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Polyradiculoneuropathies

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Synonym(s): Polyneuritis, acute or chronic polyradiculoneuritis, peripheral neuropathies, Coonhound paralysis, idiopathic polyradiculoneuritis

Introduction

  • Group of inflammatory diseases which affect the nerve roots and/or peripheral nerves.
  • Cause: immune-mediated, or infectious disease, attack on peripheral nerve or nerve roots, causing axonal degeneration and some demyelination.
  • Signs: paresis/paralysis, especially in pelvic limbs although with normal progression to involve all 4 limbs, loss of tendon reflexes, and variable muscle atrophy. Sensory function is intact as is bladder and bowel function.
  • Diagnosis: acute to chronic progressive tetraparesis to tetraplegia with normal sensation, tail, bladder and bowel function. Electrophysiology, CSF analysis, muscle and nerve biopsies and protozoal serum and CSF titers aid in diagnosis.
  • Treatment: supportive care and physical rehabilitation.
  • Prognosis: variable:
    • Good if acute polyradiculoneuritis or Coonhound paralysis Acute idiopathic polyradiculoneuritis.
    • Guarded to poor if chronic progressive radiculoneuritis or protozoal polyradiculoneuritis.

Presenting signs

  • Acute to chronic onset, paresis/paralysis, initially in pelvic limbs, progressing to all limbs, dependent on etiology.
  • Loss of tendon reflexes except perineal reflex which remains normal.
  • Reduced muscle tone.
  • Because the disease is often confined mostly to the ventral nerve roots, proprioception can remain unaffected in some cases if given enough support and provided they maintain some degree of motor function to perform the efferent pathway of this test.
  • Variable muscle atrophy.
  • Respiratory paralysis and cranial nerve VII deficits may develop in severe cases of acute polyradiculoneuritis or Coonhound paralysis.

Geographic incidence

  • Coonhound paralysis occurs relative to the distribution of raccoons (North, central and parts of South America).
  • USA and UK: infectious and idiopathic polyradiculoneuritis. Infectious causes include Neosporosis Neosporosis and Toxoplasmosis Toxoplasmosis.

Age predisposition

  • Adult dogs are primarily affected with acute and chronic polyradiculoneuropathies.
  • Neospora associated polyradiculoneuritis typically occurs in young puppies between 2-4 months old.

Breed/Species predisposition

  • Any breed in contact with raccoons can develop acute polyradiculoneuritis (Coonhound paralysis).
  • Dog breeds used in raccoon hunting would have a higher incidence, eg Coonhounds Black and Tan Coonhound, Walker hounds, Blue tick hounds, Redbone hounds.
  • Jack Russell terriers Jack Russell Terrier and West Highland White terriers West Highland White Terrier for acute idiopathic polyradiculoneuritis.

Cost considerations

  • IV immuno globulin therapy for acute polyradiculoneuritis and Coonhound paralysis is expensive.
  • Intensive care may be prolonged and expensive.
  • Long-term immunosuppressive drugs, eg cyclophosphamide, azothioprine, for chronic inflammatory polyradiculoneuritis is moderately expensive.
  • Diagnostic evaluation including electrophysiology, nerve and muscle biopsies, CSF analysis, and protozoal serology is also quite costly.

Special risks

  • The bitch can carry the neospora organism without clinical signs and continue to transmit it to successive litters.
  • The neospora and toxoplasma organisms in the dog do not have zoonotic potential.

Pathogenesis

Etiology

  • Immune response to antigen in racoon saliva (Coonhound paralysis Acute idiopathic polyradiculoneuritis ).
  • Immune response to other suspected antigens associated with upper respiratory infections, gastroenteritis (viral and bacterial), vaccination, and possible environmental antigens (acute and chronic idiopathic inflammatory polyradiculoneuritits).
  • 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.
  • Toxoplasmosis Toxoplasmosis.
  • Neosporosis Neosporosis.

Predisposing factors

General

  • Coonhounds and other raccoon hunting breeds due to the nature of their activities (Coonhound paralysis).

