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Ulnar impaction syndrome
Last revised by Yuranga Weerakkody◉ on 11 Dec 2022
Citation, DOI, disclosures and article data
Ulnar impaction syndrome, also known as ulnar abutment or ulnocarpal impaction or
loading, is a painful degenerative wrist condition caused by the ulnar head
impacting upon the ulnar-sided carpus with the injury to the triangular
fibrocartilage complex (TFCC).

Differentiation from ulnar impingement syndrome is critical, which is due to a

shortened ulna that abuts and causes radial remodelling.

Epidemiology
Ulnar impaction syndrome most commonly presents in middle-aged patients. The
majority of cases occur in association with positive ulnar variance or increased
dorsal tilt of the distal radius. This can be seen in patients with:

distal radial fracture malunion

ulnar styloid fracture nonunion

radial head resection (such as following an Essex-Lopresti fracture-dislocation)

premature radial physeal closure

congenital wrist abnormalities

Ulnar impaction syndrome is rare in the absence of such anatomic predispositions

but can occur if there is excessive repeated loading of the ulnar-carpus in daily
activity 5.

Clinical presentation
Patients present with chronic or subacute ulnar-sided wrist pain exacerbated by
activity. There is often associated swelling and limitation of forearm and wrist
movement. Anything that results in a relative increase in ulnar variance such as
firm grip, pronation, and ulnar deviation of the wrist, can exacerbate the symptoms.

Pathology
As the name suggests, ulnar impaction syndrome involves impaction of the distal
ulnar upon the ulnar-sided carpal bones, particularly the lunate. This results in a
continuum of pathologic changes which are represented in the class II subsection of
the Palmer classification of TFCC lesions 2.

IIA TFC complex wear

IIB TFC complex wear, lunate or ulnar chondromalacia

IIC TFC complex perforation, lunate or ulnar chondromalacia

IID TFC complex perforation, lunate or ulnar chondromalacia, lunotriquetral

ligament perforation

IIE TFC complex perforation, lunate or ulnar chondromalacia, lunotriquetral

ligament perforation, ulnocarpal osteoarthritis

Chronic abutment leads to tears and osteoarthritis of the TFCC.

Radiographic features
Imaging findings of ulnar impaction may precede the onset of symptoms. Recognising
the distribution pattern (ulnar, lunate, triquetral) is the key to making the
diagnosis.

Plain radiograph
Plain radiographs can appear normal in early disease. General features include:

presence of a predisposing factor

positive ulnar variance

previous distal radial fracture with shortening or dorsal tilt

distal radial resection

Madelung deformity

subchondral sclerosis and cysts in specific ulnar impaction distribution

distal ulna

proximal ulnar aspect of lunate - (see subchondral cyst of the lunate)

radial aspect of triquetrum

ulnocarpal osteoarthritis in more advanced disease

To accurately access ulnar variance, the wrist must be correctly neutrally

positioned with the shoulder abducted at 90° and the elbow flexed at 90°. Variance
can falsely be reduced in supination and exaggerated in pronation or with clenching
of the fist.

MRI
MR imaging is the investigation of choice in both the detection of early disease
and characterisation of more advanced disease. Can demonstrate the bone, cartilage
and ligamentous features of the syndrome 3.

Location of bone signal changes 4:

ulnar side of proximal lunate ~90%

radial side of proximal triquetrum ~40%

distal ulna ~10%

Types of bone signal change:

subchondral sclerosis (low T1 and T2) most common in lunate

bone oedema (high T2, low-intermediate T1)

subchondral cysts (round T2 hyperintensities)

Cartilage and ligamentous changes:

chondromalacia of distal ulnar cartilage (altered signal)

central TFCC signal increase often with tear (T2 hyperintense fluid)

lunatotriquetral ligament tear (T2 hyperintense fluid) with proximal arc offset

Treatment and prognosis

Treatment varies depending on the amount of ulnar variance, the Palmer lesion
class, the contour of the distal ulnar and the presence of lunotriquetral
instability.

Palmer class IIA and IIB lesions (no TFC perforation) are managed with open wafer
procedure (surgical resection of the distal 2-3 mm of the dome of the ulnar head)
or formal ulnar shortening (excision of a 2-3 mm slice of the ulnar shaft followed
by fixation).

When the TFC is perforated (Palmer class IIC and IID lesions), the head of the ulna
can be burred down with the help of arthroscopic instrumentation (arthroscopic
wafer procedure). This procedure is minimally invasive, highly effective, and
allows rapid return to normal activities.

Class IIE lesions are managed with salvage procedures such as complete or partial
ulnar head resection (Darrach procedure) or arthrodesis of the distal radioulnar
joint with distal ulnar pseudoarthrosis (Sauve-Kapandji procedure).

Differential diagnosis
Kienböck disease

signal change in lunate is usually more diffuse and radial sided

no ulnar or triquetral abnormality

more often with negative ulnar variance

traumatic TFCC injuries

degenerative arthritis of the wrist (SLAC wrist)

radiocarpal joint involved

intraosseous ganglia

usually radial side of the lunate or distal lunate

See also
ulnar-sided wrist impaction and impingement syndromes

References
Related articles: Wrist pathology
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Cases and figures

Case 1: T2 FS

Case 1: PD

Case 2: PD

Case 2: T2 FS

Case 3

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Imaging differential diagnosis

Kienbock disease
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MRI Web Clinics
Home 9 Web Clinic 9 Spinal Epidural Lipomatosis with Review of Visceral Fat
Deposition in Obesity
MRI Web Clinic - July 2017
Spinal Epidural Lipomatosis with Review of Visceral Fat Deposition in Obesity

Gabrielle Bergman, M.D.

Clinical history:

A 49 year-old moderately obese male with a one-year history of chronic low back
pain, numbness and sensation of weakness at bilateral thighs, without neurological
deficits on clinical exam, undergoes lumbar spine MR imaging. Comparison is made to
a prior lumbar spine MRI exam from 4.5 years ago, when the patient experienced back
pain which resolved after a few months. From the current MRI exam (1a), midline
sagittal (left) and L4/5-level axial (right) T2-weighted images without fat-
saturation are provided, together with corresponding T2-weighted images (1b) from
the earlier MRI exam.

