Intracranial lipoma
Updates to Article Attributes
Intracranial lipomas are not tumours as such, but rather a result of abnormal differentiation of embryologic meninx primitiva. They are frequently associated with abnormal development of adjacent structures.
Epidemiology
Intracranial lipomas are congenital lesions and as such are found at any age when the brain is imaged for other reasons.
Clinical presentation
They are usually asymptomatic, and either found incidentally or as a result of investigation of related malformations and their presentation (e.g. mental retardation, epilepsy, hydrocephalus etc.) 5-6.
Pathology
content pending
Radiographic features
A number of theories have been put forward to explain the development of intracranial lipomas. The favoured theory is persistence and maldifferenitation of the meninx primitiva (subarachnoid space precursor), which accounts for the subarachnoid location, associated parenchymal anomalies and traversing structures of intracranial lipomas 7,8.
Location
Intracranial lipomas are widely distributed in the intracranial compartment and although they can be found essentially anywhere, certain regions are characteristic and are discussed separately.
-
pericallosal lipoma (45%)
- associated with agenesis of the corpus callosum is ~50% of cases
- divided morphologically into tubonodular and curvilinear types
-
quadrigeminal cistern lipoma (25%)
- associated with underdevelopment of the inferior colliculus
- suprasellar cistern lipoma (15%)
-
cerebellopontine angle lipoma (10%)
- the facial nerve and vestibulocochlear nerve often courses through the lipoma
- sylvian fissure (5%)
Radiographic features
The characteristic finding on both CT and MRI is of a mass which has appearances consistent with fat.
CT
Typically appears as a mass with uniform fat density (negative HU values). It has a lobulated 'soft' appearance, conforming to adjacent anatomy. No enhancement. Some peripheral calcification may be present.
MRI
MRI with and without fat saturation are able to make the diagnosis easily. In the absence of fat saturated images, then chemical shift artefact may be useful. Signal characteristics are not surprisingly that of fat:
- T1: high signal intensity
- T2: high signal intensity
- T1 C+ (Gd): no enhancement
- fat saturated sequences: low signal
Often the lipomas are traversed by cranial nerves and adjacent vessels, best seen on high resolution sequences.
Treatment and prognosis
Intracranial lipomas are in most cases asymptomatic, and even when associated with symptomatic malformations (e.g. callosal dysgenesis) they usually require no treatment per se. In fact attempts at resection have had relatively high morbidity with little benefit 5-6. Treatment of seizures or hydrocephalus is of course necessary if these are present 5-6.
Differential diagnosis
The differential is essentially that of masses which contain fat, and therefore includes:
-
intracranial dermoid
- if: if ruptured will often have multiple droplets scattered through the subarachnoid space. Usually; usually midline. - intracranial teratoma
- lipomatous transformation of neoplasm
-: PNET, ependymoma, glioma
On MRI, if no fat saturated sequences are available then a number of other possibilities should be entertained, which also have high T1 signal.
- thrombosed berry aneurysm
-: often will have calcified rim, and haemosiderin staining on gradient echo / SWI sequences. -
white epidermoid
- rare: rare, and will restrict on DWI
-<p><strong>Intracranial lipomas </strong>are not tumours as such, but rather a result of abnormal differentiation of embryologic <a href="/articles/meninx-primitiva">meninx primitiva</a>. They are frequently associated with abnormal development of adjacent structures. </p><h4>Epidemiology</h4><p>Intracranial lipomas are congenital lesions and as such are found at any age when the brain is imaged for other reasons. </p><h4>Clinical presentation</h4><p>They are usually asymptomatic, and either found incidentally or as a result of investigation of related malformations and their presentation (e.g. mental retardation, epilepsy, hydrocephalus etc.) <sup>5-6</sup>.</p><h4>Pathology</h4><ul><li><em>content pending</em></li></ul><h4>Radiographic features</h4><p>Intracranial lipomas are widely distributed in the intracranial compartment and although they can be found essentially anywhere, certain regions are characteristic and are discussed separately.