Long-term nutritional management of an obese German Spitz with paroxysmal dyskinesia, calcium oxalate urolithiasis, and suspected pancreatitis—A case report

**Background:** Canine paroxysmal dyskinesia (PD) is a movement disorder characterized by recurrent episodes of abnormal, involuntary, self-limiting movements with preserved consciousness. While some case reports have shown clinical improvement in Border Terriers fed gluten-free diets, long-term nutritional follow-up has never been reported. This case describes the nutritional management of a dog with multiple concurrent diseases: PD, obesity, calcium oxalate (CaOx) urolithiasis, and suspected pancreatitis.

**Methods:** A 9-year-old, male entire, German Spitz (initial body weight 4.4 kg, BCS 8/9, estimated ideal body weight 3.4 kg) was referred for nutritional management after CaOx urolith removal and suspected pancreatitis. The dog had a history of neurological episodes since 3 months of age, initially misdiagnosed as epileptic seizures and treated with phenobarbital (7 mg/kg iBW BID) and potassium bromide (23 mg/kg iBW BID), with 2 years of episode-free control. A weight loss program was initiated using a low-fat, low-RSS diet (diet 3a; 2.4 g fat/kg^0.75, 70 kcal x kg iBW^0.75). After 4 months, the dog weighed 3.5 kg (BCS 5/9) with a mean weight loss rate of 1.72% BW per week. Ten months later, neurological episodes increased to 3x/week and were unresponsive to increased potassium bromide (23 mg/kg iBW morning, 46 mg/kg iBW evening). PD was diagnosed based on video evaluation showing dystonia-like movements during rest, preserved consciousness, episode duration of 1-3 minutes, and absence of post-ictal phase. A dietary trial with a commercial hypoallergenic, gluten-free, hydrolyzed protein diet with low RSS (diet 4a; 3.3 g fat/kg^0.75) was initiated. Anti-seizure drugs were gradually reduced by 25% per month after 3.5 months.

**Key Results:** During the first 3.5 months of the gluten-free diet trial, only 4 PD episodes occurred, all related to food indiscretion (2 from commercial dog treats containing gluten, 2 from accidental ice cream intake). During the 3-month ASD reduction period, the dog experienced 2 PD episodes (3 days after first reduction and 1 day after tapering). The dog remained episode-free for 4 months. A change to another gluten-free diet with higher fat content (diet 5; 3.5 g fat/kg^0.75) led to vomiting and a PD episode. Upon resuming the previous diet (diet 4b; 3.1 g fat/kg^0.75), the dog clinically improved with no further clinical signs for 5 months. At Month 37, the owner reported short-lived episodes but did not record dates.

**Clinical Implications:** This is the first reported case of PD in a German Spitz and the first with complete nutritional history and long-term follow-up. The case highlights the importance of individualized nutritional management for patients with multiple comorbidities. The clinical improvement on a gluten-free, hypoallergenic diet and deterioration after dietary challenges (gluten-containing treats, higher-fat diet) supports a dietary association with PD, though a causal relationship with gluten specifically could not be confirmed. The increase in fat intake from 3.1 to 3.5 g/kg^0.75 may have triggered vomiting and stress-induced neurological signs. The case also demonstrates the risk of misdiagnosing PD as epilepsy, leading to long-term ASD therapy that may increase pancreatitis risk. Key limitations include the lack of serological testing for anti-gliadin and anti-transglutaminase A2 antibodies, absence of a formal challenge phase, and reliance on owner-reported diaries.