Hypothyroid-associated neurologic signs in dogs


See when you should test for this disease in your patients with neuromuscular signs.

Hypothyroidism is one of the most common endocrine diseases faced in small-animal medicine.1 While many practitioners are well-acquainted with the classic manifestations of canine hypothyroidism (weight gain, alopecia, lethargy, poor appetite), those involving the central nervous system, peripheral nervous system, and muscles are less well-recognized (Table 1).

Table 1: Clinical signs reflecting neurologic dysfunction in hypothyroid dogs

Although uncommon, it is important that practitioners be aware that dogs with hypothyroidism can present with neurologic deficits as the only clinical sign. Consequently, testing of the pituitary-thyroid axis may be indicated in certain clinical scenarios despite a lack of other clinical findings suggestive of hypothyroidism.

In this article, we use case examples to illustrate a variety of clinical scenarios in which neurologic signs and clinicopathologic test results should prompt the evaluation of the pituitary-thyroid axis and a possible diagnosis of hypothyroidism. Clinical evidence that prompted pituitary-thyroid axis testing in these patients included the diagnosis of syndromes that have been known to be associated with hypothyroidism such as facial nerve paralysis or vestibular disease, blood work abnormalities such as hypercholesterolemia, or the suspicion of an ischemic infarction. Although a causal relationship between hypothyroidism and neurologic deficits is difficult to establish, the response to therapy in these three cases helped support a diagnosis of neurologic dysfunction secondary to hypothyroidism.

Case 1: A recumbent Leonberger

A 4-year-old spayed female Leonberger was presented to the Matthew J. Ryan Veterinary Hospital at the University of Pennsylvania for evaluation of an acute onset of tetraparesis.


The owners reported that the dog had been normal until the previous morning, when it had experienced pelvic limb weakness, which progressed to recumbency over the course of several hours. Once recumbent, the dog had displayed an episode of rigidity involving all four limbs and diffuse muscle fasciculation. Before the onset of clinical signs, the dog had been healthy. The dog's vaccination status was up-to-date, and the dog was receiving heartworm and tick prevention. There was no history of exposure to toxins.

Physical and neurologic examinations

Physical examination abnormalities were limited to the nervous system. The dog's body condition score was ideal at 4/9.

On neurologic examination, the dog's mentation was normal. The dog was recumbent but able to walk when assisted. When prompted to walk, the dog displayed a short-strided gait in all four limbs and occasionally would knuckle onto the dorsum of the paw of the left thoracic limb. Postural reactions were abnormal in all four limbs. However, when the dog's weight was supported, the postural reactions were normal in all four limbs.

Patellar reflexes were decreased bilaterally and withdrawal reflexes were reduced in all four limbs. The muscular tone of the limbs was reduced, and no muscle atrophy was appreciated. The dog displayed a right-sided head tilt with normal physiologic nystagmus and no abnormal nystagmus. The menace response in the right eye was absent. Palpebral reflexes, pupil size, and pupillary light reflexes were normal. No other cranial nerve deficits were noted. The dog did not exhibit pain on palpation of the vertebral column or when moving the head and neck through normal range of movement.

Differential diagnoses

Based on the gait characteristics and decreased patellar and withdrawal reflexes, lack of menace response, and head tilt, a multifocal neuroanatomic diagnosis was made with likely involvement of the neuromuscular, visual, and vestibular systems, respectively. Differential diagnoses included ischemic infarction, inflammatory disease such as polymyositis, polyneuritis, immune-mediated disease such as myasthenia gravis, infectious diseases such as Toxoplasma or Neospora species infection, and neoplasia.

Initial diagnostic tests

A complete blood count (CBC) and serum chemistry profile were performed (Table 2). The CBC disclosed a normocytic, normochromic anemia; mild thrombocytopenia; and lymphopenia. The serum chemistry panel revealed elevated aspartate transaminase (AST) and alkaline phosphatase (ALP) activities and a fasting hypercholesterolemia. The creatinine kinase activity was markedly elevated.

