Fat in the brain: Facts and features

Abstract

The presence of fat within a lesion in the brain is not only easy to identify on both CT/MRI but also can help narrow the differential. The purpose of this paper is to illustrate the spectrum of common and rare fat-containing lesions in the brain that are encountered in clinical practice. This paper intends to discuss 15 such lesions which are confirmed by MRI findings and histopathological correlation. We divided the spectrum of fat-containing lesions into lesions with adipose cells, lesions with cholesterol-rich content and tumours with lipomatous differentiation/transformation. Knowledge of these common and rare fat-containing lesions is essential for making the right diagnosis or narrowing the differential diagnosis.

Introduction

By definition, a fat-containing lesion could be an adipose-rich lesion or a cholesterol-rich lesion with high triglycerides and unsaturated fatty acids. Fat can be present in a spectrum of brain lesions including congenital, iatrogenic, neoplastic and non-neoplastic mass lesions.

On CT, pure macroscopic fat typically lies between −50 and −100 HU. ¹ Even outside this range, the presence of CT density below zero Hounsfield units (HU) must raise the possibility of fat-containing neoplasm with partial volume effect. Fat has a short relaxation time on T1 and thus appears bright on T1-weighted (T1w) sequences. Fat suppression techniques are used to suppress the high signal from fat on T1w images, confirming the presence of fat and also evaluating the underlying enhancement. The lipid peak (0.9 ppm–1.3 ppm) on MRS (MR spectroscopy) also supports the presence of fat noted on MRI. ¹

We aimed to review the spectrum of fat-containing lesions within the brain. In this review, the fatty component is evident on MRI by T1 hyperintensity (corresponding lipid peak on MRS wherever applicable) with signal suppression on fat saturation sequences and histopathological correlation.

Lesions with definite adipose cells

On histology, there is evidence of adipocyte-like cells distributed in variable proportions.

Lipoma

Intracranial lipoma (ICL) is a rare congenital malformation usually located along the midline, commonly involving the callosal cisterns (Figure 1(a)). They can also occur in cerebellopontine angles, vestibule, choroid plexus, Sylvian cisterns, suprasellar/interpeduncular, quadrigeminal/superior cerebellar cistern and hypothalamus.^2–4 The incidence of ICLs is reported to be 0.08–0.46% in an autopsy study. ⁵ Most lipomas are incidentally found but larger lesions can have varying presentations depending on the location. Persistent headaches, hearing loss, dizziness, seizures, cranial nerve palsies and developmental delay have all been reported.^2,4,6 These are assumed to result from abnormal persistence and maldifferentiation of the meninx primitiva, the mesenchymal precursor of the leptomeninges, during the development of the subarachnoid cisterns. Various brain malformations are often seen in association with ICLs, including dysplasia or agenesis of the corpus callosum, absence of the septum pellucidum, spina bifida, encephalocele, myelomeningocele, malformation of the cortex and abnormal intracranial vessels. ⁷ There are also a few cases of cortical malformations associated with ICLs in the literature (Figure 1(b)).

Figure 1.

(a and b): Pericallosal lipoma (1A) – Curvilinear hyperintense lesion on sagittal T1, T2 images (a, b) along the posterior peri callosal region, involving splenium demonstrating suppression on fat sat images (c) with lipid peak on MRS (d).

Encephalo craniocutaneous lipomatosis

Figure 2 Encephalo craniocutaneous lipomatosis is a congenital neurocutaneous disorder characterized by unilateral lipomas of the head and neck, ipsilateral lipodermoids of the eye, and an ipsilateral brain anomaly. There is no available epidemiological data on the incidence, as just a few isolated case reports are available in the literature. ⁸ Seizures and mental retardation are the most common clinical presentations. ⁹ CNS imaging features include cerebral hemispheric atrophy, ventriculomegaly, lipomas and cortical malformations such as polymicrogyria, porencephalic cysts, arachnoid cysts, leptomeningeal angiomatosis and gyral calcifications. Among these, lipomas are the commonest finding. The presence of lipomas is a conspicuous finding which with other findings will lead to the diagnosis ¹⁰ (Figure 3).

Figure 2.

Interhemispheric lipoma with cortical dysplasia (1B): Hyperintense lesion. On axial T1, T2 images (a, b) along the right interhemispheric fissure (large arrow). Showing suppression on fat sat images. There is also an adjacent thickened right. Frontal cortex (small arrow) suggestive of cortical dysplasia.

