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.

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We report a series of 14 patients who had recurrent intracerebral hemorrhage due to hypertension. These patients comprise 2.7% of all those admitted to the Soonchunhyang University Chonan Hospital for hypertensive intracerebral hemorrhage from 1985 to 1988. Women outnumbered men by 13 to 1. The mean age of the patients was 54.5 years at the time of the first hemorrhage and 55.4 years at the time of the second hemorrhage. The mean interval between attacks was 13.1 months. All patients were hypertensive on admission, and in 10 patients hypertension had been diagnosed previously. None of the patients had received regular antihypertensive therapy, even after the first hemorrhage. Hemiplegia was the most common deficit seen after both the first and second attacks. The site of the first hemorrhage was ganglionic in 9 patients, cerebellar in 3 patients, and lobar in 2 patients. The site of the second hemorrhage was ganglionic in 9 patients and lobar in 5. The site of recurrent hemorrhage was different from the initial site in all patients except one. The most common pattern of recurrence was “ganglionic-ganglionic.” The “lobar-lobar” pattern was noted in only 1 patient. The hypertensive changes of the cerebral arteries are considered to be the major cause of these recurrent hemorrhages. We believe that recurrent intracerebral hemorrhages in hypertensive patients are not rare as previously thought. Possible reasons for the increased frequency of recurrent intracerebral hemorrhage are discussed.

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