Felis ISSN 2398-2950

Spinal cord diseases: overview

Contributor(s): Laurent Garosi

Introduction

  • Although seen less commonly than in dogs, spinal diseases are important causes of disability in cats and represent a high proportion of the caseload in a neurology referral center.
  • Intervertebral disk diseases is an uncommon cause of paresis in cats.
  • Spinal column is made up of bony vertebrae (7 cervical, 13 thoracic, 7 lumbar, 3 sacral and variable number of caudal vertebrae).  Through vertebrae runs the vertebral canal inside which the spinal cord is protected.
  • Intervertebral disk is a cartilaginous pad between two adjacent vertebrae and lies beneath spinal cord. Disks give spine flexibility and act as shock absorbers.
  • Spinal cord is made of neuropil and fibers (neuronal processes) linking brain and rest of the body including limbs, anus, bladder and tail. These fibers carry a wide variety of information about movement of the limbs or tail (motor function), control of the bladder or anal function, ability to recognize position of body in space and coordination of movement (proprioception).
  • Investigations of spinal cord disease require a very accurate clinical neurolocalization Neuroanatomical diagnosis.
  • Spinal cord is divided into functional segments (8 cervical, 13 thoracic, 7 lumbar, 3 sacral and variable number of caudal). Segments contain the cell bodies of the lower motor neuron (LMN). The segments C6 - T2 and L4 - S3 contain the cell bodies of the LMN innervating the thoracic and pelvic limbs. Lesion at the level of these intumescence results in LMN signs in the corresponding limb(s).
  • Some spinal cord segments lie in the vertebra of the same annotation while others do not. Neurological lesion localization refers to spinal cord segments.
  • Two broad categories of diseases can affect spinal cord function: compressive and non-compressive diseases.

Pathogenesis

Etiology

  • Disease processes that affect nervous system classified according to pneumonic mean DAMNITV (degenerative - anomalous - metabolic - neoplastic - nutritional - inflammatory/infectious - traumatic - toxic - vascular).  Each disease process has typical signalment, onset and progression as well as distribution within the nervous system.
  • Differential diagnosis list essential for choosing and interpreting any diagnostic test however sophisticated.  Diagnostic test aimed at confirming or excluding different hypotheses, not replacing clinical evaluation.
  • Differential diagnosis should take account of:
    • Historical data.  Question owner to define onset and progression of condition.  May give clues as to:
      •  How widespread or focal disease process is in the nervous system.
      • Any evidence of asymmetry.
      • Severity of signs.
    • Neurological findings. Define:
      • Lesion localization (affected spinal cord segments) and distribution (focal, multifocal, diffuse) within nervous system.
      • Severity of the disease process when combined with results of diagnostic tests.
  • Two broad categories of diseases affect the spinal cord function: compressive and non-compressive diseases.
  • Compressive diseases include:
  • Non-compressive diseases include:
    • Spinal cord malformation (hydrosyringomyelia, meningocoele, meningomyelocoele, spinal dysraphism), inflammatory/infectious CNS disease (myelitis).
    • Degenerative disease and lysosomal storage diseases Storage disease).
    • Vascular accident (such as fibrocartilaginous embolism Fibrocartilaginous embolism) and other causes of ischemic myelopathy.
    • Acute non-compressive nuclear disk extrusion (also known as type III disk herniation or high speed/low volume disk herniation).

Pathophysiology

  • Primary injuries occur at time of injury and include:
    • Parenchymal damage (contusion, laceration, direct axono-neuronal damage).
    • Vascular damage (hemorrhage and abnormal perfusion). This primary injury is beyond control of clinician and may initiate a number of secondary pathophysiological lesions.
  • Secondary injuries are a number of interrelated biochemical pathways that act in concert to perpetuate further brain tissue damage. Occur few minutes to 24-48 hours after onset.
  • The mechanisms of secondary injuries can be summarized as energy failure, changes in membrane permeability, excitotoxicity, oxidative damage and inflammation.

Diagnosis

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Treatment

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Outcomes

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Further Reading

Publications

Refereed papers

Other sources of information

  • de Lahunta A, Glass E (2008) Veterinary Neuroanatomy and Clinical Neurology. 3rd edn. St Louis, Missouri: W B Saunders Co.
  • Olby N, Halling K B, Glick T R (2005) Rehabilitation for the neurological patient. Vet Clin North Am Small Anim Pract 35(6), 1389-13409, viii.
  • Platt S & Olby N (eds) BSAVA Manual of Canine and Feline Neurology. 3rd edn. Bristish Small Animal Veterinary Association. Chapter 24.
  • Oliver J E, Lorenz M D & Kornegay J N (1997) Handbook of Veterinary Neurology. Third edition. Philadelphia: W B Saunders Company.
  • Wheeler S J & Sharp N J H (1994) Small Animal Spinal Disorders - Diagnosis and Surgery. St Louis, W B Saunders.
  • Braund K G (1994) Clinical Syndromes in Veterinary Neurology. Second edition. St Louis: Mosby Year Book.


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