The most common cause is cerebral edema where there is a decrease in parenchymal attenuation and engorgement and dilatation of the superficial venous structures due to an increased intracranial pressure . This is seen in hypoxic-ischemic brain injury and recent resuscitation from cardiopulmonary arrest.
Other causes include:
- severe meningitis: breakdown of the blood-brain barrier allowing mildly hyperdense proteinaceous material to leak into the subarachnoid space
- venous sinus thrombosis
- bilateral large subdural hemorrhage producing effacement of sulci and basal cisterns and the false impression of blood in the subarachnoid space
- intrathecal contrast
- usually, symmetrical density confined to the basal cisterns (i.e. no sulcal density)
- 30-40 HU (cf. true acute subarachnoid hemorrhage ~60 HU)
- often seen with generalized cerebral edema or basal cistern effacement
- the appearances are thought to be due to a combination of
- cisternal effacement
- distention +/- thrombosis of vessels
- adjacent brain hypoattenuation accentuating contrast difference
Given et al. reviewed 7 cases of generalized cerebral edema accompanied by increased basal cisternal attenuation which were all found not to have subarachnoid blood at lumbar puncture or autopsy .