Submitted Successfully!
To reward your contribution, here is a gift for you: A free trial for our video production service.
Thank you for your contribution! You can also upload a video entry or images related to this topic.
Version Summary Created by Modification Content Size Created at Operation
1
Valerio D'Agostino
 -- 1910 2023-01-30 15:05:37 |
2 format correct
Conner Chen
 Meta information modification 1910 2023-01-31 07:32:57 |

Video Upload Options

We provide professional Video Production Services to translate complex research into visually appealing presentations. Would you like to try it?
No, upload directly Yes

Confirm

Are you sure to Delete?
Yes No
Cite
If you have any further questions, please contact Encyclopedia Editorial Office.
D’agostino, V.;  Petrera, M.R.;  Tedesco, G.;  Pipola, V.;  Ponti, F.;  Spinnato, P. Spinal Epidural Lipomatosis’ Etiology. Encyclopedia. Available online: https://encyclopedia.pub/entry/40595 (accessed on 15 November 2024).
D’agostino V,  Petrera MR,  Tedesco G,  Pipola V,  Ponti F,  Spinnato P. Spinal Epidural Lipomatosis’ Etiology. Encyclopedia. Available at: https://encyclopedia.pub/entry/40595. Accessed November 15, 2024.
D’agostino, Valerio, Miriana Rosaria Petrera, Giuseppe Tedesco, Valerio Pipola, Federico Ponti, Paolo Spinnato. "Spinal Epidural Lipomatosis’ Etiology" Encyclopedia, https://encyclopedia.pub/entry/40595 (accessed November 15, 2024).
D’agostino, V.,  Petrera, M.R.,  Tedesco, G.,  Pipola, V.,  Ponti, F., & Spinnato, P. (2023, January 30). Spinal Epidural Lipomatosis’ Etiology. In Encyclopedia. https://encyclopedia.pub/entry/40595
D’agostino, Valerio, et al. "Spinal Epidural Lipomatosis’ Etiology." Encyclopedia. Web. 30 January, 2023.
Spinal Epidural Lipomatosis’ Etiology
Edit
This entry is adapted from the peer-reviewed paper 10.3390/diagnostics13020322

Spinal epidural lipomatosis is defined by an excessive amount of epidural fat in the spinal canal, usually in the lumbosacral tract: a well-known cause of lumbar pain and spinal stenosis with a possible wide range of neurological symptoms.

magnetic resonance imaging obesity visceral adipose tissue

1. Introduction

Spinal epidural lipomatosis (SEL) is a condition characterized by the over-deposition of unencapsulated epidural fat in the spinal canal, usually in the lumbosacral tract. The non-invasive diagnosis of SEL can be made with Magnetic Resonance Imaging (MRI) or Computed Tomography (CT) only.
SEL, a pathologic condition, may lead to the narrowing of the spinal canal and compression of surrounding neural structures. SEL can be asymptomatic in mild–moderate disease and usually becomes symptomatic in moderate–severe cases. The clinical presentation typically involves progressive lower back pain radiating to the lower limbs, spinal claudication, radiculopathy, myelopathy, and cauda equine syndrome [1][2].
In most cases, symptoms develop over months to years but may develop acutely in some rare cases [3][4][5][6]. For unclear reasons, males are affected more commonly than females (M:F = 3:1) [7]. Moreover, more than 75% of all reported patients are obese [8]. Exceptionally, children can suffer from neurological symptoms associated with SEL, and this is often accompanied with a long history of steroid treatment [9][10][11][12].
A previous large population study based on MRI reports including 28,902 subjects reported a prevalence of SEL of approximately 2.5%. In this series, the main factors associated with the disease included being male, obese, and having a history of systemic corticosteroid use [13]. Recent work has focused attention on the ratio of radiologists’ awareness and the detection of this condition, highlighting a fairly significant underestimation of SEL in radiologists’ reports and suggesting that the actual prevalence of SEL has been underestimated so far [14]. The prevalence of SEL in this latter research study, which includes 450 subjects, was notably higher (16.7%) [14]. Another previous large series focused on lumbar MRIs and including 2528 patients found quite similar results (SEL prevalence = 20.8%) [15].
Historically, steroid excess (exogenous or endogenous) was considered the most common etiological factor associated with SEL [16][17][18]. Indeed, the first case of steroid-induced lipomatosis was reported by Lee et al. in 1975 [19].
Because obesity in adults is usually accompanied by common non-communicable diseases, such as dyslipidemia, Type 2 diabetes, hypertension, and arteriosclerosis, the high rate of obesity in patients with idiopathic SEL suggests that non-communicable diseases and SEL are causally related. The primary line of treatment is to reduce or eliminate the etiologic factors. When a clear etiologic factor cannot be ruled out, weight loss has been proposed as a conservative treatment. However, surgical decompression is the treatment of choice, especially for acute or severe cases [20][21]. Moreover, in patients with worsening or persistent neurologic symptoms, surgery should be suggested [1][21][22].
When SEL is a concause of neurological symptoms, together with other conditions (i.e., thickened yellow ligament and disc herniation), a negative prognostic impact on the surgical outcome of posterior decompression surgery has been reported [23], giving paramount importance to its correct reporting by radiologists.

