The records of 75 dogs with fibrocartilaginous embolism of the spinal cord were evaluated retrospectively. The diagnosis was confirmed histopathologically in 21 dogs (group A) and remained suspected in 54 patients (group B). The two groups were compared. Particular emphasis was placed on the description of physiotherapy procedures, recovery rates and prognostic criteria. Results demonstrated that fibrocartilaginous embolism affected mainly middle-aged, large- or giant-breed dogs. Clinical signs were peracute in onset, non-progressive and often asymmetric. Cerebrospinal fluid analysis was normal in the majority of dogs. Intramedullary swelling was the only abnormality detected on myelograms of these patients. A positive correlation was found between a poor prognosis and the involvement of intumescences, symmetrical clinical signs and decreased deep pain sensation. However, physio/hydrotherapy instituted immediately after the diagnostic work-up seemed to have a major influence on the recovery rate.

Steroid-responsive meningitis-arteritis is an immunopathological disease in dogs characterised by neck pain, pleocytosis of the cerebrospinal fluid (CSF) and increased serum and CSF immunoglobulin (Ig) A levels. A long-term treatment protocol (four to 20 months) with prednisolone was applied in 10 dogs with the condition. Clinical side effects, changes in blood and CSF values and long-term outcome were evaluated retrospectively. Eight of the 10 dogs were without clinical signs up to 29 months after the treatment was terminated. Long-term glucocorticosteroid treatment appears to result only in mild clinical side effects, such as polyuria/polydipsia, polyphagia and weight gain. All clinical and laboratory changes were reversible after the therapy was discontinued. Elevated serum and CSF IgA levels did not decrease to normal values during prednisolone treatment and were still slightly increased after the therapy was discontinued. A marked decrease in the cell count of the CSF was observed after therapy was initiated, although pleocytosis increased again during relapses of the disease. Monitoring of CSF cell count in dogs with this condition seems to be a sensitive indicator of success of treatment. In addition, older dogs with high IgA levels in the CSF and frequent relapses seem to require a longer duration of therapy and have a less favourable prognosis long term. The reason for high systemic and intrathecally produced IgA levels remains unknown, but seems not to be influenced by prednisolone treatment.

The purpose of this study was to analyse retrospectively a feline population with intracranial neoplastic diseases, to document seizure patterns in these animals and to determine whether partial seizures were more frequently associated with structural brain lesions then generalised seizures. In addition, a comparison was made within the population with intracranial neoplasia between two groups of cats: one with and one without seizures. Special emphasis was given to the evaluation of tumour type, localisation and size of the lesion and its correlation with seizure prevalence. Sixty-one cats with histopathological diagnosis of intracranial tumour were identified. Fourteen cats (23%; group A) had a history of seizure(s). Forty-seven cats (77%; group B) had no history of seizure(s). Generalised tonic-clonic seizures were seen in eight cats (57%) and were the most common seizure pattern in our cats with intracranial neoplasia. Clusters of seizures were observed in six cats. Status epilepticus was observed in one patient. The mean age of the cats was 7.9 years within group A (median 8.5) and 9.3 years (median 10) within group B. The cats with lymphoma within both groups were significantly younger than cats with meningioma. In both groups meningioma and lymphoma were confirmed to be the most frequent tumour type, followed by glial cell tumours. The prevalence of the seizures in patients with glial cell tumours was 26.7%, 26.3% in patients with lymphomas and 15% in cases with meningiomas. In 33 cases (54.1%) the tumours were localised in the forebrain, 15 tumours (24.6%) were in the brainstem, four (6.6%) in the cerebellum and nine tumours (14.7%) had multifocal localisation. Parietal lobe and basal ganglia mostly affected group A. In group B tumours were most frequently located in the parietal and frontal lobes as well as in the diencephalon. A positive association was documented between the localisation of a tumour in the forebrain and seizure occurrence.

Reports on intervertebral disc disease in cats are rare in the veterinary literature. It has been postulated that intervertebral disc protrusion is a frequent finding during necropsy in cats, without having any clinical relevance (King and Smith 1958, King & Smith 1960a, King & Smith 1960b). However, a total of six cases with disc protrusions and clinically significant neurological deficits have been reported over the past decade. (Heavner 1971, Seim & Nafe 1981, Gilmore 1983, Littlewood et al 1984, Sparkes & Skerry 1990, Bagley et al 1995). As in dogs, there are also two types of intervertebral disc disease in cats: Hansen's type I (extrusion), and type II (herniation). Cervical spinal cord involvement was more commonly recognised in cats than the lumbar or the thoraco lumbar area. Cats over 15 years were mainly affected (King & Smith 1958, King & Smith 1960a, King & Smith 1960b). We describe two cats with lumbar intervertebral disc protrusions. Emphasis is placed on differential diagnoses, treatment and follow-up.

Inherited ataxias are characterized by degeneration of the cerebellar structures, which results in progressive motor incoordination. Hereditary ataxias occur in many species, including humans and dogs. Several mutations have been found in humans, but the genetic background has remained elusive in dogs. The Finnish Hound suffers from an early-onset progressive cerebellar ataxia. We have performed clinical, pathological, and genetic studies to describe the disease phenotype and to identify its genetic cause. Neurological examinations on ten affected dogs revealed rapidly progressing generalized cerebellar ataxia, tremors, and failure to thrive. Clinical signs were present by the age of 3 months, and cerebellar shrinkage was detectable through MRI. Pathological and histological examinations indicated cerebellum-restricted neurodegeneration. Marked loss of Purkinje cells was detected in the cerebellar cortex with secondary changes in other cortical layers. A genome-wide association study in a cohort of 31 dogs mapped the ataxia gene to a 1.5 Mb locus on canine chromosome 8 (praw = 1.1×10−7, pgenome = 7.5×10−4). Sequencing of a functional candidate gene, sel-1 suppressor of lin-12-like (SEL1L), revealed a homozygous missense mutation, c.1972T>C; p.Ser658Pro, in a highly conserved protein domain. The mutation segregated fully in the recessive pedigree, and a 10% carrier frequency was indicated in a population cohort. SEL1L is a component of the endoplasmic reticulum (ER)–associated protein degradation (ERAD) machinery and has not been previously associated to inherited ataxias. Dysfunctional protein degradation is known to cause ER stress, and we found a significant increase in expression of nine ER stress responsive genes in the cerebellar cortex of affected dogs, supporting the pathogenicity of the mutation. Our study describes the first early-onset neurodegenerative ataxia mutation in dogs, establishes an ERAD–mediated neurodegenerative disease model, and proposes SEL1L as a new candidate gene in progressive childhood ataxias. Furthermore, our results have enabled the development of a genetic test for breeders.