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Spinal cord diseases: overview

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Introduction

  • Spinal diseases are important causes of disability in dogs and represent a high proportion of the caseload in a neurology referral center.
  • 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.
  • 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.

Presenting signs

  • Gait abnormality Gait analysis.
  • Spinal discomfort.
  • Abnormal gait concerns co-ordination (ataxia), strength of voluntary movement (paresis) or more often, a combination of both Ataxia.

Ataxia

  • Ataxia is defined as an uncoordinated gait. Deficit arises from either:
    • Afferent kinesthetic deficit in peripheral nerve or spinal cord (general proprioceptive or sensory ataxia).
    • Vestibular disorder (vestibular ataxia).
    • Cerebellar disorder (cerebellar ataxia).
  • Ataxia can be further divided into:
    • Hypometria (shorter protraction phase of gait).
    • Hypermetria (longer protraction phase of gait).
    • Dysmetria (combination of both hypo- and hypermetria).

Paresis

  • Paresis is defined as a loss of ability to support weight (lower motor neuron disease) or inability to generate a gait (upper motor neuron disease). Term 'paresis' implies that some voluntary movement is still present as compared to paralysis that refers to a more severe paresis with complete (-plegia) loss of voluntary movement. Depending which limbs are affected, the terms paresis/paralysis can be further defined as:
    • Tetraparesis/plegia - paresis/lysis of all four limbs resulting from lesion located cranial to T3 spinal cord segment or from a generalized lower motor neuron disorder.
    • Paraparesis/plegia - paresis/lysis of the pelvic limbs caused by lesion caudal to T2.
    • Monoparesis/plegia - paresis/lysis of one limb caused by lesion of the lower motor neuron innervating the affected limb.
    • Hemiparesis/plegia - paresis/lysis of the limbs on one side due to lesion located cranial to T2. This hemiparesis/plegia is ipsilateral to lesion located between T2 and caudal midbrain and contralateral to lesion located in rostral midbrain or cerebrum.
  • There are two types of paresis - upper motor neuron and lower motor neuron - causing a spastic or flaccid paresis, respectively:
    • UMN paresiscauses a delay in the onset of protraction (swing phase of the gait) with a resultant stride being longer than normal and a stiff quality of movement.
    • LMN paresisreflects degrees of difficulty in supporting weight and varies from a short stride, choppy gait, to complete inability to support weight, causing collapse of the limb whenever weight is placed on it.
  • Less common presentations of spinal cord disease include:
    • Lameness.
    • Urinary incontinence.
    • Fecal incontinence.

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) Spinal cord diseases: lesion localization 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 diseasesinclude:
  • Non-compressive diseasesinclude:

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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Prevention

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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.
  • McGowan C, Goff L & Stubbs N (eds) (2007)Animal Physiotherapy Assessment, Treatment and Rehabilitation of Animals.Oxford: Blackwell.
  • Olby N, Halling K B, Glick T R (2005)Rehabilitation for the neurological patient.Vet Clin North Am Small Anim Pract35(6), 1389-13409, viii.
  • Sharp N J H, Wheeler S J (2005)Spinal trauma.In:Small Animal Surgical Disorders, Diagnosis and Surgery.2nd edn. Chapter 13, pp 281-318. Elsevier Mosby.
  • 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.
  • Braund K G (1994)Clinical Syndromes in Veterinary Neurology.Second edition. St Louis: Mosby Year Book.