2. SEL’s Etiology

In the following subsections, the recognized causes of SEL are reported and discussed, with reference to the available literature.

2.1. Excessive Amount of Corticosteroids

SEL has been frequently associated with excessive use of corticosteroids, which can have an exogenous source-like steroid injection [24] or long-term corticosteroid therapy [25][26][27][28]. It is also associated with an endogenous source-like corticotropin syndrome from ACTH-secreting extra pituitary tumors (endogenous Cushing’s syndrome) [17] or from an ACTH-secreting pituitary gland adenoma (Cushing’s disease) [29][30].
Among the series that have been reported, approximately 75% of cases have been associated with exogenous steroid use [31], with great variability from case to case in terms of the doses and duration of treatments associated with this condition [32]. Mostly, moderate-to-high steroid dosages were received by patients for years before the development of symptoms.
Although relatively rare, some cases of patients who developed SEL with a long-term and low-dosage steroid treatment have been described in the literature [33].
When the treatment with steroids is both long-term and high-dosage, there is a risk of developing severe SEL, even in children, as evident in an 8-year-old patient in treatment for Crohn’s disease who suffered from myelopathy due to the SEL-induced compression of the spinal cord [34].
There have been reports of SEL associated with epidural steroid injections and even inhaled steroids, but the long-term use of oral steroids is by far the most common association [35][36][37].
Koch et al. described a case of a patient with bronchial carcinoid associated with ectopic corticotropin syndrome. The patient complained of severe back pain and leg weakness among other clinical issues. The MRI showed multiple levels of excessive epidural fat, which reverted to normal after two months of treatment with the inhibitors of steroidogenesis (metyrapone and ketoconazole). At the same time, there was a complete resolution of neurological symptoms [38].
Bathia et al. reported a similar case of ACTH-secreting bronchial carcinoid in a male farmer with Type 2 diabetes mellitus. The MRI showed multiple levels of SEL of the thoracic spine, without significant disc herniation. Since the patient’s pain was improving, despite treatment with ketoconazole, he was successfully treated with decompressive hemilaminectomy and the removal of the epidural adipose tissue (no stabilization was performed due to massive osteoporosis) [39].
A 17 yo with an ACTH-secreting adenoma of the pituitary gland, which developed after trans-sphenoidal adenectomy, experienced a sudden spastic paraparesis with a sensory deficit to the level of T5. An MRI scan showed a severe SEL of the thoracic spine, which was treated conservatively with success. This case shows that it is important to rule out SEL from a myopathy caused by hypercortisolism, starting with a proper collection of the patient’s clinical history [40].
Historically, SEL was associated with exogenous steroid use as the first cause of disease, even if recent reports suggest that obesity is becoming the major risk factor. A study by Fogel et al. reports that 55.8% of SEL cases caused by exogenous steroids affect the thoracic spine, compared to 32.7% that only involve the lumbosacral region and 11.5% that affect both [2]. This differs from the endogenous steroid disease-related SEL, which affects the thoracic and lumbosacral areas relatively the same. In addition, most obesity-related SEL (69.6%) and idiopathic-related SEL (50%) result in lumbosacral involvement.
On the other hand, a recent systematic review with meta-analyses revealed that obesity is the current leading cause of SEL [41].

