Fly-catching syndrome responsive to a gluten-free diet in a French Bulldog.

OBJECTIVE: Fly-catching syndrome (FCS) is a rare condition typically characterized by episodes during which affected dogs bite or lick the air and jump for no apparent reason. Among veterinary literature, obsessive-compulsive disorders, focal epileptic seizures, and underlying gastrointestinal diseases were considered the most likely triggering causes. Recently, gluten-sensitive dyskinesia has been described in dogs, but it has never been reported to be associated to FCS. ANIMAL: A 6-year-old male French Bulldog. CLINICAL PRESENTATION, PROGRESSION, AND PROCEDURES: The dog was presented for a 2-month history of episodes characterized by sudden onset of jumping while trying to catch something in the air without impaired consciousness or autonomic signs. The episodes could be interrupted by the owner and lasted several minutes. The dog suffered from chronic gastrointestinal signs. The neurological examination was within normal limits except for the episodes suggestive of FCS during the consultation. The serological test for anti-gliadin immunoglobulin G (AG IgG) and anti-transglutaminase-2 immunoglobulin A (ATG-2 IgA) antibodies resulted above the reference range (3.092 and 0.929, respectively; normal range < 0.6). TREATMENT AND OUTCOME: An exclusively gluten-free diet was started. Complete resolution of the episodes was reported during a 3-month follow-up. CLINICAL RELEVANCE: To the authors' knowledge, this is the first report of FCS associated to positive AG IgG and ATG-2 IgA antibodies responsive to a gluten-free diet. The typical manifestation of the episodes and response to diet support the hypothesis that FCS may be associated to gastrointestinal disorders. However, more studies are needed in order to confirm this hypothesis.

Serum anti-GM2 and anti-GalNAc-GD1a ganglioside IgG antibodies are biomarkers for immune-mediated polyneuropathies in cats.

Recent work identified anti-GM2 and anti-GalNAc-GD1a IgG ganglioside antibodies as biomarkers in dogs clinically diagnosed with acute canine polyradiculoneuritis, in turn considered a canine equivalent of Guillain-Barré syndrome. This study aims to investigate the serum prevalence of similar antibodies in cats clinically diagnosed with immune-mediated polyneuropathies. The sera from 41 cats clinically diagnosed with immune-mediated polyneuropathies (IPN), 9 cats with other neurological or neuromuscular disorders (ONM) and 46 neurologically normal cats (CTRL) were examined for the presence of IgG antibodies against glycolipids GM1, GM2, GD1a, GD1b, GalNAc-GD1a, GA1, SGPG, LM1, galactocerebroside and sulphatide. A total of 29/41 IPN-cats had either anti-GM2 or anti-GalNAc-GD1a IgG antibodies, with 24/29 cats having both. Direct comparison of anti-GM2 (sensitivity: 70.7%; specificity: 78.2%) and anti-GalNAc-GD1a (sensitivity: 70.7%; specificity: 70.9%) antibodies narrowly showed anti-GM2 IgG antibodies to be the better marker for identifying IPN-cats when compared to the combined ONM and CTRL groups (P = .049). Anti-GA1 and/or anti-sulphatide IgG antibodies were ubiquitously present across all sample groups, whereas antibodies against GM1, GD1a, GD1b, SGPG, LM1 and galactocerebroside were overall only rarely observed. Anti-GM2 and anti-GalNAc-GD1a IgG antibodies may serve as serum biomarkers for immune-mediated polyneuropathies in cats, as previously observed in dogs and humans.

Suspected Pituitary Apoplexy: Clinical Presentation, Diagnostic Imaging Findings and Outcome in 19 Dogs.

