Peripheral nerve pathology in two rottweilers with neuronal vacuolation and spinocerebellar degeneration

Neuronal vacuolation and spinocerebellar degeneration in young Rottweiler dogs is a neurodegenerative condition characterized by neuronal vacuolation of several nuclei in the central nervous system and degeneration of the spinal cord white matter. Here, we describe the morphologic and ultrastructural findings in laryngeal muscles and peripheral nerves of a 16-week-old female and a 32-week-old female Rottweiler dog affected by progressive ataxia and tetraparesis associated with laryngeal paralysis. Lesions were characterized by neurogenic muscle atrophy of the intrinsic laryngeal muscles, and a loss of large myelinated fibers in the recurrent laryngeal nerve, accompanied by demyelinating/remyelinating features affecting the small myelinated fibers. No significant changes were detected in the cranial laryngeal, vagus, phrenic, ulnar, or peroneal nerves. These findings were indicative of a selective distal neuropathy of the recurrent laryngeal nerve with early severe axonal degeneration, mainly of the large myelinated fibers.     

Equine laryngeal hemiplegia. Part IV. Muscle pathology

This study confirmed that neurogenic muscle pathology exists in intrinsic laryngeal muscles supplied by the recurrent laryngeal nerves in horses subclinically and clinically affected with laryngeal hemiplegia. An important additional observation was the occurrence in three out of four laryngeal hemiplegic horses of neurogenic muscle changes in a hindlimb muscle, the extensor digitorum longus, a muscle supplied by another long peripheral nerve. This finding suggests that a polynenropathy exists in laryngeal hemiplegic horses, and supports the classification of this disease as a distal axonopathy. Comparison of the degree of pathology in the intrinsic laryngeal muscles and that of the recurrent laryngeal nerves innervating them, demonstrated a strong correlation between the extent of damage in the distal left recurrent laryngeal nerve and the overall degree of muscle pathology. The muscle damage in clinically affected horses is a reflection of the nerve damage present in the most distal portion of the recurrent laryngeal nerve. The more variable pathological changes found in proximal levels of the left and right recurrent laryngeal nerves probably reflects the ongoing nature of the pathological process affecting nerve fibres. The existence of a subclinically affected group of horses, the earliest involvement of an adductor, the left cricoarytenoideus lateralis muscle, and the presence of changes in the right intrinsic laryngeal muscles all confirmed the findings of previous workers.     

Laryngeal paralysis-polyneuropathy complex in young related Pyrenean mountain dogs

OBJECTIVES: To characterise clinical, electrophysiological and histopathological findings. To analyse pedigree information in six young related Pyrenean mountain dogs with laryngeal paralysis-polyneuropathy complex (LP-PNC). METHODS: A retrospective study of clinical records and pedigrees of six young related Pyrenean mountain dogs with LP-PNC was carried out. RESULTS: All dogs were presented with laryngeal paralysis and concurrent megaoesophagus. Electrodiagnostic testing was performed in three dogs and showed electrophysiological abnormalities in the distal appendicular muscles. Histopathological findings of peripheral nerve samples were dominated by distal axonal degeneration. Clinical, electrophysiological and histopathological findings were supportive of a diagnosis of degenerative, sensorimotor LP-PNC, similar to that reported in young dalmatians and rottweilers. All dogs died or were euthanased by two years of age. An autosomal recessive mode of inheritance was suspected based on pedigree analysis. CLINICAL SIGNIFICANCE: Congenital LP-PNC should be suspected in any young dog presenting with laryngeal dysfunction and other concurrent neurological abnormalities. The prognosis is usually poor.     

Inability to experimentally produce a polyneuropathy in dogs given chronic oral low level lead.