2.2. SEL and Obesity

Obesity has always been considered one of the most common causes of SEL [2]. Nonetheless, in recent years, obesity is believed to be the most common cause of SEL. A recent meta-analysis confirmed that obesity should be considered the main risk factor for SEL development (52% of cases) [41].
Consistent with previous studies, there was a positive correlation between the degree of obesity and the severity of SEL [42][43][44][45].
In a large series by Theyskens et al., which included MRI scans of 28,902 patients, a BMI > 30 was independently associated with SEL in a multivariate analysis [13]. Yildirim et al. reported the strong correlation of an increased BMI with SEL in a retrospective case-matched control study including 199 patients. In this research study, the authors indicated that patients with SEL had a significantly higher median BMI than control subjects (36.7 vs. 29.4 kg/m2, p < 0.001) [46].

2.3. Non-Alcoholic Fatty Liver Disease

Non-alcoholic fatty liver disease (NAFLD) is nowadays the most common chronic liver disease in developed countries. The clinical presentation of NAFLD ranges from asymptomatic (only with elevated liver enzyme levels) to cirrhosis, with possible complications of liver failure and hepatocellular carcinoma. There is sufficient evidence supporting an association between NAFLD and metabolic syndrome [47]; interestingly, recent studies have also found an association between SEL and NAFLD [48].

2.4. Miscellaneous

Other possible risk factors for SEL development have been suggested in recent years, but their role remains controversial and needs further investigation.
The principal difficulty in defining their real role in the development of SEL is the contemporary presence of well-known risk factors such as obesity and exogenous steroid treatment. More studies are needed to assess if they can be addressed as risk factors or only associated factors.
SEL has been described as a possible manifestation of highly active antiretroviral therapy (HAART)-associated lipodystrophy in HIV-positive patients [49][50][51][52].
Androgen deprivation therapy for prostate cancer has been suggested as a possible risk factor for SEL in several case reports [53][54][55][56].
Three case reports have described an association between SEL and scoliosis [57][58][59]. The rapid progression of SEL has been reported after spinal surgery [4][5][60].
In the study by Okada et al., SEL was significantly associated with diffuse idiopathic skeletal hyperostosis (relative risk (RR), 2.6; 95% confidential interval (CI), 1.3–5.1; p < 0.01) [61].
Finally, some authors have suggested a possible association between SEL and spinal kyphotic deformities, such as congenital, Scheuermann, and tuberculotic kyphosis [62][63]; Paget disease [64][65]; hypothyroidism [66]; chronic alcoholism [67]; and Type 1 diabetes mellitus [68].

2.5. Idiopathic

Idiopathic cases of SEL have been reported in the literature since 1982 [69]. Haddad et al. first hypothesized that idiopathic SEL was a byproduct of obesity, with the gradual overgrowth of epidural fat resulting in the compression of the spinal cord and nerves [70]. Nevertheless, cases of SEL in underweight patients suggest another kind of pathogenetic mechanism for idiopathic SEL [31].
The recognition of idiopathic SEL is of paramount importance, and in absence of risk factors, the disease cannot be clinically suspected. Patients may remain undiagnosed for a long period. As a result, the longer duration of nerve root constriction may cause a relatively lower recovery rate [71].
There is disagreement in the literature regarding the definition of idiopathic SEL. Indeed, some authors refer to idiopathic diseases to indicate the SEL of an unknown cause, while others use this term to describe SEL associated with obesity or other causes that nowadays are clearly risk factors for disease development. Indeed, the term “idiopathic SEL” should be used only in patients without any other recognized risk factor (e.g., metabolic syndrome, obesity, and increased corticosteroids).
In the literature review and meta-analysis by Fogel et al., idiopathic SEL has been reported to account for 17% of the cases. This group includes those patients who did not take exogenous steroids, were not obese, and did not have an underlying endogenous steroid hormonal disease [2][72][73].
Idiopathic SEL is also reported in the pediatric age, with few reports in the literature at this regard [74][75]. Importantly, the grading of SEL (including a cut-off for diagnosis) was tested only in adult patients, while pediatric-age patients’ range of normality in terms of amount of epidural fat is still missing [15]. Indeed, the diagnosis at this age is purely qualitative depending on the MRI or CT evaluation.
Racial differences may become more prevalent when discussing the pathogenesis of SEL.
Yoo et al. reported an incidence of up to 68.8% of idiopathic SEL in the Korean population [76], while Fogel et al. reported 17% for the same SEL category in Western countries [2].
This difference may suggest a role of genetic variation in the pathogenesis of SEL.