Figure 3.

Encephalo craniocutaneous lipomatosis (ECCL) clinical picture (a) of. Patient (taken with permission to publish) showing focal alopecia (arrow), hypertrophy of bulbar conjunctiva of left eye with a soft limbal nodule encroaching. On the cornea (small arrow) and soft skin-coloured papules in the left perioral and. Periorbital area (arrowheads). Axial T1 and T2W images (b–f) show a left temporal arachnoid cyst (block arrow on c), left cerebellopontine angle lipomas (not shown in the figure) with incomplete opercularization adjacent to left Sylvian fissure (small arrow on f), dilated occipital horn of left lateral ventricle (arrowhead on e) and dural lipomatosis seen involving left frontoparietal convexity (arrows on b, d and e).

Dermoid

Dermoid tumours are epithelium-lined inclusion cysts containing dermal appendages derived from the ectoderm with the presence of lipid material, and previous reports have discussed the existence of fatty tissue peripherally and fluid centrally. ¹¹ They account for approximately 0.5% of all intracranial tumours. ¹² They are usually present in the first three decades of life. They can be found in other places besides the suprasellar or parasellar regions, such as the frontonasal region, the posterior fossa, the spine and the pineal gland fossa, despite being most frequently detected there.^13,14 Though most dermoids are asymptomatic, they can present with varying clinical features secondary to mass effect and rupture. Headache is the most common symptom, but seizures, meningitis, focal neurological deficits and hydrocephalus have all been reported. Rupture can either occur spontaneously or be preceded by trauma. Common differentials to consider are lipomas, epidermoids, immature teratoma and craniopharyngioma, depending on the location. The sebaceous lipid material within a dermoid cyst has attenuation and signal intensity characteristics that simulate those of fat on both CT scan and MRI, thus giving a characteristic hypodense appearance on CT and are predominantly T1 hyperintense on MRI. However, dermoid density may be variable. On MRI, signal characteristics vary depending on lipid content. Intracranial dermoid may obstruct the ventricular system leading to obstructive hydrocephalus and can also rupture resulting in chemical meningitis (Figure 4). Common differentials to consider are lipomas, epidermoids, immature teratoma and craniopharyngioma, depending on the location.^11,13,15

Figure 4.

Ruptured intracranial dermoid. Axial T1W image showing hyperintensities disseminated in bilateral subarachnoid spaces (a), suppressed on fat sat image post-contrast Axial T1W image (b) (arrows). Predominantly hyperintense lesion (arrows) on axial T2W (c) and axial T1W (d) images in the frontal location which is further suppressed on axial T1 fat-sat image (e) (arrow). Histopathological examination (f) shows a cyst lined by stratified squamous epithelium shows cholesterol clefts with foci of calcification.

Teratoma

Teratoma is a type of germ cell tumour containing tissue elements of each of the three germ cell layers: endoderm, mesoderm and ectoderm. ¹ Teratomas compromise just 0.3–0.6% of all intracranial tumours. They have a predilection for the paediatric age group and show a male predominance. They are commonly found in the suprasellar and pineal regions. Mature teratomas consist of well-differentiated cells while immature teratomas consist of foetal and mature tissue in varying amounts. Malignant somatic tissue is seen in the malignant transformation of teratomas. They have been further classified as mature, immature, or malignant. On MRI, there are variable contents of cystic, solid or fat components visualized within them (Figure 5). Mature teratomas appear heterointense on T1 images, with absent to moderate multilocular enhancement on T1 contrast images. Immature teratomas show heterogenous intratumoral fatty enhancement.^16,17

Figure 5.

Immature teratoma in the posterior third ventricle. Sagittal T1W and T2W images (a and b) demonstrate a cystic lesion in the location of the posterior third ventricle with curvilinear peripheral hyperintensity and show susceptibility. Artefact on axial gradient images (arrow on c) suggestive of fat. Histopathological examination (d) shows adipocytic tissue admixed with few intestinal glands having goblet cells.