Electromyographic examinations were performed at various times over a 40 week period in four mature dogs receiving chronic oral low doses of lead acetate and a control dog receiving sodium acetate. Blood lead levels in the four dogs were elevated (mean values 1.15, 2.18, 1.13 and 1.72 mumol/liter). No clinical signs of lead intoxication were present. Two dogs had evidence of a nonregenerative anemia. Neither needle electromyographic nor nerve conduction velocity studies showed evidence of a polyneuropathy. Teased nerve fiber preparations of proximal and distal segments of the ulnar and tibial nerves and muscle biopsies of distal appendicular muscles were normal in all dogs. Light microscopic examination of the brain, kidneys and liver revealed no abnormalities in the two dogs necropsied. In conclusion, a polyneuropathy was not produced experimentally in dogs ingesting low doses of inorganic lead for up to 40 weeks.     

Neuronal vacuolation, myelopathy and laryngeal neuropathy in a mixed-breed dog

A bilateral and symmetrical neuronal vacuolation associated with spinal cord white matter degeneration and laryngeal neuropathy was observed in a 12-week-old male mixed-breed dog with a history of progressive pelvic limbs ataxia. On clinical examination, signs included inspiratory stridor, spinal ataxia, tetraparesis, and proprioceptive deficits more severe in the pelvic limbs. Examination of the larynx showed bilateral laryngeal paralysis and electromyography revealed fibrillation potentials restricted to the intrinsic laryngeal muscles. Clinical and pathological findings resembled the syndrome of neuronal vacuolation and spinocerebellar degeneration described in Rottweiler dogs. This is the first report of a similar disorder in a dog different from Rottweiler.     

Experimental crush of the equine recurrent laryngeal nerve: a study of normal and aberrant reinnervation

Experimental reinnervation of the equine larynx in healthy ponies was studied after the recurrent laryngeal nerve was crushed, using endoscopic, electromyographic, and microscopic techniques. In 12 ponies, the recurrent laryngeal nerve was crushed unilaterally in the midcervical area. All showed postoperative paralysis of the larynx on the operated side. In 8 ponies, recovery of movement of the vocal folds occurred at different times (2.5 to 8 months) after surgical operation was done. These movements, which were often abnormal, included trembling and asynchronism. In 2 of these ponies, complete return of normal vocal fold function occurred. Return of function was due to reinnervation, as determined by electromyographic examination of the laryngeal muscles and microscopic evaluation of these muscles and the recurrent laryngeal nerves. In the muscles, there was evidence of fiber-type grouping, and the nerves showed regenerative activity. In 3 ponies, there was evidence of aberrant reinnervation, with adductor or abductor muscles discharging during an inappropriate phase of the respiratory cycle. Further evidence that reinnervation occurred in the larynges of these ponies was determined in microscopic sections of the recurrent laryngeal nerves and muscles, which showed regenerative activity and muscle fiber-type grouping, respectively. The endoscopic abnormalities in these ponies were compared with those seen in horses with spontaneous subclinical laryngeal paralysis. However, the possibility that the abnormal endoscopic findings in this latter group of horses are due to aberrant reinnervation is thought to be unlikely.     

Electromyographic evaluation of conduction time and velocity of the recurrent laryngeal nerves of clinically normal dogs

In 25 adult dogs of various breeds, recurrent laryngeal nerve fibers were electrically stimulated at 2 points along their extralaryngeal course. Evoked compound muscle action potentials were recorded in the ipsilateral intrinsic laryngeal muscles, using a percutaneous needle electrode. Latencies, amplitudes, and durations were measured. Latencies were correlated with neck length (r = 0.88 on left and 0.82 on right). Five of the dogs were euthanatized, and the nerve length between the 2 stimulating needle electrodes was measured; calculated conduction velocities (mean +/- SD) were 55 +/- 6 m/s (left) and 57 +/- 6 m/s (right). In 38 additional canine cadavers, the lengths of the exposed left and right recurrent laryngeal nerves were correlated with neck length (r = 0.44 on left and 0.56 on right). A linear regression model is proposed for predicting normal latencies, despite variations in neck length among different breeds of dogs.     

Insulinoma and Subclinical Peripheral Neuropathy in Two Dogs

Two dogs with diffuse, subclinical polyneuropathy associated with insulinoma are reported. Seizures were the dominant sign of central nervous system disease. One dog had clinical signs of facial nerve paralysis. Lesions in selected appendicular and cranial nerves included a mixture of demyelination, remyelination, and axonal degeneration. The incidence (range: 18-47%) of these changes far exceeded that of comparable nerves from six control dogs (range 0-11%). Myopathic and electrodiagnostic findings were compatible with the nerve changes.     

