Epileptic seizures triggered by eating in dogs.

BACKGROUND: Seizures triggered by eating (STE) behavior are very rare in humans and have not been documented previously in dogs. OBJECTIVES: To document the occurrence of STE in dogs and describe their clinical features. ANIMALS: Ten client-owned dogs with STE diagnosed at 5 European referral centers. METHODS: A call for suspected cases of STE was made online. This call was followed by a retrospective review of medical records, combined with a questionnaire to be completed by both the owner and the board-certified neurologist who made the diagnosis. Cases were included if >50% of the seizures that occurred were related to eating and if a minimum diagnostic evaluation for seizures had been performed. RESULTS: Four cases only had STE and 6 cases had both STE and spontaneous seizures. Four of the dogs were retrievers. The most common seizure type was focal epileptic seizures evolving to become generalized. Nine dogs were diagnosed with idiopathic epilepsy. One dog had a presumptive diagnosis of glioma involving the margins of the parietal, temporal, and frontal cortex (the perisylvian region), an area known to have a key role in eating-associated epilepsy in people. Treatment strategies included a combination of pharmacological management and eating habit changes. CONCLUSIONS AND CLINICAL IMPORTANCE: We have identified a form of reflex epilepsy in dogs, with STE behavior. Further studies are warranted to improve the characterization and management of STE.

Features of stimulus-specific seizures in dogs with reflex epilepsy: 43 cases (2000-2014).

OBJECTIVE To describe the occurrence and management of reflex epilepsy (ie, seizure activity triggered by exposure to specific locations or situations) in dogs. DESIGN Retrospective case series. ANIMALS 43 client-owned dogs. PROCEDURES Discussions by veterinarians participating in the Veterinary Information Network online community for the years 2000 through 2014 were reviewed to identify dogs with a diagnosis of reflex epilepsy and seizure activity in response to stimuli. History, signalment (including age at onset), the specific stimulus or stimuli that provoked seizures, treatments, and any concurrent neurologic diagnoses were recorded. RESULTS A variety of breeds were affected. Median age at onset was 5 years (range, 3 months to 11 years). Reflex seizures were reported as being repeatedly triggered by visits to a veterinary clinic (35/43 dogs), grooming facility (24/43 dogs), or boarding facility (13/43 dogs) and, less commonly, by other situations (eg, pet store or car ride). Over half of the dogs (24/43) had multiple triggers. Eight (19%) dogs had seizures at other times that were not induced by location or a specific situation. A variety of sedatives and maintenance antiepileptic drugs administered to affected dogs failed to prevent the stimulus-specific seizure activity. CONCLUSIONS AND CLINICAL RELEVANCE Results of the present study suggested that seizures provoked by specific situations or locations occur in dogs with reflex epilepsy and that common triggers were visits to veterinary and grooming facilities. Further studies are necessary to elucidate the characteristics of reflex epilepsy in dogs and to determine the most effective means to manage these patients.

Audiogenic reflex seizures in cats.

OBJECTIVES: This study aimed to characterise feline audiogenic reflex seizures (FARS). METHODS: An online questionnaire was developed to capture information from owners with cats suffering from FARS. This was collated with the medical records from the primary veterinarian. Ninety-six cats were included. RESULTS: Myoclonic seizures were one of the cardinal signs of this syndrome (90/96), frequently occurring prior to generalised tonic-clonic seizures (GTCSs) in this population. Other features include a late onset (median 15 years) and absence seizures (6/96), with most seizures triggered by high-frequency sounds amid occasional spontaneous seizures (up to 20%). Half the population (48/96) had hearing impairment or were deaf. One-third of cats (35/96) had concurrent diseases, most likely reflecting the age distribution. Birmans were strongly represented (30/96). Levetiracetam gave good seizure control. The course of the epilepsy was non-progressive in the majority (68/96), with an improvement over time in some (23/96). Only 33/96 and 11/90 owners, respectively, felt the GTCSs and myoclonic seizures affected their cat's quality of life (QoL). Despite this, many owners (50/96) reported a slow decline in their cat's health, becoming less responsive (43/50), not jumping (41/50), becoming uncoordinated or weak in the pelvic limbs (24/50) and exhibiting dramatic weight loss (39/50). These signs were exclusively reported in cats experiencing seizures for >2 years, with 42/50 owners stating these signs affected their cat's QoL. CONCLUSIONS AND RELEVANCE: In gathering data on audiogenic seizures in cats, we have identified a new epilepsy syndrome named FARS with a geriatric onset. Further studies are warranted to investigate potential genetic predispositions to this condition.

Startle disease in Irish wolfhounds associated with a microdeletion in the glycine transporter GlyT2 gene.

Defects in glycinergic synaptic transmission in humans, cattle, and rodents result in an exaggerated startle reflex and hypertonia in response to either acoustic or tactile stimuli. Molecular genetic studies have determined that mutations in the genes encoding the postsynaptic glycine receptor (GlyR) α1 and ß subunits (GLRA1 and GLRB) and the presynaptic glycine transporter GlyT2 (SLC6A5) are the major cause of these disorders. Here, we report the first genetically confirmed canine cases of startle disease. A litter of seven Irish wolfhounds was identified in which two puppies developed muscle stiffness and tremor in response to handling. Although sequencing of GLRA1 and GLRB did not reveal any pathogenic mutations, analysis of SLC6A5 revealed a homozygous 4.2kb microdeletion encompassing exons 2 and 3 in both affected animals. This results in the loss of part of the large cytoplasmic N-terminus and all subsequent transmembrane domains due to a frameshift. This genetic lesion was confirmed by defining the deletion breakpoint, Southern blotting, and multiplex ligation-dependent probe amplification (MLPA). This analysis enabled the development of a rapid genotyping test that revealed heterozygosity for the deletion in the dam and sire and three other siblings, confirming recessive inheritance. Wider testing of related animals has identified a total of 13 carriers of the SLC6A5 deletion as well as non-carrier animals. These findings will inform future breeding strategies and enable a rational pharmacotherapy of this new canine disorder.