Despite appropriate antiepileptic drug treatment, approximately one-third of humans and dogs with epilepsy continue experiencing seizures, emphasising the importance for new treatment strategies to improve the quality of life of people or dogs with epilepsy. A 6-month prospective, randomised, double-blinded, placebo-controlled cross-over dietary trial was designed to compare a ketogenic medium-chain TAG diet (MCTD) with a standardised placebo diet in chronically antiepileptic drug-treated dogs with idiopathic epilepsy. Dogs were fed either MCTD or placebo diet for 3 months followed by a subsequent respective switch of diet for a further 3 months. Seizure frequency, clinical and laboratory data were collected and evaluated for twenty-one dogs completing the study. Seizure frequency was significantly lower when dogs were fed the MCTD (2·31/month, 0–9·89/month) in comparison with the placebo diet (2·67/month, 0·33–22·92/month, P=0·020); three dogs achieved seizure freedom, seven additional dogs had ≥50 % reduction in seizure frequency, five had an overall <50 % reduction in seizures (38·87 %, 35·68–43·27 %) and six showed no response. Seizure day frequency were also significantly lower when dogs were fed the MCTD (1·63/month, 0–7·58/month) in comparison with the placebo diet (1·69/month, 0·33–13·82/month, P=0·022). Consumption of the MCTD also resulted in significant elevation of blood β-hydroxybutyrate concentrations in comparison with placebo diet (0·041 (sd 0·004) v. 0·031 (sd 0·016) mmol/l, P=0·028). There were no significant changes in serum concentrations of glucose (P=0·903), phenobarbital (P=0·422), potassium bromide (P=0·404) and weight (P=0·300) between diet groups. In conclusion, the data show antiepileptic properties associated with ketogenic diets and provide evidence for the efficacy of the MCTD used in this study as a therapeutic option for epilepsy treatment.

Background: Adult dogs with neosporosis can develop a variety of neurologic signs. No area of predilection within the nervous system so far has been identified in adult dogs. Objectives: To document neosporosis as a cause of progressive cerebellar ataxia and cerebellar atrophy in dogs. Animals: Seven client‐owned dogs. Methods: Retrospective, descriptive study. Results: Age at diagnosis ranged from 1 year 6 months to 9 years 11 months. Neuroanatomic localization indicated cerebellar and brainstem disease in 6 dogs and a central vestibular lesion in 1 dog. In all 7 dogs, there was moderate to marked bilaterally symmetrical cerebellar atrophy, with the atrophied cerebellum being surrounded by a region of T2‐weighted hyperintense and T1‐weighted hypointense signal. Cerebrospinal fluid (CSF) analysis in all but 1 dog showed mononuclear pleocytosis and high protein concentration. Polymerase chain reaction testing for Neospora caninum performed on the CSF was positive in 4/5 dogs tested and there was a high titer of serum antibodies to N. caninum (≥ 1 : 800) in all 6 dogs tested. Postmortem examination in 1 dog confirmed cerebellar atrophy and multifocal nonsuppurative encephalitis with areas of malacia and leptomeningitis. All of the remaining 6 dogs were treated with some combination of clindamycin, trimethoprim, sulfadiazine, and pyrimethamine. Two dogs were euthanized because of deterioration or relapse of neurologic signs, but treatment of the remaining 4 dogs resulted in improvement (3 dogs) or resolution (1 dog) of neurologic signs. Conclusions and Clinical importance: Neosporosis is an important cause of progressive cerebellar ataxia and cerebellar atrophy in adult dogs.

No abstract

Sustained clinical improvement can be achieved in hydrocephalus with no active underlying cause by use of ventriculoperitoneal shunting.

No abstract

Raised IL-6 but not CRP predicted cognitive decline in this population Inflammatory changes associated with cognitive decline may be specific to particular causal pathways.

No abstract

This study investigated the cross sectional area (CSA) and fat infiltration of the epaxial muscles in Dachshunds with compressive spinal cord lesions due to intervertebral disc herniation (IVDH) and in dogs with non-compressive spinal cord lesions with fibrocartilaginous embolism (FCE). The CSA and fat infiltration of the multifidi and longissimus dorsi muscles were determined from T1 weighted magnetic resonance images. Difference in CSA and fat infiltration between the lesion- and non-lesion side in the Dachshunds was assessed using mixed model analysis. Difference in CSA and fat infiltration between Dachshunds and FCE dogs was analysed with independent sample t-tests. There was no difference in CSA or fat infiltration between sides in the Dachshunds. FCE dogs had greater CSA (multifidus P = 0.036, longissimus P < 0.001) and less fat infiltration compared to Dachshunds (longissimus P = 0.017). Duration of neurological deficits, age, body size and conformation are likely to have influenced the difference between the groups.