Study Design. These case reports illustrate the neurologic manifestati
ons due to beta(2) microglobulin amyloid deposition at the lumbar spin
e level in long-term hemodialysis patients. Objective. Radiologic inve
stigations suggested the amyloid origin of extradural Soft tissue depo
sition, which was confirmed by histologic examination after surgical e
xcision. Summary of Background Data. Although cervical myelopathy is a
recently recognized complication of long-term dialysis-related beta(2
) microglobulin amyloidosis, neurologic manifestations due to amyloid
deposition at the lumbar spine level have rarely been reported. Method
s. Three case reports of cauda equina compression in long-term hemodia
lysis patients are presented. Follow-up radiography, computed tomograp
hy, and magnetic resonance imaging were performed and patients underwe
nt surgical decompression of the thecal sac. Results. In two patients,
the compression resulted from the development of a destructive spondy
larthropathy, and from the infiltration of extradural spaces and ligam
ents by an abnormal soft tissue. The third patient had lumbar spinal s
tenosis due to multiple disc protrusion and to hypertrophy of facet jo
ints acid ligamentum flavum. Multilevel laminectomies enabled excision
of an abnormal fibrous tissue responsible for the thecal sac compress
ion. Histologic examination of the excised fibrous tissues disclosed a
myloid deposits in intervertebral discs, apophysial joints, and ligame
nts. Conclusions. In long-term hemodialysis patients, cauda equina com
pression may develop as the consequence of beta(2) microglobulin amylo
id deposition in lumbar intervertebral discs, facet joints, and ligame
nts. Magnetic resonance imaging is well suited to show the extent of t
he compression and supports the argument for the amyloid origin of ext
radural soft tissue.