2.6. Epidemiological Analysis of SEL’s Etiologies

Historically, SEL was associated with exogenous steroid use as the first cause of disease [2], even if recent reports suggest that obesity is becoming the major risk factor [77]. A study by Fogel et al. reported that 55.8% of SEL cases caused by exogenous steroids affect the thoracic spine, compared to 32.7% that only involve the lumbosacral region and 11.5% that affect both [2]. This differs from the endogenous steroid disease-related SEL, which affects the thoracic and lumbosacral areas relatively the same. In addition, the majority of obesity-related SEL (69.6%) and idiopathic-related SEL (50%) result in lumbosacral involvement.
On the other hand, recently, obesity has been recognized as the main cause of SEL. Indeed, a recent systematic review and meta-analysis (time period considered 1990–2020) revealed that obesity is currently the main cause of SEL, accounting for more than a half of patients [77].

References

  1. Ferlic, P.W.; Mannion, A.F.; Jeszenszky, D.; Porchet, F.; Fekete, T.F.; Kleinstück, F.; Haschtmann, D. Patient-reported outcome of surgical treatment for lumbar spinal epidural lipomatosis. Spine J. 2016, 16, 1333–1341.
  2. Fogel, G.R.; Cunningham, P.Y., III; Esses, S.I. Spinal epidural lipomatosis: Case reports, literature review and meta-analysis. Spine J. 2005, 5, 202–211.
  3. Greenish, D.; Watura, K.; Harding, I. Spinal epidural lipomatosis following bilateral spinal decompression surgery. BMJ Case Rep. 2019, 12, e226985.
  4. Choi, K.-C.; Kang, B.-U.; Lee, C.D.; Lee, S.-H. Rapid progression of spinal epidural lipomatosis. Eur. Spine J. 2011, 21, 408–412.
  5. Youn, M.S.; Woo, Y.H.; Shin, J.K. Rapid progression of spinal epidural lipomatosis after percutaneous endoscopic spine surgery mimicking disc herniation. Int. J. Surg. Case Rep. 2020, 73, 1–4.
  6. Praver, M.; Kennedy, B.C.; Ellis, J.A.; D’Amico, R.; Mandigo, C.E. Severity of presentation is associated with time to recovery in spinal epidural lipomatosis. J. Clin. Neurosci. 2015, 22, 1244–1249.
  7. Al-Khawaja, D.; Seex, K.; Eslick, G.D. Spinal epidural lipomatosis—A brief review. J. Clin. Neurosci. 2008, 15, 1323–1326.
  8. Robertson, S.C.; Traynelis, V.C.; Follett, K.A.; Menezes, A.H. Idiopathic spinal epidural lipomatosis. Neurosurgery 1997, 41, 68–74.
  9. Papastefan, S.T.; Bhimani, A.D.; Denyer, S.; Khan, S.R.; Esfahani, D.R.; Nikas, D.C.; Mehta, A.I. Management of idiopathic spinal epidural lipomatosis: A case report and review of the literature. Childs Nerv. Syst. 2018, 34, 757–763.
  10. Caruba, T.; Brunie, V.; Bousseau, V.; Guillemain, R.; Prognon, P.; Bégué, D.; Sabatier, B. Substitution of corticosteroid with everolimus after lung transplantation: A pediatric case report. Pharm. World Sci. 2010, 32, 347–349.
  11. Möller, J.; Girschick, H.; Hahn, G.; Pessler, F. Steroid-induced spinal epidural lipomatosis in pediatric patients. Z. Rheumatol. 2010, 69, 447–449.
  12. Vazquez, L.; Ellis, A.; Saint-Genez, D.; Patino, J.; Nogues, M. Epidural lipomatosis after renal transplantation—Complete recovery without surgery. Transplantation 1988, 46, 773–774.
  13. Theyskens, N.C.; Paulino Pereira, N.R.; Janssen, S.J.; Bono, C.M.; Schwab, J.H.; Cha, T.D. The prevalence of spinal epidural lipomatosis on magnetic resonance imaging. Spine J. 2017, 17, 969–976.
