Contributors: Laurent Garosi

 Species: Feline   |   Classification: Diseases

Introduction Pathogenesis Diagnosis Treatment Outcomes Further Reading


  • 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.

Presenting Signs

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


  • 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 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 paresis causes 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 paresis reflects 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.



  • 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).


  • 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.


Client History

  • 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.
    • Factors that trigger or improve the signs.
    • Evolution of the signs (progressive, static, improving or waxing and waning).

Clinical Signs

  • Gait abnormality.
  • Paralysis. 
  • Spinal discomfort.
  • Lameness.
  • Urinary and/or fecal incontinence.

Diagnostic Investigation

  • Primary aim of neurological evaluation of patient is to answer the following questions:
    • Do clinical signs observed refer to a nervous system lesion?
    • Location of lesion within nervous system?
    • Main types of disease process that explain clinical signs?
    • Severity of disease?
  • First two questions aim to determine anatomical diagnosis (location and distribution of lesion within nervous system). 
  • With spinal cord disease, aim is to locate pathological process to specific spinal cord segments ([C1-C5], [C6-T2], [T3-L3], [L4-S3]).
  • Gait generation requires the interaction between two motor systems: upper motor neuron (UMN) and lower motor neuron (LMN) systems.

Upper motor neuron (UMN)

  • Command efferent neuron located in the brain.
  • Responsible for initiation and maintenance of normal movements and for maintenance of tone in the extensor muscle to support body against gravity.
  • Cell body lies within cerebral cortex, basal nuclei and brainstem.
  • Axon never leaves the central nervous system (CNS).
  • Travels through brain and/or spinal cord white matter and synapses indirectly (via an interneuron) with a LMN to modulate its activity (essentially inhibit).
  • Essentially responsible for initiation of movement and maintenance of tone in extensor muscles for support of body against gravity.
  • Lesion of UMN typically results in release of inhibitory effect that UMN has on LMN (disinhibition) located caudal to level of injury.  Disinhibition is usually more apparent on extensor muscles.  Clinically, the result is spastic paresis/paralysis with normal to increased reflex activity (hyperreflexia) and increased extensor muscle tone (hypertonia).  Increased resistance to passive manipulation of the limbs manifests hypertonia.

Lower motor neuron (LMN)

  • Last neuron in chain of neurons that cause muscles to contract (final common pathway to the effector).
  • If LMN are damaged, the following clinical signs are characteristically found:
    • Flaccid paresis/paralysis.
    • Reduced or absent reflexes (areflexia or hyporeflexia).
    • Reduced or absent muscle tone (atonia or hypotonia).
    • Early and severe muscle atrophy (neurogenic atrophy).
  • The CNS is arranged in a segmental way. Each spinal cord segment innervates by one spinal nerve a muscle or group of muscles (myotome).  Identification of LMN signs allows accurate clinical neurolocalization to a peripheral nerve, nerve root or motor neuron within spinal cord or brainstem.
  • Functionally the spinal cord can be divided into four regions:
    • Cranial cervical [C1 to C5].
    • Cervico-thoracic [C6 to T2].
    • Thoraco-lumbar [T3 to L3].
    • Lumbo-sacral [L4 to S3].
  • LMN cell bodies are located within gray matter of cervico-thoracic intumescence (segments C1 to C5) for thoracic limbs and lumbo-sacral intumescence (segments L4 to S3) for pelvic limbs. Lesion at level of these intumescences results in LMN signs in corresponding limb(s).
  • LMN axon leaves the central nervous system by the ventral nerve roots to join successively a spinal nerve and a peripheral nerve before it synapses with an effector muscle.


Initial Symptomatic Treatment

  • Most can be treated either medically or surgically with the exception of degeneration of spinal cord and tumors growing inside spinal cord.
  • Surgery is usually advised for disk herniation causing neurological signs, some fractures or luxations of the spine, certain spinal cord or vertebral malformations and some tumors growing on outside of spinal cord. Surgery relieves spinal cord compression and, if necessary, stabilizes spine.
  • Medical treatment used for mild disk herniation causing pain but not neurologic signs, inflammation of spinal cord, infection of intervertebral disk or vascular accident of spinal cord. 

