Neurological Manifestations of Hypothyroidism: A Retrospective Study of 29 Dogs

摘要

Neuromuscular signs in association with hypothyroidism are described in 29 dogs. Eleven dogs had lower motor neuron signs, 9 had peripheral vestibular deficits, 4 had megaesophagus, and 5 had laryngeal paralysis. Primarily older (mean = 9.5 years), large-breed dogs were affected, and there was no sex or breed predisposition. Duration of clinical signs before presentation ranged from 2 to 8 weeks (mean = 5 weeks). The diagnosis was based on (1) results of neurological examination (29 dogs); (2) electromyographic abnormalities (18 dogs), including fibrillation potentials (n = 18), positive sharp waves (n = 15), and complex repetitive discharges (n = 4); (3) high serum cholesterol concentration (10 dogs; mean = 335 mg/dL); (4) low response to thyroid-stimulating hormone (29 dogs; mean T ₄ prestimulation concentration = 0.8 μg/dL; mean T ₄ poststimulation = 1.2 μg/dL); and (5) good response to thyroxine supplementation (26 dogs). Dogs with vestibular deficits had abnormal brainstem auditory-evoked responses (BAER), including increased latencies of P ₁ -P ₆ and decreased amplitude of P _4,5 -N ₅ . Seven other dogs had similar BAER abnormalities without manifesting clinical signs of vestibular involvement. Three dogs with vestibular signs had fibrillation potentials and positive sharp waves without exhibiting lower motor neuron signs. All dogs were supplemented with levothyroxine (0.02 mg/kg P0 bid). The follow-up period ranged between 6 and 30 months (mean, 14 months). Serum T ₄ concentrations were measured at least 3 times for each dog every 2 months (mean T ₄ concentration = 2.6 μg/dL). All but 1 dog with lower motor neuron signs and 1 dog with vestibular signs recovered after 2 months (mean, 57 days). Signs of megaesophagus became progressively less severe over 4 months. Dogs with laryngeal paralysis improved partially after 5 months. We suggest that either vestibular or lower motor neuron signs, megaesophagus, or laryngeal paralysis may be the only clinical signs of an underlying, more generalized polyneuropathy associated with hypothyroidism. Electro-diagnostic abnormalities may be detected before clinical disease develops.