  14. Spinnato, P.; D’Agostino, V.; Fiorenzo, D.; Barakat, M.; Vara, G.; Ponti, F.; Filonzi, G.; Crombé, A.; Tetta, C.; Miceli, M. Underreporting of spinal epidural lipomatosis: A retrospective analysis of lumbosacral MRI examinations from different radiological settings. Diagn. Interv. Imaging 2022, 103, 251–257.
  15. Borré, D.G.; Borré, G.E.; Aude, F.; Palmieri, G.N. Lumbosacral epidural lipomatosis: MRI grading. Eur. Radiol. 2003, 13, 1709–1721.
  16. Fassett, D.R.; Schmidt, M.H. Spinal epidural lipomatosis: A review of its causes and recommendations for treatment. Neurosurg. Focus 2004, 16, 1–3.
  17. Bodelier, A.; Groeneveld, W.; Van Der Linden, A.; Haak, H. Symptomatic epidural lipomatosis in ectopic Cushing’s syndrome. Eur. J. Endocrinol. 2004, 151, 765–769.
  18. Schurmann, D.; Rademaker, J.; Trottenberg, T.; Bergmann, F.; Wesselmann, H.; Suttorp, N. Spinal epidural lipomatosis: A manifestation of HAART-associated lipodystrophy. AIDS 2005, 19, 2052–2054.
  19. Lee, M.; Lekias, J.; Gubbay, S.S.; Hurst, P.E. Spinal cord compression by extradural fat after renal transplantation. Med. J. Aust. 1975, 1, 201–203.
  20. Noh, E. An unusual complication of morbid obesity: Epidural lipomatosis. Am. J. Emerg. Med. 2015, 33, 742.e3–742.e4.
  21. López-González, A.; Giner, M.R. Idiopathic spinal epidural lipomatosis: Urgent decompression in an atypical case. Eur. Spine J. 2008, 17, 225–227.
  22. Mallard, F.; Buni, M.; Nolet, P.S.; Emary, P.; Taylor, J.A.; Moammer, G. Lumbar spinal epidural lipomatosis: A case report and review of the literature. Int. J. Surg. Case Rep. 2021, 78, 71–75.
  23. Fujita, N.; Ishihara, S.; Michikawa, T.; Suzuki, S.; Tsuji, O.; Nagoshi, N.; Okada, E.; Yagi, M.; Tsuji, T.; Kono, H.; et al. Negative impact of spinal epidural lipomatosis on the surgical outcome of posterior lumbar spinous-splitting decompression surgery: A multicenter retrospective study. Spine J. 2019, 19, 1977–1985.
  24. Jaimes, R., III; Rocco, A.G. Multiple epidural steroid injections and body mass index linked with the occurrence of epidural lipomatosis: A case series. BMC Anesthesiol. 2014, 14, 70.
  25. Zentner, J.; Buchbender, K.; Vahlensieck, M. Spinal epidural lipomatosis is a complication of prolonged corticosteroid therapy. J. Neurosurg. Sci. 1995, 39, 81–85.
  26. Pinsker, M.O.; Kinzel, D.; Lumenta, C.B. Epidural thoracic lipomatosis induced by long-term steroid treatment case illustration. Acta Neurochir. 1998, 140, 991–992.
  27. Kotilainen, E.; Hohenthal, U.; Karhu, J.; Kotilainen, P. Spinal epidural lipomatosis caused by corticosteroid treatment in ulcerative colitis. Eur. J. Intern. Med. 2006, 17, 138–140.
  28. Koch, C.A.; Doppman, J.L.; Patronas, N.J.; Nieman, L.K.; Chrousos, G.P. Do glucocorticoids cause spinal epidural lipomatosis? When endocrinology and spinal surgery meet. Trends Endocrinol. Metab. 2000, 11, 86–90.
  29. Mukhtar, N.; Alzahrani, A.S. Spinal epidural lipomatosis: A rare and frequently unrecognized complication of Cushing syndrome. Endocrine 2022, 76, 218–223.
