Single or double-level compression of the lumbosacral nerve roots located i
n the dural sac results in a polyradicular symptomatology clinically diagno
sed as cauda equina syndrome. The cauda equina nerve roots provide the sens
ory and motor innervation of most of the lower extremities, the pelvic floo
r and the sphincters. Therefore, in a fully developed cauda equina syndrome
, multiple signs of sensory disorders may appear. These disorders include l
ow-back pain, saddle anesthesia, bilateral sciatica, then motor weakness of
the lower extremities or chronic paraplegia and, bladder dysfunction. Mult
iple etiologies can cause the cauda equina syndrome. Among them, non-neopla
stic 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 arachnoi
ditis and other infectious etiologies. The use of canine, porcine and rat m
odels mimicking the cauda equina syndrome enabled discovery of the effects
of the compression on nerve root neural and vascular anatomy, the impairmen
t of impulse propagation and the changes of the neurotransmitters in the sp
inal cord after compression of cauda equina. The involvement of intrinsic s
pinal cord neurons in the compression-induced cauda equina syndrome include
s anterograde, retrograde and transneuronal degeneration in the lumbosacral
segments. Prominent changes of NADPH diaphorase exhibiting, Fos-like immun
oreactive and heat shock protein HSP72 were detected in the lumbosacral seg
ments in a short-and long-lasting compression of the cauda equina in the do
g. Developments in the diagnosis and treatment of patients with back pain,
sciatica and with a herniated lumbar disc are mentioned, including many tre
atment options available. (C) 2001 Elsevier Science Ltd. All rights reserve
d.