formaldehyde-treated than for alcohol-treated limbs. Histologic evaluation showed preservation of nerve fiber alignment with an intact epineurium, loss of axons, axon degeneration, fibrosis, and inflammation in alcohol-treated and formaldehyde-treated nerves. Conclusions and Clinical Relevance—Results suggested that intraneural injection of either ethyl alcohol or formaldehyde in the palmar digital nerves of horses resulted in substantial, but partial, heel analgesia that persisted for at least 112 days. No advantage of formaldehyde over alcohol was found, and formaldehyde resulted in greater soft tissue inflammation.

Objective-To assess gait abnormalities associated with selective anesthesia of the suprascapular nerve (SSN) achieved by use of perineural catheterization and thereby determine the function of that nerve as it relates to gait in horses. Animals-3 adult horses with no preexisting clinically apparent lameness at a walk. Procedure-Each horse was anesthetized; the right SSN was exposed surgically for placement of a perineural catheter to permit delivery of 1 mL of 2% mepivacaine hydrochloride. Six hours after recovery from anesthesia, each horse was videotaped while walking (50-step data acquisition period) before and after administration of mepivacaine. Videotapes were reviewed and the proportion of abnormal steps before and after selective SSN anesthesia was assessed. A step was considered abnormal if a marked amount of scapulohumeral joint instability (ie, lateral luxation of the proximal portion of the humerus) was observed during the weight-bearing phase of the stride. Results-Clinically apparent gait dysfunction was detected in all 3 horses following perineural administration of the local anesthetic agent. Anesthesia of the SSN resulted in scapulohumeral joint instability as evidenced by consistent lateral excursion of the shoulder region during the weight-bearing phase of gait at a walk. The proportion of abnormal steps before and after SSN anesthesia was significantly different in all 3 horses. Conclusions and Clinical Relevance-These data support the role of the SSN in shoulder joint stability in horses and define SSN dysfunction as 1 mechanism by which the syndrome and gait dysfunction clinically referred to as sweeny may develop.

Intraocular pressure (IOP) was measured, using applanation tonometry, in both eyes of 20 horses after topical application of 0.5% proparacaine to the cornea. Ultrasonic pachymetry was used to measure central, mid-peripheral, and peripheral corneal thickness (CT) in all 4 quadrants of both eyes of 25 horses. All measurements were repeated after auriculopalpebral nerve block, sedation by IV administration of xylazine, or combination of nerve block and sedation. Mean IOP after topical anesthesia of the cornea was 20.6 +/- 4.7 mm of Hg for the left eye and 20.35 +/- 3.7 mm of Hg for the right eye. Mean central CT was 793.2 +/- 42.3 micrometers. The peripheral part of the cornea was significantly (P < 0.05) thicker, on average, than the central part of the cornea. Auriculopalpebral nerve block had no significant effect on IOP or CT. Intravenous administration of xylazine resulted in a significant (P < 0.05) decrease in IOP, but had no effect on CT.

A method yielding functional diaphragmatic variables in conscious animals is crucially needed to determine whether concepts and conclusions drawn from deeply anesthetized, highly instrumented clinically normal animals can be extrapolated to patients. Transdiaphragmatic pressure (Pdi) was, therefore, measured in 20 conscious calves during supramaximal transvenous bilateral stimulations of the phrenic nerves (pulse duration, 0.2 milliseconds; pulse frequency, 1, 10, 20, 30, 40, 70, and 100 Hz). Constancy of phrenic activation and precontraction length and geometry was ensured by respectively monitoring the amplitudes of right and left mass action potentials and triggering each activation train at end-expiratory lung volume against an occluded airway. Repeated phrenic activation and pressure recording procedures were well tolerated, safe, specific, and able to achieve constant and symmetric diaphragmatic tetanic contractions for prolonged periods. The Pdi increased with frequency of stimulation, so that, at 10, 20, 40, and 70 Hz, the mean +/- SD generated Pdi was 33 +/- 5, 65 +/- 8, 82 +/- 6, and 94 +/- 6% of Pdi at 100 Hz, respectively. The general shape of the Pdi-frequency relation and the absolute values of the generated Pdi were reproducible at 10-hour intervals despite CO2- or resistor-induced substantial changes in breathing pattern. It is concluded that this experimental model provides a reliable assessment of diaphragm function in conscious animals and can be used to study diaphragmatic contractility.

Maximal conduction velocities of compound action potentials evoked by stimuli of 2 times threshold in the caudal cutaneous sural (CCSN) and medial cutaneous antebrachial (MCAN) nerves were determined by averaging potentials evoked and recorded through percutaneous needle electrodes. Mean maximal conduction velocities of compound action potentials were: CCSN = 61.3 +/- 2.0 meters/second (m/s) and MCAN = 56.4 +/- 2.8 m/s. To confirm accuracy of our percutaneous recordings, compound action potentials were recorded through bipolar chlorided silver electrodes from the exposed surfaces of fascicles of the CCSN and the MCAN. The maximal conduction velocities of these potentials were in agreement with the conduction velocities of compound action potentials that were evoked and recorded through percutaneous needle electrodes. The specificity of stimulating and recording sites was verified by recording before and after section of the nerves. Stimuli from 3 to 5 times threshold evoked a second, longer latency, compound action potential that consisted of a variable number of components in the CCSN and MCAN. The configurations and conduction velocities of the shorter latency potentials were the same as those of the single compound action potentials evoked by stimuli of 2 times threshold. Mean conduction velocities of the longer latency potentials were: CCSN = 24.4 +/- 2.6 m/s and MCAN = 24.5 +/- 2.2 m/s. Needle electrode and direct stimulation of either the CCSN or the MCAN at 3 to 5 times threshold failed to evoke contractions of limb muscles. Therefore, action potentials that contributed to the evoked compound potentials recorded in these horses arose, most likely, from afferent nerve fibers.