Angiolipoma

Angiolipomas which are mesenchymal hamartomas composed of abnormal blood vessels and mature adipose tissue are extremely rarely located in the central nervous system (CNS). ¹⁸ Reported locations of these lesions are sellar – the parasellar region, cerebral hemispheres, cerebellopontine angle, intraosseous and spine. Clinical presentations include haemorrhage, seizures, cranial nerve palsy, headache and double vision. Only eight intracranial angiolipomas are reported to date. On MRI, these tumours are iso- or hyperintense on T1-weighted sequences and hyperintense on T2-weighted sequences and show post-gadolinium enhancement^19–21 (Figure 6).

Figure 6.

Suprasellar angiolipoma. Axial T1W image shows an isointense lesion in the sellar and right parasellar region (a) with few hyperintensities (arrows). MRS (b) shows the lipid peak at 1.2 ppm (arrow). Coronal post-contrast T1W image (c) demonstrates homogenous enhancement with contrast. Coronal T2W image (d) shows hyperintensity within the lesion. Magnified sagittal T1 and post-contrast fat-suppressed T1 image (e, f) showing suppressed areas of fat (arrows) within the lesion. (g) Post-contrast T1W coronal image demonstrates persistent enhancement with contrast. Histopathological image (h) confirms the diagnosis of angiolipoma.

CSF fat dissemination

Although rare, operative seepage and dissemination of fat into the cerebrospinal fluid pathway can occur following a recent paraspinal or intraspinal surgical procedure. Radiologists should be aware of this potential complication and consider it in the differential diagnosis when fat is encountered in the subarachnoid spaces. Surgical fixation of fractures increases intramedullary pressure and hence causes mobilization of marrow fat which results in fat dissemination ²² (Figure 7). Such a finding can also occur in the post-operative period after the resection of dermoid, epidermoid cyst, acoustic neuroma and meningioma. Fat grafts used in transsphenoidal surgeries can also result in a similar appearance. This condition must be correctly diagnosed, as complications such as hydrocephalus, ischaemia and aseptic chemical meningitis can occur in the immediate post-operative period.^23–25

Figure 7.

Dissemination of fat in post-operative status. Sagittal CT of the cervical spine (a) in a patient with trauma shows type III odontoid fracture with left pars interarticularis fracture, grade III listhesis of C2 over C3 vertebra. (b) CT angio was unremarkable. The patient underwent surgery including C3 corpectomy with grafting and C2-4 screw plate fixation and C1 to C5 fusion. Post-op day 10, the patient became unresponsive and axial CT brain images (c, d) demonstrating multiple foci of hypo densities (arrows) were noted in subarachnoid spaces. Repeat MRI axial T1W image (e) shows hyperintense foci in the subarachnoid spaces (arrows) that are suppressed on axial fat sat T1 image (f) confirming fat as a result of marrow fat mobilization due to increased intramedullary pressure secondary to surgical fixation of fractures.

Lesions with cholesterol-rich content

Epidermoid

Signal intensity in epidermoid cysts can be variable depending on the relative amount of lipids, cholesterol, keratin and proteins. But ‘white epidermoid’ is rare, has high protein content and may appear hyperdense on CT scans. When compared to the classic epidermoid cyst, white epidermoid shows high signal intensity on T1-weighted images (cholesterol-rich) and low or high signal intensity on T2-weighted images. “White” epidermoid cysts are rare and constitute about 3–8% of all epidermoids. Timmer et al. ²⁶ found a high lipid content in the white epidermoid which could attribute to the high signal seen on T1W images. White epidermoids also have a rich protein content like black epidermoids. However, they commonly have higher lipid content with mixed triglycerides containing polyunsaturated fatty acids, and no cholesterol leading to high viscosity. Owing to these contents, epidermoids which are ‘white’ are hyperintense on T1 and are usually hypointense on T2; and demonstrate no diffusion restriction (unlike protein rich-black epidermoids) (Figure 8).

Figure 8.

Epidermoid cyst in the right medulla and peri medullary cistern. Axial T1W (a) and T2W (b) images show an intramedullary lesion extending to the premedullary cistern. Post-contrast sagittal T1 (c) image shows no enhancement of the lesion. Axial diffusion and ADC images (d and e) reveal restricted diffusion in the posterior component of the lesion. The posterior aspect of the lesion is hypo. Intense on T1 and hyperintense on T2 images and correlates with the appearance of a usual epidermoid cyst which restricts diffusion (black epidermoid). The anterior aspect of the lesion is hyperintense on T1 and hypointense on T2W images and shows no restriction of diffusion and corresponds to ‘white epidermoid’ which is rare in occurrence. The existence of both varieties (usual ‘black’ and rarer ‘white’ epidermoid) in a single lesion is an infrequent finding in imaging. Histopathological examination (f) shows concentric lamellae of anucleate keratin.

