Diffusion-weighted imaging of traumatic subdural hematoma in the subacute stage.

Five cases of traumatic subdural hematomas in the subacute stage (from 7 to 20 days after head injury) were treated in one male and four females, aged from 63 to 82 years, with evacuation via craniotomy in three and aspiration via burr hole surgery in two. All hematomas were evaluated by T1-, T2-, and diffusion-weighted magnetic resonance imaging, and measurement of the apparent diffusion coefficient (ADC). Diffusion-weighted imaging showed the hematoma as a crescent high intensity area with a low intensity rim close to the brain surface (two-layered structure) in four cases and as high intensity with low intensity components in one case. The high intensity areas under the dura mater on diffusion-weighted imaging appeared as homogeneous high intensity on T1- and T2-weighted imaging in four cases, and inhomogeneous high intensity on T1- and isointensity on T2-weighted imaging in one case. The mean ADC value of the high intensity areas was 0.58 +/- 0.23 (mean +/- standard deviation) x 10(-3) mm2/sec. The operative findings revealed the high intensity areas as solid clots. The low intensity areas on diffusion-weighted imaging appeared as homogeneous high intensity in four cases and inhomogeneous isointensity with high intensity components in one case on T1- and T2-weighted imaging. The mean ADC value of the low intensity areas was 2.03 +/- 0.27 x 10(-3) mm2/sec. The operative findings revealed the low intensity areas as mixtures of resolved clot and cerebrospinal fluid. Diffusion-weighted imaging showed the characteristic two-layered structure in traumatic subdural hematomas in the subacute stage, and analysis of the ADC values was useful for differentiating solid from liquid hematoma and for selection of the surgical procedure.

Subdural hyperintense band on diffusion-weighted imaging of chronic subdural hematoma indicates bleeding from the outer membrane.

The diffusion-weighted magnetic resonance (MR) imaging characteristics of chronic subdural hematoma and the correlation between hematoma liquidity and apparent diffusion coefficient (ADC) were investigated in 26 consecutive patients, 16 males and 10 females aged 42 to 92 years (mean +/- SD 73.3 +/- 13.1 years), with 31 chronic subdural hematomas. The chronic subdural hematomas were divided into homogeneous, separate, and trabecular types based on diffusion-weighted MR imaging findings. Almost all hematomas were low intensity on diffusion-weighted imaging, and the mean ADC value was 1.81 +/- 0.79 x 10(-3) mm2/sec. The high intensity areas in the subdural hematomas consisted of several types: high intensity line along the dura mater (subdural hyperintense band), high intensity along the intrahematoma septum, and laminar shape along the inner membrane. The subdural hyperintense bands accounted for almost all high intensity areas in the subdural hematomas. The mean ADC value of the high intensity areas was 0.76 +/- 0.24 x 10(-3) mm2/sec, close to that of the normal brain. The subdural hyperintense bands were considered to be intracellular and/or extracellular methemoglobin based on the T1- and T2-weighted imaging and intraoperative findings. The subdural hyperintense band is an important finding indicating relatively fresh bleeding from the outer membrane. Diffusion-weighted imaging shows liquid subdural hematoma as low intensity, and measurement of the ADC values can differentiate between liquid and solid components of the chronic subdural hematoma.

Diffusion-weighted magnetic resonance imaging of organized subdural hematoma--case report.

A 59-year-old male presented with a left organized subdural hematoma. The hematoma appeared as a homogeneous low density area on brain computed tomography and as hyperintense and isointense area on both fluid-attenuated inversion recovery and T2-weighted magnetic resonance (MR) imaging. Echo-planar diffusion-weighted MR imaging showed a crescent hyperintense area under the dura mater and an irregular hypointense area over the brain surface in the left subdural space. The apparent diffusion coefficient (ADC) values of the solid and liquid hematoma were 0.86 +/- 0.32 x 10(-3) and 2.56 +/- 0.39 x 10(-3) mm2/sec, respectively. The ADC value of the solid hematoma was similar to acute subdural or intraparenchymal hematoma, and that of the liquid was similar to cerebrospinal fluid. Burr-hole surgery failed to remove all the hematoma, and he complained of persistent headache. The hematoma was removed through a craniotomy without further neurological deficits. Organized subdural hematoma often requires craniotomy for evacuation because of its solid content. Diffusion-weighted MR imaging and measurement of ADC values can differentiate solid from liquid hematoma, so are useful for selection of the surgical procedure.

[A case of organized chronic subdural hematoma presented with transient neurologic deficits].

A 59-year-old diabetic male presented with transient motor aphasia and monoparesis of the right upper limb. Brain CT scan showed a low density area in the left subdural space with a mild midline shift. Magnetic resonance (MR) T2-weighted and fluid-attenuated inversion recovery (FLAIR) imagings revealed homogenous hyperintensity with a hypointense web-like structure in the subdural hematoma. Cervical MR angiography showed no abnormal lesion at the bifurcation of the bilateral common carotid arteries. Conventional cerebral angiography showed an avascular, crescent, space-occupying mass over the left hemisphere without an etiologic lesion of cerebral ischemia. CT perfusion imagings indicated reduced cerebral blood flow (CBF) and prolonged mean transit time (MTT) in the left middle cerebral artery territory underneath the subdural hematoma. No epileptic discharge was found in electroencephalogram. Operative findings indicated that the hematoma was encapsulated with thickened outer and inner membranes including paste-like materials, and the brain surface was intact. Postoperative CT perfusion imagings revealed normal CBF and MTT. The pathophysiological mechanism which the chronic subdural hematoma produces the transient neurological deficit is still uncertain. The mechanical pressure of the hematoma on the neighboring cerebral vessels may cause impairment of blood flow leading to cerebral ischemia and paralysis of function. Our case indicated the transient neurological deficits attributed to a decreased CBF around the subdural hematoma and a change in pressure exerted by the hematoma during changes of head position and increased blood viscosity.