Progressive axonopathy: an inherited neuropathy of Boxer dogs. 1. Further studies of the clinical and electrophysiological features

Abstract

The clinical and electrophysiological findings in 14 Boxer dogs with progressive axonopathy (PA) are described. The salient clinical features are hind‐limb ataxia which may later involve forelegs, proprioceptive defects, hypotonia, patellar areflexia, absence of muscle atrophy and, in a few instances, ocular tremor and head bobbing. The outward signs are often observed by 2–3 months of age but clinical testing can reveal patellar areflexia at 1 month of age. After an initial progression, the signs may stabilize and dogs are alive at 4 years of age having shown no deterioration over the previous 2 years. The electrophysiology shows reduced motor nerve conduction velocities and evoked potential amplitudes after about 4 months of age. The F‐wave latency is considerably increased. Sensory nerves also show a marked reduction in the amplitude of their evoked potentials and eventually cease to conduct. Abnormal spontaneous activity is not a feature on electromyography. The conduction defects probably reflect to some degree the reduced nerve fibre diameters and myelin sheath changes found in PA although other factors may also be operating. The study shows that PA can be diagnosed with reasonable confidence by routine clinical testing at an early age.

Clinical aspects of 27 cases of neosporosis in dogs

“…Labradors and boxers were well represented, but both are popular breeds, and breeders of boxers have received information about neosporosis, owing in part to the similarity of the clinical signs of neosporosis and progressive axonopathy (Griffiths 1985), and this publicity may have increased the number of samples received from this breed.…”

Progressive Axonopathy: An Inherited Neuropathy of Boxer Dogs. 2. The Nature and Distribution of the Pathological Changes

“…Both sensory and motor fibres are affected, with involvement of dorsal and ventral roots and cutaneous nerves. However, the proportion of motor fibres undergoing degeneration is small at any given time as indicated by the lack of spontaneous activity at electromyography, the absence of gross muscle atrophy (Griffiths, 1985) and the minor degree of histological atrophy. The majority of atrophic muscle fibres are seen in more distal limb muscles as might be expected from the pattern of nerve degeneration.…”

“…Proprioceptive defects, hypotonia and loss of tendon reflexes are also demonstrable but muscle atrophy is not a feature of the disease. The clinical signs and electrophysiological features have been summarized recently (Griffiths, 1985).…”

Hereditary polyneuropathy in the Alaskan Malamute

“…Since the late 1970s various case reports about hereditary polyneuropathies in different canine breeds have been described such as the giant axonal neuropathy in German shepherds (11,12), the progressive axonopathy in Boxers (16), the hypomyelinating polyneuropathy in the Golden retriever (3), the laryngeal paralysispolyneuropathy complex in Bouviers de Flandre (24), young Dalmatians (6), young Rottweilers (17) and Siberian Huskies (21), the distal sensorimotor polyneuropathy in the Rottweiler (5), the hypertrophic neuropathy in the Tibetan terrier (8) and Mastiff (22), the sensory neuropathies in the English pointer (9,10) and Dachshund (13), and the distal symmetric polyneuropathy in the Great Dane (2). A recent review was provided by Granger (15).…”