Table 2: Case 1 CBC and serum chemistry profile abnormalities on preliminary examination

Administration of edrophonium hydrochloride did not result in clinical improvement. Because of the hypercholesterolemia, as well as the suspicion of infarction, pituitary-thyroid axis testing was performed (Table 2). The serum total thyroxine (T4) and free T4 concentrations were decreased, and the thyroid-stimulating hormone (TSH) concentration was increased. Since less than 5% of euthyroid-sick dogs will have an elevated TSH concentration, the results of thyroid testing in this dog were strongly consistent with primary hypothyroidism.2 Imaging of the brain to investigate the cause of the menace deficit and head tilt was not pursued based on the owner's financial constraints.

Despite the lack of improvement in strength after administration of edrophonium, titers for autoantibodies directed against the acetylcholine receptor (AchR) were assessed and found to be negative, excluding myasthenia gravis from consideration. Other causes for hypercholesterolemia such as diabetes mellitus, nephrotic syndrome, hyperadrenocorticism, and hypertriglyceridemia were not suspected in this patient because of a lack of relevant blood work abnormalities and clinical signs associated with these disease processes. Although primary hyperlipidemia was a differential diagnosis for this dog, a triglyceride concentration was not measured.


Levothyroxine sodium was initiated (0.02 mg/kg orally twice daily). Within 24 hours, the head tilt and menace response deficit resolved, the postural reactions and reflexes improved, and the gait normalized. Based on thyroid hormone concentrations and TSH measurement combined with the rapid improvement after supplementation with T4, along with the exclusion of other etiologies to explain the multifocal neurologic deficits, neurologic and muscular dysfunction secondary to hypothyroidism was presumptively diagnosed. However, the self-limiting nature of ischemic lesions could have also accounted for the dog's rapid improvement.

The patient was discharged with instructions to return in two weeks for a recheck. The owners had traveled a long distance and did not want to return for the recheck visit, so personal communication at two weeks revealed that the patient's gait and strength were mildly improved. The advising clinician instructed the owners to return in seven to 10 days to have the patient reevaluated.

Second presentation

Ten days later (about one month after initial examination), the dog was presented for evaluation of acute respiratory distress. The patient had not been reevaluated since initial hospitalization. On physical examination, the patient was dyspneic and tachypneic and had pale mucous membranes. Neurologic examination showed that the dog was mentally dull and was ambulatory. The dog still displayed generalized weakness, but its muscle tone and reflexes seemed slightly improved from one month prior. Postural reactions were normal, and cranial nerve function was normal.

A CBC and serum chemistry panel were performed (Table 3). A normocytic, normochromic anemia and thrombocytopenia were still present. In addition, elevated AST, alanine transaminase (ALT), ALP, and gamma-glutamyl transpeptidase (GGT) activities and an elevated total bilirubin concentration were detected. The serum cholesterol concentration had normalized.

Table 3: Case 1 CBC and serum chemistry profile abnormalities on second examination

Differential diagnoses for the dog's acute respiratory distress included aspiration pneumonia and pulmonary thromboembolism. In addition, the markedly elevated hepatocellular and cholestatic enzyme activities suggested a degree of acute liver dysfunction, most likely hypoxic damage. The owner declined diagnostic testing and treatment and elected euthanasia.


A gross necropsy and subsequent histologic evaluation of tissues were performed. The thyroid gland showed evidence of marked lymphoplasmacytic thyroiditis. Fibrinous thrombi were found in the hepatic sinusoids. The spleen, kidneys, and lungs contained atherosclerotic vasculature. Additionally, multiple infarcts were found in the vasculature of the lung. Appendicular skeletal musculature displayed evidence of myofiber necrosis that was consistent with ischemic damage.

