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Table of Contents    
Year : 2013  |  Volume : 61  |  Issue : 1  |  Page : 56-59

Susceptibility artifacts in lipomas

1 Department of Diagnostic and Interventional Radiology, Narayana Hrudayalaya and Muzumdar Shaw Cancer Center, Bangalore, Karnataka, India
2 Department of Imaging Sciences and Interventional Radiology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Medical College, Trivandrum, Kerala, India

Date of Submission20-Nov-2012
Date of Decision09-Dec-2012
Date of Acceptance20-Jan-2013
Date of Web Publication4-Mar-2013

Correspondence Address:
Dayananda Lingegowda
Department of Diagnostic and Interventional Radiology, Narayana Hrudayalaya and Muzumdar Shaw Cancer Center, Health City No. 2/4 2/8, 3, Bommasandra Industrial Area, Anekal Taluk, Bangalore - 99
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.108012

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 » Abstract 

Background: Intracranial lipomas are uncommon tumors, which produce susceptibility artifacts on susceptibility weighted images. The cause for the susceptibility artifact on SWI images remains speculative. Our purpose was identifying the possible causes of susceptibility artifacts in lipoma. Materials and Methods: We retrospectively reviewed 15 cases harboring 16 lipomas of head region. All the lipomas are evaluated on SWI images for the presence of blooming and types of blooming artifacts. Computed tomography (CT) images were evaluated for presence of calcification. Results: All three pericallosal tubulonodular lipomas showed peripheral rim-like susceptibility artifacts. All the curvilinear lipomas (four cases) showed complete blooming. Five out of eight nodular lipomas showed peripheral susceptibility artifacts, whereas, one showed complete blooming. Two nodular lipomas showed peripheral and central susceptibility artifacts. Scalp and craniovertebral lipomas (four in number) showed peripheral susceptibility artifacts. Specks of calcification were identified in two out of seven cases on CT scan. Conclusions: Contribution of the macroscopic calcification to susceptibility blooming appears to be insignificant. Microscopic mineralization and chemical shift artifact appears to be a major cause of susceptibility blooming.

Keywords: Blooming, lipoma, susceptibility weighted imaging

How to cite this article:
Lingegowda D, Rajashekar C, Belaval VV, Thomas B, Keshavdas C, Kapilamoorthy. Susceptibility artifacts in lipomas. Neurol India 2013;61:56-9

How to cite this URL:
Lingegowda D, Rajashekar C, Belaval VV, Thomas B, Keshavdas C, Kapilamoorthy. Susceptibility artifacts in lipomas. Neurol India [serial online] 2013 [cited 2023 Dec 7];61:56-9. Available from:

 » Introduction Top

Intracranial lipomas are uncommon intracranial neoplasms. [1] Lipomas are easily identified by virtue of their characteristic signals on magnetic resonance imaging (MRI) sequences. Interestingly, lipomas shows susceptibility blooming artifact on susceptibility weighted images. The blooming in lipomas seems to be independent of calcification identified on the computed tomography (CT) scan. To the best of our knowledge, the cause for blooming in lipomas is not clearly established. The intention of the present study was to identify the patterns of susceptibility blooming on susceptibility weighted imaging (SWI), and also to identify the possible causes of blooming. We also discuss the relevant pathogenesis of the intracranial lipomas and also histopathology literature, which will possibly help to understand causes of susceptibility blooming.

