Ruptured intracranial dermoid cyst.

I ntracranial dermoid cystic tumors account for <1% of all intracranial masses. Dermoids are nonneoplastic, congenital ectodermal inclusion cysts that contain varying amounts of ectoderm derivatives to include apocrine, sweat, and sebaceous cysts as well as hair follicles, squamous epithelium, and possibly teeth. Th ey are not to be confused with an epidermoid cyst, which contains only squamous epithelium. Teratomas, although similar in some respects, are a separate entity. Teratomas are true neoplasms that contain tissue from all three embryonic germ cell layers (1). Dermoid cystic tumors arise from the inclusion of ectodermally committed cells at the time of neural tube closure during the third to fi fth week of embryogenesis. Th ese lesions are slow growing due to the active production of hair and oils from the internal dermal elements (2). Th e presentation of dermoid tumors is quite variable. Occasionally they are incidental fi ndings discovered on brain computed tomography (CT) or magnetic resonance imaging (MRI) for otherwise unrelated clinical complaints, or they are discovered during imaging investigation of unexplained headaches, seizures, and rarely olfactory delusions (3, 4). When dermoid cystic tumors rupture and spread their contents into the ventricles and subarachnoid and/or subdural spaces, the most common clinical presentation is that of headache and seizures. Headache may be the consequence of compression of adjacent neural structures, chemical meningitis from cyst content irritation, or perhaps the eff ects of hydrocephalus if present.