Neurology Networks tries to offer broad exposure to various topics that may be presented on the veterinary neurology board exam.

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Vascular - FCE & other spinal cord infarctive disease

“Spinal Shock – Comparative aspects and clinical relevance”  REVIEW

Smith and Jeffery

J Vet Intern Med 2005;19:788–793


Presents a case of a dog with signs consistent with an FCE.  Signs of UMN lesion but poor withdrawal despite good patellar reflexes (does not specify if sciatic myotatic reflexes are also poor).  MRI showed T12-13 parenchymal lesion typical of probable type III disc.  The dog recovered slight withdrawal in the next few days and ambulation over 4 weeks.

Spinal shock in humans:

Phase 1 (<24H):  slow return of polysynaptic reflexes (like bulbocavernosis).

Phase 2 (1-3 days):  slow return of cutaneous reflexes.  Limb myotatic reflexes usually still absent

Phase 3 (1-4 weeks):  slow return of deep tendon reflexes followed by withdrawal. 

Phase 4 (1-12 months):  development of exaggerated reflexes and increased muscle tone progressing to spasticty.


Spinal shock in cats and dogs:

(10-15 minutes):  anal sphincter reflex reappears

(30-120 minutes):  patellar reflex

(2-12 hours):  withdrawal reflex

(24-48 hours):  spasticity

(1-2 weeks):  crossed extensor


Difference between primate and non-primate wiring:

The pyramidal tract (cortical spinal tract) in humans is directly connected to motor neurons.  This allows very fine motor control for things like playing the piano but also makes humans more susceptible to difficult recovery from spinal cord injury. 

In dogs and cats, these CST axons project to the dorsal horn and interneurons before reaching most motor neurons.  Recovery is medicated by plasticity of interneuron function. 


After spinal cord transaction:


Spinal reflexes are lost after transection of the spinal cord because descending facilitatory inputs are lost, causing a

hyperpolarization of spinal motor neurons and a reduction in their excitability.  This happens with anything that can block conduction including toxins, hypothermia, and injury from trauma. 


Most of the positive input comes from the dorsal raphe (serotonergic) and locus ceruleus (noradrenergic) nuclei in the pons.  Serotonin and noradrenaline agonists may therefore help with return of reflex strength (lab studies). 


Recovery of reflexes:

This is a result of different adaptations at the level of the spinal cordàallows cord to function better without as much supraspinal control (plasticity).

  1. Denervated neurons become hypersensitive which allows them to better respond to a given input. 
    1. Inhibition of neurotransmitter uptake
    2. Increased receptor production, less degradation, and modifications to enhance responsiveness
  2. Previously silent synapses may be activated to start functioning to reawaken motor activity
  3. NMDA receptor modification (by phosphorylation and by increasing receptor production) after loss of supraspinal input enhances responses in chronic pain and may also be involved in improving sensitivity of synapses after spinal cord injury.



Development of hyperreflexia:

  1. Generation of new excitatory synapses on motor neuronsàslow due to slow nature of axonal transport
    1. Can come from interneurons (earlier wave of new synapses b/c shortest neurons for transport)
    2. Can come from primary segmental afferent fibers (later wave b/c longer neurons and slower transport of new receptors/ organelles, etc)
    3. Dependence on length of neurons may help explain why cats get better so much faster than people?
  2. What evidence is there for new synapse formation?
    1. Electron microscopy has shown that synaptic organization on motor neurons is altered after spinal cord transaction
    2. Sprouting of primary segmental afferent fibers into deeper layers of the dorsal horn occurs after SCI in both rats and cats, and it seems reasonable to suggest that these new nerve fibers can form new synapses on motor neurons.
    3. The stimulus for sprouting might be growth factors expressed within the damaged spinal cord:

*Growth factor expression is upregulated after cord injury, both at the injury site and, to a lesser extent, along the rest of the cord

*Anti-bodies to growth factors can inhibit sprouting of small nerve fibers

*Sprouting of larger fibers is much better in the lumbar region than in the thoracic region, where neurons respond poorly to certain growth factors


Autonomic functions:

Supraspinal control of spinal output includes autonomic nervous system neuronal populations.  For example the sympathetic output from the spinal cord below the injury is often eliminated then progressively increases like what we see with motor neurons.  Loss of sympathetic innervation to the heart with preservation of vagal tone (from the unaffected brainstem) leads to bradycardia and can lead to AV block. This can drop blood pressure which is exacerbated by poor peripheral vessel sympathetic tone. 

Normally, spinal cord perfusion is autoregulated to keep perfusion stable between 45-165 mm Hg. Spinal cord trauma damages spinal arterioles and abolishes this intrinsic regulation, so that cord perfusion becomes dependent on mean arterial pressure. Spinal cord perfusion is poor during spinal shock, and the initial spinal injury can be markedly worsened as ischemia and hypoxia develop. Maintaining normal arterial pressure after spinal injury is therefore crucial to limiting neuronal damage as much as possible.