 » Materials and Methods Top

We retrospectively reviewed 22 cases of lipomas of the head region done between January 2005 and July 2010. The study had local ethics committee approval. Informed consent was not obtained from patients. We excluded five cases of lipomas since the SWI images were not available. Two cases of high frontal convexity scalp lipomas were excluded, since the area of interest was not included in the SWI images. Diagnosis of intracranial lipoma was made in all these cases on the basis of hyperintense appearance on T1-weighted (T1W) images and turbo spin T2-weighted (T2W) images. All the lipomas showed complete suppression on fat suppressed T1W images. None of the patients underwent surgical resection. The lipomas are classified as pericallosal, prepontine, ambient cistern, quadrigeminal plate, sylvian fissure, cortical, and falcine lipomas. The pericallosal lipomas are further subclassified into tubulonodular and curvilinear lipomas. Tubulonodular lipomas are defined as rounded or lobular lesions measuring >1 cm in thickness. Curvilinear pericallosal lipomas are defined as elongated lipomas with thickness < 1 cm. Lipomas in other locations are also subclassified as curvilinear (length twice that of thickness) and nodular or oval variety. All the lipomas were evaluated on SWI images for the presence of blooming. Blooming artifacts are classified as complete blooming of the lesion, only peripheral, and peripheral with irregular central blooming. Peripheral blooming is subclassified into complete ring and incomplete ring. We also looked into associated intracranial anomalies, displacement of nerves, and vessels. The CT scan was available in seven cases. CT images were evaluated for presence of calcification.

All magnetic resonance imaging (MRI) studies were obtained on a 1.5-tesla scanner (Avanto Tim SQ engine, Siemens, Erlangen, Germany). The pulse sequences and parameters were as follows: (1) T1 spin echo; TR: 450 ms; TE: 11 ms; slice thickness: 5 mm; matrix size: 230 × 230; FOV: 230 mm; flip angle: 90°, (2) T2 Turbo spin echo: TR: 4500 ms; TE: 95 ms; slice thickness: 5 mm; matrix size: 160 × 256; FOV: 230 mm; flip angle: 150°, (3) SWI: TR: 49 ms; TE: 40 ms; slice thickness: 2.1 mm; matrix size: 512 × 256; FOV: 220 mm; flip angle: 20°; bandwidth: 80 kHz, acquisition time: 2.58 min, 4)Fat saturated T1 spin echo; TR: 847 ms; TE: 11 ms; slice thickness: 5 mm; matrix size: 230 × 230; FOV: 230 mm; flip angle: 90°.

 » Results Top

In total, 15 cases harboring 16 lipomas were studied (12 intracranial, 3 scalp, and 1 craniovertebral junction intradural lipoma). Salient findings are summarized in [Table 1] [Figure 1], [Figure 2], [Figure 3], [Figure 4]. Age group was ranging between 6-72 years with mean age of 32.4 years (Male-8, female-7). Out of 12 intracranial lipomas, five lipomas were located in pericallosal location (41.66%), four were in quadrigeminal cistern (33.33%), one in ambient cistern (8.3%), one in Sylvian cistern (8.3%), and one in parafalcine region (8.3%). All the intracranial lipomas showed peripheral, complete or mixed pattern of blooming. Five out of nine tubulonodular and nodular lipomas showed peripheral susceptibility artifacts where as two showed complete blooming. Rest of the lipomas showed mixed susceptibility blooming (two lipomas). The nodular lipomas with complete blooming are smaller then 7 mm. All the curvilinear lipomas showed compete blooming (the mean thickness of the curvilinear lipomas is 4.2 mm). All the extra cranial lipomas showed very thin rim of peripheral susceptibility artifacts (mean thickness of the rim is 1 mm). In cases of intracranial lipomas, peripheral hypointensity was thicker (mean thickness 4 mm) than that of the extra cranial lipomas. The cervicomedullary lipoma showed peripheral thick susceptibility changes. The CT was available in seven cases. Only two tubulonodular lipomas showed specks of calcification on CT. No curvilinear or bracket type of calcification was observed in our series.
Table 1: Summary of findings in intracranial lipoma

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Figure 1: (a) Axial CT image showing corpus callosal lipoma with specks of calcification, (b and c) Corresponding Axial T1 weighted with and without fat saturated images, (d) SWI images showing predominantly peripheral blooming

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Figure 2: (a) Axial T1 weighted image showing small nodular lipoma, (b) in tectal plate region which shows complete blooming on SWI image, (c) T1 weighted axial images of another patient, (d) showing relatively large tectal plate lipoma which shows peripheral blooming on SWI image