  30. Benamou, P.H.; Hilliquin, P.; Chemla, N.; Chevrot, A.; Cormier, C.; Menkès, C.J. Epidural lipomatosis not induced by corticosteroid therapy. Three cases including one in a patient with primary Cushing’s disease (review of the literature). Rev. Rhum. Engl. Ed. 1996, 63, 207–212.
  31. Stern, J.D.; Quint, D.J.; Sweasey, T.A.; Hoff, J.T. Spinal epidural lipomatosis: Two new idiopathic cases and a review of the literature. J. Spinal Disord. 1994, 7, 343–349.
  32. Fessler, R.G.; Johnson, D.L.; Brown, F.D.; Erickson, R.K.; Reid, S.A.; Kranzler, L. Epidural lipomatosis in steroid-treated patients. Spine 1992, 17, 183–188.
  33. Tobler, W.D.; Weil, S. Epidural lipomatosis and renal transplantation. Surg. Neurol. 1988, 29, 141–144.
  34. Muñoz, A.; Barkovich, J.A.; Mateos, F.; Simón, R. Symptomatic epidural lipomatosis of the spinal cord in a child: MR demonstration of spinal cord injury. Pediatr. Radiol. 2002, 32, 865–868.
  35. McCullen, G.M.; Spurling, G.R.; Webster, J.S. Epidural lipomatosis complicating lumbar steroid injections. J. Spinal Disord. 1999, 12, 526–529.
  36. Roy-Camille, R.; Mazel, C.; Husson, J.L.; Saillant, G. Symptomatic spinal epidural lipomatosis induced by long-term steroid treatment. Review of the literature and report of two additional cases. Spine 1991, 16, 1365–1371.
  37. Sandberg, D.I.; Lavyne, M.H. Symptomatic spinal epidural lipomatosis after local epidural corticosteroid injections: Case report. Neurosurgery 1999, 45, 162–165.
  38. Koch, C.A.; Doppman, J.L.; Watson, J.C.; Patronas, N.J.; Nieman, L.K. Spinal epidural lipomatosis in a patient with the ectopic corticotropin syndrome. N. Engl. J. Med. 1999, 341, 1399–1400.
  39. Bhatia, K.; Frydenberg, E.; Steel, T.; Ow-Yang, M.; Ho, K.; Grainger, E. Spinal epidural lipomatosis due to a bronchial ACTH-secreting carcinoid tumour. J. Clin. Neurosci. 2010, 17, 1461–1462.
  40. Ahmad, S.; Best, T.; Lansdown, A.; Hayhurst, C.; Smeeton, F.; Davies, S.; Rees, A. Spinal epidural lipomatosis: A rare association of Cushing’s disease. Endocrinol. Diabetes Metab. Case Rep. 2020, 2020, 20-0111.
  41. Zhang, B.; Yuan, H.; Hu, L.; Saad, M. Obesity is a risk factor for epidural lipomatosis. A meta-analysis. J. Orthop. Surg. 2021, 29, 1–8.
  42. Shimada, Y.; Ishikawa, Y.; Miyakoshi, N.; Suzuki, T.; Hongo, M.; Kasukawa, Y.; Okada, K.; Itoi, E. Decompression of idiopathic lumbar epidural lipomatosis: Diagnostic magnetic resonance imaging evaluation and review of the literature. J. Neurosurg. Spine 2006, 4, 24–30.
  43. Kumar, K.; Nath, R.K.; Nair, C.P.V.; Tchang, S.P. Symptomatic epidural lipomatosis secondary to obesity. Case report. J. Neurosurg. 1996, 85, 348–350.
  44. Sugaya, H.; Tanaka, T.; Ogawa, T.; Mishima, H. Spinal epidural lipomatosis in lumbar magnetic resonance imaging scans. Orthopedics 2014, 37, e362–e366.
  45. Spinnato, P.; Ponti, F.; De Pasqua, S. MRI Diagnosis of Obesity-Related Spinal Epidural Lipomatosis. Can. J. Neurol. Sci. 2020, 47, 124–125.
  46. Yildirim, B.; Puvanesarajah, V.; An, H.S.; Novicoff, W.M.; Jain, A.; Shen, F.H.; Hassanzadeh, H. Lumbosacral Epidural Lipomatosis: A Retrospective Matched Case-Control Database Study. World Neurosurg. 2016, 96, 209–214.
  47. Yki-Järvinen, H. Non-alcoholic fatty liver disease as a cause and a consequence of metabolic syndrome. Lancet Diabetes Endocrinol. 2014, 2, 901–910.