Comparison of Three Clinical Techniques for the Diagnosis of Laryngeal Paralysis in Dogs

Objectives— To evaluate laryngeal function using 3 diagnostic techniques: echolaryngography (EL), transnasal laryngoscopy (TNL), and laryngoscopy per os (LPO).
Study Design— Prospective clinical study.
Animals— Dogs with laryngeal paralysis (n=5) and control dogs (n=10); 5 age- and breed-matched dogs and 5 young, breed-matched dogs.
Methods— Laryngeal function was evaluated in conscious dogs using EL. All examinations were recorded and evaluated by separate, blinded observers upon completion of the study. The methods were compared with a standard evaluation incorporating all clinical knowledge of the case (STD) using sensitivity, specificity, positive, and negative predictive values.
Results— Three dogs with bilateral laryngeal paralysis requiring surgery were diagnosed as unilaterally affected or normal on EL. Three dogs had paradoxic motion on TNL and LPO, 2 of those were considered normal on EL, and 1 had no motion on EL. Paralysis was diagnosed in 1 age-matched and 3 young control dogs on EL. LPO and TNL falsely diagnosed lack of arytenoid movement in 2 age-matched controls and 1 young control. Two age-matched and 1 young control dog were misdiagnosed as paralyzed with TNL and LPO.
Discussion— Direct observation of the larynx allowed better evaluation of laryngeal function compared with EL. TNL did not require induction of anesthesia, but did not improve the ability to assess laryngeal function compared with LPO.
Conclusions— EL was not as effective as direct observation of the larynx. TNL did not improve the evaluation of laryngeal function compared with LPO.
Clinical Relevance— We use LPO combined with knowledge of the clinical history and physical examination to diagnose laryngeal paralysis in preference to EL and TNL.     

Dysphagia in Bouviers associated with muscular dystrophy; evaluation of 24 cases

Twenty-four Bouviers with dysphagia were examined between October 1986 and October 1988. The type of dysphagia was characterised by the results from the clinical examination, the videofluorographic examination and the electromyographic recordings from the oral, pharyngeal, and esophageal muscles. Electromyography indicated neurogenic as well as myogenic causes of dysphagia. Tissues from 10 dogs were available for histopathologic examination. In nine dogs there was a progressive muscular degeneration of the pharyngeal and/or esophageal muscles, resembling muscular dystrophy. In two of these dogs the same abnormalities were also noticed in the masseter and temporalis muscles and in the intrinsic laryngeal muscles. In one dog small areas with hyalin degeneration and fragmentation of muscle fibres were found in the cricopharyngeal muscle. No abnormalities in nerve tissue were found. Muscular dystrophy is a hereditary disease. The mode of transmission in these Bouviers is not yet known.     

Bilateral laryngeal paralysis in the horse

Four two-year-old Thoroughbreds suffered an acute gastrointestinal illness shortly after dosing with mineral oil which was thought to have been contaminated with an organophosphate compound. Three weeks later all four were noted to be dyspnoeic and endoscopic examination showed that they had developed bilateral laryngeal paralysis. Two of the horses died during severe bouts of dyspnoea six and eight months later and the third was killed shortly thereafter. Examination of the left and right recurrent laryngeal nerves from these horses showed a severe loss of myelinated fibres distally, especially in the left nerve. A similar but less severe lesion was seen in other long peripheral nerves, including the phrenic and digital nerves of the third horse. The spinal cord in two horses showed evidence of mild axonal degeneration which was not related to a particular tract or location. The fourth horse had bilateral laryngeal paralysis two years later. The acute clinical signs and delayed neurological sequelae seen in these horses were strongly suggestive of accidental organophosphate toxicity.     

