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.

4
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).

5
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).

7
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).

8
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).

9
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.

15
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

17
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 posterior to the lumbar spine, a normally thin and low-signal fibrous subcutaneous fascia, located within the subcutaneous fat layer, divides the superficial fat from the deep fat (Figures 5, 12a, 13a). In obesity, fat deposition often occurs preferentially within the deep layer, seen as a more prominent thickening of the 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

18
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

19
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

  1. 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
  2. Spinal epidural lipomatosis: case reports, literature review and meta-analysis. Fogel GR, Cunningham PY lll, Esses SI. Spine J 2005:5(2):202-211
  3. Idiopathic spinal epidural lipomatosis. Robertson SC, Traynelis VC, Follett KA et al. Neurosurgey 1997: 41(1);68-74
  4. 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
  5. Lumbosacral epidural lipomatosis: MRI grading. Borre’ DG, Borre’ GE, Aude F, Palmieri GN. European Journal of Radiology 2003 Jul;13(7):1709-21
  6. 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
  7. 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
  8. 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
  9. 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
  10. 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
  11. 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
  12. 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/
  13. 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/
  14. 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
  15. Case 148: Thoracic epidural lipomatosis. Venkatanarasimha N, Parrish RW. Radiology Aug 2009:252(2). Free full text: https://doi.org/10.1148/radiol.2522080365
  16. Unusual spinal epidural lipomatosis and lumbosacral instability. Ruiz Picaso D, Villaescusa JR. Case Reports in Orthopedics, Vol 2016, Article ID 3094601, 4 pages Free full text: https://www.hindawi.com/journals/crior/2016/3094601/
  17. Focal spinal epidural lipomatosis after a single epidural steroid injection. Danielson KD, Harrast MA. Physical Medicine & Rehabilitation June 2011:3(6):590-593
  18. 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
  19. Inflammatory mechanisms in obesity. Gregor MF, Hotamisligil GS. Annual Rev Immunol 2011;29:415-445
  20. 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
  21. 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
  22. 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
  23. 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/
  24. 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/
  25. 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

More on this topic