They are frequently observed in the middle and posterior cranial fossae, as well as the sellar/suprasellar region. Frontal lobe and brain stem “white” epidermoid lesions have been reported as well. The most common presentation is headache, but vomiting, ataxia, while visual and hearing disturbances can also occur depending on the region of occurrence.^27–31

Craniopharyngioma

Craniopharyngiomas account for 1–3% of all intracranial tumours and arise from squamous epithelial rests along remnants of Rathke’s cleft and have two histological subtypes: the Adamantinomatous type and the papillary type. Adamantinomatous tumours appear cystic but may have both solid and cystic components. The cyst content is rich in cholesterol, which is typically described as machine-oil. ⁸ MR spectroscopy shows prominent peaks at 1–1.5 ppm, which corresponds to lipid (cholesterol) peaks (Figure 9). The papillary type is solid and spherical, shows no calcification and usually affects the adult age group. Most commonly they present with headaches, visual disturbances and endocrine abnormalities. ³²

Figure 9.

Suprasellar craniopharyngioma. Sagittal T1W and coronal T2W images (a and b) show solid cystic lesions (pink block arrows) where the cyst is hyperintense on T1, T2 images (cholesterol-rich contents) in the suprasellar region extending into the left temporal region with lipid peak (blue arrow at 1.2 ppm) on MRS (c). Fat-suppressed post-contrast sagittal T1 image (d) shows mild suppression of the T1 hyperintense cystic contents with the enhancement of solid components and rim enhancement of the cyst. Histopathological examination (e) demonstrates cholesterol crystals, consistent with the imaging diagnosis.

Atypical intracranial dermoid

The recognition of atypical imaging features in the dermoid cyst can avoid diagnostic pitfalls and is clinically relevant for overall surgical management. Kumaran et al. ³³ reported two such cases which were hyperdense on CT with corresponding T2 hypo intensity on MRI and this was thought to be due to a combination of saponification of lipid/keratinized debris with secondary microcalcification in suspension, partially liquefied cholesterol, high protein content, and hemosiderin or iron-calcium complexes relating to previous episodes of haemorrhage within the cyst. They also reported the presence of fat (hyperintense on T1 and suppressed on fat saturation image) along the peripheral aspect of the lesion in one of the cases (Figure 10).

Figure 10.

Atypical intracranial dermoid in left cerebellum. Axial T1W, T2W and post-contrast T1W MRI (a–c) showed a non-enhancing lesion in the left cerebellum. The lesion is predominantly hypointense on T1 and homogenously hypointense on T2 with peripheral mural nodule which shows a heterogeneous signal. Diffusion and ADC images (d and e) show no restricted diffusion within the lesion. Axial non-contrast CT image (f) shows a homogeneously hyperdense lesion (large arrow) with peripheral areas of calcification (small arrow) and fat density (curved arrow). In correlation with CT, the hyperintense signal in the peripheral mural nodule on T1 and T2 images (short arrows on a, b) correspond to fat. Histopathological study (g) shows keratinized stratified squamous epithelium with proliferating sebaceous gland (arrow).

Petrous apex cholesterol granuloma

Cholesterol granulomas are the commonest lesions encountered in the petrous apex. They are filled with cholesterol crystals and viscous brown fluid, surrounded by a thick fibrous capsule and chronic inflammation. They are classically seen in patients with a pneumatized petrous apex and chronic otitis media.

They commonly present with hearing loss, vestibular symptoms, tinnitus, headache and VII-VIII CN symptoms.

Since they are long-standing, CT demonstrates erosions and bony remodelling. On T1 and T2 sequences of MRimaging, they appear hyperintense due to the cholesterol content. They do not show any enhancement or diffusion restriction (Figure 11). Important differential to be considered includes an asymmetrical pneumatization where fatty marrow signal can be misinterpreted for a lesion (Figure 12). Other differential diagnoses include: petrous apex effusion, petrous apicitis and cholesteatoma. Fat-suppressed sequences can be utilized for accurate diagnosis, as the fatty marrow signal in asymmetrical pneumatization will suppress, while in cholesterol granulomas it remains hyperintense.^34,35

Figure 11.

