Felis ISSN 2398-2950

Peripheral neuropathies

Synonym(s): Neuropathy

Contributor(s): Laurent Garosi

Introduction

  • Uncommon peripheral nerve disease in which the primary changes appear in the nerve cell body.
  • Includes motor neuron disease, mixed motor and sensory neuropathies, sensory neuropathies and autonomic neuropathies   Feline dysautonomia  .
  • Cause: often unknown; can be hereditary, toxic, idiopathic, metabolic, paraneoplastic, infectious or inflammatory.
  • Signs: progressive neurological deficits.
  • Treatment: high quality nursing.
  • Prognosis: poor because generally progressive.

Pathogenesis

Etiology

  • Causes:
    • Hereditary.
    • Toxic.
    • Inflammatory.
    • Traumatic
    • Infectious.
    • Immune-mediated.
    • Idiopathic.
    • Ischemic.
    • Metabolic.
    • Paraneoplastic.

Pathophysiology

  • Premature degeneration and death of neuronal cell populations in the spinal cord and/or interruption of nerve to target organ   →   decreased or absent function of target organ.
  • Classification based on
  • Anatomical position
    • Distal or proximal axonopathy.
    • Motor or sensory.
  • Pathological change
    • Axonal degeneration.
    • Segmental demyelination.
  • Etiology
    • Inherited.
    • Acquired.
Wallerian degeneration
  • Usually follows nerve trauma   Peripheral nerve: trauma  .
  • Distal to the site of trauma axons die and myelin sheaths degenerate.
  • Schwann cells remain intact for some time in the distal stump of a transected nerve, and proliferate to form columns of denervated Schwann cells also known as bands of Bungner.
  • Regenerating sprouts from the intact axons in the proximal stump penetrate the distal stump with the denervated Schwann cells that serve to guide the regenerating nerve fiber back to target site.

Axonal degeneration (wallerian-like degeneration)

  • Degeneration of axon and myelin sheath starts from distal extremity.
  • Mainly affects large myelinated axonsdistal axonopathy(dying-back process).
  • Regeneration may occur or adjacent axons may reinnervate denervated muscle fibers.
  • Secondary segmental demyelination  →   affected axons atrophy prior to degeneration.
  • The sprouting of healthy axons, and their reinnervation of denervated muscle fiber, results in expansion of the motor units and loss of the normal mixing of fibers that make up the units.

Demyelination

  • Axon remains intact but myelin sheath lost along whole or part of length (segmental demyelination).
  • Primary site of damage can be either the Schwann cell or its myelin sheath.
  • Recovery is possible if adjacent Schwann cells proliferate and remyelinate axons.

Timecourse

  • Variable, depends on entity involved.

Diagnosis

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Treatment

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references fromPubMed.
  • Coates J R, O'Brien D P (2004)Inherited peripheral neuropathies in dogs and cats.Vet Clin North Am Small Anim34, 1361-1401.
  • Dickinson P J, LeCouteur R A (2004)Feline neuromuscular disorders.Vet Clin North Am Small Anim34, 1307-1359.
  • Chrisman C L (2000)Polyneuropathies of cats.JSAP41, 3840389.
  • Braund K G (1996)Degenerative causes of neuropathies in dogs and cats - Part I.Vet Med91722-739.
  • Braund K G (1996)Endogenous causes of neuropathies in dogs and cats - Part II.Vet Med91740-754.
  • Braund K G (1996)Idiopathic and exogenous causes of neuropathies in dogs and cats - Part III.Vet Med91755-769.

Other sources of information

  • Duncan I D (1989)Canine and feline polyneuropathies.In:Manual of Small Animal NeurologyWheeler S (Ed), BSAVA, Cheltenham pp243.


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