What are the findings? What is your diagnosis?

1a

1b

Figure 1:

1a and 1b

Findings:

2a

2b

Figure 2:

There has been interval mild narrowing at the dural sac (2a) (arrows) compared to
the prior examination (2b), slight at L3 and L4 (arrowheads)and mild at the L5 and
S1 levels (arrows). No significant interval change is noted in the L4-5 mild
diffuse disc bulge and mild facet and ligament degeneration. The dural sac
narrowing is less well demonstrated on T2-weighted images than on T1-weighted
images (Figure 3), due to the similar high T2 signal of both CSF fluid and epidural
fat tissue.

3a

3b

Figure 3:

Corresponding T1-weighted sagittal (left) and axial (right) images from the current
exam (3a) and the earlier MRI exam (3b) better demonstrate the interval decrease in
A/P diameter of the dural sac between the two MRI exams (arrows), due to the
difference between the high T1 signal of epidural fat and the intermediate-to-low
T1 signal of CSF. Axial (right) image from the current exam (3a) shows interval
change to a “stellate” configuration at the dural sac (arrowheads). Interval
increase in thickness of the subcutaneous fat tissues at posterior lumbar region
(asterisk) compatible with patient’s interval weight gain to 245 lbs and a BMI of
35.2, from a body weight of 218 lbs at the earlier MRI exam.

Diagnosis:
Spinal Epidural Lipomatosis.

Introduction:
Spinal Epidural Lipomatosis (SEL) is a relatively rare disorder where the small
amount of fat tissue normally present within the epidural space becomes excessive,
and thereby limits the size of the dural sac within the osseous spinal canal. This
may lead to symptomatology related to compressive myelopathy or radicular symptoms,
depending on the severity of involvement and the spinal levels affected. These
symptoms cannot be well distinguished from the clinical symptoms related to the
much more frequent degenerative lumbar disc disease. SEL can be well demonstrated
on MR imaging of the spine.

The prevalence of SEL in the general population is not known. While the vast
majority of obese individuals never develop SEL, obesity is almost always present
in patients who are diagnosed with SEL, and often there is a history of
corticosteroid medication, or less frequently of endocrinopathy such as endogenous
overproduction of glucocorticoids. In view of the current epidemic of obesity
affecting all age groups, SEL is likely to become increasingly frequently
encountered in clinical practice.

Weight-loss has been reported to often result in symptomatic improvement or full

resolution of symptoms in patients with SEL, and reduction or discontinuation of
corticosteroid therapy as tolerated has also been associated with clinical
improvement. Patients exhibiting severe or rapidly progressing neurologic symptoms
have been treated successfully in several reported cases with spinal decompressive
surgery.

MRI of the lumbar spine often allows the diagnosis of the presence or absence of
significant obesity, through evaluation of the posterior subcutaneous tissues for
subcutaneous type of obesity, and if the field-of-view of the sagittal localizer
images includes the trunk, there is an opportunity to also evaluate for the
presence of visceral (intra-abdominal) type of fat deposition. This evaluation may
influence patient management, as the visceral type of fat deposition is associated
with significant increases in patient morbidity related to diabetes, cardiovascular
disease and metabolic syndrome.

Epidemiology and Etiology

Since the first case of SEL was reported in the medical literature in 19751,
several more usually single clinical case descriptions of this disorder have become
available, and also a few smaller patient series; a meta-analysis of reported cases
in 2005 included more than 100 patients with SEL.2. It has been stated that SEL
occurs almost exclusively in the obese population.3 The prevalence of SEL in the
general population is however not currently known. In an attempt to determine the
prevalence of severe and symptomatic cases of lumbar or sacral SEL in a
subpopulation of patients with low back pain sent for MRI exam of the lumbar spine,
severe (grade 3) epidural lipomatosis was identified in 0.33 % of 1498 patients.4
However if also the milder grades of SEL detected on the MR imaging exam had been
included, the prevalence would have been much higher. At another investigation with
retrospective review of lumbar spine MRI exams, the authors described a grading
system for SEL severity of involvement on MR images, and identified 2.1% of lumbar
spine exams demonstrating a severe grade of SEL, 6.5% with moderate grade and 12.2%
with mild grade; they also found that all patients with the severe grade of SEL
were symptomatic, but only 14.5% of patients with moderate SEL exhibited symptoms
likely related to this disorder, and none of the patients with mild grade of SEL on
MRI findings exhibited related clinical symptoms.5 Other authors have verified the
use of the grading classification for imaging diagnosis, however did not establish
a distinct correlation between the grading classification and the severity of
clinical symptoms in a large retrospective study.6

MRI features of SEL have been demonstrated in patients ranging in age from children
to the elderly, with predominant occurrence in middle-aged and older individuals.7
Most authors suggest a mild predominance in males over females, and a similar
frequency of involvement of the lumbar/sacral and the thoracic vertebral levels.

It remains unclear why some individuals develop SEL. Nearly all patients diagnosed
with SEL are obese, and an association with the complexities of fat metabolism and
endocrine functions, directing fat storage beyond subcutaneous regions to also
involve non-subcutaneous centripetal fat tissue regions, is likely to be
implicated. Approximately half of reported cases of spinal epidural lipomatosis
have been observed in patients on corticosteroid medication, usually both long-term
and high-dose, while a small number of cases have been reported after only a few
months of corticosteroid medication duration and utilizing a low dose.7 Less
frequently, SEL has been diagnosed in individuals with endogenous overproduction of
glucocorticoids, and very rarely in patients with other endocrine disorders,
including hypothyroidism. The second largest percentage group of reported patients
with SEL consists of obese individuals not on corticosteroid medication or with an
endocrine disorder. There have also been rare reports of epidural lipomatosis
occurring in non-obese non-corticosteroid-medicating individuals.7

Clinical signs and Diagnostic Exams

SEL has been reported to occur at the thoracic, lumbar or sacral levels of the
spine, where normally a small amount of fat tissue is present, with no cases of
cervical involvement in SEL reported and no epidural fat normally present there.