A nerve muscle pedicle (NMP) graft was placed in the cricoarytenoideus dorsalis (CAD) muscle of 6 horses with induced left laryngeal hemiplegia. The NMP graft was created by use of the first cervical nerve and omohyoideus muscle. In 1 horse (control), the first cervical nerve was transected after placement of the NMP graft. One year after the surgical procedure, horses were examined endoscopically and then anesthetized. While the larynx was observed endoscopically, the first cervical nerve was stimulated. Horses were subsequently euthanatized, and the larynx was harvested. Prior to anesthesia, the endoscopic appearance of the larynx of all horses was typical of laryngeal hemiplegia. During anesthesia, stimulation of the first cervical nerve produced vigorous abduction of the left arytenoid in principal horses but not in the control horse. The right cricoarytenoideus lateralis and CAD muscles were grossly and histologically normal. Also, the left cricoarytenoideus lateralis was atrophic in all horses as was the left CAD muscle of the control horse. In contrast, the left CAD muscle harvested from principal horses had evidence of reinnervation with type 1 or type 2 fiber grouping. One year after the NMP graft procedure, horses with left laryngeal hemiplegia had reinnervation of the left CAD muscle. In another study, reinnervation was sufficient to allow normal laryngeal function during exercise. Combined, these data suggest that the NMP graft procedure is a viable technique for the treatment of left laryngeal hemiplegia in horses.

A morphologic and morphometric study was carried out on the facial nerve: to determine normal histologic data in myelinated fibers of clinically normal young adult dogs; to establish reference values for mean fiber diameter, and to delineate the relative diameter frequency distribution curve. Few degenerative changes were observed in single teased-nerve fibers and semithin cross-sectional nerve preparations. Statistical difference was not observed between left and right facial nerves. The distribution of fiber diameters in the facial nerve was unimodal. Mean (+/- SD) fiber diameter of the facial nerve was 3.92 +/- 1.18 micromole. Approximately 89% of fibers in the facial nerve had diameter between 3 and 6 micromole. Fiber diameter ranged from 2 to 12 micromole; however, < 1% of fibers had diameter > 8 micromole.

Evoked potentials were induced by transcranial stimulation and recovered from the spinal cord, and the radial and sciatic nerves in six dogs. Stimulation was accomplished with an anode placed on the skin over the area of the motor cortex. Evoked potentials were recovered from the thoracic and lumbar spinal cord by electrodes placed transcutaneously in the ligamentum flavum. Evoked potentials were recovered from the radial and sciatic nerves by surgical exposure and electrodes placed in the perineurium. Signals from 100 repetitive stimuli were averaged and analyzed. Waveforms were analyzed for amplitude and latency. Conduction velocities were estimated from wave latencies and distance traveled. The technique allowed recovery of evoked potentials that had similar characteristics among all dogs. Conduction velocities of potentials recovered from the radial and sciatic nerves suggested stimulation of motor pathways; however, the exact origin and pathway of these waves is unknown.

Continous electromyographic recordings of pharyngeal muscle activity were made in 5 clinically normal control dogs and in 7 dogs 3 years after partial denervation of the pharyngeal muscles. Electromyographic recordings were made of the sequence of actions of each muscle and of the combined muscle activity, at rest and during swallowing of food. During 30-second periods, the recordings were digitalized and stored on diskette for further analysis. All control dogs had a distinct pattern of muscle activity during swallowing, the onset being in a constant order (hyopharyngeal, thyropharyngeal, and cricopharyngeal) and bilaterally synchronous. While eating, each dog had about 5 to 12 short periods of synchronous activity in each muscle, between the swallowing actions. During the resting period, there were longer periods of activity, which were synchronous with respiration. In each denervated dog, there were normal and irregular swallowing actions. Swallowing activity was recognized, but the sequence of hyopharyngeal, thyropharyngeal, and cricopharyngeal muscle activity was irregular and different from that in control dogs. Partial denervation of the pharyngeal muscles does not seriously impair motor activity of the muscles, but does alter the sequence of activity in the pharyngeal muscles during swallowing.

Sensory nerve conduction velocity was measured in the lateral palmar nerve of 8 horses. The limb temperature was manipulated by external means and monitored. Alterations in the nerve conduction velocity related to limb temperature variation were identified at both increased and decreased temperatures. These were quantified and a mean value of 2.15 +/- 0.2 m/s/degree Celsius was determined. The effect of altered limb temperature should be considered in nerve conduction velocity determinations.