In human medicine, pituitary apoplexy (PA) is a clinical syndrome characterised by the sudden onset of neurological signs because of haemorrhage or infarction occurring within a normal or tumoral pituitary gland. The diagnosis is usually performed combining neurological signs and imaging findings. The aim of the present study is to describe the abnormal neurological signs, the diagnostic imaging findings, based on Computed Tomography (CT) and/or Magnetic Resonance Imaging (MRI), and the outcome in a population of dogs with suspected PA. Clinical cases were retrospectively reviewed. Nineteen cases of suspected PA were included. The majority of dogs showed behavioural abnormalities (11/19). Neurological signs more frequently identified were obtundation (7/19), vestibular signs (7/19) and epileptic seizures (6/19). The onset of neurological signs was per-acute in 14 out of 19 cases. Data regarding CT and MRI were available in 18 and 9 cases, respectively. Neurological signs resolved in less than 24 h in seven patients. The short-term prognosis was defined as favourable in the majority of our study population. The median survival time was of 7 months from the time of PA diagnosis. This is the first description of neurological signs, imaging findings and outcome in a large group of dogs with PA.

Neurological abnormalities in 97 dogs with detectable pituitary masses.

Background: Pituitary tumours are common neoplasms of the sellar region in small animals. However, detailed information regarding the spectrum and severity of possible neurological signs are lacking. Objective: To retrospectively describe the neurological abnormalities in a population of dogs with a detectable pituitary mass (DPM) and relate them with the size of the mass and magnetic resonance imaging (MRI) signs of brain compression (BC). Client-owned dogs were included in the study if they had MRI showing a DPM and a detailed neurological examination. The neurological signs were evaluated in relation to the pituitary height/brain ratio (P:B ratio) and the presence/absence of brain compression. Results: Ninety-seven dogs were enrolled. Besides abnormal mentation and behaviour (77%), gait (61%) and cranial nerve abnormalities (44%), other unreported neurological signs observed included postural abnormalities (21%), pain and/or hyperesthesia (25%) and abnormal postural and proprioceptive reactions (49%). The majority of dogs with DPM had signs of BC. The presence of a high pituitary height/brain area and BC represented a risk factor for developing mental status abnormalities. Conclusion: Neurological signs recorded in DPM-affected dogs include not only the typical forebrain signs but also gait disturbances and hyperesthesia. Neurological signs are positively associated with increased P:B ratio and MRI signs of brain compression.

Structural, functional, and behavioral insights of dopamine dysfunction revealed by a deletion in SLC6A3.

The human dopamine (DA) transporter (hDAT) mediates clearance of DA. Genetic variants in hDAT have been associated with DA dysfunction, a complication associated with several brain disorders, including autism spectrum disorder (ASD). Here, we investigated the structural and behavioral bases of an ASD-associated in-frame deletion in hDAT at N336 (∆N336). We uncovered that the deletion promoted a previously unobserved conformation of the intracellular gate of the transporter, likely representing the rate-limiting step of the transport process. It is defined by a "half-open and inward-facing" state (HOIF) of the intracellular gate that is stabilized by a network of interactions conserved phylogenetically, as we demonstrated in hDAT by Rosetta molecular modeling and fine-grained simulations, as well as in its bacterial homolog leucine transporter by electron paramagnetic resonance analysis and X-ray crystallography. The stabilization of the HOIF state is associated both with DA dysfunctions demonstrated in isolated brains of Drosophila melanogaster expressing hDAT ∆N336 and with abnormal behaviors observed at high-time resolution. These flies display increased fear, impaired social interactions, and locomotion traits we associate with DA dysfunction and the HOIF state. Together, our results describe how a genetic variation causes DA dysfunction and abnormal behaviors by stabilizing a HOIF state of the transporter.

Atypical dopamine efflux caused by 3,4-methylenedioxypyrovalerone (MDPV) via the human dopamine transporter.

Synthetic cathinones are similar in chemical structure to amphetamines, and their behavioral effects are associated with enhanced dopaminergic signaling. The past ten years of research on the common constituent of bath salts, MDPV (the synthetic cathinone 3,4-methylenedioxypyrovalerone), has aided the understanding of how synthetic cathinones act at the dopamine (DA) transporter (DAT). Several groups have described the ability of MDPV to block the DAT with high-affinity. In this study, we demonstrate for the first time a new mode of action of MDPV, namely its ability to promote DAT-mediated DA efflux. Using single cell amperometric assays, we determined that low concentrations of MDPV (1nM) can cause reverse transport of DA via DAT. Notably, administration of MDPV leads to hyperlocomotion in Drosophila melanogaster. These data describe further how MDPV acts at the DAT, possibly paving the way for novel treatment strategies for individuals who abuse bath salts.