Cholesterol granuloma. Axial T1W image shows a homogenously hyperintense lesion along the right petrous apex (arrow in a) with no restricted diffusion on B1000 image (b). Location with imaging characteristics (hyperintense on T2 with no restriction on diffusion images) confirmed the diagnosis. As the patient was not symptomatic for this lesion, this was not operated and was periodically followed-up.

Figure 12.

Asymmetrical pneumatization with fatty marrow signal (normal variant). There is evidence of asymmetrical pneumatization. In the left petrous apex on non-contrast CT (arrow in a) as compared to the right side. The corresponding area shows fatty marrow signal with T1 hyperintensity (arrow in b) that is further suppressed on post-contrast fat saturation T1 sequence (arrow in c).

Tumours with lipomatous differentiation/transformation

Mesenchymal differentiation although rare is documented in primary brain neoplasms. Lipolytic differentiation with the coalition of fat droplets forming a single vacuole that displaces the nucleus to the cytoplasmic margin can occur in a variety of primary brain tumours. This mechanism is different from the lipidization or xanthomatous change with small vacuoles scattered throughout the cytoplasm without nuclear peripheralization. Such differentiation may present in tumours such as cerebellar neurolipocytomas or as variants of established tumour types such as central neurocytomas, medulloblastomas, ependymomas, mixed glial neuronal tumours, glioblastomas and gliosarcomas. Lipid accumulation is a result of a metabolic abnormality of the neoplastic cells.^36–39

Lipohamartoma

It represents the subcutaneous tumour of the scalp, clinically often diagnosed as a lipoma. It is quite a rare entity, with as few as 18 published case reports. It is most commonly seen in the posterior scalp and the occipital midline. Alopecia can often be a presenting feature. ⁴⁰ Histologically, the tumour consisted of mature connective tissue elements, adipose tissue, blood vessels and clusters of cuboidal or polygonal cells with scant eosinophilic or amphophilic cytoplasm and regular nuclei. Gregová et al. ⁴¹ reported a similar case of hamartoma of scalp. When there is predominant adipose tissue, it is labelled as lipohamartoma (Figure 13).

Figure 13.

Meningeal lipohamartoma of scalp. Sagittal T1W and coronal T2W images (a and b) showing a lesion in the right parietal scalp with fat component (large arrows) visualized as a hyperintense signal on T1 and T2. Axial T1 and post-contrast fat-suppressed T1W image (c and d) demonstrate the suppressed fat on fat-sat images and enhancing soft tissue component in the centre of the lesion (small arrows). Histopathological evaluation (e, f, and g) suggests predominant adipose tissue with a minor component of meningioma. The meningioma component showed EMA IHC positivity and adipose tissue showed S-100 positivity.

Lipomatous meningioma

Lipomatous meningioma is a rarer variant with the presence of fat within meningioma cells, leading to a particular challenge in histopathological diagnosis, since each has a different treatment strategy and prognosis. To the best of our knowledge, only 49 case reports have been published. Commonly reported locations are frontal, frontotemporal and parietal regions. Symptomatology depends on the location, with headaches and seizures being the common presenting complaints. ⁴² Imaging characteristics of lipomatous meningiomas are intratumoral fat accumulations, which are seen on computerized tomographic (CT) as hypodense and are hyperintense on T1-weighted MRI ³⁸ (Figure 14).

Figure 14.

Grade I lipomatous meningioma. Axial T1W and T2W images (a and b) show a heterogeneous dural-based lesion along left frontal convexity. Post contrast coronal T1W image (c) reveals heterogeneous enhancement with a dural tail and a lipid peak at 1.2 ppm (arrow) on MRS (d) suggestive of a subtle fat component on histopathological correlation (e and f) shows meningothelial cells interspersed between the adipocytes. Meningioma component showing EMA IHC highlighting the meningothelial cells.

Liponeurocytoma

The cerebellar liponeurocytoma (LNC), as per WHO guidelines, is a “rare, well-differentiated neurocytic tumour of the cerebellum that arises in adults and typically shows focal or regional lipomatous differentiation. ⁴³ More than 40 cases are reported in the literature. Both supratentorial intraventricular and fourth ventricular liponeurocytoma have also been reported. Symptoms include headache, nausea, vomiting, dizziness, ataxia and CSF flow obstruction. ³⁹ It is challenging to differentiate these tumours histologically from medulloblastoma and oligodendroglioma. ⁴⁴ LNC has a more favourable prognosis when compared to medulloblastoma (MDB), and thus needs to be distinguished. On MRI scan, these tumours are often heterogeneous, iso- or hypointense on T1-weighted images, with areas of high signal intensity (fat) which suppress fat suppression sequences (Figure 15).

