Seroprevalence of various infectious agents in dogs with suspected acute canine polyradiculoneuritis.

BACKGROUND: Acute canine polyradiculoneuritis (ACP) is considered to be an animal model of the acute axonal form of Guillain-Barré syndrome (GBS) in humans. Various antecedent events have been associated with GBS, including bacterial or viral infection. The relationship between ACP and previous infection requires additional attention. HYPOTHESIS: We hypothesized a relationship between ACP and serological evidence of exposure to Ehrlichia canis, Borrelia burgdorferi, Toxoplasma gondii, Neospora caninum, Campylobacter jejuni, and canine distemper virus (CDV). ANIMALS: Eighty-eight client-owned dogs, 44 with ACP, 44 age-matched controls. METHODS: Retrospective study with stored serum samples. Serum antibodies against the target organisms were measured with commercially available assays. Sera from dogs with and without ACP that were positive for T. gondii IgG by ELISA were assayed by an IgG heavy chain-specific, Western blot immunoassay. RESULTS: Dogs with ACP (55.8%) were more likely to have T. gondii IgG serum antibody titers than dogs without ACP (11.4%). Serum antibodies from 8 affected dogs and 11 control dogs bound to T. gondii antigens with apparent molecular masses of 67, 61, 58, 45, 33, 24, 9, and 6 kDa. An antigen with an apparent molecular mass of 36 kDa was recognized by 2 dogs with ACP but none of the control dogs. CONCLUSIONS: Results of this study suggest that ACP in some dogs, like GBS in some humans, may be triggered by T. gondii and a prospective study should be performed to further evaluate this potential association.

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.

Nemaline rods in canine myopathies: 4 case reports and literature review.

The diagnosis of nemaline rod myopathy (NM) is based on the presence of numerous pathognomonic rods within a fresh frozen muscle biopsy specimen. Three forms of congenital NM have been described in humans, and rods have been found to occur in various other conditions. A similar myopathy was described in 1986 in a family of cats. In this report, we describe a case of congenital NM in a 10-month-old Border Collie, an adult-onset NM in an 11-year-old Schipperke, and 2 acquired myopathies with nemaline rods in adult dogs associated with hypothyroidism and Cushing's syndrome. Common clinical features included exercise intolerance, abnormal electromyography, and the presence of nemaline rods in fresh, frozen, and glutaraldehyde-fixed biopsies from proximal appendicular limb muscles. Staining of cryostat sections of muscle biopsy specimens by the modified Gomori trichrome technique disclosed numerous rod bodies that were localized to type 1 fibers by the histochemical adenosine triphosphatase reaction. Accumulation of rods also was demonstrated by electron microscopy in 2 of the cases with localized enlargement and streaming of Z lines. Documentation of NM in a young Border Collie and the adult-onset form in the Schipperke alerts clinicians to the existence of this disorder in these breeds.

Myelin mosaicism and brain plasticity in heterozygous females of a canine X-linked trait.

The shaking (sh) pup, an animal model of Pelizaeus-Merzbacher disease, is characterized by severe central nervous system dysmyelination in affected males, and myelin mosaicism in some female heterozygotes as a result of X-linked inactivation. Heterozygous females develop a tremor of varying severity that usually disappears at 4 to 6 weeks, whereas male hemizygotes have severe, generalized tremor that persists throughout life. We have used these two myelin-deficient models to study the potential for recovery with time as reflected by brainstem auditory evoked responses (BAERs). At set time points, the state of myelination in the trapezoid body was studied microscopically. Sequential BAERs demonstrated consistently prolonged interpeak latencies during the period of gross tremor in heterozygotes, with the trend continuing to a lesser extent after tremor cessation. The random nature of X-linked inactivation resulted in variable myelin mosaicism that was reflected in variations in BAER changes within animals in the same litter. In most heterozygotes, the tremor resolved with time, the BAERs returned to near normal, and myelin mosaicism was lost. In contrast, in the affected males, the severity of tremor and lack of recovery was demonstrated by consistent abnormalities in BAER waves at all times studied, and severe and persistent myelin deficiency in the trapezoid body. These findings show that despite the normal tightly programmed temporal development of myelin in the brain in the heterozygous mosaic state, sufficient plasticity persists during the neonatal period for late-stage myelination to occur.

Electrophysiologic assessment of acute polyradiculoneuropathy in dogs: comparison with Guillain-Barré syndrome in people.

Electrophysiologic investigations of motor and sensory nerve as well as ventral nerve root function were performed on 12 dogs with suspected acute canine polyradiculoneuropathy (ACP) at different stages and with different severity of disease. The most reliable electrophysiologic indicators of ACP were electromyographic changes (occurring in 100% of affected dogs), significantly decreased compound muscle action potential amplitudes (in 75, 90, and 100% of affected dogs at all sites along the sciatic/tibial, radial, and ulnar nerves, respectively), increased minimum F-wave latencies (67%), increased F ratios (92%), and decreased F-wave amplitudes (67%). These findings suggest that ACP represents a peripheral motor axonopathy, with demyelination and axonal involvement also occurring in ventral nerve roots. Evidence of peripheral demyelination was present in some dogs although it was overshadowed by the prominent axonopathy. ACP more closely resembles the acute axonal or intermediate forms of Guillain-Barré syndrome in people.

Myelination of the canine central nervous system by glial cell transplantation: a model for repair of human myelin disease.

There is a lack of effective means of promoting remyelination of the central nervous system (CNS) in humans with chronic demyelinating disease. We have investigated the ability of transplanted glia to myelinate areas of the CNS equivalent to focal demyelinated lesions in multiple sclerosis (MS). In these studies we show that transplantation of oligodendrocytes or their progenitors into the CNS of a neonatal or adult canine myelin mutant results in repair of large areas similar in size to many MS plaques. Progenitor or pre-progenitor cells of the oligodendrocyte lineage have the greatest capacity for myelination following grafting, although cells of neonatal origin may also be used. Such an approach may therefore have therapeutic value in the repair of focal lesions in human myelin disease.