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Figure 3: (a) Axial T1 weighted images showing large lipoma over right frontal convexity, (b) showing both peripheral and central blooming on SWI images. (c) Axial T1 weighted images of another patient, (d) showing
small curvilinear lipoma, which shows complete blooming on SWI images

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Figure 4: (a) Axial T1 weighted images showing small subcutaneous lipoma, (b) Corresponding SWI images shows thin linear peripheral hypointensity, (c) Axial T1 weighted images of the another patient showing intradural cervical lipoma, (d) which shows thin rim of hypointensity on SWI images

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 » Discussion Top

Intracranial lipomas are rare tumors with incidence of 0.1-0.5% of all intracranial tumors. [1],[2] Pericallosal lipomas account for 50% of all intracranial lipomas. [3] The quadngeminal/superior cerebellar lipomas account for 25% of the cases followed by suprasellar/interpeduncular (14%), cerebellopontine angle (9%), and sylvian (5%) cisterns lipomas. [3] Cerebral hemispheric lipomas are extremely rare. Hemispheric lipomas are commonly associated with other congenital anomalies like agenesis/dysgenesis of the corpus callosum, absence of septum pellucidum, cranium bifidum, spina bifida, encephalocele, myelomeningocele, hypoplasia of vermis, malformation of the cortex, and abnormal intracranial vessels. [4],[5] Lipomas show typical appearance on CT and MR images. On CT scan they show marked hypodensity with a Hounsfield units (HU) value between −40 and −100. [6] Lipomas appears hyperintense on T1W images and show complete suppression of signal after fat saturation pulse. [6] The signal intensity of lipoma decreases as the repetition time (TR) and echo time (TE) increases. [6]

Chemical shift artifact is commonly observed in large lipomas situated in interhemispheric fissure. Blooming of lipomas on the susceptibility-weighted images remains speculative. To the best of our knowledge, the causes of blooming on SWI images are not well-established in literature. Contribution of the macroscopic calcification to susceptibility blooming appears to be insignificant in our series. The reason being all the lipomas showed susceptibility blooming, irrespective of whether or not calcification, was identified on CT scan. Even in cases where the calcification was identified on our series, it did not correlate with the pattern of blooming on susceptibility images [Figure 1] and [Figure 4].

Small accretions of calcium in the capsule as well as with in the lipomas are reported in histopathology literature. [7] It appears that these microscopic calcifications are visible only on susceptibility-weighted images. Chemical shift artifact also appears be have significant contribution for the blooming on the susceptibly-weighted images. If the chemical environment is significantly different between adjacent structures, a shift in the precessional frequency of nuclei can occur. [8] The chemical shift phenomenon is most noticeable at lipid and water interface, which are exaggerated on gradient echo sequences. The approximate chemical shift between the lipid and water is 3.5 ppm which translates to 224 Hz separation at 1.5 T field strength. [8] The chemical misregistration is a result of the inability of the system to identify the frequency displacement caused by chemical shift and special frequency encoding. This misregistration causes dark or bright band at interfaces. Findings in our series suggest the chemical shift artifact is the likely cause of blooming. Five out of nine tubulonodular lesions showed predominant peripheral blooming artifacts that are at the interfaces of lipid and cerebrospinal fluid (CSF). Two out of five tubulonodular lesions showed peripheral blooming artifacts along with central blooming [Figure 2] and [Figure 3]. The two small (mean short diameter 4 mm) tubulonodular lipomas showed complete blooming. Since the size of the lipomas were so small, we believe this complete blooming is due to merging of peripheral blooming from the opposite walls creating the appearance of complete blooming. It is also important to note that all four curvilinear lipomas (with mean thickness 4.2 mm) showed full blooming. This also supports our assumption that complete blooming is due to merging of peripheral chemical shift artifacts, since they are placed very close to each other. There is also significant difference in the thickness of the peripheral blooming noted in the subcutaneous lipomas (mean 1 mm thickness peripheral susceptibility artifact) as compared to the intracranial lipomas (mean 4 mm thick peripheral blooming). This difference in peripheral blooming can be explained by the fact that in case of scalp lipomas the interfaces is subcutaneous fat to lipoma fat as oppose to lipid and CSF in intracranial lipomas [Figure 4]. Since there is no significant difference in interfaces in subcutaneous lipoma the chemical shift artifact is minimal. The combination of significant difference in interfaces and gradient echo sequences, exaggerated the chemical shift artifact in intracranial lipomas. It is not possible to explain central blooming with chemical shift artifacts alone. Two large lipomas in our series showed central and peripheral susceptibility blooming. We looked into histopathological and embryogenesis of lipomas which may explain the central blooming.

