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  • Author or Editor: Terrell A. Holliday x
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Summary

Eleven horses (3 mares, 7 stallions, 1 gelding) with clinical and biochemical evidence of hyperkalemic periodic paralysis were studied. Each horse had history of episodic weakness, muscular tremors, or collapse, which lasted for periods of a few minutes to hours. Diagnosis was based on hyperkalemia in association with a spontaneous episode of paralysis or by precipitation of an episode by oral administration of potassium chloride. Clinical and biochemical events were documented during spontaneous and induced episodes of muscular weakness. During episodes, electrocardiographic findings were consistent with hyperkalemia. Electromyography performed between episodes revealed fibrillation potentials and positive sharp waves, complex repetitive discharges, and myotonic discharges. Histologic changes in muscle biopsy specimens varied from no overt changes in some horses to vacuolation in type-2B fibers with mild degenerative changes in other horses. Electron microscopy of myofibers revealed dilatations of the sarcoplasmic reticulum.

Analysis of blood samples taken serially during induced attacks in 5 horses revealed marked hyperkalemia (5.5 to 9.0 mEq/L), with normal acid-base status, hemoconcentration, and modest changes in muscle-derived enzymes. Close correlation (r 2 = 0.882) between total plasma protein and plasma potassium concentrations was observed and indicated a shift of fluid out of the extracellular fluid compartment. Treatment of either spontaneous or induced episodes by iv administration of calcium, glucose, or bicarbonate resulted in rapid recovery. Dietary management or daily administration of acetazolamide effectively controlled episodes.

An affected mare was bred to an affected stallion, and 3 affected offspring were produced by embryo transfer. Blood samples from another extended family of affected horses were analyzed for identification of a genetic marker. Blood typing, including 22 loci, revealed no linkage with erythrocytic or serum markers. Lymphocyte typing for equine lymphocytic antigen markers also failed to reveal any linkage.

Free access
in Journal of the American Veterinary Medical Association

SUMMARY

The compound nerve action potential (cnap) of the superficial peroneal nerve of dogs was investigated to determine: (1) the influence of the stimulation technique on the configuration of the cnap, with particular attention to late components; (2) the fiber diameter (fd) distribution; and (3) the relationship between fd distribution and cnap configuration, by reconstruction of cnap made on the basis of fd distributions.

The cnap were evoked in 9 dogs under halothane anesthesia by 2 stimulation methods: percutaneous needle electrode stimulation and direct stimulation of the exposed superficial peroneal nerve. Recordings were made with percutaneous needle electrodes. Full nerve cross sections of 7 superficial peroneal nerves were prepared for fd morphometric analysis. Reconstruction of cnap were made on the basis of the fd distributions.

Late components of the cnap could be evoked with either stimulation method, but only with a stimulus intensity of 3 to 5 times maximal for the main (early) component of the cnap. The fd histograms of 7 analyzed nerves had bimodal distribution. In 5 nerves, peaks were at 4.2 to 4.5 μm and 9.0 to 10.0 μm, with 60% of the fibers in the small-diameter group. In 2 nerves with lower maximal conduction velocities, peaks were shifted toward smaller values.

The cnap reconstructions made by use of fd data closely resembled actual recordings when a fifth-order polynomial function was applied to the relationship between nerve conduction velocity and fd. Reconstructions made by use of 1 or 2 linear functions did not accurately resemble actual recordings.

The results indicate clinical sensory electroneurographic recordings can provide accurate information regarding both large- and small-diameter fibers, if adequate stimulus intensities are used. To understand the recorded potential more completely, further studies are needed to determine the effects of volume conduction on configuration of the cnap. It should then be possible to estimate fd distributions even more accurately by analyzing cnap of normal nerves, or of diseased nerves in which the normal relation between fd and conduction velocity is preserved.

Free access
in American Journal of Veterinary Research