</p><ul>- +<p><strong>Intracranial lipomas </strong>are not tumours as such, but rather a result of abnormal differentiation of embryologic <a href="/articles/meninx-primitiva">meninx primitiva</a>. They are frequently associated with abnormal development of adjacent structures. </p><h4>Epidemiology</h4><p>Intracranial lipomas are congenital lesions and as such are found at any age when the brain is imaged for other reasons. </p><h4>Clinical presentation</h4><p>They are usually asymptomatic, and either found incidentally or as a result of investigation of related malformations and their presentation (e.g. mental retardation, epilepsy, hydrocephalus etc.) <sup>5-6</sup>.</p><h4>Pathology</h4><p>A number of theories have been put forward to explain the development of intracranial lipomas. The favoured theory is persistence and maldifferenitation of the <a title="Meninx primitiva" href="/articles/meninx-primitiva">meninx primitiva</a> (subarachnoid space precursor), which accounts for the subarachnoid location, associated parenchymal anomalies and traversing structures of intracranial lipomas <sup>7,8</sup>. </p><h5>Location</h5><p>Intracranial lipomas are widely distributed in the intracranial compartment and although they can be found essentially anywhere, certain regions are characteristic and are discussed separately.</p><ul>
-</ul><p>The characteristic finding on both CT and MRI is of a mass which has appearances consistent with fat. </p><h5>CT</h5><p>Typically appears as a mass with uniform fat density (negative HU values). It has a lobulated 'soft' appearance, conforming to adjacent anatomy. No enhancement. Some peripheral calcification may be present. </p><h5>MRI</h5><p>MRI with and without fat saturation are able to make the diagnosis easily. In the absence of fat saturated images, then <a href="/articles/chemical-shift-artifact-1">chemical shift artefact</a> may be useful. Signal characteristics are not surprisingly that of fat: </p><ul>- +</ul><h4>Radiographic features</h4><p>The characteristic finding on both CT and MRI is of a mass which has appearances consistent with fat. </p><h5>CT</h5><p>Typically appears as a mass with uniform fat density (negative HU values). It has a lobulated 'soft' appearance, conforming to adjacent anatomy. No enhancement. Some peripheral calcification may be present. </p><h5>MRI</h5><p>MRI with and without fat saturation are able to make the diagnosis easily. In the absence of fat saturated images, then <a href="/articles/chemical-shift-artifact-1">chemical shift artefact</a> may be useful. Signal characteristics are not surprisingly that of fat: </p><ul>
-<a href="/articles/intracranial-dermoid-cyst-1">intracranial dermoid</a> - if ruptured will often have multiple droplets scattered through the subarachnoid space. Usually midline. </li>- +<a href="/articles/intracranial-dermoid-cyst-1">intracranial dermoid</a>: if ruptured will often have multiple droplets scattered through the subarachnoid space; usually midline</li>
-<li>lipomatous transformation of neoplasm - <a href="/articles/primitive-neuroectodermal-tumour-of-the-cns">PNET</a>, <a href="/articles/ependymoma">ependymoma</a>, <a href="/articles/glioma">glioma</a>- +<li>lipomatous transformation of neoplasm: <a href="/articles/primitive-neuroectodermal-tumour-of-the-cns">PNET</a>, <a href="/articles/ependymoma">ependymoma</a>, <a href="/articles/glioma">glioma</a>
-<li>thrombosed <a href="/articles/saccular-cerebral-aneurysm">berry aneurysm </a>- often will have calcified rim, and haemosiderin staining on gradient echo / SWI sequences. </li>- +<li>thrombosed <a href="/articles/saccular-cerebral-aneurysm">berry aneurysm</a>: often will have calcified rim, and haemosiderin staining on gradient echo / SWI sequences. </li>
-<a href="/articles/white-epidermoid">white epidermoid</a> - rare, and will restrict on <a href="/articles/dwi">DWI</a>- +<a href="/articles/white-epidermoid">white epidermoid</a>: rare, and will restrict on <a href="/articles/dwi">DWI</a>
References changed:
- 7. McLendon RE, Rosenblum MK, Bigner DD. Russell & Rubinstein's Pathology of Tumors of the Nervous System. CRC Press. ISBN:0340810076. <a href="http://books.google.com/books?vid=ISBN0340810076">Read it at Google Books</a> - <a href="http://www.amazon.com/gp/product/0340810076">Find it at Amazon</a><span class="auto"></span>
- 8. Tumors of the Central Nervous System, Volume 13: Types of Tumors, Diagnosis, Ultrasonography, Surgery, Brain Metastasis, and General CNS Diseases. Springer. ISBN:9400776012. <a href="http://books.google.com/books?vid=ISBN9400776012">Read it at Google Books</a> - <a href="http://www.amazon.com/gp/product/9400776012">Find it at Amazon</a><span class="auto"></span>
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