The intracranial lipomas are resultant of differentiation of persistent menix premitiva. [3] Osseous metaplsia with in lipoma also reported on histopathology. [3],[9] We suggest that, microscopic mineralization during the process of ossification is also a cause for blooming.

Smaller sample size is limitation of our study. However, to the best of our knowledge, no large studies available in literature describing susceptibility blooming with out macroscopic calcification. None of the patient underwent surgical excision to test our hypothesis is also major limitation of our study. Since the intracranial lipomas are incidental detected in all cases and lipomas did not explain the patient symptoms, patient are not subjected to surgery. Hence, the histopathological proof for our hypothesis could not be established.

Awareness of blooming on SWI images is very important, since the lesion shows similar MRI characteristic of hematoma. Both hematoma and lipomas appear hyperintense on T1 and shows blooming on SWI images. Fat suppressed T1 weighted imaging will help to differentiate the both the lesions. Lipoma appear hypointense on fat suppressed T1 weighted images, where as hematoma maintains its hyperintense signal.

In conclusion , contribution of the macroscopic calcification to susceptibility blooming appears to be insignificant. Microscopic mineralization and chemical shift artifact appear to be the major cause of susceptibility blooming. Osteolipoma should also be considered as a cause for blooming especially in the tuber cinereum region.

 » References Top

1.Faerber EN, Wolpert SM. The value of computed tomography in the diagnosis of intracranial lipomata. J Comput Assist Tomogr 1978;2:297-9.  Back to cited text no. 1
2.Kazner E, Stochdorph O, Wende S, Grumme T. Intracranial lipoma. Diagnostic and therapeutic considerations. J Neurosurg 1980;52:234-45.  Back to cited text no. 2
3.Truwit CL, Barkovich AJ. Pathogenesis of intracranial lipoma: An MR study in 42 patients. AJR Am J Roentgenol 1990;15:855-64.  Back to cited text no. 3
4.Sasaki H, Yoshida K, Wakamoto H, Otani M, Toya S. Lipomas of the frontal lobe. Clin Neurol Neurosurg 1996;98:27-31.  Back to cited text no. 4
5.Saatci I, Aslan C, Renda Y, Besim A. Parietal lipoma associated with cortical dysplasia and abnormal vasculature: Case report and review of the literature. AJNR Am J Neuroradiol 2000;21:1718-21.  Back to cited text no. 5
6.Yildiz H, Hakyemez B, Koroglu M, Yesildag A, Baykal B. Intracranial lipomas: Importance of localization. Neuroradiology 2006;481:1-7.  Back to cited text no. 6
7.Wallace D. Lipoma of the corpus callosum. J Neurol Neurosurg Psychiatry 1976;39:1179-85.  Back to cited text no. 7
8.Hood MN, Ho VB, Smirniotopoulos JG, Szumowski J. Chemical shift: The artifact and clinical tool revisited. Radiographics 1999;19:357-71.  Back to cited text no. 8
9.Park YS, Kwon JT, Park US. Interhemispheric osteolipoma with agenesis of the corpus callosum. J Korean Neurosurg Soc 2010;47:148-50.  Back to cited text no. 9


  [Figure 1], [Figure 2], [Figure 3], [Figure 4]

  [Table 1]

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