Figure 15.

Cerebellar liponeurocytoma. Axial T1W and T2W images (a and b). Demonstrating T1 isointense and T2 hyperintense lesion with central linear hyper. Intensities, which shows susceptibility artefact on axial gradient images (c) and suppress on post-contrast fat sat axial T1 images (d) suggestive of fat. There is a lipid peak on MRS (e). Multiple non-enhancing T2 hyperintense lesions were additionally noted in the cerebellum on coronal T2W images (b). Histopathological examination (f, g, h and i) shows (f) glioneuronal component with focal immunopositivity for glial fibrillary acidic protein (inset), lipomatous areas (straight arrow), (g) microvascular proliferation (curved arrow) with focal strong positivity for synaptophysin in neuronal component (Inset), (h) eosinophilic neuropil-like matrix between the tumour cells and (i) focal oligodendroglia-like areas with a perinuclear halo with MIB-1 labelling index of approximately 6%.

Lipoastrocytoma

Lipocytic differentiation in lower-grade astrocytic lesions has started to be recognized as lipoastrocytomas. As few as 15 case reports are available in the literature. It usually presents in adult age, commonly occurring in the supratentorial compartment, posterior fossa and spine. No sex predilection is evident in these small spectra of cases. Fat globules may accumulate within the cytoplasm of tumour cells as fat droplets, revealing a xanthomatous appearance. This phenomenon is different from lipomatous tumour cells that have fat droplets coalescing into a single clear vacuole which causes displacement of the nucleus to the cytoplasmic margin and resembles a mature adipocyte. ³⁷ MRI shows fat as T1 hyperintensity and may also show a lipid peak. They may be cystic and do not show a fat signal at all and in such cases, the diagnosis is established on histopathology (Figure 16). Histologically, the tumour shows glial cells that contained lipid droplets and immunohistochemically the tumour cells strongly express GFAP and S-100 protein.

Figure 16.

Lipoastrocytoma. Axial T1W and T2W images (a and b). Reveal a heterogeneous lesion in the left frontal cortex. Axial post-contrast T1W image (c) shows heterogeneous contrast enhancement. Owing to the cortical location, attempted MRS was non-contributory to the diagnosis. Imaging did not show any evidence of fat within the lesion and the likely diagnosis presumed was a low-grade glioma. Histopathological evaluation (e, f and g) showed a glial neoplasm with a focal perivascular arrangement. Several large clear cells (adipocytes) are admixed amidst the glial cells and immunohistochemistry for glial fibrillary acidic protein and S-100 protein is positive in tumour cells.

Glioblastoma with fatty transformation

Lipidization in CNS tumours is a rare histologic finding but sometimes could be prominent. Johnson et al. ³⁶ reported a case of glioblastoma with lipidization. Radiologically and histologically, the enhancing component of MRI is classic for a glioblastoma and the bright foci on T1 correlate to tumour cells which resemble adipose tissue (Figure 17).

Figure 17.

Glioblastoma with fatty transformation. Axial T1W and T2W images (a and b) demonstrate a left temporal intraaxial cortical lesion, iso on T1 with some T1 hyperintensities (arrows), suppressed on axial gradient fat sat image (c). Coronal post-contrast T1 image (d) shows heterogeneous enhancement and multivoxel MRS (e) centred on the T1 hyperintensities shows a lipid peak at 1.2 ppm (arrow). On histopathological evaluation (f and g): The tumour was composed of cells with moderate cellular and nuclear pleomorphism areas of necrosis, pseudo palisading, glomeruloid vascular proliferation and mitotic activity were noted. There was evidence of focal lipomatous change and a diagnosis of glioblastoma with lipidization was established.

The primary differential diagnosis to consider is pleomorphic xanthoastrocytoma both radiologically and pathologically. ⁴⁵

Vascular pathology

Cerebral fat embolism

Cerebral fat embolism usually occurs in traumatic long-bone fractures or orthopaedic surgery, presenting with the classic triad of confusion, respiratory distress and petechiae. The incidence of this condition is about 1–2 % post-trauma. Symptoms usually occur 48–72 hours after injury. Presentations can range from having an indolent course to respiratory distress.

