This case suggests that adhering to currently recommended guidelines in stroke protocols might at times lead to potentially serious consequences. A literature review disclosed at least 2 recent reports of "CT-negative" ICH.8,9 Features common to these cases, including ours, were the lack of plausible explanations, such as severe anemia, that might have accounted for the negative CT findings, and the fact that the hematomas were subacute rather than very recent in onset. The latter is not surprising, since the density of ICH on CT images steadily decreases, by an average of 0.7 Hounsfield units per day, from the initial hyperdensity of approximately 40 to 50 Hounsfield units to CT isodensity with the brain tissue, and ultimately to hypodensity.10 In contrast to the relatively large size of the lobar hemorrhage detected in our case, previously reported hemorrhages were relatively small and involved the basal ganglia. Of the 3 CT-negative ICHs reported, 2 were related to previous traumatic brain injury and 1 to chronic hypertension. The mechanism of the recurrent ICHs in our patient remains uncertain. The lack of evidence of intracranial vascular lesions with bleeding potential, history of cranial irradiation, or cerebral metastases suggested cerebral amyloid angiopathy as their underlying mechanism, possibly precipitated by the head trauma that preceded her first ICH. However, that diagnosis was not confirmed by histologic examination of tissue obtained at the time of the surgical drainage of her second ICH. In the absence of an autopsy study, however, we cannot rule out cerebral amyloid angiopathy as the underlying cause of her ICHs.