ULTRASONOGRAPHY OF PERIPHERAL NERVES DURING WALLERIAN DEGENERATION AND REGENERATION FOLLOWING TRANSECTION

Ultrasonography was performed on sciatic, tibial and/or peroneal nerves and interosseous muscles in 7 dogs using a ultrasound machine with a 7.5 MHz linear array transducer. A tibial nerve was transected near the distal aspect of the bellies of the gastroenemius muscle. Serial neurologic examinations, electromyography, and ultrasonography were performed before and after surgery. Dogs were euthanized at variable intervals and histopathology performed on nerve samples. In sagittal images, normal nerves had hyperechoic walls with multiple internal linear echoes. In transverse images, the nerves were round or oval hyperechoic structures with internal punctate echoes. After transection, the proximal stump was consistently seen whereas the distal stump and nerve were harder to identify. Neuromas were present in all 5 dogs followed beyond 2 days and appeared as hypoechoic bulbous swellings most apparent at 3 weeks after surgery. Only 1 dog developed a neuroma large enough to be considered of potential clinical significance. Four dogs were followed beyond 2 months. Regeneration was evidenced by a steady growth of nerve with an irregular outline (2 dogs) or by a knobby connection between the proximal and distal stumps (1 dog). Regeneration was not detected in 1 dog.     

Bilateral thyroarytenoid cartilage lateralization and vocal fold excision with mucosoplasty for treatment of idiopathic laryngeal paralysis: 67 dogs (1998-2005)

Objective— To evaluate combined bilateral thyroarytenoid cartilage lateralization, vocal fold excision, and mucosoplasty technique (BTAL) through ventral median laryngotomy for treatment of laryngeal paralysis in dogs.
Design— Retrospective study.
Animals— Dogs (n=67) with laryngeal paralysis.
Methods— Medical records were reviewed for dogs with idiopathic laryngeal paralysis that had BTAL between January 1998 and March 2005. Retrieved data included signalment, history, physical and laryngoscopic examination findings, clinicopathologic tests, and results of recheck examination findings.
Results— BTAL was performed by a single surgeon. Short-term (<6 months) follow-up information was available for 67 dogs and long-term (>12 months) for 40 dogs. Major postoperative complications were surgical failures (13; 7 short term, 6 long term) and aspiration pneumonia (1). Mean recurrence of clinical signs was at 19 weeks (range, 2–30 weeks). Minor complications occurred in 22 (33%) dogs including occasional coughing or gagging, stridorous breathing during exercise, panting, noisy or heavy breathing, and aspiration pneumonia (3 dogs) that did not require hospitalization. All owners reported an improved quality of life and had no regrets with surgical outcome.
Conclusions— BTAL is seemingly an effective procedure for treatment of laryngeal paralysis.
Clinical Relevance— BTAL is associated with a low incidence of aspiration pneumonia; however, there is substantial risk of recurrence of clinical signs associated with narrowing of the glottis. Consequently, unilateral arytenoid lateralization currently represents the accepted approach to the treatment of laryngeal paralysis.     

Examination of the laryngeal musculature and recurrent laryngeal nerves of zebra (Equus burchelli) for evidence of idiopathic laryngeal hemiplegia

AIMS: This study was undertaken in order to determine whether wild Burchell's Zebra (Equus burchelli) are affected by Idiopathic Laryngeal Hemiplegia (ILH). ILH has a high prevalence in the domestic horse and a negative control population has not been identified. METHODS: The work was conducted in two phases on two large farms in central Kenya during routine culls. The larynges of 42 zebra were removed and the left and right intrinsic laryngeal adductor and abductor muscles and recurrent laryngeal nerves were isolated. The muscles were weighed and biopsy samples of left and right recurrent laryngeal nerve and cricoarytenoideus lateralis muscles from 16 animals were taken for histological examination. RESULTS: Left adductor muscles were observed to be significantly lighter than right adductor muscles (p = 0.001). There was no significant difference between the weights of left and right laryngeal abductors (p = 0.260). There was no light microscopic evidence of pathological changes consistent with ILH in any of the muscle or nerve samples. CONCLUSIONS: Zebra do not appear to suffer from ILH and equids unaffected by ILH can have significantly lighter muscles on the left of the larynx. CLINICAL RELEVANCE: Mild asymmetries of the larynx on palpation may not be a reliable indicator of ILH. Zebra may be a potentially useful negative control animal for observational ILH studies.     

