A 9.5 yo MN Terrier Cross presented for dental evaluation and at this time the owner reported intermittent episodes of shaking and being unsteady on his feet for around 12 months, approximately every 2 months. The episodes were usually very short but had been progressive and more recently had lasted up to 2 minutes. In between episodes the dog was completely normal, and no other clinical signs were reported. A video of one of these episodes was provided.
General blood tests including haematology and biochemistry were performed and identified a mild increase in ALkP only. Abdominal imaging was performed as a result of this finding and found normal hepatic architecture, and only a small nodule was seen within the splenic parenchyma. Samples were collected which were consistent with a vacuolar hepatopathy and mild extramedullary haematopoiesis respectively.
The primary care vet contacted VetCT to discuss the presentation and the hepatic findings with our Internal Medicine Team.
- How would you describe these episodes?
- What are your top three differentials?
The video was reviewed by our Neurology Team, and showed an episode characterised by a sustained involuntary muscle contraction, mild head shaking and flexion of the right thoracic limb on standing position with maintenance of normal mentation. While attempting to walk, generalised stiffness and intermittently unsteady gait is seen As the primary care vet had reported, there was no ptyalism, but a few drops of saliva were noted likely reflecting muscle discomfort associated with the sustained contraction or stress. There was also no loss of control of urinary or defaecatory function.
Within the veterinary literature, paroxysmal dyskinesia is poorly characterized, and whilst particular syndromes in specific breeds are suspected or identified to be genetic, or appear to be related to gluten intolerance, it remains important to ensure there is no obvious extra-cranial metabolic or endocrine causes. This may well be particularly for cases that fall outside those recognised breed-related conditions, or that display an older onset of clinical signs, as for this case. Importantly, other clinical presentations might mimic the findings of paroxysmal dyskinesia. A minimum database of haematology, serum biochemistry (including ionized calcium ideally), and urinalysis is therefore reasonable.
In this case the main finding in preliminary testing was a mild hepatopathy, that on sampling of the liver was compatible with a vacuolar hepatopathy. This was considered most likely incidental given a lack of other clinical signs. However, consideration was given to evaluating blood pressure and potentially testing for hypercortisolaemia in case transient ischaemic attacks secondary to hypertension or minor embolic events due to hypercoaguability were contributing factors.
Similar to this case, other specific testing for individual metabolic conditions or endocrinopathies might be indicated if there is a significant index of suspicion based upon the individual patient and diagnostic test results (B12 concentrations, basal cortisol, D-Dimers and FDPs).
An MRI scan and CSF analysis can help to further exclude structural abnormalities.
How do we manage paroxysmal dyskinesia?
Border Terrier’s have been identified to have gluten intolerance associated with paroxysmal dyskinesia and an antibody test can be undertaken, and/or a treatment trial with a gluten free diet can resolve their clinical presentation. A dietary trial can also be tried for other breeds, but largely response to gluten in other breeds or cross-breeds is not seen. Cavalier King Charles Spaniels with episodic falling syndrome, a specific paroxysmal hypertonicity disorder in this breed, respond to acetazolamide. The natural history of the disorder in all other dogs is that episodes are generally self-limiting and spontaneous remission can be seen in 30-40% of cases. Dogs with cluster events might show less likelihood of remission or improvement.
However beyond this, and where no underlying cause is seen that can be concurrently managed, no specific treatment has been shown to impact the clinical signs. Response to anti-epileptic therapies is generally not seen, but can be tried for those patients with frequent or more progressive episodes.
As Rhaja was a terrier of unknown mix, he was trialled on a gluten free diet, but after several weeks continued to have intermittent episodes with no further progression or other clinical signs. His owners elected not to pursue further diagnostic testing.
- Lowrie and Garosi. (2017) Classification of involuntary movements in dogs: Paroxysmal dyskinesias. The Veterinary Journal 220 (2017) 65–71
- Manso-Calderon, R (2019) The spectrum of paroxysmal dyskinesia. Future Neurology. 14(3), FNL26
- Blakeley and Jankovic (2002). Secondary Paroxysmal Dyskinesia. Movement Disorders. Vol. 17, No. 4, 2002, pp. 726–734