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Presumptive paroxysmal dyskinesia in 41 dogs: is the diet change enough?
Henry Mendo Reyes1, Greta Galli1, Evelina Burbaitè1,2
1Neurology Division, San Marco Veterinary Clinic and Laboratory, Veggiano, Italy.
Background:
Paroxysmal dyskinesia (PD) in dogs comprises episodic, involuntary, nonepileptic movement disorders. Recent evidence suggests that PD may be associated with gluten sensitivity, paralleling human gluten-related neurologic syndromes.
Hypothesis/Objectives:
Characterize clinical features, gastrointestinal comorbidities, gluten-related serology, and response to a gluten-free diet (GFD) in dogs with presumptive gluten-sensitive PD. We hypothesized that dietary modification would decrease episode frequency, particularly in dogs with gastrointestinal signs, seropositivity for anti-gliadin and anti-transglutaminase-2 immunoglobulin A antibodies or both.
Animals:
Forty-one client-owned dogs with presumptive PD.
Methods:
Retrospective review of dogs diagnosed with presumptive PD at a single institution between 2019 and 2023. Inclusion criteria included > 1 episode, video-documented episodes, normal interictal neurologic examination, serum gluten-related antibody titers, and ≥ 6 months of follow-up after transition to GFD.
Results:
Gastrointestinal signs were reported in 33/41 (80.5%) dogs; 21/41 (51.2%) had at least 1 positive antibody titer. After dietary change, 24/41 (58.5%) dogs achieved complete resolution, 15/41 (36.6%) showed partial response, and 2/41 (4.9%) remained unchanged, regardless of antibody status. All owners reported gastrointestinal improvement. Nine dogs relapsed after initial response: 6 after gluten ingestion, 1 associated with stress, and 2 despite strict GFD. Response to GFD was not significantly associated with gastrointestinal signs or antibody status.
Conclusions And Clinical Importance:
Although dietary response was not significantly associated with antibody status or gastrointestinal signs, GFD led to substantial clinical improvement in most dogs with PD across multiple breeds, supporting a potential link between gluten sensitivity and PD, and a possible role of the gut-brain axis in disease pathogenesis.
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