The diagnosis was lymphoplasmacytic thyroiditis consistent with hypothyroidism with pulmonary infarcts; atherosclerosis of the vasculature of the spleen, lungs, and kidneys; and skeletal muscle myofiber necrosis. Although a primary myopathy cannot be completely excluded, given the atherosclerosis and infarctions found elsewhere, an ischemic myopathy secondary to hypothyroidism was most likely. In our experience, the marked inflammation of the thyroid gland is a common pathologic finding in dogs with immune-mediated hypothyroidism.

The brain and spinal cord were unfortunately not examined. However, while speculative, it is probable that the observed neurologic deficits represented ischemic infarction involving the brain secondary to atherosclerosis given the rest of the necropsy findings. Ischemic infarction involving the prosencephalon and brainstem may have explained the menace deficit and head tilt, respectively.

Dogs with hypothyroidism have been reported to be hypercoagulable and at risk for thromboembolic events due to atherosclerosis of the vasculature of the brain.3-7 Similarly, the elevated creatinine kinase activity and thrombocytopenia suggested a possible embolic event manifesting as ischemic myopathy and consumptive coagulopathy. Recovery was unlikely given the dog's severe respiratory compromise and the recurrent nature of its disease.

Case 2: Facial nerve dysfunction in a mixed-breed dog

An 8-year-old spayed female mixed-breed dog was presented to Red Bank Veterinary Hospital in Tinton Falls, New Jersey, for evaluation of ocular discharge and conjunctivitis in the right eye.


The dog had initially been evaluated by the referring veterinarian. Treatment had consisted of topical ophthalmic solution containing a corticosteroid-antibiotic combination (neomycin-polymyxin-dexamethasone). After five days, the signs had failed to improve, and the dog had been referred to Red Bank Veterinary Hospital.

Physical and neurologic examinations

Physical examination abnormalities were limited to the nervous system. The dog's body condition score was 6/9, subjectively. No abnormalities were seen on an otoscopic examination.

Neurologic examination revealed bilateral drooping of the lips and drooping of the pinna of the right ear as well as a lack of palpebral reflex in the right eye. Response to stimulation of the nares was normal bilaterally. The neuroanatomic diagnosis was consistent with dysfunction of cranial nerve VII (facial nerve).

Differential diagnoses

Differential diagnoses included ischemic infarction, idiopathic facial nerve paralysis, infection such as otitis media, neoplasia, and trauma. The latter seemed unlikely given the lack of history of any traumatic event.

Initial diagnostic tests

A CBC and serum chemistry profile were performed. The CBC results were normal, and the serum chemistry profile revealed hypercholesterolemia (440 mg/dl; reference range = 110 to 320 mg/dl).

Based on neurologic deficits and hypercholesterolemia, total T4, free T4, and TSH concentrations were measured. As in the previous case, a triglyceride concentration was not measured.

While pending results of the thyroid function testing, the dog developed a right-sided vestibular ataxia. In addition to the previous neurologic deficits, neurologic examination at the time of the development of vestibular ataxia revealed normal mentation and gait, no postural reaction deficits, normal reflexes and tone, and no abnormal nystagmus. The neuroanatomic diagnosis was consistent with right-sided cranial nerve VIII (vestibulocochlear nerve) as well as cranial nerve VII. Magnetic resonance imaging (MRI) of the head revealed no abnormalities. Because of this lack of MRI abnormalities and owner preference, a cerebrospinal fluid analysis was not performed.

Table 4: Case 2 pituitary-thyroid axis testing results

The total T4 and free T4 concentrations were decreased, and the TSH concentration was increased, consistent with primary hypothyroidism (Table 4). However, there is a small possibility that the thyroid gland itself was normal but being suppressed by the corticosteroid in the ocular preparation that cannot be ruled out. But the elevated TSH concentration makes this possibility less likely.

Treatment and follow-up

Supplementation with levothyroxine (0.02 mg/kg orally twice daily) was initiated. The dog experienced improvement of the vestibular dysfunction and the facial paralysis over the next seven days. However, the owner reported that the dog was restless, as evidenced by frequent pacing and reluctance to sleep. A total T4 concentration was rechecked because of the suspicion of oversupplementation, and the concentration was elevated (7.1 µg/dl; reference range = 1 to 4 µg/dl). Consequently, the dose of levothyroxine was reduced by 50%.