Cerebral manifestations include confusion and encephalopathy-like features. The pathophysiology is usually a combination of occlusive arteriolar disease and consequent neurotoxicity. As a result of this, there is no visualization of a fatty signal or any requisition for fat saturation sequences on imaging. CT may not show any changes but widespread low signal intensity foci should raise the possibility. MR is the most sensitive investigation revealing multiple T2 FLAIR hyperintense foci involving the grey and white matter. Scattered diffusion-restricting foci can be seen, typically described as a ‘Starfield’ pattern. Corpus callosum involvement is quite common. Profuse susceptibility foci are noted on T2 * sequences in the ‘Walnut Kernel’ pattern.^46,47

Normal structures which can demonstrate fat

Fatty cerebral falx

Fatty falx dura is a benign condition where fat is situated between the two visceral layers of the falx. It is a commonly encountered finding in routine practice, with an incidence of 7.3%. Patients usually are asymptomatic. It appears hypodense on CT and T1/T2 hyperintense. No enhancement is seen. A differential to consider is the osseous metaplasia of falx, where the fat within the medullary space might have a similar appearance. ⁴⁸

Fat in the dural sinus

Fat is an incidental finding in the dural venous sinus, especially in the superior sagittal sinus and torcula. Adipose tissue within the sinuses is hypothesized to be the reason for the appearance. On CT/MR, typical imaging features of fat are seen. They are asymptomatic and need no intervention. ⁴⁹

Advanced imaging

Advanced sequences are not required to identify a fat-containing intracranial lesion. This is best done on non-contrast CT, T1 and fat-suppressed MR sequences. It is important to know that-not all fat-containing lesions in the brain are T1 hyperintense, especially if the fat component is small/microscopic in nature. To the best of our knowledge, there has been no large-scale study to understand the role of in-phase and out-phase imaging sequences in the brain, though commonly performed in the spine. Advanced sequences such as MRS (MR spectroscopy), DTI (diffusion tractography and perfusion imaging (ASL (Arterial spin labelling), Dynamic susceptibility-weighted (DSC) and Dynamic contrast enhanced (DCE)) help in further characterization of the intracranial lesions.

Conclusion

As only a spectrum of lesions demonstrate fat on imaging, their identification plays an important role in the diagnosis. Fat-containing intracranial lesion can be made easily recognized on both CT/MRI. Fat-containing lesions can be: lesions with adipose cells, lesions with cholesterol-rich content and tumours with lipomatous differentiation. Fatty transformation within a neoplasm does not alter the WHO grading in histopathological diagnosis. Lipomatous transformation within the neoplasm is not always visualized on MRI as it depends on the content of fat-composition within the lesion. Lipomatous transformation within the neoplasm (such as lipomatous meningioma) can make a ‘neoplasm with typical imaging appearance’ look ‘unusual’ on imaging. Some neoplasms such as lipoastrocytoma are rare in occurrence and have varied imaging appearances. However, if ‘fat’ is encountered within these rare neoplasms on imaging, it would compel radiologists to include these tumours in the preoperative diagnosis.

A table has been formulated listing the typical locations, most common age during diagnosis, relevant imaging aspects and differential diagnosis (Table 1).

Table 1.

Showing the spectrum of fat-containing intracranial lesions with age prediction, key imaging findings and common differentials wherever required.

