Abstract.A disorder of central nervous white matter in Norwegian-bred silver foxes is described from the case histories of 2 1 clinically affected foxes. The main presenting sign of this disorder was caudal limb ataxia, which appeared between 2% and 4 months of age and progressed over the next 4-8 weeks. Only four affected foxes were allowed to live beyond this period, but they showed moderate to marked improvement.Light microscopic examination of specimens from 16 affected foxes necropsied between 3% and 6% months of age revealed lesions that were restricted to the white matter of brain and spinal cord. The lesions were characterized by a symmetrical spongy change with vacuoles of varying sizes and included significant myelin deficiency. There was a relative preservation of axons and nerve cells and no significant inflammation or vascular reaction. An astrocytic hypertrophy was usually associated with the spongy change.Ultrastructural examination of central nervous tissue from two, perfusion-fixed, 6-month-old foxes showed intramyelin vacuoles resulting from splitting of the myelin lamellae at the intraperiod line and was interpreted as indicating myelin edema. Expanded extracellular spaces and watery astrocytic processes also contributed to the vacuolar appearance. Astrocytic processes in affected areas were hypertrophic and contained abundant filaments.Although the 16 silver foxes had severe clinical signs, their lesions had features in common with the juvenile form of Canavan's disease in children and a spongy degeneration reported in Labrador Retrievers; however, the clinical course in the foxes was not uniformly progressive.

A three‐month‐old female basset hound was referred to the Norwegian College of Veterinary Medicine with a history of progressive paresis of the pelvic limbs. Following neurological examination and the study of myelograms, extradural masses causing spinal cord compressions at the T12.13 and T13‐L1 junctions were diagnosed. At necropsy bone‐tissue of the vertebral laminae was found to have formed stenoses of the vertebral canal producing compressions of the spinal cord. Irreversible tissue‐damage was observed in histological sections prepared from the compressed areas of the spinal cord.

Spongy degeneration of white matter in silver foxes is a naturally occurring, hereditary disorder. We report ultrastructural findings in the upper cervical cord of five perfusion-fixed foxes that were examined between 5 weeks and 2 1/4 years after the onset of clinical signs. Large cytoplasmic vacuoles in oligodendrocytes were present in the foxes examined 5, 12 and 20 weeks after the onset. Other early features of the disease were severe vacuolation of myelin sheaths, demyelination, expansion of extracellular spaces and hypertrophy of astrocytes. Evidence of partial demyelination as well as demyelination of entire internodes was found. In the later stages of the disease, the vacuolation was largely resolved but a marked astrogliosis persisted and numerous remyelinated axons were present in the gliotic areas. Vacuolation of oligodendrocytes and partial demyelination has not previously been seen together in a single disease process. The relationship between oligodendrocyte vacuolation, myelin sheath vacuolation and demyelination is discussed. It is concluded that the present condition is due to a primary damage to oligodendrocytes; however, the underlying biochemical lesion is not known.

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