SUMMARY Fifty patients with spontaneous lobar haematomas were reviewed. Thirty-two were normotensive and eighteen were hypertensive. Vomiting, seizures, and altered consciousness were more common in hypertensive than in normotensive patients. Haematoma size (greater than 4-0 cm) and intraventricular extension occurred most commonly in hypertensive and rarely in normotensive patients. Twenty-eight per cent of hypertensive patients died, whereas none of the normotensive patients died.The majority of intracerebral haematomas are hypertensive in aetiology. These are usually located in the thalamic or basal ganglionic region; less commonly, they are in the cerebellum, brain stem, or subcortical white matter of the cerebral hemispheres (lobar haematomas). The finding of a lobar haematoma should initiate a thorough investigation for a specific neuropathological aetiology for the haemorrhage such as angioma, aneurysm, neoplasm, or an underlying medical condition (for example bleeding disorder, collagen vascular disease).The present report is an analysis of the clinicalcomputed tomographic correlations in 50 patients with non-traumatic acute lobar haematoma in whom a thorough clinical and laboratory investigation did not demonstrate a specific aetiology for the intracranial haematoma.
Methods and patientsOf 489 consecutive patients who were studied prospectively with CT evidence of intracerebral haematoma, there were 68 patients with lobar haematomas. There were 18 patients in whom neurodiagnostic findings, laboratory studies and/or pathological findings showed a specific aetiology for the lobar haematomas ( There were 50 other patients with CT evidence of lobar haematoma in whom no aetiology was determined by CT findings, angiography, laboratory studies, and in some cases by surgical or necropsy studies. Patients with a history of trauma were excluded from this analysis. In an effort to ensure that patients with traumatic haemorrhagic contusions were not included, patients in whom trauma was even a remote consideration were excluded. The clinical and CT findings were reviewed by the author. The diagnostic criteria used by Kase et al' to support the diagnosis of lobar haematoma were used. These included: (1) absence of clinically detectable cardiac source of cerebral embolism; (2) CT evidence of a hyperdense lesion located in the subcortical white matter which extended beyond a specific arterial territory; (3) the haematoma was sometimes surrounded by an irregularly marginated hypodense region (representing oedema), but the irregular margination of the hypodense component excluded the diagnosis of infarction; (4) there was sometimes ventricular extension; (5) ring enhancement was sometimes seen if scan was performed 7 to 28 days after the haemorrhage; (6) when performed, angiogram showed evidence of an avascular mass and not a cortical branch occlusion (which would be consistent with cerebral embolism). Haematomas which appeared to originate in the ganglionic-thalamic region and then secondarily extended into the white m...