Laryngeal paralysis in a Rottweiler with neuroaxonal dystrophy
Laryngeal paralysis in a Rottweiler with neuroaxonal dystrophy
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DOI:
10.1111/j.1751-0813.1997.tb15650.x
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发表时间:
1997-11-01
影响因子:
1.1
通讯作者:
Clarke, RE
中科院分区:
文献类型:
--
作者:
Bennnett, PF;Clarke, RE
Case reports arytenoid6 and a biopsy of the cricothyroid muscle was taken as all laryngeal musculature was markedly atrophied. The stridor, dyspnoea and cough were less severe in the postoperative period, but at no stage was the dog’s respiration totally normal. Histological examination of the muscle biopsy showed active muscle degeneration, with excess connective tissue and scant regeneration. The dog recovered well and over the following 3 weeks showed good exercise tolerance with minimal increase in respiratory sounds. It was noted at these visits that the dog’s hindlimb gait was abnormal. At times the leg rised with some difficulty and the dog had a bunny-hopping hindlimb gait when running. No proprioceptive or other neurological deficits could be elicited on neurological examination. Four weeks after surgery the dog was presented after it had suffered a collapse while exercising. The owners reported that it had displayed hindlimb weakness, involuntarily voided urine and frothed at the mouth. An increase in respiratory noise for about 10 days prior to the collapse had been noticed. At presentation the dog was bright and alert, with no abnormalities except a soft cough and inspiratory stridor. It was not possible to visualise the larynx. A tentative diagnosis of a failure of the arytenoid lateralisation and a syncopal episode induced by the exercise was made. Because the owners did not wish to hospitalise the dog, they were instructed to keep it strictly confined and under close observation. The dog was re-presented 12 hours later, when it had again collapsed, this