Cerebral fat embolism (CFE) is an uncommon incomplete type of fat embolism syndrome (FES), characterized by purely cerebral involvement. It usually occurs 12–72 hours after the initial trigger, mainly represented by closed, long-bone multiple fractures of the lower extremities. Neurological manifestations are mainly characterized by headache, confusion, seizures, focal deficit, and alteration of the consciousness state up to coma onset. It represents a diagnostic challenge, above all when secondary to uncommon nontraumatic causes, because neurological signs and symptoms are variable and nonspecific, not satisfying the Gurd and Wilson’s criteria, the diagnostic features most widely used today for FES diagnosis. Neuroimaging (mainly MRI, but in some cases, brain computed tomography too) can hasten the diagnosis, avoiding other unnecessary investigations and treatment. Usually self-limiting, CFE may sometimes be fatal. Treatment is to date mainly supportive and prophylactic strategies are considered an important tool to decrease the development of fat embolism and, consequently, the rate of CFE.

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The combination of EEG/SEP findings allows prediction of good and poor outcome (within 12 h after CA) and of poor outcome (after 48-72 h). Recording of EEG and SEPs in the same patients allows always an increase in the number of cases correctly classified, and an increase of the reliability of prognostication in a single patient due to concordance of patterns.