  48. Abe, T.; Miyazaki, M.; Ishihara, T.; Kanezaki, S.; Notani, N.; Kataoka, M.; Tsumura, H. Spinal epidural lipomatosis is associated with liver fat deposition and dysfunction. Clin. Neurol. Neurosurg. 2019, 185, 105480.
  49. Billings, F.; Hoyt, M. Epidural lipomatosis causing new debilitating back pain in a patient with human immunodeficiency virus on highly active antiretroviral therapy. Int. J. Obstet. Anesth. 2012, 21, 367–370.
  50. Vince, G.H.; Brucker, C.; Langmann, P.; Herbold, C.; Solymosi, L.; Roosen, K. Epidural spinal lipomatosis with acute onset of paraplegia in an HIV-positive patient treated with corticosteroids and protease inhibitor: Case report. Spine 2005, 30, E524–E527.
  51. Cersósimo, M.G.; Lasala, B.; Folgar, S.; Micheli, F. Epidural lipomatosis secondary to indinavir in an HIV-positive patient. Clin. Neuropharmacol. 2002, 25, 51–54.
  52. Ebright, J.R.; Stellini, M.A.; Tselis, A.C. Spinal epidural lipomatosis in a human immunodeficiency virus-positive patient receiving steroids and protease inhibitor therapy. Clin. Infect. Dis. 2001, 32, e90–e91.
  53. Mattei, T.A.; Goulart, C.R.; Rai, S.S.; Rehman, A.A.; Williams, M.; Mendel, E. Rapid development of spinal epidural lipomatosis after treatment of metastatic castration-resistant prostate cancer with second-generation androgen receptor antagonists. World Neurosurg. 2019, 125, 222–227.
  54. Awwad, A.; Adam, R.E.I.; Patel, C.; Thomas, J.D. Symptomatic spinal epidural lipomatosis after combined hormonal and steroidal palliative therapy of prostate cancer. Spinal Cord Ser. Cases 2018, 4, 75.
  55. Tulloch, I.; Laban, J.T.; Martin, A.J. A proposed link between spinal epidural lipomatosis, prostate cancer, and androgen deprivation therapy. J. Clin. Urol. 2018, 11, 299–301.
  56. Grayling, M.; Jardine, D.L.; Mcclintock, A.D.; Spar, J.; Wilton, G.N. Symptomatic epidural lipomatosis following cyproterone acetate therapy. Aust. N. Z. J. Surg. 2000, 70, 233–235.
  57. Han, S.R. Scoliosis associated with idiopathic lumbosacral epidural lipomatosis. J. Spine Surg. 2016, 2, 72–75.
  58. Sabharwal, S.; Mahmood, F. Thoracic spinal epidural lipomatosis associated with adolescent scoliosis. J. Spinal Disord. Tech. 2006, 19, 217–221.
  59. Kurt, E.; Bakker-Niezen, S.H. Neurogenic claudication by epidural lipomatosis: A case report and review of literature. Clin. Neurol. Neurosurg. 1995, 97, 354–357.
  60. Neal, M.T.; Patra, D.P.; Lyons, M.K. Surgical management of thoracic myelopathy from long-segment epidural lipomatosis with skip hemilaminotomies: Illustrative case. J. Neurosurg. Case Lessons 2021, 2, CASE21595.
  61. Okada, E.; Ishihara, S.; Azuma, K.; Michikawa, T.; Suzuki, S.; Tsuji, O.; Nori, S.; Nagoshi, N.; Yagi, M.; Takayama, M.; et al. Metabolic Syndrome is a Predisposing Factor for Diffuse Idiopathic Skeletal Hyperostosis. Neurospine 2021, 18, 109–116.
  62. Zhang, Z.; Liu, Z.; Zhu, Z.; Qiu, Y. Spinal epidural lipomatosis—An easily ignored secondary intraspinal disorder in spinal kyphotic deformities. BMC Musculoskelet. Disord. 2017, 18, 112.
  63. Abul-Kasim, K.; Schlenzka, D.; Selariu, E.; Ohlin, A. Spinal epidural lipomatosis: A common imaging feature in Scheuermann disease. J. Spinal Disord. Tech. 2012, 25, 356–361.
