Duncan I D, Griffiths I R, Carmichael S, Henderson S
Muscle Nerve. 1981 May-Jun;4(3):223-7. doi: 10.1002/mus.880040309.
To date, a single case of canine giant axonal neuropathy (GAN) has been recorded. The present report describes the disease in 3 more dogs from the second litter produced by the parents of the original case. Regular clinical and electrophysiological examinations were carried out on all 11 dogs of the second litter. At 14--16 months of age, 3 dogs developed slight posterior ataxia which progressed to a severe lower motor neuron disturbance involving only the hind legs. During this period, each dog began to regurgitate food as a result of megaesophagus. From 12 months of age, there was a progressive reduction in the amplitude of the evoked muscle action potential. Biopsy of the tibial fascicular nerve at 16 months of age confirmed that all 3 dogs had GAN, with numerous swollen unmyelinated fibers and less frequent enlarged myelinated fibers containing accumulated neurofilaments.
迄今为止，仅记录到一例犬巨大轴索性神经病（GAN）。本报告描述了另外3只患该病的犬，它们来自首例病例父母所生的第二窝幼犬。对第二窝的所有11只犬进行了定期的临床和电生理检查。在14至16月龄时，3只犬出现轻微的后躯共济失调，进而发展为仅累及后肢的严重下运动神经元功能障碍。在此期间，每只犬因巨食管开始出现食物反流。从12月龄起，诱发肌肉动作电位的幅度逐渐降低。在16月龄时对胫束神经进行活检，证实所有3只犬均患有GAN，有大量肿胀的无髓纤维，含有积聚神经丝的有髓纤维肿大的情况较少见。
