Anna Dellwig, Nina Meyerhoff, Casey B Rogers, Holger A Volk, Andrea Tipold, Jasmin N Nessler
Seventy dogs met inclusion criteria. Suspected idiopathic forms predominated (61.4%), followed by genetic (suspected and confirmed; 22.9%) and gluten-sensitive (12.9%) forms, whereas reactive and structural causes were rare (1.4% each). Across groups, dystonia with concurrent tremor and episodic gait or postural abnormalities represented the dominant clinical topographical distribution. Neither age at onset nor topographical distribution of signs reliably differentiated etiologies. Body weight differed significantly between groups.
INTRODUCTION: Canine paroxysmal dyskinesia is an episodic movement disorder characterized by transient dystonia, dyskinesia and tremor in dogs with preserved consciousness, yet its differentiation from focal epilepsy remains challenging and a structured diagnostic framework comparable to that used in epilepsy is lacking.
METHODS: This retrospective, single-center study evaluated the distribution of etiologies in dogs presenting with paroxysmal dyskinesia to a tertiary referral center between 2012 and 2023. Medical records were systematically screened, and dogs were included if episodic abnormal movements fulfilled established clinical criteria while cases with impaired consciousness, postictal signs or insufficient documentation were excluded. Diagnostic data comprised history, neurological examination, laboratory testing, serology for gluten sensitivity, advanced imaging and cerebrospinal fluid analysis when available, and cases were categorized into suspected idiopathic, genetic (suspected and confirmed), gluten-sensitive, reactive or structural groups.
RESULTS: Seventy dogs met inclusion criteria. Suspected idiopathic forms predominated (61.4%), followed by genetic (suspected and confirmed; 22.9%) and gluten-sensitive (12.9%) forms, whereas reactive and structural causes were rare (1.4% each). Across groups, dystonia with concurrent tremor and episodic gait or postural abnormalities represented the dominant clinical topographical distribution. Neither age at onset nor topographical distribution of signs reliably differentiated etiologies. Body weight differed significantly between groups.
DISCUSSION: These findings demonstrate that most cases represent diagnoses of exclusion and that clinical presentation alone is insufficient for etiological classification, underscoring the need for a standardized, tiered diagnostic strategy integrating basic laboratory evaluation, targeted genetic testing in predisposed breeds and early assessment for gluten sensitivity, with advanced diagnostics reserved for selected cases.