This patient was initially referred to our epilepsy clinic at the age of 22 for evaluation of absence spells. She had been diagnosed with absence epilepsy at the age of 6 and was treated with valproic acid between the ages of 11 and 18. An old brain MRI report mentioned the presence of an interhemispheric lipoma with dysgenesis of the corpus callosum. Routine electroencephalograms (EEGs) in her childhood were supposedly normal. Family history of epilepsy was positive in one of her grandmothers. She had no personal history of major head trauma or central nervous system infection.

At the time of presentation to our clinic, she was taking levetiracetam 500 mg twice daily and valproic acid 500 mg twice daily for her spells. She described these as staring spells with behavioral arrest and occasional jaw movements, which could last up to 20 minutes. Neurological exam was normal.

The patient was admitted for a 48h scalp EEG monitoring, during which four seizures were recorded. These seizures were focal aware and began in the right frontal and temporal leads. The longest seizure lasted 95 s and occurred during sleep. The three other seizures had a stereotypical semiology of vague malaise, anxiety and hyperventilation. She was discharged from the epilepsy monitoring unit and eventually benefited from satisfactory seizure control with oxcarbazepine 750 mg twice daily and clobazam 10 mg once daily.

Two MRIs were performed since her referral to our clinic, the latest within the last year due to increasing headaches. These MRIs identified a large, 3.8 cm (transverse) × 6.5 cm (anteroposterior) × 5.7 cm (craniocaudal) interhemispheric lipoma with peripheral calcifications associated with dysgenesis of the corpus callosum. The lipoma did not significantly increase in size between MRIs, the latest MRI being presented in Figure 1.

Figure 1.

Brain MRI (A) T1-weighted, (B) T2-weighted FLAIR, (C) T1-weighted with gadolinium injection, (D) DWI and ADC and (E) SWI images showing a large interhemispheric lipoma. 3T brain MRI was performed with and without gadolinium injection, with (A) 3D T1-weighted axial, coronal and sagittal images with MPR reconstructions, (B) a T2-weighted FLAIR axial image with fat saturation, (C) a 3D T1-weighted gadolinium-enhanced axial image with MPR reconstructions, (D) DWI and ADC axial images and (E) a SWI axial image. A large fat-containing lesion measuring 3.8 cm (transverse) × 6.5 cm (anteroposterior) × 5.7 cm (craniocaudal) is demonstrated along the interhemispheric fissure, closely related to the corpus callosum, consistent with a lipoma. The lesion is non-enhancing, demonstrates no diffusion restriction and has a dark peripheral rim on SWI, probably representing peripheral calcification and blooming due to the fat-water interface. The lipoma invaginates between the lateral ventricles with secondary ventricular compression. Dysgenetic corpus callosum is displaced inferiorly to the lipoma. No other epileptogenic lesions are identified.

Intracranial lipomas account for less than 0.5% of primary brain tumors and are mostly located at or near the midline. ^{Reference Gossner1,Reference Truwit and Barkovich2} These lipomas are congenital and usually asymptomatic, but some have been reported to be epileptogenic. ^{Reference Loddenkemper, Morris, Diehl and Lachhwani3} More than half of cases of intracranial lipomas are accompanied by dysgenesis or agenesis of the corpus callosum. ^{Reference Osborn and Boyer4}

Intracranial lipomas can grow to large sizes, albeit extremely rarely, with the largest reported such lesion measuring 12 × 10 × 9 cm in a 3-year-old child. ^{Reference Jha, Jain and Ajaya5} We report a case of an interhemispheric intracranial lipoma measuring 3.8 × 6.5 × 5.7 cm presenting in a young adult with focal epilepsy and headaches. No other etiology for her epilepsy was identified. Although intra-axial lesions are more frequently epileptogenic, extra-axial lesions such as intracranial lipomas, especially when large and compressing cortical structures, can also be epileptogenic. ^{Reference Akeret, Serra and Rafi6} In our case, it is difficult to confirm if seizures were due to the lipoma itself or due to dysgenesis of the corpus callosum, or both. ^{Reference Unterberger, Bauer, Walser and Bauer7}

In conclusion, we have highlighted the archetypal imaging characteristics of intracranial lipomas in hopes that they aid clinicians in recognizing these lesions and considering them as a potential, albeit uncommon, cause of epilepsy, particularly in patients with associated corpus callosum anomalies.