Sl. no	Lesion	Typical location	Age group	Typical imaging findings	Differential diagnosis
1	Lipoma	Pericallosal, quadrigeminal, suprasellar, cerebellopontine cistern	No specific age predilection	CT – fat density MRI: DWI – no restriction T1 – hyperintense T2 – hyperintense T1 + C – no enhancement SWI – blooming may occur due to susceptibility artefact	None
2	Encephalo craniocutaneous lipomatosis	Imaging findings are seen ipsilateral to the scalp lipoma	Infancy	Cerebral hemispheric atrophy ICLs polymicrogyria intracranial cysts Leptomeningeal angiomatosis porencephalic cysts	None
3	Dermoid	Midline sellar and suprasellar, parasellar, frontonasal region, posterior fossa	First three decades	CT – fat density MRI: DWI – no restriction T1 – hyperintense T2 – variable signal T1 + C – generally no enhancement SWI – no blooming	ICL, epidermoid, immature teratoma Craniopharyngioma
4	Teratoma	—	Predominantly in the foetal period. Uncommon in adulthood	CT – fat, soft tissue and calcification seen MRI – DWI – immature and malignant teratomas may show restricted diffusion T1 – mixed T2 – mixed T1 + C – heterogenous enhancement of the solid component and the septae SWI – shows calcification and haemorrhage	Intraaxial – atypical rhabdoid/teratoid tumour (AT/RT), embryonal tumour with multilayered rosettes (RTRT), extra axial – lipoma, dermoid, pineal region tumours
5	Angiolipoma	Sellar – parasellar region, cerebral hemispheres, cerebellopontine angle	Both in children and adults	CT – fat density with prominent flow voids MRI – T1 – fat component: Hyperintense vascular component: Hypointense T2 – fat and vascular components: Hyperintense T1 + C – avid enhancement SWI - microhaemorrhages	Sellar – parasellar region – Rathke’s cleft cyst, pituitary adenoma with apoplexy and pituitary xanthogranuloma
6	CSF fat dissemination	—	—	Sulcal and intraventricular spaces show fat attenuating content on CT/MRI	Ruptured dermoid and epidermoid
7	White epidermoid	Middle and posterior cranial fossae, sellar/suprasellar region	Adult population	CT – hyperdense MRI – DWI – no diffusion restriction T1 – hyperintense T2 – variable T1 + C – no enhancement SWI – no blooming	Dermoid, lipoma, cystic tumours
8	Adamantinomatous craniopharyngioma	Sellar – suprasellar region	Paediatric population	CT – soft tissue, calcification, and cystic components MRI – T1 – Iso-hyperintense T2 – variable T1 + C – solid component: Vivid enhancement SWI - calcifications	Rathke’s cleft cyst, pituitary macroadenoma, pituitary apoplexy
9	Petrous apex cholesterol granuloma	Petrous apex	Young to middle age	CT – well-delineated, expansile lesion MRI – DWI – no restricted diffusion T1 – hyperintense T2 – hyperintense T1 + C – no enhancement SWI – no haemorrhage/calcification	Asymmetrical pneumatisation, petrous apex effusion, petrous apicitis and cholesteatoma
10	Lipohamartoma	Posterior scalp	No age predilection	The fat component shows classical signal changes on CT/MR.	Lipoma
11	Lipomatous meningioma	Frontal, frontotemporal and parietal regions	No age predilection	The fat component shows classical signal changes on CT/MR.	Lipoma, dermoid, xanthomous and osseous meningioma
12	Liponeurocytoma	Cerebellum, supratentorial intraventricular and fourth ventricular	No age predilection	The fat component shows classical signal changes on CT/MR.	Medulloblastoma and oligodendroglioma
13	Lipoastrocytoma	Supra tentorial compartment, posterior fossa	No age predilection	The fat component shows classical signal changes on CT/MR.	Lipoma, dermoid, pleomorphic xanthoastrocytoma
14	Glioblastoma with fatty transformation	No specific location	No age predilection	The fat component shows classical signal changes on CT/MR. The solid component of the tumour will show heterogenous enhancement	Lipoma, dermoid, pleomorphic xanthoastrocytoma
15	Cerebral fat embolism	Subcortical and deep white matter	No age predilection	Mimics stroke on imaging CT – multifocal, hypodensity MRI – DWI – restricted diffusion T1 – hypointense T2 – hyperintense T1 + C – may show contrast enhancement SWI - microbleeds	Diffuse axonal injury, septic emboli, disseminated intravascular coagulation
16	Fatty falx dura	Falx	No age predilection	CT – fat density MRI – DWI – no restricted diffusion T1 – hyperintense T2 – hyperintense T1 + C – no contrast enhancement SWI - no haemorrhage/calcification	Osseous metaplasia of falx
17	Fat in the dural sinus	Superior sagittal sinus, torcula	No age predilection	CT – fat density MRI – DWI – no restricted diffusion T1 – hyperintense T2 – hyperintense T1 + C – no contrast enhancement SWI - no haemorrhage/calcification	None

ORCID iDs

Sunitha Palasamudram Kumaran https://orcid.org/0000-0001-5524-0229

Shreyas Reddy K https://orcid.org/0000-0002-5908-6385