Paroxysmal Dyskinesia in Norwich Terrier Dogs

Abstract

Background: Episodic muscular hypertonicity in Norwich terrier dogs was first reported in a brief communication in 1984. Since then, the condition has remained poorly characterized.

Objectives: The aims of this study were to characterize the phenomenology, clinical course, and family history of paroxysmal dyskinesia in the Norwich terrier and to estimate its prevalence in the United Kingdom.

Methods: The owners of Norwich terrier dogs born since January 1, 2000 were invited to complete a specifically designed questionnaire aimed at identifying affected and unaffected dogs and investigating the clinical characteristics of this paroxysmal dyskinesia. Pedigrees were collected and reviewed.

Results: The questionnaire was returned for 198 Norwich terrier dogs. Of these, 26 (13%) were classified as affected by paroxysmal dyskinesia after revision of the questionnaires and after obtaining videos of the episodes, veterinary medical records, and telephone interviews with the owners. All dogs were neurologically normal between episodes. No significant abnormalities were detected on diagnostic investigations. Mean age at the first episode was 3 years. The episodes were characterized by sustained muscular hypertonicity in the pelvic limbs, lumbar region, and thoracic limbs, impairing posture and locomotion without loss of consciousness. Episode frequency varied both between and within individuals. Stress, anxiety, excitement, and variation in daily routine were recognized as episode triggers in 13 dogs. Episode duration generally was from 2 to 5 minutes (range, from < 2 to 30 minutes). The majority of affected dogs were related.

Conclusions: Paroxysmal dyskinesia segregates in an extended pedigree of Norwich terrier dogs and thus is potentially an inherited disorder in this breed.

Keywords: Norwich terrier dogs; genetic; movement disorder; paroxysmal dyskinesia.

Figure 1

Extended pedigree containing UK Kennel Club‐registered Norwich terrier dogs. Affected cases are marked in solid black, individuals of unknown phenotype are indicated with question marks, and 3 clinically unaffected dogs are marked with gray dots. All but 1 of the affected cases are connected through the extended pedigree, potentially suggesting an inherited component to the disease. The separate family of 3 could not be linked to the main pedigree with the 5‐generation pedigree data available for each individual.