Ten rottweilers presenting with spinal arachnoid pseudocysts were investigated. In six dogs, the lesions were localised dorsally at C2-C3; in three dogs, dorsally and ventrally at C5-C6; and, in one dog, dorsally and ventrally at C6-C7. Clinical signs were consistent with focal compression of the affected spinal cord segments. The animals showed ataxia of all four limbs, with truncal ataxia and marked hypermetria in cases of C2-C3 involvement, or ambulatory tetraparesis in cases of C5-C6 or C6-C7 involvement. Other than signs indicative of spina bifida in one dog, no abnormalities could be detected on plain radiographs. Myelography was used to define the localisation and extent of the pseudocysts. Additional information was obtained using magnetic resonance imaging in five dogs. Five dogs underwent a dorsal laminectomy; in three cases, the pseudocyst was treated by marsupialisation and, in two, by durectomy.

Results indicated that ventriculoperitoneal shunt implantation is a viable option for treatment of dogs or cats with congenital hydrocephalus. Because complications are most likely to develop in the first 3 months after surgery, repeated neurologic and imaging evaluations are warranted during this period.

No abstract

In this population of dogs, we were not able to identify any significant difference in remission or survival times between dogs with lymphoma treated with a continuous, multiagent chemotherapeutic protocol and dogs treated with a short-term single-agent protocol involving doxorubicin.

The polyneuropathy of juvenile Greyhound show dogs shows clinical similarities to the genetically heterogeneous Charcot-Marie-Tooth (CMT) disease in humans. The pedigrees containing affected dogs suggest monogenic autosomal recessive inheritance and all affected dogs trace back to a single male. Here, we studied the neuropathology of this disease and identified a candidate causative mutation. Peripheral nerve biopsies from affected dogs were examined using semi-thin histology, nerve fibre teasing and electron microscopy. A severe chronic progressive mixed polyneuropathy was observed. Seven affected and 17 related control dogs were genotyped on the 50k canine SNP chip. This allowed us to localize the causative mutation to a 19.5 Mb interval on chromosome 13 by homozygosity mapping. The NDRG1 gene is located within this interval and NDRG1 mutations have been shown to cause hereditary motor and sensory neuropathy-Lom in humans (CMT4D). Therefore, we considered NDRG1 a positional and functional candidate gene and performed mutation analysis in affected and control Greyhounds. A 10 bp deletion in canine NDRG1 exon 15 (c.1080_1089delTCGCCTGGAC) was perfectly associated with the polyneuropathy phenotype of Greyhound show dogs. The deletion causes a frame shift (p.Arg361SerfsX60) which alters several amino acids before a stop codon is encountered. A reduced level of NDRG1 transcript could be detected by RT-PCR. Western blot analysis demonstrated an absence of NDRG1 protein in peripheral nerve biopsy of an affected Greyhound. We thus have identified a candidate causative mutation for polyneuropathy in Greyhounds and identified the first genetically characterized canine CMT model which offers an opportunity to gain further insights into the pathobiology and therapy of human NDRG1 associated CMT disease. Selection against this mutation can now be used to eliminate polyneuropathy from Greyhound show dogs.