Three days after the dose reduction, the facial paralysis returned, and an intermediate dose of levothyroxine supplementation was instituted. The clinical signs of facial paralysis and vestibular ataxia resolved.

The patient had follow-up blood work performed by the referring veterinarian; results were not available, but recorded personal communication with the owner revealed that the dog was doing well on the intermediate dose. In this patient, a reduced initial dose of 0.1 mg/kg twice daily might have avoided the clinical signs of hyperthyroidism.

Based on results of the thyroid testing, lack of other disease processes that could explain dysfunction of cranial nerves VII and VIII, and response to thyroid hormone supplementation, hypothyroid-induced cranial neuropathy was presumptively diagnosed.

Case 3: A tetraparetic and ataxic rottweiler

A 10-year-old spayed female rottweiler was presented to Red Bank Veterinary Hospital for evaluation of acute tetraparesis and ataxia.

Physical and neurologic examinations

Physical examination abnormalities were limited to the nervous system. The dog's body condition score was 5/9, subjectively.

On neurologic examination, the dog's mentation was normal. The dog walked with a tendency to lean and fall to the right. Additionally, there was a left-sided dysmetria primarily evidenced by an over-reaching of the left limbs and excessive flexion of the carpus. There were left-sided postural reaction deficits. Spinal reflexes were normal. There was thoracic limb extensor rigidity. A cranial nerve examination revealed a right-sided head tilt. No abnormal nystagmus or strabismus was present.

The remainder of the cranial nerve examination findings were normal.

Differential diagnoses

The neuroanatomic diagnosis was consistent with a left-sided paradoxical central vestibular dysfunction. Differential diagnoses included ischemic infarction, neoplasia, infectious disease (e.g. Neospora caninum or Toxoplasma gondii infection), a noninfectious inflammatory disease such as granulomatous meningoencephalitis, and trauma. The latter seemed unlikely given the lack of history of any traumatic event.

Initial diagnostic tests

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.

Table 5: Case 3 pituitary-thyroid axis testing results

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.

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.

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 µg/dl (reference range = 1 to 4 µg/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 µg/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.

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


The link between hypothyroidism and neurologic disorders remains difficult to prove definitively. Consequently, a presumptive diagnosis of neurologic dysfunction secondary to hypothyroidism is challenging, especially when other supporting clinicopathologic data are not present. These three cases indicate that clinicians should consider pursuing thyroid testing in dogs with neurologic deficits that are unexplained through a basic diagnostic work-up.

Although the dogs in the aforementioned cases had blood work changes consistent with hypothyroidism, this is not the case with all dogs in the literature.9-11,13,16 In addition, the dogs reported herein did not have clinical signs or a presenting complaint that is often attributed to thyroid hormone deficiency.

In particular, dogs with dysfunction of the neuromuscular system, dogs with multiple cranial nerve deficits primarily involving cranial nerves VII and VIII, and dogs with clinicopathologic data and imaging findings consistent with ischemic injury to the central nervous system should undergo appropriate testing of the pituitary-thyroid axis. These tests should accompany a systemic work-up including a CBC, a serum chemistry profile, a urinalysis, and an otoscopic examination in dogs with vestibular involvement or facial nerve deficits. Moreover, exclude from consideration euthyroid-sick syndrome, the impact of drugs that can alter thyroid hormone concentrations, and other etiologies to which the observed neurologic deficits could be attributed to before making a presumptive diagnosis.

Ultimately, in dogs with a definitive diagnosis of hypothyroidism and unexplained neurologic deficits, empirical thyroid hormone supplementation followed by close monitoring of the resolution of neurologic deficits should be judiciously undertaken.

