Spinal epidural lipomatosis (SEL)
Magnetic resonance imaging (MRI) of the thoracic spine was performed in
the axial and sagittal planes using T1-weighted (T1W), T2weighted (T2W),
and short tau inversion recovery sequences. MRI revealed a prominence
of the epidural fat along the posterior aspect of the thecal sac from T5
through T10, greatest at the T8–T9 level, with a sagittal epidural fat
thickness of approximately 8 mm at this level. There was also associated
ventral displacement of the spinal cord (Figure 1). Axial T1W and T2W
images also showed the prominence of the epidural fat with ventral
displacement of the spinal cord and narrowing of the spinal canal at the
T8 level (Figure 2).
Spinal epidural lipomatosis is characterized by pathological
hypertrophy of adipose tissue located in the spinal epidural space
producing thecal sac compression. It was ﬁrst described by Lee et al1 in
1975 in a patient after renal transplantation. Since then, reports have
drawn a distinct correlation between long-term administration of
steroid and hypertrophy of adipose in the extradural space, associating
this with the general increase in adipose tissue deposition associated
with Cushing’s syndrome.2 Spinal epidural lipomatosis has
been associated with Cushing’s disease, Cushing’s syndrome,
hypothyroidism, pituitary prolactinoma, radiotherapy, obesity, and
idiopathic causes.2,3 However, it is most commonly caused by
long-term steroid use (most often via oral administration), which is
found in approximately 75% of reported cases.4 Its occurrence is unpredictable and does not correspond to the dosage or duration or steroid use.5 It
is considered rare, but there have been more reported cases than
previously thought. The prevalence of SEL is unknown, but many
well-documented cases exist.3 Spinal epidural lipomatosis is
found more often in males (75%) than females with a mean age of 43
years, but has been reported in boys as young as 6 years of age who were
on high-dose steroid treatment.2
manifestations most commonly include back pain followed by lower
extremity weakness, which is usually slowly progressive but may also
include numbness and bladder or bowel dysfunction. Symptoms depend on
region of canal compromise. The thoracic region is most commonly
involved, which produces myelopathic effects, while lesions in the
lumbar region tend to cause radiculopathic effects. On physical
examination, lower extremity weakness is the most common ﬁnding,
although decreased pinprick sensation and altered reﬂexes have also been
found.6-8 Direct compression of the spinal cord and its
resulting symptoms require further investigation into differential
diagnoses, aside from the imaging modalities that can point to SEL.
imaging modality of choice for SEL is spinal MRI. On conventional
spin-echo MRI, fat shows increased signal intensity on noncontrast T1W
images and intermediate signal intensity on T2W images. The MRI ﬁndings
have typically shown sagittal epidural fat thickness between 7 and 15 mm
(normal is 3 to 6 mm) with subsequent thecal sac compression. Spinal
epidural lipomatosis is most commonly found at the T6–T8 levels of the
thoracic spine and at the L4–L5 levels of the lumbosacral region, with
approximately 60% of cases involving the thoracic cord and 40% with
lumbar involvement.4,6,7 However, idiopathic SEL has no predominance of either thoracic or lumbar regions.6,9,10 MRI
of SEL typically shows the adipose tissue located posterior and
posterolateral to the dural sac, compressing the cord anteriorly.11,12 The
high contrast between adipose tissue and the thecal sac on T1W MRI
permits an accurate evaluation of the extent of pathologic epidural
adipose tissue overgrowth in the spinal canal, thus making MRI ideal for
diagnosis of this condition.13 According to a study by Quint et al,11 epidural lipomatosis should be considered when:
- A complete posterior block is seen at myelography;
- Computed tomography (CT) or MRI reveals only fat contiguous to a ventrally displaced dural sac;
- There is a history of chronic steroid use;
- There are myelopathic or radicular symptoms referable to the level of the abnormality; or
- There are no other structural lesions that could help explain the symptoms and imaging ﬁndings.
scanning shows a soft tissue extradural mass with low attenuation.
Gross and histological examinations show a normal, diffuse
unencapsulated deposit of adipose tissue in SEL, which distinguishes it
from a well-deﬁned, focal encapsulated extradural lesion, such as
lipoma, infection, cyst, or neoplasm.10,12
treatment for steroid-induced SEL includes the reduction of
glucocorticoid excess and an increase in physical activity. The
treatment for SEL associated with obesity is weight loss, but it has
been reported that a weight reduction of ≥15 kg is necessary.6
cases unresolved by the above treatments or cases with severe cord
compression and neurological deﬁcits, decompressive laminectomy with
excision of epidural fat is recommended. In addition, in patients with
compression fracture secondary to steroid-induced osteoporosis, fusion
surgery may be necessary to improve spinal stability.5 For
patients with SEL who do not respond to conservative methods of
treatment, this remains the optimal mode of management for relief of
symptoms. Such surgery has an approximately 80% success rate6;
however, it also has a 22% postoperative mortality, which is most
likely due to the immunocompromised status induced by steroid 7,10 Postoperatively, repeat images and close follow-up are necessary.
For a patient who presents with persistent back pain or leg weakness,
pain, or paresthesias, SEL should be included in the list of
differential diagnoses and investigated via MR imaging. Speciﬁc
attention should be directed to the appearance of the epidural fat in
order to make a prompt diagnosis, so that appropriate treatment may be
initiated and complications of cord compression can be avoided.
- Lee M, Lekias J, Gubbay SS, Hurst PE. Spinal cord
compression by extradural fat after renal transplantation. Med J
- Fassett DR, Schmidt MH. Spinal epidural
lipomatosis: A review of its causes and recommendations for treatment.
Neurosurg Focus. 2004; 16(4):E11.
- Fan CY, Wang ST, Liu CL, et al. Idiopathic spinal epidural lipomatosis. J Chin Med Assoc. 2004;67:258-261.
JD, Quint DJ, Sweasey TA, Hoff JT. Spinal epidural lipomatosis: Two new
idiopathic cases and a review of literature. J Spinal
- Chen CC, Lee WY, Cho DY. Spinal epidural lipomatosis. Zhonghua Yi Xue Za Zhi (Taipei).2002;65:86-89.
SC, Traynelis VC, Follett KA, Menezes AH. Idiopathic spinal epidural
lipomatosis. Neurosurgery. 1997;41:68-74; discussion 74-75.
RG, Johnson DL, Brown FD, et al. Epidural lipomatosis in
steroid-treated patients. Spine. 1992;17:183-188; comment in: Spine.
- Roy-Camille R, Mazel C, Husson JL, Saillant G.
Symptomatic spinal epidural lipomatosis induced by a long-term steroid
treatment. Review of the literature and report of two additional
cases. Spine. 1991;16:1365-1371.
- Randall BC, Muraki AS, Osborn
RE, Brown F. Epidural lipomatosis with lumbar radiculopathy: CT
appearance. J Comput Assist Tomogr. 1986; 10:1039-1041.
- Kumar K,
Nath RK, Nair CP, Tchang SP. Symptomatic epidural lipomatosis secondary
to obesity. Case report. J Neurosurg. 1996;85:348-350.
- Quint DJ, Boulos RS, Sanders WP, et al. Epidural lipomatosis. Radiology. 1988;169:485-490.
- Greiner FG, Takhtani D. Neuroradiology case of the day. Extradural lipomatosis. RadioGrapics. 1999;19:1397-1400.
- Lee RKT, Chau LF, Yu KS, Lai CW. Idiopathic spinal epidural lipomatosis. A case report. J HK Coll Radiol. 2002;5:105-108.