Single or double-level compression of the lumbosacral nerve roots located in the 
dural sac results in a polyradicular symptomatology clinically diagnosed as 
cauda equina syndrome. The cauda equina nerve roots provide the sensory and 
motor innervation of most of the lower extremities, the pelvic floor and the 
sphincters. Therefore, in a fully developed cauda equina syndrome, multiple 
signs of sensory disorders may appear. These disorders include low-back pain, 
saddle anesthesia, bilateral sciatica, then motor weakness of the lower 
extremities or chronic paraplegia and, bladder dysfunction. Multiple etiologies 
can cause the cauda equina syndrome. Among them, non-neoplastic compressive 
etiologies such as herniated lumbosacral discs and spinal stenosis and spinal 
neoplasms play a significant role in the development of the cauda equina 
syndrome. Non-compressive etiologies of the cauda equina syndrome include 
ischemic insults, inflammatory conditions, spinal arachnoiditis and other 
infectious etiologies. The use of canine, porcine and rat models mimicking the 
cauda equina syndrome enabled discovery of the effects of the compression on 
nerve root neural and vascular anatomy, the impairment of impulse propagation 
and the changes of the neurotransmitters in the spinal cord after compression of 
cauda equina. The involvement of intrinsic spinal cord neurons in the 
compression-induced cauda equina syndrome includes anterograde, retrograde and 
transneuronal degeneration in the lumbosacral segments. Prominent changes of 
NADPH diaphorase exhibiting, Fos-like immunoreactive and heat shock protein 
HSP72 were detected in the lumbosacral segments in a short-and long-lasting 
compression of the cauda equina in the dog. Developments in the diagnosis and 
treatment of patients with back pain, sciatica and with a herniated lumbar disc 
are mentioned, including many treatment options available.