Subsequent Management


  • Bladder management: micturition problems can be seen in patients with either a lesion of the sacral spinal cord segments, their respective nerve roots and peripheral nerves (LMN bladder), or with a spinal cord lesion cranial to the sacral spinal cord segments (UMN bladder).  Patients with either UMN or LMN bladder may not be able to store and/or eliminate urine effectively and voluntarily. The patients bladder should be checked at regular intervals (every three to four hours). Bladder size and urinary status should be documented throughout the day and this should not be solely based on the presence of urine on the bedding. Patients with urinary incontinence should either have their bladder manually expressed or have a urinary catheter placed. 
  • Gastro-intestinal complications: gastro-intestinal problems such as diarrhea and/or vomiting are not unusual during the recovery period of spinal injury due to possible development of colonic and gastro-duodenal ulceration and pancreatitis. Administration of corticosteroids (dexamethasone Dexamethasone in particular) and/or non-steroidal anti-inflammatory medications, will increase the risk of gastro-intestinal problems. Furthermore diarrhea and vomiting will increase the risks of complications such as urinary tract infections and aspiration pneumonia, respectively, emphasising the importance of preventing and treating rapidly such gastro-intestinal disturbances. Symptomatic treatment is recommended as a first line approach by discontinuing anti-inflammatory treatment, withholding food for 24 h, administering intravenous fluids, and administration of gastric acid secretion inhibitors.
  • Respiratory complications: patients with C1-C6 spinal cord injury can experience hypoventilation leading to hypercapnia Hypercapnia. Oxygen supply by facial mask, nasal catheters or flow-by delivery should be provided in patients where mild hypoventilation is confirmed, with the method of delivery dependent on the particular circumstances. In severe cases, mechanical ventilation will be required. Atelectasis refers to collapse of part of the lung. It may include a lung subsegment or the entire lung. It is most commonly seen in patients with prolonged recumbency preventing lung expansion. Patients showing signs of atelectasis may be tachypneic, dyspnoeic and cyanotic. To prevent pulmonary atelectasis patients should be maintained in either complete sternal recumbency, sternal at the front with the hind limbs moved from side to side every 4-6 hours, or for those patients that cannot stay in sternal, turned between left and right lateral recumbency a minimum of every 2-4 hours.
  • Bedding: the most important aspect of the bedding is that it is non-retentive to allow urine to drain away from the patient. Recumbent patients require a well padded non-retentive bed to prevent pressure sores (decubitus ulcers). This can be provided by a waterproof foam mattress, a memory foam orthopedic mattress or multiple thick blankets covered by a non-retentive bed.
  • Prevention of decubitus ulcers: decubitus ulcers are an ulceration of skin and underlying tissue caused by pressure that limits the blood supply to the affected area. They are caused by the prolonged pressure and friction on the body surface by the underlying bed. Prevention of decubitus ulcers is easier than treatment. Recumbent patients are at risk of developing these ulcers and therefore require a well padded non-retentive bed; the patient should be turned every 2-4 hours ideally and massage applied to the bony prominences to help promote circulation. Areas at high risk of ulceration can be protected using circular padding or doughnuts of foam, cotton wool or bubble wrap. Recumbent patients, where possible, should be lifted into a normal standing position at least twice daily with the use of a hoist or sling.
  • Pain management: a well designed analgesia regimen is mandatory, particularly for the post-surgical management of patients. The most common drugs used alongside non-steroidal anti-inflammatories to manage spinal or neurogenic pain include buprenorphine Buprenorphine, morphine Morphine, methadone Methadone, fentanyl Fentanyl (parenteral), ketamine Ketamine, medetomidine Medetomidine, dexmedetomidine Dexmedetomidine, lidocaine Lidocaine and gabapentin. The patients level of pain should be assessed every 2-4 h using an appropriate pain scoring system Pain: management Pain: assessment.
  • Physical rehabilitation Physical rehabilitation (after fracture stabilization): it is essential that a thorough examination of the patient is undertaken before starting any treatment, to avoid deterioration of any pre-existing conditions during treatment, and to detect any abnormalities which may contraindicate further treatment. The clinical diagnosis should be discussed with the physiotherapist before starting any therapy.



  • Prognosis of spinal cord disease depends on variable factors including:
    • Rate of onset.
    • Duration.
    • Degree of spinal cord dysfunction (in particular loss and duration of loss of conscious pain perception).
    • Underlying etiology.
  • In general, animals that have lost conscious pain perception (nociception) have a poor prognosis, especially if it has been for more than 48 hours. For pain to be consciously perceived, the sensory component of peripheral nerves and their spinal cord segments, spinal cord and brainstem pain pathways and related thalamocortical system must all be intact and functional. Pain can often be elicited by heavy pressure to bones of digits of thoracic or pelvic limbs with fingers or a hemostat even when cutaneous pain sensation is diminished or lost. Pathways that carry deep pain sensation are located deep in spinal cord white matter and project to both sides of spinal cord, forming a multisynaptic, bilateral nerve network. A severe bilateral deep pain spinal cord lesion therefore only impairs the modality of pain. Therefore testing of deep pain is a useful prognostic indicator in case of spinal cord disease. Assess conscious pain perception on all four limbs, tail and perineal region.   Expected reaction is a behavioral response such as turning head, trying to bite or vocalization. Withdrawal of limb is only the flexor reflex and should not be taken as evidence of pain sensation.
  • Degeneration and tumors inside spinal cord, incurable with a very poor prognosis.
  • Prognosis very poor for cat with spinal fracture presented with absent nociception.
  • Feline infectious peritonitis virus causing myelitis Feline infectious peritonitis carries a very poor prognosis.
  • Lymphoma Spinal lymphoma affecting the spinal cord carries a fair prognosis if it manifests as an extradural mass that can be removed surgically and follow-up treatment by means of chemotherapy.
  • Disk herniation, fair to good prognosis as long as animal has retained nociception. When nociception is lost, prognosis depends on time elapsed between loss of pain sensation and surgery.
  • Vascular accident such as fibrocartilaginous embolism (FCE), fair prognosis as long as animal's nociception, retained. However, prognosis usually poor if intumescence is affected.
  • Non-infectious causes of inflammation of spinal cord (myelitis) can be treated but aim of treatment is to control disease rather cure it.

Expected Response to Treatment

Reasons for Treatment Failure

Further Reading


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.

Other Sources of Information