Progressive back pain is the most commonly reported symptom in individuals with
SEL. When thoracic levels are involved, there may be signs of myelopathy. With
lumbar or sacral involvement, often there will also be slowly progressive weakness
of the hips and lower extremities, as well as sensory changes with numbness and
paresthesias, and sometimes radicular symptoms.7 These clinical findings are not
specific for SEL, and usually the pre-MRI clinical concern is for a disc herniation
and possible spinal stenosis. If MR imaging of the spine shows features of moderate
or severe SEL, without co-existing significant disc or other spine pathology, SEL
often becomes the clinical diagnosis of exclusion.

SEL cannot be diagnosed on radiographic or ultrasound imaging exams. While CT

scanning can provide a limited evaluation, MR imaging is the modality which best
demonstrates the extent of the increased epidural fat tissue, and signs of mass
effect upon the size and configuration of the dural sac and nerve roots. MR imaging
can also demonstrate the presence of often coexisting spine pathology such as disc
and facet joint degeneration, or vertebral malalignment.

Normal anatomy and function of spinal epidural fat tissue

The epidural space is a thin elongated compartment within the spinal central canal,
and it contains neural and vascular structures, subtle anchoring ligaments, and
interspersed fat tissue (Fig 4). Its outer border consists of cortical bone, disc
and ligamentous walls of the spinal canal, and its inner border consists of the
outer aspect of the cylindrical-shaped dural sac.

4a

Figure 4:

A 3D graphic lateral view at the level of the conus demonstrates the boundaries and
contents of the spinal canal.

The normal dural sac usually has an even diameter, with distal tapered termination
at the sacral canal, usually at the S2 vertebral level, with the fat within the
epidural space extending further distally within the sacral canal (Fig 5).

5a

Figure 5:

Sagittal midline T1-weighted image of a 46 year-old male demonstrates the normal

distribution of epidural fat tissue, with a small amount present posterior to and
along the dural sac, interrupted at each vertebral level laminar junction
(asterisks). In addition there is a normal small amount of fat tissue anterior to
the dural sac at the S1 level (arrowhead), and fat tissue present within the sacral
canal distal to the dural sac termination (blue asterisk). Note the normal conus
termination at T12-L1 level (long arrow), and the normal dural sac termination at
S1-2 level (short arrow).

The neural elements within the lumbar epidural space consist of nerve roots at each
segment, extending between the dural sac and the neural foramina. The vascular
elements within the epidural space consist of multiple small segmental arterial
spinal branches coursing along the nerve roots and through the dural sac to join
the anterior and posterior spinal arteries, and intradural spinal venous braches
which exit along the nerve roots into a venous plexus within the epidural space.
The epidural venous plexus is more prominent anterior than posterior to the dural
sac, and includes longitudinal as well as segmental transverse branches.
Subtle ligamentous elements within the epidural space are suggested to have a
function to connect and loosely anchor the dural sac to the inner aspects of the
vertebral canal, while also allowing some degree of positional change depending on
flexion-extension of the spine, and position of the body related to gravitational
forces. These very thin and short anchoring meningo-vertebral ligaments extend from
the dural sac periphery to the osseous or capsular structures at the inner margins
of the central spinal canal. Anatomic studies have shown these subtle ligaments to
have a distribution similar to the spokes of a wheel, or likened to the hours on a
clock-face,8 but to be inconsistently present and with individual variability in
expression at different vertebral levels; the ligaments tended to be more prominent
anterior than posterior to the dural sac.8

Fat tissue is normally present between the vascular, neural and ligamentous
structures of the epidural space. In the large majority of individuals, the amount
of fat tissue within the epidural space does not appreciably change with age, or as
the individual becomes obese or underweight. The epidural fat tissue does not
normally demonstrate even thickness in any plane, but varies according to available
space. Epidural fat tissue is unencapsulated, does not normally demonstrate mass
effect upon adjacent structures such as the dural sac and nerve roots, and is
considered to have a “bolstering” effect in protecting the neural structures and
cushioning the pulsatile movements of the dural sac. There is no free fluid within
the epidural space, although some reports in the anesthesiology literature have
described a sometimes semi-fluid feature of lumbar epidural fat detected during
epidural needle placement and injections for therapeutic procedures.9 It has also
been suggested that epidural fat tissue represent a functional rather than
incidental tissue which facilitates sliding movements of the dural sac relative to
the periosteum of the vertebrae during spinal flexion-extension.10

MRI findings of normal epidural fat tissue

The MR signal of normal epidural fat tissue is at all aspects and on all imaging
sequences identical to the signal of normal posterior subcutaneous fat, and
demonstrates homogeneous high signal on T1-weighted images (Fig 5; Fig 6a-d).

6a

6b

6c

6d

Figure 6:

(6a) In the same patient as Fig. 5, an axial T1-weighted image obtained at L1-2
disc level shows the small amount of epidural fat tissue normally located posterior
to the dural sac (arrow).

(6b) Also in the same patient as Fig. 5, an axial T1-weighted image obtained at the
L2 inferior endplate level shows the normal absence of epidural fat tissue
posterior to the dural sac at the level of the laminar junction (arrow).
(6c) In the same patient as Fig. 5, an axial T2-weighted image at the mid-L3
vertebral body level shows the central canal and pedicles/posterior elements at the
segmental level where there are bony margins around the central canal. Minimal
epidural fat is seen posterior to the dural sac (arrowhead), and epidural veins are
demonstrated between the pedicles and the lateral margin of the dural sac (arrows).

(6d) In the same patient as Fig. 5, an axial T1 weighted image at the level of the
S1 superior endplate just below the disc demonstrates the normal small amount of
epidural fat tissue anterior to the dural sac. For SEL grading purposes (see
below), anteroposterior diameter of this normal epidural fat tissue (1) measures 3
mm, the dural sac (2) measures 12 mm, and the bony central canal (3) 15 mm, for a
normal ratio of dural sac to fat of 4.0, and a normal percentage of epidural fat to
spinal canal A/P dimensions of 20%.

