To characterize the recurrence of bleeding in patients who had hypertensive intracerebral hemorrhage (HICH), the authors reviewed 989 patients who underwent treatment for HICH between 1989 and 1995. Fifty-three patients (5.4%) had two episodes of HICH within a median interval of 22.9 ± 16.3 months (range 1.5–72 months), and of these 3 (5.7%) had three episodes of HICH. The recurrence of bleeding most commonly occurred within 2 years of the first hemorrhage: in 66% of the 53 patients the second hemorrhage occurred soon after the first (within 1 year in 34%, within 1–2 years in 32.1%). The site of the second hemorrhage was different from the initial site in all patients. Only 1 patient had a third hemorrhage in the same site as the second hemorrhage. The common patterns of recurrence were ‘ganglionic (putamen/caudate nucleus)-thalamic’ in 26.8% and ‘ganglionic-ganglionic’ in 21.4%. The ‘lobar-lobar’ pattern was noted in only 2 patients. The volume of the hematoma was increased at the second hemorrhage. The overall mortality was 28.3%. The risk of recurrent hemorrhage significantly increased in the patients who had antihypertensive therapy of less than 3 months after the initial attack compared to those with further long-term therapy (p < 0.005). Long-term regular control for hypertension is needed to prevent recurrent hemorrhage.

ObjectiveDensity of the chronic subdural hematoma (cSDH) is variable. It often appears to be mixed density. Multiple densities of cSDH may result from multiple episodes of trauma. We investigated the frequency of mixed density and the causes of head injuries representing each density.MethodsWe could collect 242 cases of chronic SDH. The cSDHs were classified into four groups; hypodensity, homogeneous isodensity, layered type, and mixed type on the basis of CT scans.ResultsThe density of cSDH was isodense in 115 patients, hypodense in 31 patients, mixed in 79 cases, and layered in 17 cases. The cSDH was on the left side in 115 patients, on the right side in 70 patients, and bilateral in 40 patients. The history of trauma was identifiable in 122 patients. The etiology could be identified in 67.7% of the hypodense hematomas, while it was obscure in 59.5% of the mixed hematomas.ConclusionMixed density of cSDH results from multiple episodes of trauma, usually in the aged. It is hard to remember all the trivial traumas for the patients with the mixed density cSDHs. Although there were membranes within the mixed density hematomas, burr-holes were usually enough to drain the hematomas.

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Acute subdural hematoma (ASDH), chronic subdural hematoma (CSDH) and subdural hygroma (SDG) occur in the subdural space, usually after trauma. We tried to find a certain relationship among these three traumatic subdural lesions in 436 consecutive patients. We included all subdural lesions regardless of whether they were main or not. We evaluated the distribution, age incidence and interval from injury to diagnosis of these lesions, and the frequency of new subdural lesions in each lesion. ASDH constituted 68.6%, SDG 15.8%, and CSDH 15.6%, Age incidence of CSDH was similar to that of SDG, but differed from that of ASDH. Mean interval from injury to diagnosis was 0.4 days in ASDH, 13.4 days in SDG, and 51.6 days in CSDH. Focal brain injuries accompanied in 37.5% of ASDH, 5.8% of SDG, and no CSDH. In ASDH, 2 recurrent ASDHs, 17 SDGs and 9 CSDHs occurred. In SDG, 3 postoperative ASDHs and 8 CSDHs occurred. In CSDH, 2 postoperative ASDHs, 2 SDGs and 1 CSDH occurred. These results suggest that the origin of CSDH is not only ASDH, but also SDG in upto a half of cases. SDG is produced as an epiphenomenon by separation of the dural border cell layer when the potential subdural space is sufficient. A half of CSDHs may originate from ASDHs. ASDH may occur in CSDH by either a repeated trauma or surgery. Such transformation or development of new lesions is a function of a premorbid condition and the dynamics between the absorption capacity and expansile force of the lesion.

The sequential change in density (attenuation coefficient) of subdural hematomas (SDHs) in computed tomography (CT) is important in understanding the pathogenesis and evolution of SDHs. We retrospectively investigated the age of SDHs by CT in 446 cases. We included 30 cases of chronic SDHs, in whom the density was directly measured in the CT. The density of acute (within 7 days) SDH was hyperdense in 98.6%, isodense in 1.1%, and hypodense in 0.3% of the cases. In subacute (8-22 days) SDHs, it was hypodense in 45.7%, isodense in 42.9%, and hyperdense in 11.4%. In chronic (over 22 days) SDHs, 86.7% was isodense and only 13.3% was hypodense. In hypodense SDHs, 64.0% was the subacute, and 73.2% of the isodense SDHs was the chronic one. The mean interval from injury to CT was 0.5 +/- 1.6 days in hyperdense SDHs, 20.9 +/- 20.7 days in hypodense SDHs, and 54.9 +/- 44.0 days in isodense SDHs. In 30 cases of chronic SDH, the average density was 38.0 +/- 6.9 Hounsfield number(H) in 20 approximately 30 days, 43.8 +/- 12.8 H in 31 approximately 60 days, 51.8 +/- 5.1 H in 61 approximately 90 days, and 44.2 +/- 8.3 H in over 90 days. The density of acute SDH is usually hyperdense. It becomes hypodense within 3 weeks. Then the density progressively increases by the repeated microhemorrhage, which is the mechanism of enlargement of chronic SDH. The density of chronic SDH increases with time up to 90 days, then decreases again after maturation of the neomembrane, which is the mechanism of spontaneous resolution.