  64. Oikonomou, A.; Birbilis, T.; Gymnopoulou, E.; Prassopoulos, P. Paget disease of the spine manifested by thoracic and lumbar epidural lipomatosis: Magnetic resonance imaging findings. Spine 2007, 32, E789–E792.
  65. Koziarz, P.; Avruch, L. Spinal epidural lipomatosis associated with Paget’s disease of bone. Neuroradiology 2002, 44, 858–860.
  66. Toshniwal, P.K.; Glick, R.P. Spinal epidural lipomatosis: Report of a case secondary to hypothyroidism and review of literature. J. Neurol. 1987, 234, 172–176.
  67. Kim, S.-S.; Lim, D.-J. Epidural lipomatosis with cauda equina syndrome in chronic alcoholic patient: A case report. Int. J. Surg. Case Rep. 2017, 33, 12–15.
  68. Lotan, I.; Charlson, R.W.; Fatterpekar, G.M.; Shapiro, M.; Smith, M.L.; William, C.; Kister, I. Progressive myelopathy associated with spinal epidural lipomatosis in three nonobese patients with type 1 diabetes mellitus. J. Neurol. Sci. 2020, 411, 116688.
  69. Badami, J.P.; Hinck, V.C. Symptomatic deposition of epidural fat in a morbidly obese woman. Am. J. Neuroradiol. 1991, 3, 664–665.
  70. Haddad, S.F.; Hitchon, P.W.; Godersky, J.C. Idiopathic and glucocorticoid-induced spinal epidural lipomatosis. J. Neurosurg. 1991, 74, 38–42.
  71. Miyakoshi, N.; Shimada, Y.; Suzuki, T.; Hongo, M.; Kasukawa, Y.; Okada, K.; Itoi, E. Factors related to long-term outcome after decompressive surgery for ossification of the ligamentum flavum of the thoracic spine. J. Neurosurg. 2003, 99, 251–256.
  72. Eap, C.; Litre, C.F.; Duntze, J.; Theret, E.; Noudel, R.; Graftieaux, J.-P.; Rousseaux, P. Compression médullaire lente par lipomatose épidurale thoracique idiopathique: Cas clinique et revue de la littérature . Neurochirurgie 2010, 56, 55–58.
  73. Sato, M.; Yamashita, K.; Aoki, Y.; Hiroshima, K. Idiopathic spinal epidural lipomatosis. Case report and review of literature. Clin. Orthop. Relat. Res. 1995, 320, 129–134.
  74. Al-Yafeai, R.; Maghrabi, Y.; Malibary, H.; Baeesa, S. Spinal cord compression secondary to idiopathic thoracic epidural lipomatosis in an adolescent: A case report and review of literature. Int. J. Surg. Case Rep. 2017, 37, 225–229.
  75. Lee, S.-B.; Park, H.-K.; Chang, J.-C.; Jin, S.-Y. Idiopathic thoracic epidural lipomatosis with chest pain. J. Korean Neurosurg. Soc. 2011, 50, 130–133.
  76. Yoo, J.C.; Choi, J.J.; Lee, D.W.; Lee, S.P. Spinal epidural lipomatosis in Korean. J. Korean Neurosurg. Soc. 2014, 55, 365–369.
  77. Alomari, S.; Lubelski, D.; Khalifeh, J.M.; Sacino, A.N.; Theodore, N.; Witham, T.; Bydon, A. Etiologies and Outcomes of Spinal Epidural Lipomatosis: Systematic Review of the Literature and Meta-Analysis of Reported Cases. Clin. Spine Surg. 2022, 35, 383–387.
More
© Text is available under the terms and conditions of the Creative Commons Attribution (CC BY) license; additional terms may apply. By using this site, you agree to the Terms and Conditions and Privacy Policy.
Upload a video for this entry
Information
Subjects: Neuroimaging
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Valerio D’Agostino
,
Miriana Rosaria Petrera
,
Giuseppe Tedesco
,
Valerio Pipola
,
Federico Ponti
,
Paolo Spinnato
View Times: 471
Revisions: 2 times (View History)
Update Date: 31 Jan 2023
Table of Contents
    1000/1000
    Hot Most Recent
    ScholarVision Creations
    Feedback