Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0152025 (polyneuropathy)
 7,862 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Laryngeal paralysis is a common cause of upper airway obstruction in older, large-breed dogs and is likely associated with a generalized polyneuropathy in most animals. Surgical therapy is frequently indicated, and UAL is currently the recommended treatment. Respiratory signs significantly improve in most patients after surgery; however, postoperative complication rates can be high, and patients have a lifelong risk of developing respiratory tract disease.
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PMID:Laryngeal paralysis in dogs. 1951 15

Laryngeal paralysis is the effect of an inability to abduct the arytenoid cartilages during inspiration, resulting in respiratory signs consistent with partial airway obstruction. The aetiology of the disease can be congenital (hereditary laryngeal paralysis or congenital polyneuropathy), or acquired (trauma, neoplasia, polyneuropathy, endocrinopathy). The most common form of acquired laryngeal paralysis (LP) is typically seen in old, large breed dogs and is a clinical manifestation of a generalised peripheral polyneuropathy recently referred to as geriatric onset laryngeal paralysis polyneuropathy. Diagnosing LP based on clinical signs, breed and history has a very high sensitivity (90%) and can be confirmed bylaryngeal inspection. Prognosis after surgical correction depends on the aetiology: traumatic cases have a good prognosis, whereas tumour-induced or polyneuropathy-induced LP has a guarded prognosis. Acquired idiopathic LP is a slow progressive disease, with dogs reaching median survival times of 3-5 years after surgical correction.
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PMID:Laryngeal paralysis in dogs: an update on recent knowledge. 2371 78

Laryngeal paralysis associated with a generalized polyneuropathy (LPPN) most commonly exists in geriatric dogs from a variety of large and giant breeds. The purpose of this study was to discover the underlying genetic and molecular mechanisms in a younger-onset form of this neurodegenerative disease seen in two closely related giant dog breeds, the Leonberger and Saint Bernard. Neuropathology of an affected dog from each breed showed variable nerve fiber loss and scattered inappropriately thin myelinated fibers. Using across-breed genome-wide association, haplotype analysis, and whole-genome sequencing, we identified a missense variant in the CNTNAP1 gene (c.2810G>A; p.Gly937Glu) in which homozygotes in both studied breeds are affected. CNTNAP1 encodes a contactin-associated protein important for organization of myelinated axons. The herein described likely pathogenic CNTNAP1 variant occurs in unrelated breeds at variable frequencies. Individual homozygous mutant LPPN-affected Labrador retrievers that were on average four years younger than dogs affected by geriatric onset laryngeal paralysis polyneuropathy could be explained by this variant. Pathologic changes in a Labrador retriever nerve biopsy from a homozygous mutant dog were similar to those of the Leonberger and Saint Bernard. The impact of this variant on health in English bulldogs and Irish terriers, two breeds with higher CNTNAP1 variant allele frequencies, remains unclear. Pathogenic variants in CNTNAP1 have previously been reported in human patients with lethal congenital contracture syndrome and hypomyelinating neuropathy, including vocal cord palsy and severe respiratory distress. This is the first report of contactin-associated LPPN in dogs characterized by a deleterious variant that most likely predates modern breed establishment.
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PMID:A CNTNAP1 Missense Variant Is Associated with Canine Laryngeal Paralysis and Polyneuropathy. 3326 Nov 76