| Ridgebacks by Kat |
 |  |  |  |  |  |  |  |  |  |
| Hypothyroid |
| Hypothyroid Neuropathy by K.G. Braund |
with immune-mediated lymphocytic thyroiditis/idiopathic thyroid atrophy [256,257]. A hypothyroid-associated neuropathy
commonly occurs in mature to middle-aged dogs, usually of the large-breed variety. The few cases reported in the
literature [258-261] do not reflect the prevalence of this metabolic neuropathy, based on muscle and nerve biopsy
material that we have examined (both at the Scott-Ritchey neuromuscular laboratory at Auburn University and at my
peripheral nerve laboratory) from numerous hypothyroid dogs. Sub-clinical cases have been recognized [534]. Clinical
signs may include exercise intolerance, progressive weakness (e.g., paraparesis, tetraparesis), muscle atrophy (mainly
appendicular) and depressed spinal reflexes. Other signs may include pelvic limb proprioceptive deficits, Hypothryroidism
is common in dogs but rare in cats and most cases of acquired canine hypothyroidism are associated unilateral/bilateral
facial nerve paresis/paralysis, ventrolateral strabismus, and decreased corneal/facial sensitivity. Intermittent forelimb
lameness is less commonly reported [533]. In one comprehensive study of the neurological manifestations of
hypothyroidism in 29 dogs, lower motor neuron signs were seen in 11 dogs, 9 dogs had peripheral vestibular deficits, 4
had megaesophagus, and 5 had laryngeal paralysis [260]. Peripheral neuropathy has been seen in several hypothyroid
dogs with megaesophagus and myasthenia gravis [261]. Electrodiagnostic studies in appendicular muscles have revealed
multifocal patterns of fibrillation potentials, positive sharp waves, decreased motor and sensory semithin sections are
typically characterized by mixed pathology involving demyelination/remyelination and axonal necrosis. The underlying
pathology appears to be a sensorimotor polyneuropathy and, based on my experiences, at least some of these cases
have a distal distribution (i.e., distal sensorimotor polyneuropathy).
Diagnosis is based on serological evidence of hypothyroidism (low serum T4 concentration and inadequate response to
thyroid-stimulating hormone administration) [260]. Prognosis is often favorable. In one study involving 29 dogs, most dogs
recovered within 2 to 3 months of thyroid hormone supplementation (20 mg/kg of L-thyroxine PO bid). Dogs with
megaesophagus improved over 4 months, while dogs with laryngeal paralysis showed partial improvement after 5 months.
One caveat is that we have encountered a number of dogs in which there is less dramatic or no clinical response to
long-term thyroid hormone supplementation.
Note that affected dogs may also have generalized signs of hypothyroidism, including thinning of the haircoat, alopecia,
dry skin with epidermal scales and flaking, etc.
The pathophysiology surrounding hypothyroid neuropathy remains unexplained [262]. In people with hypothyroidism, a
mild peripheral neuropathy is relatively common and may include facial mononeuropathy, sensorineural hearing loss,
distal sensory neuropathy, and sensorimotor polyneuropathy [103,263]. One study reported changes in nerves consistent
with a dying back process and possible underlying slow axonal transport [264]. There may be preferential loss of larger
caliber myelinated fibers [265]. Carpal tunnel syndrome (median nerve mononeuropathy at the wrist) is the most common
mononeuropathy encountered [103]. As we have seen in dogs, the relative proportions of axonal degeneration
(secondary to disturbance of neuronal metabolism?) and demyelination (primary Schwann cell involvement?) varies from
case to case [264,266,267]. Onion bulb formations are infrequently found. Ultrastructural changes in affected human
nerves include prominent cluster formations and excessive glycogen deposition in Schwann cells, myelinated and
unmyelinated axons, endothelial cells, and perineurial cells [265,268].
commonly occurs in mature to middle-aged dogs, usually of the large-breed variety. The few cases reported in the
literature [258-261] do not reflect the prevalence of this metabolic neuropathy, based on muscle and nerve biopsy
material that we have examined (both at the Scott-Ritchey neuromuscular laboratory at Auburn University and at my
peripheral nerve laboratory) from numerous hypothyroid dogs. Sub-clinical cases have been recognized [534]. Clinical
signs may include exercise intolerance, progressive weakness (e.g., paraparesis, tetraparesis), muscle atrophy (mainly
appendicular) and depressed spinal reflexes. Other signs may include pelvic limb proprioceptive deficits, Hypothryroidism
is common in dogs but rare in cats and most cases of acquired canine hypothyroidism are associated unilateral/bilateral
facial nerve paresis/paralysis, ventrolateral strabismus, and decreased corneal/facial sensitivity. Intermittent forelimb
lameness is less commonly reported [533]. In one comprehensive study of the neurological manifestations of
hypothyroidism in 29 dogs, lower motor neuron signs were seen in 11 dogs, 9 dogs had peripheral vestibular deficits, 4
had megaesophagus, and 5 had laryngeal paralysis [260]. Peripheral neuropathy has been seen in several hypothyroid
dogs with megaesophagus and myasthenia gravis [261]. Electrodiagnostic studies in appendicular muscles have revealed
multifocal patterns of fibrillation potentials, positive sharp waves, decreased motor and sensory semithin sections are
typically characterized by mixed pathology involving demyelination/remyelination and axonal necrosis. The underlying
pathology appears to be a sensorimotor polyneuropathy and, based on my experiences, at least some of these cases
have a distal distribution (i.e., distal sensorimotor polyneuropathy).
Diagnosis is based on serological evidence of hypothyroidism (low serum T4 concentration and inadequate response to
thyroid-stimulating hormone administration) [260]. Prognosis is often favorable. In one study involving 29 dogs, most dogs
recovered within 2 to 3 months of thyroid hormone supplementation (20 mg/kg of L-thyroxine PO bid). Dogs with
megaesophagus improved over 4 months, while dogs with laryngeal paralysis showed partial improvement after 5 months.
One caveat is that we have encountered a number of dogs in which there is less dramatic or no clinical response to
long-term thyroid hormone supplementation.
Note that affected dogs may also have generalized signs of hypothyroidism, including thinning of the haircoat, alopecia,
dry skin with epidermal scales and flaking, etc.
The pathophysiology surrounding hypothyroid neuropathy remains unexplained [262]. In people with hypothyroidism, a
mild peripheral neuropathy is relatively common and may include facial mononeuropathy, sensorineural hearing loss,
distal sensory neuropathy, and sensorimotor polyneuropathy [103,263]. One study reported changes in nerves consistent
with a dying back process and possible underlying slow axonal transport [264]. There may be preferential loss of larger
caliber myelinated fibers [265]. Carpal tunnel syndrome (median nerve mononeuropathy at the wrist) is the most common
mononeuropathy encountered [103]. As we have seen in dogs, the relative proportions of axonal degeneration
(secondary to disturbance of neuronal metabolism?) and demyelination (primary Schwann cell involvement?) varies from
case to case [264,266,267]. Onion bulb formations are infrequently found. Ultrastructural changes in affected human
nerves include prominent cluster formations and excessive glycogen deposition in Schwann cells, myelinated and
unmyelinated axons, endothelial cells, and perineurial cells [265,268].