Presumed acquired neuromyotonia of unknown cause in a cat with hyperthyroidism

A 16-year-old spayed female domestic shorthair cat with methimazole-treated hyperthyroidism presented with a chronic progressive history of a stiff gait progressing to recumbency. A neurological examination revealed continuous excessive muscle tone with myokymia, which exacerbated with exercise and persisted during general anaesthesia. An electromyographic study revealed myokymic discharges in all tested muscles, as well as complex repetitive discharges, fibrillation potentials and positive sharp waves. Blood tests, urinalysis and abdominal ultrasound did not reveal significant abnormalities. A histological examination of a muscle biopsy showed no specific abnormalities. A clinical diagnosis of acquired neuromyotonia with myokymia was formulated. Phenytoin treatment resulted in temporary improvement, but excessive muscle tone recurred resulting in episodes of dyspnoea. Euthanasia was elected 3 weeks after presentation.

To the best of the authors' knowledge, this is the second report of an acquired neuromyotonia in a cat. In contrast with the previous report, treatment with phenytoin resulted in only partial and temporary improvement of signs. Subsequent progression of the disease, including signs of dyspnoea and dysuria, led to the decision to euthanase the cat. In humans, acquired neuromyotonia (Isaacs syndrome) is usually due to an autoimmune response to proteins associated with voltage-gated potassium channels. More rarely, it has also been described in humans with thyroid disorders. A link with methimazole treatment or hyperthyroidism in the cat reported here could not be excluded.