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.


Initial diagnostic tests

Table 5: Case 3 pituitary-thyroid axis testing results
The results of a CBC were normal. A serum chemistry profile revealed an elevated cholesterol concentration (1,028 mg/dl; reference range = 110 to 320 mg/dl) on a fasted sample. A pituitary-thyroid axis test was performed given the suspicion of infarction and the hypercholesterolemia (Table 5). The total T4 and free T4 concentrations were decreased, and the TSH concentration was increased, consistent with primary hypothyroidism.

Figure 1. A transverse T2-weighed MRI at the level of the cerebellum from a rottweiler with an acute onset of central vestibular dysfunction reveals a single, well-demarcated, hyperintense wedge-shaped lesion in the left cerebellar hemisphere (arrow) consistent with an ischemic infarction involving the rostral cerebellar artery.
MRI of the brain revealed a well-defined, wedge-shaped lesion in the left cerebellar hemisphere that was hyperintense on T2-weighted and T2-weighted fluid-attenuated inversion recovery sequences (Figure 1). An additional lesion with similar MRI characteristics was noted in the left thalamus. Cerebrospinal fluid analysis was declined by the owner.

Based on the acute onset of clinical signs and MRI findings, an ischemic infarction of the cerebellum and thalamus was suspected, although inflammation or a neoplastic lesion could not be excluded. Given the results of thyroid function testing, the infarction was likely secondary to hypothyroidism.

Treatment and follow-up

The dog was treated with levothyroxine. Over the course of five days, the neurologic signs improved, supporting the hypothesis that the observed lesions were secondary to vascular compromise.

The patient was rechecked in two weeks, and its total T4 concentration was elevated at 5 g/dl (reference range = 1 to 4 g/dl); however, the clinical signs had resolved, and the dose was not altered.

Three months later, full blood work was performed—the serum cholesterol concentration had decreased to 279 mg/dl, and the total thyroid concentration was normal at 3.5 g/dl. No abnormalities were detected on the CBC or serum chemistry profile.


These three cases illustrate variations in neuromuscular dysfunction associated with a hypothyroid state. Although a causal relationship between the neurologic deficits and hypothyroidism could not be definitively established in any of the cases, a strong presumptive diagnosis was suggested by establishing the existence of a hypothyroid state, excluding other etiologies to explain the neurologic deficits, and achieving resolution of the deficits with supplementation with levothyroxine. All dogs had clinicopathologic testing results consistent with hypothyroidism.

Although the dog in case 1 showed initial improvement with supplementation but ultimately developed progression of its disease, the other two cases showed full resolution of clinical signs when T4 supplementation was initiated. In further support of this argument, the dog in case 2 experienced recurrence of neurologic signs after decreasing supplementation with levothyroxine and resolution of signs upon increasing the dosage of T4 supplementation again. However, we cannot attribute the improvement of the dog in case 3 to T4 supplementation alone when considering the tendency for cerebrovascular accidents to be self-limiting and resolve with or without treatment.


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