Specific

  • Pregnant bitch harboring the neospora organism in her placenta (Neospora polyradiculoneuritis).
  • Previously affected dogs are at greater risk of developing Coonhound paralysis than the general canine population.
  • Consumption of raw chicken for acute idiopathic polyradiculoneuritis.
  • 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.
  • Exposure to offending antigen → immune response directed against proteins or lipoids in antigen (raccoon saliva, bacterial cell wall, etc) → cross-reaction with similar proteins and/or lipoids in canine peripheral nerves:
    • For acute and chronic inflammatory polyradiculoneuritis: → immune mediated attack on nerve roots and peripheral nerves → demyelination and axonal degeneration → impaired nervous supply to limbs → decreased muscle tone/tendon reflexes → muscular atrophy.
    • For Neospora and Toxoplasma: → exposure to offending protozoa → localization of protozoal cysts in peripheral nerve roots → initiates inflammatory response around them → secondary inflammation of peripheral nerve roots → demyelination and axonal degeneration → impaired nervous supply to limbs → decreased muscle tone/tendon reflexes → muscular atrophy.
  • Lipopolysaccharides from Campylobacter contain a ganglioside-like epitope that resembles elements of peripheral nerve gangliosides. Molecular mimicry 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.

Timecourse

  • Coonhound paralysis and acute idiopathic polyradiculoneuritis:
    • Signs appear 7-14 days after exposure to antigen.
    • Initial progression of tetraparesis to tetraplegia occurs over 4-5 days (occasionally <10 days) then stabilizes. Duration of neurological dysfunction ranges from several weeks to 4 months depending on initial severity of neurological dysfunction.
    • Incomplete recovery and lack of improvement have been observed.
  • Chronic progressive polyradiculoneuritis:
    • Insidious onset with slow progression over many weeks to months (even years).
    • Can have relapsing course or relentlessly progressive course.
  • Neospora polyradiculoneuritis:
    • Acute to subacute onset with rapid progression over 1-2 months.

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 (1), 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 (8), 437-443 PubMed.
  • Laws E K, 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 59 (4), 222-7 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 catsNeuromuscul Disord 26 (12), 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 (1), 111 PubMed.
  • Añor S (2014) Acute lower motor neuron tetraparesis. Vet Clin North Am Small Anim Pract 44 (6), 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 (1), 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 (5), 299-309 PubMed.
  • Holt N, Murray M, Cuddon P A et al (2011) Seroprevalence of various infectious agents in dogs with suspected acute canine polyradiculoneuritis. J Vet Intern Med 25 (2), 261-266 PubMed.
  • Cuddon P A (1998) Electrophysiologic assessment of acute polyradiculoneuropathy in dogs - comparison with Guillain-Barre 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.
  • Cuddon P et al (1992) Neospora caninum infection in English Springer Spaniel littermates - diagnostic evaluation and organism isolation. J Vet Int Med 6 (6), 325-332 PubMed.
  • Cummings J F et al (1988) Canine protozoan polyradiculoneuritis. Acta Neuropathol (Berl) 76 (1), 46-54 PubMed.
  • Bichsel P et al (1987) Chronic polyneuritis in a Rottweiler. JAVMA 191 (8), 991-994 PubMed.
  • Northington J W, Brown M J (1983) Acute canine idiopathic polyneuropathy. A Guillain-Barre-like syndrome in dogs. J Neurol Sci 56 (2-3), 259-273 PubMed.
  • Cummings J F et al (1974) Chronic relapsing polyradiculoneuritis in a dog - a clinical, light and electron microscope study. Acta Neuropathol 28 (3), 191-204 SpringerLink.

Other sources of information

  • Olby NJ (2013) Tetraparesis. In: Platt S R, Olby N J (eds). BSAVA Manual of Canine and Feline Neurology. 4th edition. Gloucester (United Kingdom): British Small Animal Veterinary Association; pp 271-296.
  • Merck Veterinay Manual (1998) 8, pp 914.
  • Cuddon P (1997) Coonhound paralysis (polyradiculoneuritis, idiopathic). The 5 Minute Veterinary Consult - Canine and Feline. pp 476-477
  • Oliver J E (1997) Handbook of Veterinary Neurology 3 pp 187-188.
  • Ettinger S J (1995) Textbook of Veterinary Internal Medicine 4. 1), 715-716.
  • Dees C (1984) The immunologic basis of Coonhound paralysis. Federation proceedings 43(7), 1993.
  • DeLahunta A (1983) Veterinary Neuroanatomy and Clinical Neurology 2. pp 74-77.
  • Hawe R S (1979) Acute idiopathic polyradiculoneuritis in a dog (a case report and discussion). Small Animal Clinician 74(5), 675-682.