Effects of doxapram HCl on laryngeal function of normal dogs and dogs with naturally occurring laryngeal paralysis

OBJECTIVES: To compare the effects of IV doxapram on glottic size and arytenoid motion in normal dogs and in dogs with laryngeal paralysis. STUDY DESIGN: Prospective experimental and clinical trials. ANIMALS: Six healthy dogs weighing 24.5 +/- 3.9 kg and six dogs weighing 27.4 +/- 11.5 kg suspected of having laryngeal paralysis. METHODS: Dogs were pre-medicated with acepromazine and butorphanol, and a light plane of anesthesia was induced with isoflurane by mask. Videoendoscopic examination of laryngeal function was recorded before (baseline) and after IV doxapram administration. Normalized glottal gap area (NGGA) at maximal inspiration and expiration, and percentage change in height, width, area, and NGGA were calculated with measurements from digitized images of the glottal gap. RESULTS: Active arytenoid motion was present in all normal dogs at baseline. After doxapram administration, depth of respiration appeared greater, but arytenoid motion, as measured by percentage change in NGGA, and in area and width, did not significantly increase in normal dogs. No arytenoid motion was detected in dogs with laryngeal paralysis at baseline; however, rima glottidis NGGA of dogs with laryngeal paralysis was greater at inspiration and expiration than normal dogs. After doxapram administration, dogs with laryngeal paralysis developed paradoxical arytenoid motion and significant, negative percentage change in area (-61%) and NGGA (-145%) because of inward collapse of the arytenoids during inspiration. CONCLUSIONS AND CLINICAL RELEVANCE: Administration of doxapram during laryngeal examination is useful for differentiating normal dogs from dogs with laryngeal paralysis. Dogs with laryngeal paralysis may suffer extreme glottic constriction with vigorous respirations, and may require intubation during examination.     

Pathological aspects of Australian Stringhalt.

Nine horses with clinical signs of Australian Stringhalt were killed and tissues collected for a detailed pathological study. Lesions were limited to peripheral nerves and muscles. The most severely affected nerves were the superficial and deep peroneal, distal tibial, plantar digital, volar and recurrent laryngeal nerve with changes characterised by a selective loss of large diameter myelinated fibres with various degrees of demyelination, fibrosis, Schwann cell proliferation and onion-bulb formation. A routine evaluation of the brain and spinal cord by light microscopy failed to reveal any consistent abnormalities. Morphometric analysis of deep peroneal and recurrent laryngeal nerves confirmed the reduced number of large diameter myelinated axons. Teased fibre preparations of these nerves did not show any abnormalities in internodal distance. The most severe muscle lesions were in the long and lateral digital extensors, cranial tibial, dorsal cricoarytenoid, gracilis and lateral deep digital flexor with extensive atrophy of fibres and diffuse fibrosis. Histochemical evaluation of the long digital extensor from 3 affected horses showed an abnormally wide distribution in fibre size and a reduction in type II fibres compared with controls. These lesions are consistent with a distal axonopathy leading to neurogenic muscle atrophy. The distribution of neuromuscular lesions in Australian Stringhalt may be explained by the susceptibility of longer, larger myelinated nerve fibres to injury, but the cause for this distal axonopathy remains unknown.     

Electrophysiological evaluation of traumatic forelimb paralysis of the dog

The results of clinical neurological, electromyographic and electroneurographic examinations in 26 dogs with traumatic forelimb paralysis are presented. The results of neurological examination varied considerably among the cases. Electromyographic evidence of denervation in the epaxial muscles was observed in 22 dogs. A post ganglionic dorsal root lesion was diagnosed in 14 cases by the presence of an evoked sensory nerve action potential in association with loss of conscious pain perception in the appropriate area. Motor nerve studies in the ulnar nerve were not helpful in discriminating root lesions from spinal nerve involvement. It was concluded that electromyographic examination of the ipsilateral epaxial muscles under general anaesthesia is essential for the detection of root involvement. Sensory conduction studies in the radial nerve are indicated if conscious pain perception is absent in the fifth digit. Motor and sensory conduction studies of the ulnar nerve system seldom provide additional diagnostic information seldom provide additional diagnostic information. The absence of electrophysiological signs of root involvement does not exclude a post ganglionic dorsal root lesion.     