MRI findings in Spinal Epidural Lipomatosis

The MRI diagnosis of epidural lipomatosis requires demonstration of an increased

amount of fat within the epidural space, and also the demonstration of mass effect
by the epidural fat tissue. For these purposes, a grading system of the severity of
fat deposition can be utilized, and alteration of the axial configuration of the
dural sac may suggest mass effect through the “stellate” or “Y“ signs at the lumbar
and sacral levels, and anteroposterior dural sac flattening at the thoracic levels.

In SEL the excessive fat deposition tends to occur posteriorly at the thoracic
levels, and posteriorly and sometimes also anteriorly and at lateral aspects of the
dural sac when the lumbar or sacral levels are involved. While it has been stated
that epidural adipose tissue with an anteroposterior thickness of 7 mm or greater
is a diagnostic criterion for SEL,3 also in the absence of features to suggest mass
effect by the fat tissue, a drawback of absolute measurements is that they somewhat
depend on osseous canal size for relevance, and do not take into account the
possibility of normally occurring asymmetry of epidural fat deposition in cases of
vertebral malalignment such as with scoliosis.

SEL Grading System

A grading system for SEL utilizing ratios has been described (Ref 5). The grades
include Normal (0), Mild (1), Moderate (2), and Severe (3), and are based on ratios
obtained from anteroposterior measurements at the spinal canal midline. The authors
performed their measurements for SEL grading at the S1 vertebral level, near the
upper endplate, and although there is little data in the literature correlating
these measurements at other spinal levels with symptoms, the same measurements and
ratios can be performed at other spinal levels, and on sagittal as well as axial
images (Fig 6d).

The Borre’ classification utilizes 3 measurements: the anteroposterior length of

the dural sac, the epidural fat, and the spinal canal. They then calculate the
ratio of dural sac to epidural fat (“dura/fat ratio”); and percentage of epidural
fat to spinal canal (“fat % of spinal canal”).

Normal (Grade 0): dura/fat ratio: 1.5 or more; fat % of spinal canal: 40% or less
(Fig 7a).

Mild epidural fat overgrowth (Grade 1): dura/fat ratio: 1.0-1.5; fat % of spinal
canal: 41-50%. This grade included no symptomatic patients in their study (Fig 7b).
Moderate epidural fat overgrowth (Grade 2): dura/fat ratio: 0.34-1.0; fat % of
spinal canal: 50-75%. This grade included 14.5 % of patients with related symptoms
(Fig 7c).

Severe epidural fat overgrowth (Grade 3): dura/fat ratio: 0.33 or less; fat % of
spinal canal: more than 75%. All cases in this grade were symptomatic (Fig 7d).

7a

Figure 7:

Sagittal T1-weighted images in 4 different patients illustrate grades 0 to 3 of

SEL, with measurements and ratios.

(7a) Bony canal (green): 17 mm, dural sac (red): 13 mm, leaves 4 mm for the
epidural fat. Ratios: 3.3 and 24%: Grade 0 (Normal).

(7b) Bony canal (green): 16 mm, dural sac: 9 mm (red), epidural fat (blue): 7 mm.
Ratios: 1.2 and 43%: Grade 1 (Mild).

(7c) Spinal canal (green): 17 mm, dural sac (red): 5 mm, epidural fat: 12 mm.
Ratios: 0.42 and 71%. Grade 2 (Moderate)

(7d) Spinal canal (green) 20 mm, Dural sac (red): 2 mm, epidural fat: 18 mm.
Ratios; 0.11 and 90%. Grade 3 (Severe).

MRI sign of mass effect upon the dural sac on axial images

Changes in the normally rounded to oval configuration of the dural sac in the axial
plane may occur due to mass effect from any extradural mass lesion. In SEL at
lumbar and sacral levels the dural sac configuration is usually polygonal,
stellate, or Y- or V-shaped (Fig 8a-c).8,11 These configurations do not tend to
occur at thoracic levels.

The polygonal and stellate configurations demonstrate a tented appearance of the

dural sac margins corresponding to the meningo-osseous ligament insertions (Fig 8a-
b). The Y-sign (Fig 8c) has been described as a trifid cross-sectional
configuration of the dural sac, with 3 rays emanating from a central core.
Sometimes the configuration is more similar to the letter V (Fig 10b), especially
at sacral levels. When epidural lipomatosis is very extensive, there is flattening
with near-obliteration of the dural sac (Fig 8d).

8a

Figure 8:

(8a) Polygonal configuration of the dural sac.

(8b) Stellate configuration of the dural sac.

(8c) Y-configuration of the dural sac.

(8d) Near-obliteration configuration of the dural sac.

The epidural fat deposition in SEL is usually symmetric left to right. More rarely
it is asymmetric (Fig 9).

9a

Figure 9:

Axial T1-weighted images, obtained at 2 contiguous lower lumbar vertebral levels,

shows asymmetric predominantly right-sided epidural fat deposition in SEL. Note the
relative prominence of the meningo-osseous ligaments on the side of the predominant
fat deposition (arrows).

In cases of thoracic level involvement by SEL, the axial configuration is usually

oval with a mild degree of anteroposterior flattening of the cord, and effacement
of the CSF, as evidence of mass effect by the epidural fat (Fig 10a-c).

10a

10b

10c

Figure 10:

(10a-c) Sagittal T1-weighted (A) and T2-weighted (B) images in a 38 year-old woman
with mid-thoracic back pain demonstrate prominent epidural fat tissue posteriorly
from T2 through the T7 level (asterisks). There is obliteration of the CSF at the
corresponding levels (arrows), while CSF is present above and below the level of
SEL (arrowheads). On an axial T2-weighted image obtained at the T6-7 disc level
(C), there is oval to mildly flattened configuration of the cord and dura, which
measures 6 mm in A/P dimension at midline (red) while the epidural fat measures 9
mm (blue) and the spinal canal measures 15 mm (green), corresponding to a cord to
epidural fat ratio of 0.66, and fat percentage of the spinal canal of 60%,
indicating Grade 2 (moderate) SEL.

