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Acute idiopathic polyradiculoneuritis
Synonym(s): Coonhound paralysis
Introduction
- One of most common polyneuropathies.
- Signs: similar to distal denervating disease Distal denervating disease, an acute rapidly progressive generalized lower motor neuron flaccid paresis to paralysis with stabilization of signs after 10 days.
- Diagnosis:
- Acute progressive flaccid tetraparesis to tetraplegia with normal bladder and tail function and normal pain sensation.
- Electrophysiology and lumbar CSF analysis aid in diagnosis.
- Treatment: supportive care, intense physical rehabilitation.
- Prognosis: often recover within 3-5 weeks with adequate supportive care.
Presenting signs
- Rapidly progressive, weakness usually starting in pelvic limbs with hyporeflexia and areflexia.
- Rapid involvement of thoracic limbs.
Geographic incidence
- High incidence in countries with raccoons, eg United States, central and parts of South America.
- The disease occurs in countries without raccoon populations presumably caused by etiologies other than raccoon saliva.
- Worldwide.
Age predisposition
- Adult dogs are primarily affected.
- >3 months old.
Breed/Species predisposition
- Raccoon hunting breeds are more at risk due to the diseases associated with raccoon saliva Black and Tan Coonhound.
- Jack Russell terriers Jack Russell terrier and West Highland White terriers West Highland White Terrier.
Cost considerations
- Treatment with IV immune globulins (rarely done).
- Assisted ventilation/intensive care for dogs with respiratory paralysis.
- Intensive care may be prolonged and expensive.
Special risks
- The effects of idiopathic polyradiculoneuritis on the fetus of an affected bitch are unknown.
Pathogenesis
Etiology
- Strong association with contact with raccoon saliva in some cases.
- Raw chicken meat consumption is a risk factor in dogs for the development of acute polyradiculoneuritis which potentially is mediated by infection with Campylobacter spp Campylobacter jejuni.
- Possibly related as well to upper respiratory infections.
- Possibly associated with modified live rabies vaccine and distemper-hepatitis-parvovirus-leptospirosis combination vaccine.
- Dogs with acute polyradiculoneuritis have significantly lower serum 25-hydroxy vitamin D3 concentration compared to a control group. The cause and significance of this altered vitamin D status in dogs with polyradiculoneuritis are unclear and require further investigations.
Specific
- Possibly vaccination.
- Contact with raccoons and raccoon saliva.
- Possibly upper respiratory or gastrointestinal infections.
- Consumption of raw chicken.
- Odds of developing acute idiopathic polyradiculoneuritis possibly greater in the autumn and winter compared to spring in one study.
Pathophysiology
- Disease affects ventral spinal nerve roots more severely with minimal dorsal nerve root involvement.
- Immune response directed against proteins or lipids in raccoon saliva, bacteria or viruses → immune response cross reaction with similar proteins or lipids found in canine peripheral nerves → axonal degeneration with some demyelination → impaired nerve impulse → decreased muscle tone and tendon reflex → muscular atrophy.
- Lipopolysaccharides from Campylobacter contain a ganglioside-like epitope that resembles elements of peripheral nerve gangliosides. Molecular minicry and a cross-reactive immune-response may play a role in the pathogenesis.
- Anti-GM2 ganglioside antibodies in dogs affected with acute polyradiculoneuritis has been demonstrated, reinforcing the hypothesis that this condition is the canine counterpart of Guillain-Barre syndrome in humans.
- Immune responses directed either at Schmidt-Lanterman clefts, the paranode-node complex or both.
- Based on infiltrative and non-inflammatory changes, 4 subtypes and/or stages are distinguished, some of which indicate localization of primary target antigens while others represent convergent late stage pictures, as a consequence to epitope spreading.
Timecourse
- Duration of neurologic dysfunction ranges from several weeks to 4 months and depends on initial severity of neurologic involvement.
- Histopathological changes in nerves seen within 7-10 days of onset of signs.
- Signs appear 7-14 days after initiating incident.
- Paralysis lasts several weeks to 4 months.
- Incomplete recovery and lack of improvement have been observed.
- Tetraparesis occurs 24-48 hours after neurological signs first develop.
- Initial progression of signs occurs over 4-5 days <10 days.
