Physical and Neurological Examination
Physical assessment revealed a bright, alert, responsive dog with severe, generalized muscle atrophy that was most profound in the pelvic limbs. Posture was characterized by a crouched stance in the pelvic limbs, valgus appearance distal to the hocks, and hyperextension of the carpal joints (see Fig. 1). The dog was tetraparetic, had a short-strided gait with concurrent bunny hopping, and was moderately ataxic. Postural reaction deficits were present in all limbs and the cranial tibial, gastrocnemius, patellar, and withdrawal (rear and forelimb) reflexes were significantly reduced. Palpation of the limbs revealed contractures at the stifle and hock joints. History and physical findings suggested generalized neuromuscular disease

Fig 1. Note crouched stance in pelvic limbs and valgus appearance distal to the hocks

Diagnostic Testing
Differential diagnoses included congenital, infectious and non-infectious inflammatory, degenerative, and toxic disease of the motor unit. Diagnostic tests performed during the course of hospitalization were limited to a complete blood count (CBC), serum biochemistry profile, urinalysis, radiography, electrophysiology, cerebrospinal fluid analysis, several infectious disease titers, and muscle and nerve biopsies.

CBC – Mild lymphocytosis

Serum biochemistry profile – Not remarkable except for a mildly elevated creatine kinase (584 IU/L; reference range 68-400)

Urinalysis – No abnormal findings

Cerebrospinal fluid analysis via cerebellomedullary cistern collection – No abnormal findings

Survery radiographs of the carpi, tarsi, pelvis, and lumbar vertebrae – Within normal limits

Antibody titers for Toxoplasma gondii and Neospora caninum – Negative

Electrodiagnostics (See Fig. 2)

Electromyography (EMG)– Electromyography demonstrated generalized grade IV/IV spontaneous activity consisting of positive sharp waves, fibrillation potentials, and occasional complex repetitive discharges (Fig. 2A) These findings are supportive of myopathic or neuropathic disease, although not specific for either process.

Peroneal and ulnar motor nerve conduction velocity (MNCV)– Significantly reduced (34.1 m/sec and 32.7 m/sec respectively; reference range mean for 3-6 month old dog: 53 m/sec S.D. 2.8 and 54.1 m/sec S.D. 2.3 respectively).1 (Fig. 2B) A reduction in MNCV is most commonly seen in myelinopathies (demyelination, hypomyelination, dysmyelinogenesis) and axonopathies that involve selective loss of large diameter fibers.

Proximal compound motor unit action potential (CMAP) amplitude– Markedly lower than normal (peroneal 1.58 mV and ulnar 1.65 mV; reference peroneal 19.5mV S.D. 1.5 and ulnar 22.9 mV S.D. 1.6) suggesting axonopathy, severe myelinopathy (usually temporal dispersion seen), or myopathy.2

Peroneal sensory nerve conduction velocity (SNCV)– Peroneal SNCV were likely diminished (32.3 m/sec at the stifle; reference mean for adult dogs 55 m/sec S.D. 5).3 Low SNCV has similar causes as reduced MNCV. Sensory nerve action potentials had substantial polyphasia, which is the result of physiological or pathological (i.e. caused by myelinopathy) temporal dispersion.

Fig. 2.

A. EMG showing positive sharp waves and fibrillation potentials recorded from the cranial tibial muscle.
B. Peroneal MNCV recorded from the extensor digitorum brevis with stimulation sites at the hock (A1), stifle (B1), and hip (C1).
C. Peroneal SNCV recorded at the hock (A1), stifle (A2), hip (A3), and over L4-5 (cord dorsum A4).

Muscle and Nerve Biopsies
Fresh frozen biopsy specimens from the biceps femoris and gastrocnemius muscles showed variability in myofiber size with large groups of round, atrophic fibers (Fig. 3). Immunohistochemistry for dystrophin and related proteins were similar to control tissue (not shown). Resin embedded sections from the peroneal nerve showed an unusual pattern of myelin splitting with expanded Schwann cell cytoplasm (arrows, Fig. 4). Axons were normal in appearance.

Fig.3: H& E

Fig.4

Clinical Course
Results of the neurological examination, electrodiagnostic testing and muscle and nerve biopsies supported the presence of mixed myopathic and neuropathic disease in this dog. Given the history, signalment, and clinical data, the dog was placed on clindamycin 10 mg/kg PO TID for 1 month for possible protozoal polyneuritis-polymyositis while awaiting the results of the biopsies and titers.4,5 The dog exhibited a marked improvement over the next 2-3 months following treatment and at four months there was no evidence of weakness according to the owner. Although serology did not reveal the presence of antibodies to any infectious agents and cellular infiltrates were not identified within the muscles or nerve, a protozoal infection cannot be ruled out. Other causes of demyelinating neuropathy (infectious, immune, post-vaccine) and spontaneous remission can also not be ruled out.

References

Swallows J, Griffiths IR. Age related changes in the motor nerve conduction velocity in dogs. Res Vet Sci 1977;23:29-32

Walker TL, Redding RW et al. Motor nerve conduction velocity and latency in the dog. Am J Vet Res 1979;40:1433-1439

Redding R, Ingram JT et al. Sensory nerve conduction velocity of cutaneous afferents of the radial, peroneal, and tibial nerves of the dog: Reference values. Am J Vet Res 1982;43:517-521

Barber JS. Clinical aspects of 26 cases of neosporosis in dogs. Vet Rec 1996;139:439-443.

Barber JS, Payne-Johnson CE, Trees AJ. Distribution of Neospora caninum within the central nervous system and other tissues of six dogs with clinical neosporosis. J Small An Pract 1996;37:568-574.