11a

11b

Figure 11:

(11a) Sagittal T1-weighted image in a 48 year-old male with back pain shows the
presence of both SEL at the L4 to S2 levels and a L5-S1 disc bulge.

(11b) Axial T1-weighted image in the same patient, obtained at the S1 level near
the superior endplate, demonstrates a Y-sign characteristic of SEL.

Sometimes the focal prominence of epidural fat tissue located next to a disc bulge
or herniation has a configuration suggesting that it is compensatory, such as when
fat occupies the small triangular region seen on sagittal images anterior to the
dural sac, next to where a disc bulge or herniation displaces the dural sac
posteriorly. If this finding is present in association with a normal rounded axial
dural sac configuration, without signs of external mass effect, this does not
suggest SEL (Fig 12).
12a

12b

Figure 12:

(12a) Sagittal T1-weighted image in a non-obese 33 year-old man with back pain and
left leg weakness, demonstrate a small caudal central to left paracentral disc
extrusion, with a triangular configuration of the adjacent mildly increased
epidural fat just above and below the extrusion (arrows).

(12b) Axial midline image in the same patient, obtained at mid-L5 level (see
dotted-line on A), demonstrates a normal rounded configuration of the dural sac at
the level of the fat tissue incidental prominence, not suggesting a diagnosis of
SEL.

Similarly, incidental epidural fat without signs of mass effect upon the dural sac
may occur at regions of segmental enlargement of the spinal canal, such as with
pars defects and anterolisthesis where the dural sac remains of normal size while
the increased volume within the epidural space is occupied by epidural fat; this
does not fulfill the SEL criterion of evidence of dural sac compression (Fig 13a-
b). With vertebral malalignment such as scoliosis or prominent kyphosis, there will
also often be compensatory asymmetric distribution of the epidural fat related to
the altered osseous and dural sac configurations.

13a

13b

Figure 13:

(13a) Sagittal midline image in an obese 16 year-old male with low back pain and
known bilateral pars defects at L5, shows grade 1 anterolisthesis at L5-S1 with a
widened osseous spinal canal, and compensatory prominence of epidural fat both
anterior and posterior to the dural sac (asterisks).

(13b) An axial T2-weighted image in the same patient shows the increased
anteroposterior diameter of the osseous spinal canal, the prominence of epidural
fat tissue, and the normal rounded configuration of the dural sac (arrows), without
evidence for extrinsic compression.

Differential diagnosis

The presence of increased amounts of fat within the spinal epidural space is
usually readily identified on T1-weighted MR images, due to the high T1 signal of
normal fat tissue. In SEL this fat tissue is unencapsulated and the MR signal is
homogeneous, without transition boundaries between the excessive fat deposition
regions and regular epidural fat tissue. If instead a region of fat tissue
prominence shows a marginated focal mass, with homogeneous normal fat signal or
sometimes with minor intralesional strands of fibrous tissue, the lesion likely
represents an intra-spinal epidural lipoma (Fig 14a-b), or less commonly an
epidural angiolipoma. Up to half of intraspinal angiolipomas have been described to
exhibit a predominance of fat tissue, with a sometimes much smaller component of
vascular tissue; this vascular component demonstrates low signal intensity on T1-
weighted images and high signal intensity on T2-weighted images, the opposite of
the fat tissue component.12 Angiolipomas also demonstrate post-contrast
enhancement, which is not a feature of lipomas, or of epidural lipomatosis.

14a

14b

Figure 14:

(14a-b) Sagittal T1-weighted (a) and axial fat-saturated (b) T1-weighted images at
the T12-L1 level, in a 67-year old male with low back pain and bilateral leg
weakness. The Lumbar spine MRI exam showed a marginated extradural mass (long
arrow), with high T1 signal throughout the mass similar to that of the subcutaneous
fat (asterisk). The mass is located within the right side of the central canal, and
measures 3.8 cm in length. A few thin septations are present within the lesion
(arrowheads). Findings suggested an epidural lipoma, but to exclude an angiolipoma,
a post-contrast MRI exam was performed (b) which demonstrated a non-enhancing
lesion (long arrow) with mass effect upon the cord (short arrow).

Clinical therapy and reported results

Conservative therapy is almost always advocated in patients with symptoms

attributed to SEL. Rarely, invasive procedures may be used in cases of severe pain
or neurologic deficits, or when patients experience rapid progression of symptoms.

Due to the relatively small number of patients with symptomatic SEL described in
the medical literature, available data regarding results of conservative versus
operative therapies is limited, often representing case reports, without clinical
trial data available. Obesity, idiopathic or related to exogenous or less commonly
endogenous corticosteroid actions, is present in nearly all patients reported with
SEL. If the patients who are taking corticosteroid medication can tolerate a dose
decrease, this change has been associated with halting progression or reversing
symptoms. Sometimes, however, the patient’s underlying disease (such as asthma,
COPD, renal transplant) does not permit tapering or discontinuity of corticosteroid
therapy. Patients with endocrinopathy have been reported to improve after the
underlying disorder has been treated. In patients with obesity without underlying
endocrinopathy, clinical improvement and sometimes reversal of both clinical
symptoms and MRI features of SEL have been demonstrated after moderate weight loss
has been achieved.13,14

In individuals with SEL who are experiencing severe sensory or reflex loss, or with
severe pain attributed to SEL, surgery with decompressive laminectomy and fat
tissue debridement has been advocated to achieve pain control or to avoid permanent
function loss (Ref 6, 14). In several reports and a few smaller series in the
medical literature, operative therapy for SEL has been shown to lead to a decrease
in severity or resolution of neurological symptoms. Other reports have described
successful surgical procedures addressing symptomatic SEL and co-existing disorders
such as disc herniation or spondylolysis with listhesis.15,16

Epidural steroid injection therapy has sometimes led to symptomatic improvement in

SEL, but have been cautioned against in some reports due to technical issues, and
concern for possible local stimulation of further fat tissue deposition.17
Review of Visceral Fat deposition in Obesity, related Anatomy and MRI findings, and
Metrics applied to spinal MR images
When a mild to moderate grade of SEL is diagnosed on MRI in a patient with back
pain (Fig 1a), it can often leave doubts as to whether the excessive deposition of
epidural fat is indeed the likely cause of or even related to the patient’s
symptoms. Fat tissue has generally been associated with a cushioning, protective
function around nerve structures, not with mass effect serious enough to cause
compressive neuropathy. Of interest, almost all cases of SEL occur in obese
patients, often with centripetal abdominal/visceral type of obesity (Fig 15), where
excessive fat tissue is somewhat similarly deposited in locations that normally
have a smaller amount of fat present, such as the omentum and the small bowel
mesentery.

