Physical and Neurological Examination
On presentation, the cat was bright and alert. However, head and trunk movements looked somewhat jerky to one observer. Exploratory behaviour and reactions to stimuli were judged normal. A slight plantigrady involving both pelvic limbs was obvious and the cat could not jump on furniture. Clinical examination was normal without obvious muscle atrophy. Hopping and placing reactions were normal in the front limbs while they were delayed and hypermetric (overflexion of proximal articulations) in the pelvic limbs. Muscle tone and stretch reflexes were difficult to assess due to a lack of cooperation.

Diagnostic Testing
Hematology disclosed a lymphocytic (51%) leucocytosis (18.6 103 WBC/mm3). Serum chemistry and enzymes were in the normal range. Tests for FIP, FIV, Toxoplasmosis and FeLV (Ag p27) were all negative.

Electromyography: An electromyographic study was carried out under medethomidine/ketamine anesthesia. The pelvic limb muscles were electrically silent on concentric needle exploration except in two locations in the cranial tibial muscle where a rare positive sharp wave was found. Tibial nerve stimulation at the hock level gave a normal response in the plantar interosseous muscles (amplitude: 15 mV, latency: 2.65 ms), while stimulation at the hip level gave a severely attenuated and dispersed response (amplitude: 2.5 mV, reference 7.6 mV; duration: 16 ms, reference 11.2 ms; latency: 6.95 ms). The calculated motor nerve conduction velocity was below the minimal normal value (44.8 m/s, reference 52 m/s 2). Thoracic limbs were not tested. Slowing of the motor nerve conduction velocity and dispersion of the muscle compound action potential suggested a myelin abnormality. Rare spontaneous activities on electromyography and the absence of muscle atrophy suggested relative preservation of the nerve fibres.

Muscle and peripheral nerve biopsies: During the same anesthesia, the lateral head of the gastrocnemius muscle was biopsied with one specimen frozen in liquid nitrogen and a second immersion fixed in buffered glutaraldehyde. The common peroneal nerve was also biopsied and immersion fixed in buffered glutaraldehyde. Muscle histology was unremarkable. The nerve sample was post-fixed in osmium tetroxide, epon embedded, and semithin sections were prepared. Teased nerve fiber preparations were also performed. On semithin sections, several inappropriately thinly myelinated fibers were present (Fig. 1A). Macrophages stripping the myelin sheath could be seen. Occasional axonal degeneration and myelin ovoids could also be recognized. In some places, supernumerary Schwann cells wrapped around poorly myelinated fibres suggested early onion bulb formation (Fig. 1B). On teased nerve preparation, thin and irregular myelin sheaths were frequent (fig 2A,B). Teased nerve fibers from a control cat is shown in Fig. 2C.

A

B

C          10um

Fig 1. Semithin sections from the common peroneal nerve (toluidine blue stain). A. A macrophage is stripping a myelin sheath (arrow) and there is possible myelin ovoid formation (arrowhead). B. supernumerary Schwann cells around poorly myelinated fibers support early onion bulb formations (arrowheads). C. Common peroneal nerve from an age-matched control cat.

A.

B.

C.

Fig. 2. Teased nerve fiber preparation from the common peroneal nerve in the affected cat (A,B) and in an age-matched control cat (C).

Clinical Course
The clinical and histological presentation in this case share some features with two cases reported by Dahme et al, and with a single case reported by Summers et al, classified as feline hypertrophic neuropathy. The prominent myelin involvement and the onion bulb formations are shared points. The two reports differed since the latter included spinal cord white matter alterations not reported in the former. A major difference between the present case and those reported previously is the relatively mild disabling and stable condition. This raises the question of clinical variability within a single entity or the coexistence of several demyelinating /remyelinating degenerative conditions in cats. One author (GDS) has recently evaluated nerve biopsies from several cats with a chronic relapsing form of demyelinating neuropathy. The cat of this report did not received any specific therapy. The cat’s condition remained stable with no progression of clinical weakness, according to a telephone follow-up with the owner 6 months following presentation. Recurrence of epileptiform activity was not reported.

References

Dahme E, Kraft W, Scabell J. Hypertrophische Polyneuropathie bei der Katze. J Vet Med (A) 1987; 34:271-288.

Malik R, Ho S. Motor nerve conduction parameters in the cat. J Small Anim Pract 1989; 30:396-400.

Pillai SR, Steiss JE. Age-related changes in peripheral nerve conduction velocities of cats. Prog Vet Neurol 1991;2:95-104.

Summers BA, Cummings JF, deLahunta A. Diseases of the peripheral nervous system. In Veterinary Neuropathology, Mosby 1995. pp 402-501.