Facial Paralysis Secondary to Hypothyroidism in a Dog
Background: Secondary neurological disorders hypothyroidism is unusual in dogs, especially when compared with other clinical signs, such as lethargy, weight gain and dermatological alterations. When manifested, these signals refer to the peripheral or central nervous system and the most common include: vestibular disease, seizures, laryngeal paralysis, polyneuropathy and paralysis of the facial nerve. Several reports of neurological disorders associated with hypothyroidism are found in literature, basically international. In the national literature, however, there are few reports on the subject. Thus, the aim of this study was to report a case of facial paralysis associated with hypothyroidism in a dog.
Case: A male canine, the boxer race, with 7-year-old were referred to the Veterinary Medical Teaching Hospital of the UFSM with a history of difficult water and food intake and asymmetry of the face for seven days. On neurological examination, the animal found itself alert and locomotion, postural reactions and segmental reflexes without changes. In the evaluation of the cranial nerves, there was a menace response absent the right side, however with preserved vision, palpebral and lip ptosis of the right side and reflection palpebral absent on the same side. Opposite the historical, clinical, neurological and laboratory test findings, the diagnosis was facial paralysis secondary to hypothyroidism. As differential diagnoses were listed, inner otitis neoplasm in inner ear, trauma and idiopathic facial paralysis. After the diagnosis, clinical treatment was instituted with levothyroxine sodium, at a dose of 0.02 mg kg orally every 12 h, being observed total improvement of clinical signs (no changes for water intake and food, menace response and reflection palpebral normal and symmetry of the face) in 32 days.
Discussion: The diagnosis of facial paralysis associated with hypothyroidism was based on the history, clinical and neurological examination findings, laboratory assessment of thyroid function by observing low serum free T4 and high concentrations of TSH, the therapeutic response after supplementation levothyroxine sodium, and exclusion of other possible causes, such as otitis interna and traumatic. The pathogenesis of this change associated with hypothyroidism is not completely understood, although it is believed that cranial nerve paralysis (trigeminal, facial and vestibulocochlear) may result from the resulting compression of myxedema deposit nerve or in the tissues of the head and neck, demyelination caused by disordered metabolism of Schwann cells, decreased blood perfusion of the inner ear secondary to hyperlipidemia and increased blood viscosity or metabolic defects ranging from change in axonal transport to severe axonal loss. Treatment consists of supplementation of levothyroxine and most dogs with neurological disorders associated with hypothyroidism will present partial or total improvement of clinical signs between two and four months, generally being observed improvement within the first week of treatment. In the dog this report, after the beginning of treatment, improvement was observed partial and total clinical signs in 15 and 32 days, respectively. Therefore, with appropriate treatment, hypothyroidism is a disease with an excellent prognosis. The report brings to clinical relevance, the importance of hypothyroidism in the differential diagnosis of facial paralysis in dogs with face asymmetry history, the laboratory evaluation of thyroid function and response to therapy with levothyroxine sodium supplementation essential for definitive diagnosis.
Keywords: neurology, facial nerve, peripheral neuropathy, dogs.
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