Hypothyroid-associated neurologic signs in dogs - Veterinary Medicine
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Hypothyroid-associated neurologic signs in dogs
Explore three cases of dogs with neurologic signs that were found to have hypothyroidism, and see when you should test for this disease in your patients with neuromuscular signs.


VETERINARY MEDICINE


Peripheral neuropathies

Involvement of the neuromuscular system was evident in the dog in case 1, which displayed decreased patellar reflexes, a short-strided gait, and hypotonia. In general, large-breed dogs affected by peripheral neuropathies develop pelvic limb paresis progressing to tetraparesis or paralysis over the course of weeks to months.8,9

The dogs in cases 1 and 3 had a more acute onset of paresis, and their clinical progressions were much shorter. This could reflect their underlying diseases as well as the prompt recognition of their diagnoses and treatments. Affected dogs with polyneuropathies secondary to hypothyroidism typically show initial signs of improvement in 24 hours and complete resolution by one to two months.10-12

Cranial nerve involvement

Facial paralysis, as seen in the dog in case 2, has been frequently reported in hypothyroid dogs13-17 and in a horse.18 The parasympathetic component of cranial nerve VII may also be affected.

Theories behind the involvement of cranial nerves in hypothyroid dogs include myxedematous deposits surrounding the nerve and decreased perfusion to the inner ear.15 Decreased axonal transport due to lack of T4 hormone-induced adenosine triphosphatase (ATPase)9,11 will lead to nerve degeneration. Thyroid hormone also influences the expression of proteins such as dynein and tubulin that are needed for microtubule structure and transport function.13 As in the dog in case 2, clinical signs have been shown to resolve with supplementation with levothyroxine.

Ischemic injury

The dog in case 3 was presented with acute paradoxical vestibular disease, which is a manifestation of a central vestibular disorder. Central vestibular dysfunction and altered mentation are frequently attributed to ischemic infarction of the brain caused by atherosclerosis and hypercoagulability.1,5,7,10-15 Other causes of ischemic infarction confirmed on histologic examination include septic, neoplastic, or parasitic emboli and cardiac thromboembolism.

A previous MRI study reported that 50% of dogs with brain infarction had an underlying systemic disease, the most common of which were hyperadrenocorticism, chronic renal failure, hypothyroidism, and hypertension.17 In hypothyroid dogs, the accumulation of plasma lipids and cholesterol can lead to atherosclerosis because thyroid hormone is not present to stimulate uptake of lipoproteins in tissues.3

Additionally, an increase in cholesterol concentrations increases blood viscosity and the risk of thromboembolic events. Thromboemboli have been reported in hypothyroid dogs at necropsy and with abdominal ultrasonography and can lead to multifocal areas of hypoxia and necrosis of the brain and muscles.3-6,8 The reports of atherosclerotic plaques seen at necropsy4 support the hypothesis that neurologic deficits are related to an ischemic infarction in the brain.

Dogs with central vestibular disease secondary to hypothyroidism may display abnormal nystagmus, a head tilt contralateral to the observed postural reaction deficits, paresis, and ataxia. In affected dogs, central vestibular disease is related to ischemic infarction as detected by MRI.19,20


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Source: VETERINARY MEDICINE,
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