Metabolic encephalopathies.

Numerous metabolic derangements originate from outside the CNS that potentially can have a profound effect on cerebral function. The pathogenesis of the resultant dysfunction to the cerebrum and other regions of the brain is extremely varied. However, the CNS can only react in limited ways to these results. Therefore, the veterinarian should recognize the clinical patterns of neurologic signs associated with the metabolic encephalopathies, sift through the multiple potential causes with the aid of other accompanying extracranial clinical signs and clues from biochemical data, understand the underlying pathogenesis of the cerebral dysfunction, and, finally, formulate a rational plan of treatment. Though immediate attention is often directed at restoring homeostasis to the CNS, success is only ultimately achieved via correct and timely treatment of the underlying metabolic disease. Only then does strong potential exist for a permanent reversal of the neurologic deficit.

Familial occurrence of narcolepsy in miniature horses.

In an investigation of 2 closely related Miniature Horses with a history of excessive sleepiness, depression and episodes of collapse, a diagnosis of narcolepsy was made on the basis of neurological examination and pharmacological testing. Further investigations included electroencephalographic examination (EEG), and analysis of protein content, cell count and monoamine metabolite concentrations of lumbosacral cerebrospinal fluid (CSF). There were no abnormalities noted in the EEGs, and no consistent changes in CSF neurotransmitter metabolites in the narcoleptic horses when compared with 3 normal, unrelated Miniature Horses and 2 related, clinically unaffected animals. The breeding background of the 2 affected horses was investigated and a limited survey of Miniature Horse breeders in North America was conducted. These investigations have shown that narcolepsy is a rare but distinct syndrome in the Miniature Horse, and that the cases described here appear to represent a familial occurrence of the disease.

Preferential denervation of the adductor muscles of the equine larynx. I: Muscle pathology.

The laryngeal muscles of 18 horses were examined histologically. The neurogenic changes found in each muscle were scored by four reviewers and the results evaluated statistically. Fifteen of these horses had endoscopic evidence of abnormal laryngeal function, three of which were defined as having adductor paralysis. Measurement of muscle fibre area in two horses with idiopathic laryngeal hemiplegia (ILH) was performed. In the quantitative study of neurogenic change, the adductor muscles were more significantly affected than the abductor muscle. This was also true in the clinical cases of ILH where measurement of muscle fibre area demonstrated that the lateral cricoarytenoid (adductor) muscles showed a wider range of pathological changes than the dorsal cricoarytenoid muscle (abductor). Those horses with the most severe muscle pathology also had the most abnormal endoscopic findings. The propensity for denervation of the adductor muscles should provide clues as to the pathogenesis and natural history of horses with sub-clinical laryngeal disease and ILH.

Polyneuropathy in feline Niemann-Pick disease.

Two related cats, aged 5 months and 7 months, and 1 unrelated cat, aged 4 months, presented with signs of a progressive neuromuscular disease. Detailed electrophysiological studies suggested a primary demyelinating polyneuropathy, which was confirmed by muscle and nerve biopsies and on necropsy examination. Light and electron microscopic findings indicated a lysosomal storage disease, which was diagnosed as sphingomyelinase deficiency (Niemann-Pick disease) by enzyme analysis and lipid fractionation, although significant biochemical differences existed between the 2 related cats and the third cat. Several lines of evidence suggest that these 2 related cats were affected with a variant of type A Niemann-Pick disease, whereas cat 3 represented classic Niemann-Pick disease type A.

Motor fibers in the canine distal caudal cutaneous sural nerve--dual innervation of the hind limb plantar muscles.

The function of the communicating branch of the distal caudal cutaneous sural (DCCS) nerve to the tibial nerve was investigated in 7 adult dogs and was found to contain the motor component of this nerve. This function was studied by direct visualization of the contraction of the hind limb plantar muscles and by direct electrophysiologic recording of motor unit action potentials in these muscles, following stimulation of the DCCS nerve. Contraction of all of the mm. interossei, the mm. lumbricales, the m. adductor digiti quinti and the m. adductor digiti secundi was observed with the stimulation of either the tibial or the DCCS nerves, although there was a qualitative variability in the plantar muscles exhibiting the strongest contraction with stimulation of the latter nerve. This communicating branch was not found in one of the experimental dogs, suggesting some individual variability in the DCCS nerve anatomy and subsequent function. This study conclusively demonstrated that the canine DCCS nerve contains both motor and sensory nerve fibers, which is similar to this nerve in the rat, but anatomically and functionally different to that in the human and the cat.

Acquired scoliosis associated with hydromyelia and syringomyelia in two dogs.

Progressive scoliosis resulting from hydromyelia and syringomyelia was found in 2 dogs. In one dog, hydromyelia was associated with pachymeningeal fibrosis, with adhesions in the cervical portion of the spinal cord. In the other case, a cause was not established. Neither dog had congenital CNS malformations. The clinicopathologic findings in the 2 dogs are described, and the etiology and pathogenesis of hydromyelia and syringomyelia are discussed.

Myasthenia gravis and polymyositis in a dog following fetal hematopoietic cell transplantation.

Myasthenia gravis and focal polymyositis occurred in a dog following successful transplantation of DLA-identical fetal liver hematopoietic cells. There was no evidence of acute or chronic graft-versus-host disease. Antibodies to acetylcholinesterase receptor and immune complexes reactive with myoneural junctions were demonstrated, as well as focal inflammation with perifascicular and type 2 muscle atrophy. The dog responded to treatment with prednisolone and pyridostigmine.