15a

Figure 15:

A sagittal gradient echo scout view for lumbar spine MRI, obtained at the midline
with the umbilicus and lumbar spinous processes visible (arrows), in a 62 year-old
man with lumbar spine pain, demonstrates prominent visceral fat deposition
(asterisk), while there is a normal amount of subcutaneous fat tissue posteriorly
(arrowheads), compatible with abdominal/visceral type of obesity.

Instituted conservative therapy leading to weight loss in obese patients with SEL
has been reported to have the potential to reverse clinical symptoms, and follow-up
MRI exams have shown a decrease or reversal of the increased epidural fat
deposits.13,14 This may relate to decrease in mass effect upon the dural sac and
nerve roots, or it could instead be related to other local effects of the excessive
fat tissue deposits, such as being a cause of low-grade inflammation. A parallel
could be drawn to the mass effect shown on MRI of an acute disc herniation upon a
lumbar nerve root, in which the patient’s symptomatology is also known to be
affected by metabolic changes, not visualized on the MR images, mediated by enzymes
released locally at the site of a ruptured disc.

In has been stated that in the last decades the understanding of the physiological
and pathophysiological role of fat tissue, and specifically the adipocyte, has
dramatically changed away from fat tissue being seen as a “passive” type of
connective tissue storing excess energy for future use, and with a “cushioning”
passive effect on adjacent structures.18 Extensive research in the field of fat
tissue and obesity has established adipose tissue as an endocrine organ coupling
neuro-endocrine and metabolic signaling (Ref 18). Furthermore is has been
established that adipocytes and adipocytokines are involved in primary inflammatory
processes and diseases. Special types of regional adipocytes have been identified
in subdermal, visceral, synovial and bone marrow fat tissues.18 The low-grade
chronic inflammatory reaction associated with excessive fat deposition in obesity
has been termed “metaflammation”19 to distinguish it from the conventional acute
signs of clinical inflammation (dolor, rubor, calor, tumor).

It has been well established that obesity is a non-homogeneous condition, and that
regional distribution of excessive fat tissue appears to be an important clue to
understanding the relation of obesity to disturbances in glucose and lipid
metabolism, and the association with metabolic and cardiovascular disease.20

Visceral obesity and insulin resistance are considered the main features behind the
increased incidence of cardiovascular and diabetes in metabolic syndrome, and
obesity is considered to have a leading role in causing a low-grade inflammatory
state that leads to insulin resistance as well as endothelial and microvascular
dysfunction.21

In most instances obesity is readily diagnosed on clinical exam, and has

traditionally been graded using BMI. However, in patients with predominantly
abdominal (visceral) fat deposition and without significant increases in
subcutaneous deposits of fat tissue, the obesity may not always be recognized on
clinical exam, or may be underestimated. BMI has been shown to be less sensitive
for visceral type obesity, potentially delaying the opportunity for conservative
therapy. Other anthropometric indicators have been developed, as well as imaging
techniques including MRI, suitable for assessment of several phenotypes of human
obesity. Some of these assessments may be performed on MR images of the lumbar
spine, at the time of diagnosis of SEL.

Anatomy of Intra-abdominal fat deposition in obesity

Visceral fat depositions are mainly located within the omental, mesenteric and
retroperitoneal structures.

The greater omentum (Fig 16a-b) is a large 4-layered folded visceral peritoneal
structure, described as “apron-like”, extending caudally from the gastric greater
curvature, located anterior to the small intestine and immediately deep to the
abdominal wall, and doubling back up to the transverse colon. Normally quite thin,
it has protective functions and harbors mast cells important for immune function;
the omentum can move towards regions of bowel tissue compromise, to wall-off
perforations and prevent peritonitis. The lesser omentum similarly hangs down from
the liver to the lesser curvature of the stomach.

16a

16b

Figure 16:

(16a) This 2D graphical depiction of a lateral view of the abdomen indicates the
locations of visceral fat deposition within the greater and lesser omentum, the
small bowel mesentery, and the retroperitoneum.

(16b) Midline sagittal localizer in a 53 year-old man with low back pain and
bilateral sciatica, and MRI showing severe lumbar and sacral SEL (blue asterisks).
There is both subcutaneous and visceral abdominal obesity. The greater omentum
(long arrows) is seen deep to the linea alba and abdominal fascia (arrowheads) and
superficial to the transverse colon (red asterisk). The prehepatic fat pad is
apparent higher up (blue arrow). Abdominal anteroposterior diameter (SAD) at
umbilical level is 33.0 cm. The posterior perirenal fat thickness (not shown)
measured 4.0 cm.

The mesentery is a fan-shaped 2-layered peritoneal fold, with function to contain

and suspend the jejunal and ileal bowel loops, with accompanying veins, nerves and
lymphatic structures. The mesenteric root anchors it to the posterior abdominal
wall. There is continuity between the mesenteric root and the pararenal spaces
bilaterally.

The retroperitoneal space is divided into anterior pararenal, perirenal, and

posterior pararenal spaces by the thin perirenal fascia. The largest of these is
the perirenal space, which communicates with the opposite side perirenal space
across the midline, and contains fat tissue surrounding the kidneys; fat tissue is
present also within the smaller posterior pararenal space.