Abigail Bertalan, VMD

School of Veterinary Medicine

University of Pennsylvania

Philadelphia, PA 19104

Eric N. Glass, DVM, MS, DACVIM (neurology)

Red Bank Veterinary Hospital

197 Hance Ave.

Red Bank, NJ 07701

Marc Kent, DVM, DACVIM (internal medicine, neurology)

School of Veterinary Medicine

University of Georgia

Athens, GA 30602

Alexander de Lahunta, DVM, PhD, DACVIM (neurology), DACVP

Department of Biomedical Sciences

College of Veterinary Medicine

Cornell University

Ithaca, NY 14853


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2. Kantrowitz LB, Peterson ME, Melian C, et al. Serum total thyroxine, total triiodothyronine, free thyroxine, and thyrotropin concentrations in dogs with nonthyroidal disease. J Am Vet Med Assoc 2001;219(6):765-769.

3. Hess RS, Kass PH, Van Winkle TJ. Association between diabetes mellitus, hypothyroidism or hyperadrenocorticism, and atherosclerosis in dogs. J Vet Intern Med 2003;17(4):489-494.

4. Liu SK, Tilley LP, Tappe JP, et al. Clinical and pathologic findings in dogs with atherosclerosis: 21 cases (1970-1983). J Am Vet Med Assoc 1989;189(2):227-232.

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6. Bagley RS, Anderson WI, de Lahunta A, et al. Cerebellar infarction caused by arterial thrombosis in a dog. J Am Vet Med Assoc 1988;192(6):785-787.

7. Blois SL, Poma R, Stalker MJ, et al. A case of primary hypothyroidism causing central nervous system atherosclerosis in a dog. Can Vet J 2008;49(8):789-792.

8. Garosi LS, McConnell JF. Ischaemic stroke in dogs and humans: a comparative review. J Small Anim Pract 2005;46(11):521-529.

9. Budsberg, SC, Moore GE, Kiappenbach K. Thyroxine-responsive unilateral forelimb lameness and generalized neuromuscular disease in four hypothyroid dogs. J Am Vet Med Assoc 1993;202(11):1859-1860.

10. Indrieri RJ. Whalen LR, Cardinet GH, et al. Neuromuscular abnormalities associated with hypothyroidism and lymphocytic thyroiditis in three dogs. J Am Vet Med Assoc 1987;190(5):544-548.

11. Dewey C. Neuromuscular dysfunction in five dogs with acquired myasthenia gravis and hypothyroidism. Prog Vet Neurol 1995;6(4):117-123.

12. Levine JM, Bergman RL, Coates JR, et al. Myasthenia gravis and hypothyroidism in a dog with meningomyelitis. J Am Anim Hosp Assoc 2005;41(4):247-251.

13. Jaggy A, Oliver JE, Ferguson DC, et al. Neurological manifestations of hypothyroidism: a retrospective study of 29 dogs. J Vet Intern Med 1994;8(5):328-336.

14. Bichsel P, Jacobs G, Oliver JE Jr. Neurologic manifestations associated with hypothyroidism in four dogs. J Am Vet Med Assoc 1988;192(12):1745-1747.

15. Panciera DL. Hypothyroidism in dogs: 66 cases (1987-1992). J Am Vet Med Assoc 1994;204(5):761-766.

16. McKeown HM. Hypothyroidism in a boxer dog. Can Vet J 2002;43(7):553-555.

17. Garosi LS. Cerebrovascular disease in dogs and cats. Vet Clin North Am Small Anim Pract 2010;40(1):65-79.

18. Schwarz BC, Sallmutter T, Nell B. Keratoconjunctivitis sicca attributable to parasympathetic facial nerve dysfunction associated with hypothyroidism in a horse. J Am Vet Med Assoc 2008;233(11):1761-1766.

19. Higgins MA, Rossmeisl JH Jr, Panciera DL. Hypothyroid-associated central vestibular disease in 10 dogs: 1999-2005. J Vet Intern Med 2006;20(6):1363-1369.

20. Vitale CL, Olby NJ. Neurologic dysfunction in hypothyroid, hyperlipidemic Labrador retrievers. J Vet Intern Med 2007;21(6):1316-1322.

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