Diagnosis
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Treatment
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Prevention
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Outcomes
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Further Reading
Publications
Refereed papers
- Recent references from PubMed and VetMedResource.
- Martinez-Anton L, Marenda M, Firestone S M et al (2018) Investigation of the role of Campylobacter infection in suspected acute polyradiculoneuritis in dogs. J Vet Intern Med 32, 352-360 PubMed.
- Laws E J, Harcourt-Brown T R, Granger N et al (2017) An exploratory study into factors influencing development of acute canine polyradiculoneuritis in the UK. JSAP 58, 437-443 PubMed.
- Laws E J, Kathrani A, Harcourt-Brown T R, Granger N et al (2017) 25-Hydroxy vitamin D3 serum concentration in dogs with acute polyradiculoneuritis compared to matched controls. JSAP Nov 24. Doi:10.1111/jasp.12791. [Epub ahead of print] PubMed.
- Gross S, Fisher A, Rosati M et al (2016) Nodo-paranodopathy, internodopathy and cleftopathy: Target based reclassification of Guillain-Barre-like immune-mediated polyradiculoneuropathies in dogs and cats. Neuromuscul Disord 26, 825-836 PubMed.
- Stanciu G D, Slocan G (2016) Acute idiopathic polyradiculoneuritis concurrent with acquired myasthenia gravis in a West Highland white terrier dog. BMC Vet Res 12, 111 PubMed.
- Anor S (2014) Acute lower motor neuron tetraparesis. Vet Clin North Am Small Anim Pract 44, 1201-1222 PubMed.
- Rupp A, Galban-Horcajo F, Bianchi E et al (2013) Anti-GM2 ganglioside antibodies are a biomarker for acute canine polyardiculoneuritis. J Periph Nerv Syst 18, 75-88 PubMed.
- Hirschvogel K, Jurina K, Steinberg T A et al (2012) Clinical course of acute canine polyradiculoneuritis following treatment with human IV immunoglobulin. JAAHA 48, 299-309 PubMed.
- Cuddon P A (1998) Electrophysiologic assessment of acute polyradiculoneuropathy in dogs - comparison with Guillain-Barré syndrome in people. J Vet Intern Med 12 (4), 294-303 PubMed.
- High M E (1996) Acute canine polyradiculoneuritis. Can Vet J 37 (5), 305 PubMed.
- McGlennon N J (1990) Polyradiculoneuritis and polymyositis due to a toxoplasma-like protozoan - diagnosis and treatment. JSAP 31 (2), 102-104 VetMedResource.
- Cummings J F et al (1988) Canine protozoan polyradiculoneuritis. Acta Neuropathol (Berl) 76 (1), 46-54 PubMed.
- Cummings J F et al (1982) Coonhound paralysis. Further clinical studies and electron microscopic observations. Acta Neuropathol (Berl) 56 (3), 167-178 PubMed.
- Northington J W et al (1982) Acute canine idiopathic polyneuropathy. A Guillain-Barré-like syndrome in dogs. J Neurol Sci 56 (2-3), 259-273 PubMed.
- Northington J W et al (1981) Acute idiopathic polyneuropathy in the dog. JAVMA 179 (4), 375-379 PubMed.
- Chrisman C L (1975) Differentiation of tick paralysis and acute idiopathic polyradiculoneuritis in the dog using electromyography. JAAHA 11 (4), 455-458 VetMedResource.
Other sources of information
- Merck Veterinary Manual. (1998) 8, 914.
- Oliver J E (1997) Handbook of Veterinary Neurology 3. pp 187-188.
- Cuddon P (1997) Coonhound paralysis (polyradiculoneuritis, idiopathic). The 5 minute veterinary consult - canine and feline. pp 476-477.
- Ettinger S J (1995) Textbook of Veterinary Internal Medicine. 4(1), 716.
- Schrauwen E (1995) Postvaccinal acute polyradiculoneuritis in a young dog. Prog Vet Neur 6(2), 68-70.
- Dees C (1984) The immunological basis of Coonhound paralysis. Fed Proc 43(7), 1993.
- DeLahunta A (1983) Veterinary Neuroanatomy and Clinical Neurology (2), 74-77.