MRI demonstration of obesity types, on images from Lumbar spine MRI exams

17a

Figure 17:

(17a) Localizer gradient echo sagittal image in a 68 year-old man with back pain
and bilateral L4 pars defects with L4-5 anterolisthesis, demonstrates subcutaneous
and visceral fat tissue amount within normal limits. Abdominal anteroposterior
diameter at umbilical level: 20.5 cm. Posterior perirenal fat thickness (measured
on axial images, not included): 0.5 cm.

(17b) Sagittal T1-weighted image in a 15 year-old obese male with lumbar pain and a
L4-5 moderate disc extrusion, demonstrates the presence of subcutaneous obesity,
without visceral obesity. Abdominal anteroposterior diameter at umbilical level:
23.9 cm.

(17c) Sagittal localizer image in 59 year-old man demonstrates visceral obesity

(omental thickening and fat signal: asterisks; mesenteric fat deposition:
arrowheads) but not subcutaneous type obesity. Abdominal anteroposterior diameter
at umbilical level: 28.1 cm.

(17d) Sagittal localizer image in a 59 year-old woman with low back and right leg
pain, demonstrates the presence of both subcutaneous and visceral types of obesity.
Abdominal anteroposterior measurement at umbilical level: 32.0 cm.

At the subcutaneous tissues
signal fibrous subcutaneous
divides the superficial fat
fat deposition often occurs
prominent thickening of the
posterior to the lumbar spine, a normally thin and low-
fascia, located within the subcutaneous fat layer,
from the deep fat (Figures 5, 12a, 13a). In obesity,
preferentially within the deep layer, seen as a more
layer deep to the subcutaneous fascia (Fig: 1a-b; 18a).

A frequent finding on MR images of the lumbar spine in obese individuals is the

presence of edema within posterior subcutaneous fat, located along the subcutaneous
fascia and within the deep fat layer (Fig 18a-b). This finding has no known
corresponding clinical symptoms or significance except for that it could be
mistaken for pathology, and is considered to be due to the less organized and more
widely spaced fascial septae in the deep fat tissue when compared to the
superficial fat tissue where the septae are more uniformly and closely spaced.22

18a

Figure 18:

Sagittal T1- weighted (left) and fat-suppressed T2-weighted (right) images in a 59

year-old obese woman, demonstrates the incidental finding of focal edema centered
along the subcutaneous fascia (arrows).
MRI metrics of intra-abdominal fat deposition in obesity

In addition to MRI, other imaging modalities have been used for evaluation of
regional obesity and identifying the type of fat tissue deposition, including
ultrasound, CT scan, DXA scan, and more recently Bioelectric Impedance.

Among anthropometric measures used for detection and grading of obesity, the most
widely known is the BMI (body mass index), using only the patient’s weight and
height for calculation of a score. While easy to perform, BMI has been shown to not
consistently identify the presence of visceral obesity.23 Body measurements which
have been shown to correlate well with the presence of visceral obesity include
measurement of the waist circumference at umbilical level, with the patient
upright, and supine A/P measurement of the trunk (SAD, sagittal abdominal diameter,
or “abdominal height”) also obtained at the level of the umbilicus, L4-5. The waist
circumference measurement has been standardized on individuals in the upright
position, and technically does not readily lend itself to measurement on MRI
images; the cutoff for obesity has been set at 102 cm for men and 88 cm for women.
The SAD however can be obtained on the localizer images for Lumbar spine MRI exams
if the field-of-view permits (Fig 19 A-B). Studies have found that an A/P
measurement of less than 22 cm in men and 20 cm in women can be used as cutoff to
identify metabolically obese individuals who would benefit from intervention.24

19a

Figure 19:

The sagittal scout image from lumbar spine MRI exams in a 62 year-old man with
visceral obesity and SAD 28.0cm (left), and a 46 year-old man without obesity
demonstrating SAD 18.0 cm (right).

Other metrics which may be available for measurement on MR images are the pre-
peritoneal as well as the anterior subcutaneous fat tissue. In a clinical study of
non-obese patients, the pre-peritoneal fat tissue measured up to 10 mm in
thickness, while the anterior subcutaneous tissue ranged up to 10 mm in men and 15
mm in women, establishing useful cutoff measurements for obesity in these
regions.25

Direct measurement of the thickness of the perirenal fat tissue is also usually
feasible on MR images of the lumbar spine. This measurement, obtained at the level
of the renal artery, has been found to correlate well with the total volume of
perirenal fat tissue, and also to correlate with visceral fat volumes but not with
subcutaneous fat volumes.23 Cutoff numbers have not been well established in this
region.

Conclusion
Spinal epidural lipomatosis is a relatively rare disorder which involves increased
fat deposition into the epidural space, and may involve shorter or longer segments
of the lumbosacral or thoracic spine. Almost all cases of SEL are seen in obese
patients, and a large percentage of SEL patients have a history of corticosteroid
use. When there is a limited extent of SEL, it is thought to be not clinically
significant. When more prominent and associated with features of mass effect upon
the dural sac, symptoms indistinguishable from those related to disc herniations or
degenerative central stenosis have been attributed to SEL. Conservative therapy
such as weight loss has led to symptomatic improvement and even a few cases
demonstrating MRI resolution.
While the mass effect related to epidural fat tissue may result in symptoms from
nerve root compression, it is also possible that the excessive deposition of fat
causes symptoms related to the low-grade chronic inflammation present within fat
tissue in obese individuals. This has been called “metaflammation” to distinguish
it from the manifestations of acute inflammation.

The spinal MR images may in addition to the detection of SEL also provide
information regarding the presence and type of obesity. The visceral type of
obesity has shown a strong association with increased risks for cardiovascular
disease, diabetes and metabolic syndrome. MRI detection and grading of SEL, as well
as detection of visceral obesity, may be helpful in identifying patients at earlier
stages of the disorder when weight loss therapy may be especially beneficial to
both prevent future SEL-related back pain, and to avoid the increased health risks
associated with the visceral type of obesity.

