The diagnosis of traumatic intracerebral hematoma is made quickly and accurately with CT or MRI.
A chronic subdural hematoma is dynamic; therefore, its appearance on CT is dependent on the phase of the development. In the week after the initial hemorrhage, the acute blood is hyperdense to normal brain, then generally isodense to normal brain for a period of 1 to 3 weeks after the initial bleed, and finally hypodense to normal brain after 3 weeks in the chronic phase. Isodense hematomas may be detected indirectly, that is, by evidence of mass effect manifested by sulci displacement, gray-white matter inward displacement, deformation of the ventricular anatomy, and obliteration of the cisterns. Intravenous iodinated contrast agents are often helpful in the detection of isodense subdural hematoma. Contrast enhancement is usually detected in the inner membrane and at the cortical surface (where there may be enhancement of the brain and cortical vessels). A delay in scanning of 3 to 6 hours after contrast injection allows accumulation of contrast in the hematoma and direct visualization of the hematoma cavity itself.
Differentiation of subacute hemorrhage and chronic hemorrhage from isodense brain is sometimes difficult with CT. Thus, in a subacute or chronic situation, MRI is often the most informative and precise study (Williams and Hogg 2000). MRI signal intensity may vary with time, but chronic subdural hematomas are generally hyperintense on both T1- and T2-weighted scans. Rarely, a chronic subdural hematoma is isointense on T1 images due to methemoglobin, which is related to the age of the extravasated blood. Often, on either CT or MRI, one sees a subdural hematoma that is heterogenous or with layering of blood; these types are secondary to mixing of fresh blood (from intermittent hemorrhages from the external membrane) with the chronic subdural fluid. On T2-weighted MRI scans, a black band is frequently observed on the inner membrane of symptomatic chronic subdural hematomas (Imaizumi et al 2003). The band is rarely observed in asymptomatic collections and tends to disappear after successful surgical drainage.
Diagnosis in children is usually made by CT or MRI scan, the results of which resemble those in adults. One finding, uncommon except in children, is expansion of the subarachnoid space beneath the hematoma, presumably the result of impaired CSF absorption at the sagittal sinus (Aronyk 1994). Intentional injury must be considered in any child with chronic subdural hematoma. Retinal hemorrhages, traumatic skin lesions, long bone and rib fractures, and a vague or contradictory parental history should alert one to this possibility (Duhaime et al 1992).
Subdural hygroma resembles chronic subdural hematoma on neuroimaging studies. Hygromas may be proteinaceous and appear slightly denser than cerebrospinal fluid on CT, as well as isointense or hyperintense to cerebrospinal fluid on MRI (Hasegawa et al 1992). However, the hygroma fluid is more likely to resemble cerebrospinal fluid. Furthermore, unlike subacute and chronic subdural hematoma, there is little or no blood in a subdural hygroma. CT scans may miss small subdural hematomas in small infants; MRI may be necessary in suspicious cases (Datta et al 2005).
Electroencephalographic abnormalities are common. In a study that included 24 patients, 21 patients had electroencephalographic abnormalities, 13 had midline epileptiform discharges, and 9 had periodic lateralized epileptiform discharges. Both types of epileptiform discharges were significantly associated with the degree of midline shift on neuroimaging. Poor early outcomes were associated with the presence of bilateral, midline, and bilateral independent multifocal discharges (Rudzinski et al 2011).