Intracranial subarachnoid dissemination of fat material may occur during the preoperative or postoperative course of dermoid and epidermoid cysts. Aseptic meningitis or other complications such as hydrocephalus, seizures, or cranial nerve deficits also may occur owing to spillage of intracranial cyst contents into the subarachnoid space. MRI can detect the presence of fat drops that may adhere to the surrounding structures or migrate with the cerebrospinal fluid flow. Intracranial disseminated fat particles can remain silent without radiological or neurological change, justifying a wait-and-see approach. During long-term postoperative follow-up, however, regular MRI studies and clinical examinations are necessary to avoid potential complications.

Cerebellopontine angle lipomas are rare and attempts at surgical excision are associated with significant morbidity. Lipomatosis of nerve, the fatty infiltration of nerves, is a distinct entity. We present a case of intractible trigeminal neuralgia caused by lipomatosis of the trigeminal nerve. Clinical case: A 25-year-old male presented with severe right-sided trigeminal neuralgia. Imaging showed a lesion involving the trigeminal nerve with signal characteristics of fat. At surgery the lesion was found to be a fatty infiltration of the nerve itself. Surgery was therefore limited to arachnoid adhesiolysis. The patient remains symptom-free and neurologically intact to date. Correctly identifying these lesions as lipomatosis of nerve rather than lipoma of the cerebellopontine angle make it clear that even partial surgical excision will inevitably result in neurological deficit and should not be attempted. However, in the case of intractable trigeminal neuralgia we demonstrate that surgery can still play a role.

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Cellular senescence is a stable proliferative arrest state. Pituitary adenomas are frequent and mostly benign, but the mechanism for this remains unknown. IL-6 is involved in pituitary tumor progression and is produced by the tumoral cells. In a cell autonomous fashion, IL-6 participates in oncogene-induced senescence in transduced human melanocytes. Here we prove that autocrine IL-6 participates in pituitary tumor senescence. Endogenous IL-6 inhibition in somatotroph MtT/S shRNA stable clones results in decreased SA-β-gal activity and p16INK4a but increased pRb, proliferation and invasion. Nude mice injected with IL-6 silenced clones develop tumors contrary to MtT/S wild type that do not, demonstrating that clones that escape senescence are capable of becoming tumorigenic. When endogenous IL-6 is silenced, cell cultures derived from positive SA-β-gal human tumor samples decrease the expression of the senescence marker. Our results establish that IL-6 contributes to maintain senescence by its autocrine action, providing a natural model of IL-6 mediated benign adenoma senescence.