References
Spinal cord compression by extradural fat after renal transplantation. Lee M,
Lekias J, Gubbay SS et al. Med J Aust 1975;1(7):201-203 ↩
Spinal epidural lipomatosis: case reports, literature review and meta-analysis.
Fogel GR, Cunningham PY lll, Esses SI. Spine J 2005:5(2):202-211 ↩
Idiopathic spinal epidural lipomatosis. Robertson SC, Traynelis VC, Follett KA et
al. Neurosurgey 1997: 41(1);68-74 ↩
Spinal epidural lipomatosis in Lumbar Magnetic Resonance Imaging Scans. Sugaya H,
Tanaka T, Ogawa T et al. Healio Feature article. Free full text: April 2014 –
Volume 37 · Issue 4: e362-e366 ↩
Lumbosacral epidural lipomatosis: MRI grading. Borre’ DG, Borre’ GE, Aude F,
Palmieri GN. European Journal of Radiology 2003 Jul;13(7):1709-21 ↩
Is spinal epidural lipomatosis an MRI-based diagnosis with clinical implications? A
retrospective analysis. Pinkhardt EH, Sperfeld A-D, Bretschneider V et al. Acta
Neurologica Scandinavica June 2008;117(6):409-414 ↩
Spinal Epidural Lipomatosis: A review of its causes and recommendations for
treatment. Fassett DR, Schmidt MH. Neurosurg Focus 2004;16(4). Free full text:
http://www.medscape.com/viewarticle/474908 ↩
Polygonal deformation of the dural sac in lumbar epidural lipomatosis: anatomic
explanation by the presence of meningovertebral ligaments. Geers C, Lecouvet FE,
Begets C et al. Am J Neuroradiology 2003;24(7):1276-82. Free full text:
http://www.ajnr.org/content/24/7/1276 ↩
Posterior lumbar epidural fat as a functional structure? Histologic specificities.
Beaujeux R, Wolfram-Gabel R, Kehrli P et al. Spine 1997:22(11):1264-1268 ↩
Epidural fat in various diseases: contribution of magnetic resonance imaging and
potential implications for neuro-axial anesthesia (article in Spanish). Reina MA,
Pulido P, Castedo J et al. Rev Esp Anesthesiol Reanim 2007 Mar;54(3):173-183 ↩
Lumbar epidural lipomatosis: the “Y” sign of the thecal sac compression. Kuhn MJ,
Youssef HT, Swan TL et al. Computerized Medical Imaging and Graphics – Sept/Oct
1994:18(5):367-72 ↩
MRI features of spinal epidural angiolipomas. Su Hu, Chun-hong Hu, Xiao-yun Hu et
al. Korean J Radiol 2013 Sept-Oct; 14(5):810-817 Free full text:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3772264/ ↩
Epidural lipomatosis. Boutsen Y, Donckier J. Postgrad Med J 2000 Jan;76(891):60-61.
Free full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1741453/ ↩
Cauda equine compression by epidural lipomatosis in obesity. Pouchot J, Si-Hassen
C, Damade R et al. Effectiveness of weight reduction. J Rheumatology Sep 1995,22
(9);1771-1775 ↩
Case 148: Thoracic epidural lipomatosis. Venkatanarasimha N, Parrish RW. Radiology
Aug 2009:252(2). Free full text: https://doi.org/10.1148/radiol.2522080365 ↩
Unusual spinal epidural lipomatosis and lumbosacral instability. Ruiz Picaso D,
Villaescusa JR. Case Reports in orthopaedics, Vol 2016, Article ID 3094601, 4 pages
Free full text: https://www.hindawi.com/journals/crior/2016/3094601/ ↩
Focal spinal epidural lipomatosis after a single epidural steroid injection.
Danielson KD, Harrast MA. Physical Medicine & Rehabilitation June 2011:3(6):590-593
↩
Role of adipose tissue as an inflammatory organ in human diseases. Schaffler A,
Muller-Ladner U, Scholmerich J et al. Oxford Academic Endocrine Reviews
(2006)27(5):449-467 Free full text:
https://academic.oup.com/edrv/article-lookup/doi/10.1210/er.2005-0022 ↩
Inflammatory mechanisms in obesity. Gregor MF, Hotamisligil GS. Annual Rev Immunol
2011;29:415-445 ↩
Subcutaneous and visceral adipose tissue: their relation to the metabolic syndrome.
Wajchenberg, BL. Endocrine Reviews 2000;21(6):697-738. Free full text:
https://doi.org/10.1210/edrv.21.6.0415 ↩
Inflammation as a link between obesity and metabolic syndrome. Faloia E, Grazia M,
De Robertis M et al. Journal of Nurition and Metabolism, Volume 2012(2012), Article
ID476380, 7 pages Free full text:
https://www.hindawi.com/journals/jnme/2012/476380 ↩
MR Imaging of the lumbar spine: relation of posterior soft-tissue edema-like signal
and body weight. Shi H, Schweitzer ME, Carrino JE et al. Am J of Roentgenology
2003:180:81-86. Free full text:
http://www.ajronline.org/doi/full/10.2214/ajr.180.1.1800081 ↩
Perirenal fat thickness measured with computed tomography is a reliable estimate of
perirenal fat mass. Favre G, Grangeon-Chapon C, Rafaelli C et al. PLoS One 2017 Apr
19:12(4):e0175561. Free full text: www.ncbi.nlm.nih.gov/pmc/articles/PMC5396915/ ↩
Sagittal abdominal diameter as a screening tool in clinical research: cutoffs for
cardiometabolic risk. Rise’rus U, de Faire U, Berglund L et al. Journal of Obesity
2010(2010) Article ID757939, 7 pages. Free full text:
https://www.hindawi.com/journals/jobe/2010/757939/ ↩
Preperitoneal fat thickness determined by ultrasonography is correlated with
coronary stenosis and lipid disorders in non-obese male subjects. Tadokoro N,
Murano S, Nishide T et al.International Journal of Obesity April 2000:24(4):502-507
Free full text: http://www.nature.com/ijo/journal/v24/n4/full/0801187a.html#tbl2 ↩
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