Equine Neurology by Martin Furr, Stephen Reed

By Martin Furr, Stephen Reed

Equine Neurology, moment version offers a completely up to date new version of the single equine-specific neurology booklet, with complete, clinically orientated info. * deals an entire scientific connection with neurologic stipulations in equine sufferers * Takes a problem-based method of current a clinically orientated standpoint * provides new chapters on imaging the worried process, neuronal body structure, sleep problems, head shaking, differential analysis of muscle trembling and weak spot, and cervical articular method joint affliction * Covers the fundamental ideas of neurology, scientific subject matters similar to the preliminary examination, differentials, and neuropathology, and particular stipulations and issues * contains entry to a better half web site providing videos demonstrating featuring symptoms

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An abrupt increase in blood bicarbonate concentration, such as that associated with intrave­ nous infusion of sodium bicarbonate to treat acidosis for example, can result in a paradoxical decrease in 30 Section 1: Foundations of Clinical Neurology CSF pH due to the rapid movement of CO2 into the CSF, and the slower accumulation of bicarbonate. These paradoxical reactions are usually transient and last only a few minutes to hours [18]. Their signifi­ cance in clinical practice is unknown and they may be only laboratory curiosities.

Arch Neurol Psychiatry, 32, 523–553. C. (1966) The production of cerebrospinal fluid in man and its modification by acetezolamide. J Neurosurg, 25, 430–436. H. B. (1977) Equine cerebrospinal fluid: reference values of normal horses. Am J Vet Res, 38, 1271–1274. M. M. (1993) Effect of hypercapnia or xylazine on lateral ventricle and lumbosacral cerebrospinal fluid pressures in pentobarbital‐anesthe­ tized horses. Vet Surg, 22, 151–158. U. et al. (2002) Direct measurement of intracranial pressure in adult horses.

Potential sources of the increased enzyme activity in the CSF include diffusion across a damaged BBB or blood–CSF barrier, and release of enzymes from cells within the CNS such as inflammatory cells, micro­ organisms, and tumors, or directly from damaged nerve cells and myelin. CK exists as three isoenzymes—CK‐MM (CK1) for muscle, CK‐MB (CK2) for cardiac muscle, and CK‐BB (CK3) for nervous tissue. The CSFck has been reported to be a sensitive but nonspecific marker of nervous system disease [34, 35].

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