Presence of thoracic and lumbar vertebral malformations in pugs with and without chronic neurological deficits.

Congenital vertebral malformations (CVMs) are common in brachycephalic dogs such as the pug, and are often considered incidental findings. However, specific CVMs have been suggested to be associated with neurological deficits in pugs. The objective of this study was to investigate the clinical importance of CVMs in the pug by comparing computed tomography studies of the thoracolumbar spine from pugs without neurological deficits with those from pugs with a confirmed T3-L3 spinal cord lesion and neurological deficits consistent with a chronic T3-L3 myelopathy. A total of 57 pugs were recruited into the study from Sweden (n=33), United Kingdom (n=21) and Norway (n=3); 30 with neurological deficits and 27 without. Focal T3-L3 pathology was confirmed in all pugs with neurological deficits by magnetic resonance imaging (n=29) and/or pathology (n=15). Computed tomography studies of the thoracolumbar spine from pugs with and without neurological deficits were compared to investigate possible associations between presentation of neurological deficits consistent with chronic T3-L3 pathology and signalment variables, presence of CVMs and type of CVMs. Congenital vertebral malformations were as common in pugs with, as in pugs without, neurological deficits. Regardless of neurological status, the majority of pugs (96%) presented with one or more CVM. An association between presence, or type of CVM in the T1-L3 vertebral column, and neurological deficits consistent with T3-L3 pathology could not be confirmed.

Acquired equine polyneuropathy of Nordic horses: A conspicuous inclusion body schwannopathy.

Acquired equine polyneuropathy (AEP), formerly also known as Scandinavian knuckling syndrome, is one of the most prevalent polyneuropathies in equids in Norway and Sweden, with more than 400 cases registered since first observations in 1995. Despite geographical clustering and an association to forage feeding, its aetiology remains unknown. Clinically AEP is characterized by knuckling due to dysfunction of metatarsophalangeal extensor muscles. This neuropathological study aimed to gain further insights in the pathobiology of AEP and its underlying aetiopathogenesis. We thereby confirmed that all affected horses suffered from similar large fibre neuropathy, exhibiting conspicuous Schwann cell inclusions in most samples, suggestive of a primary disruption of Schwann cell metabolism leading to inclusion body schwannopathy with secondary inflammatory changes. The degree of nerve pathology was not predictive of clinical outcome.

Long-term follow-up of Norwegian horses affected with acquired equine polyneuropathy.

BACKGROUND: Acquired equine polyneuropathy (AEP), a neurological disease clinically characterised by knuckling of metatarsophalangeal joints, has been described in numerous Nordic horses during the last 20 years. Although clinical recovery has been reported, large-scale data on long-term follow-up of survivors have been lacking. OBJECTIVES: To describe long-term survival of AEP affected horses registered in Norway, with a focus on athletic performance and possible residual clinical signs connected to the disease. STUDY DESIGN: A retrospective cohort study. METHODS: The study includes 143 horses recorded with AEP in Norway from 2000 to 2012, with the follow-up period continuing until 2015. Participating owners of survivors completed a standardised questionnaire, providing information on disease and convalescence, management, performance-level and possible residual clinical signs. To investigate the follow-up of survivors, we performed 2 multivariable linear regression models. RESULTS: The follow-up time of survivors was 1.0-14.5 years (median 5.3, interquartile range 2.5-7.2). Fifty-seven horses survived and all but 3 horses returned to previous or higher level of performance. However, possible disease-related residual clinical signs were reported in 14/57 horses. Forty-nine of the survivors were in athletic use at time of contact. The majority of survivors were categorised with low severity-grades at time of diagnosis and the initial grade was significantly associated with time to resumed training. Only 3 horses had experienced relapse/new attack during the follow-up period. MAIN LIMITATION: Athletic performance was judged by owners, which renders a possible source of bias. CONCLUSIONS: Although AEP is a potential fatal disease, most survivors will recover and return to minimum previous level of athletic performance. Some horses display residual clinical signs, but often without negative effect on performance and relapse of disease is rare.

Cervical spinal intradural arachnoid cysts in related, young pugs.

Seven related young pugs were diagnosed with cervical spinal intradural arachnoid cysts by magnetic resonance imaging (n = 6) and myelography (n = 1). All dogs were presented with skin abrasions on their thoracic limbs and non-painful neurological deficits, indicating a C1-T2 myelopathy. In all six dogs examined by magnetic resonance imaging not only the spinal arachnoid cyst but also a concomitant, most likely secondary, syringohydromyelia was confirmed. Pedigree analysis suggested a genetic predisposition for spinal arachnoid cysts in this family of pugs. Generalised proprioceptive deficits more pronounced in the thoracic limbs suggesting a focal cervical spinal cord lesion, with concomitant skin abrasions on the dorsal aspect of the thoracic limbs in a young pug, should alert veterinarians to the possibility of cervical spinal arachnoid cysts.

Inherited polyneuropathy in Leonberger dogs.

BACKGROUND: Although reporting the same clinical phenotype, inherited polyneuropathy in Leonberger dogs (ILPN) has been attributed to various modes of inheritance. HYPOTHESIS: The ILPN is one disease with a major risk factor on chromosome X. ANIMALS: Dogs affected by ILPN (n = 104). METHODS: Pedigree analyses were performed by means of a case-control approach. Data were retrieved either from medical records of cases diagnosed by the first author (n = 13), from breeders (n = 18) or from different registries publishing data on affected dogs (n = 73). A comparison was made between the X-chromosome ancestry of fathers of affected male dogs and the ancestry of the X-chromosomes of mothers of affected dogs of either sex. A systematic random sample, obtained from an international database of registered Leonberger dogs, served as a reference population regarding ancestry. RESULTS: Having one particular female, born 1943, in the X-chromosomal lineage is a major risk factor for developing ILPN. Sex distribution among affected dogs is in favor of a risk factor on the X-chromosome and contradicts a monogenic autosomal or mitochondrial inheritance. CONCLUSIONS AND CLINICAL IMPORTANCE: The ILPN is considered most likely to be one disease, and the inheritance of ILPN is best explained by an underlying X-linked mode of transmission for the phenotype. However, age at onset and severity of signs might be determined by contributing loci. This has consequences in molecular genetic studies and for breeding strategies aimed at eliminating this disease.