MAGNETIC RESONANCE IMAGING OF ACQUIRED TRIGEMINAL NERVE DISORDERS IN SIX DOGS

The medical records and magnetic resonance (MR) images of dogs with an acquired trigeminal nerve disorder were reviewed retrospectively. Trigeminal nerve dysfunction was present in six dogs with histologic confirmation of etiology. A histopathologic diagnosis of neuritis (n=2) or nerve sheath tumor (n=4) was made. Dogs with trigeminal neuritis had diffuse enlargement of the nerve without a mass lesion. These nerves were isointense to brain parenchyma on T1-weighted (T1W) precontrast images and proton-density-weighted (PDW) images and either isointense or hyperintense on T2-weighted (T2W) images. Dogs with a nerve sheath tumor had a solitary or lobulated mass with displacement of adjacent neuropil. Nerve sheath tumors were isointense to the brain parenchyma on T1W, T2W, and PDW images. All trigeminal nerve lesions enhanced following contrast medium administration. Atrophy of the temporalis and masseter muscles, with a characteristic increase in signal intensity on T1W images, were present in all dogs.     

Assessment of dorsal nerve root and spinal cord dorsal horn function in clinically normal dogs by determination of cord dorsum potentials

OBJECTIVE: To establish normal predictive values for cord dorsum potential (CDP) onset latency after thoracic and pelvic limb sensory or mixed nerve stimulation in adult dogs. ANIMALS: 26 clinically normal adult dogs. PROCEDURE: Sensory nerve action potentials (SNAP) were recorded proximally from tibial and lateral superficial radial nerves after distal stimulation. The CDP were recorded from the L4-L5 interarcuate ligament for the tibial nerve and from the C7-T1 interarcuate ligament for the radial nerve. Linear regression analyses were performed for CDP onset latency, and mean +/- SD was calculated for CDP onset to peak latency differences and sensory nerve conduction velocities (SNCV). RESULTS: For the tibial nerve, expected CDP onset latency (CDPOL) = -1.194 + 0.014 X pelvic limb length (mm; R2 = 0.912); CDPOL = -2.156 + 0.011 X pelvic limb/spinal length (mm; R2 = 0.911); and CDPOL = 0.941 + 2.197 X tibial nerve SNAP latency (milliseconds; R2 = 0.903). For the radial nerve, CDPOL = -0.9 + 0.014 x thoracic limb length (mm; R2 = 0.873); and CDPOL = 1.454 + 1.874 X radial nerve SNAP latency (milliseconds; R2 = 0.903). Mean +/- SD for CDP onset to peak latency difference for tibial and radial nerves was 3.1+/-0.3 and 3.0+/-0.4 milliseconds, respectively. CONCLUSIONS: Strong linear associations exist between CDPOL and a number of easily measured peripheral independent variables in dogs. There is also a narrow range of normal values for CDP onset to peak latency differences that is independent of limb length. CLINICAL RELEVANCE: CDP evaluation can be used to accurately assess functional severity and distribution of abnormalities in proximal sensory nerves, dorsal nerve roots, and spinal cord dorsal horns in dogs with suspected neuropathy, radiculopathy, or myelopathy involving the brachial or lumbosacral intumescences.     

Neurological Manifestations of Hypothyroidism: A Retrospective Study of 29 Dogs

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 T₄ prestimulation concentration = 0.8 μg/dL; mean T₄ 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 P₁-P₆ and decreased amplitude of P_4,5-N₅. 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 T₄ concentrations were measured at least 3 times for each dog every 2 months (mean T₄ 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.