Lobar hemorrhage

Ravindra Kumar Garg MD (Dr. Garg of King George's Medical University in Lucknow, India, has no relevant financial relationships to disclose.)
Steven R Levine MD, editor. (

Dr. Levine of the SUNY Health Science Center at Brooklyn has no relevant financial relationships to disclose.

Originally released September 15, 1994; last updated April 26, 2020; expires April 26, 2023

This article includes discussion of lobar hemorrhage, cerebral hemorrhage, intraparenchymal hemorrhage, and spontaneous cerebral hemorrhage. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.


In lobar variety of intracerebral hemorrhage, hematoma is located in one of the cerebral lobe (frontal, parietal, temporal, or occipital). Lobar hemorrhage is the major clinical manifestation of cerebral amyloid angiopathy. Hypertension continues to be an important factor in pathogenesis of lobar intracerebral hemorrhage. Patients treated with oral anticoagulants have an increased risk of intracerebral lobar hemorrhage. Carriers of apolipoprotein E2 and E4 also have an increased risk of intracerebral hemorrhage in lobar regions, presumably because of the effects of these gene variants on risk of cerebral amyloid angiopathy. Cerebral amyloid angiopathy is a risk factor for thrombolysis and anticoagulant-related intracerebral hemorrhage as well. Cerebral microbleeds detected by gradient-echo MRI suggest the presence of advanced microangiopathy with potential for intracerebral hemorrhage. In the patients with lobar hemorrhage, microbleeds are associated with a 2- or 3-fold increase in hematoma and a large hematoma size. Finger-like projections within hemorrhage, convexity subarachnoid hemorrhage, and subdural hemorrhage are frequently observed neuroimaging abnormalities in cerebral amyloid angiopathy-related lobar hemorrhage. Cortical superficial siderosis, a distinct neuroimaging pattern, is shown to be associated with occurrence first-ever symptomatic lobar hemorrhage, early lobar hemorrhage recurrence, and a greater hematoma expansion. Findings of the STICH II trial suggest that early surgery may have a small survival benefit for patients with superficial lobar intracerebral hemorrhage. Oral anticoagulants following lobar hemorrhage can be resumed as they decrease thromboembolic complications and long-term mortality without increasing bleeding risks. In this article, the author has reviewed in detail the different aspects of lobar intracerebral hemorrhage.

Key points


Lobar hemorrhages occur either within the subcortical white matter or at the junction of the hemispheric gray-white matter.


• Cerebral amyloid angiopathy, anticoagulation, coagulopathies, fibrinolytic therapy, microbleeds, and vascular malformations are common causes.


• Hypertension is a less common risk factor in lobar hemorrhage.


• Recombinant activated factor VII can limit ongoing bleeding and improve outcomes when administered within 3 hours.


• Surgical evacuation of hematoma is not beneficial.


• Hematoma size and Glasgow coma scale score are important determinants of prognosis.

Historical note and terminology

The first complete description of an intracerebral hemorrhage was published in 1658 by Wepfer in his treatise on apoplexy (McHenry 1969). In that article he noted intracerebral hemorrhage and subarachnoid hemorrhage in different patients. In 1938 Scholz, for the first time, described pathological changes of cerebral amyloid angiopathy. In 1960 Neumann reported a case of cerebral amyloid angiopathy in a 45-year-old woman who had multiple lobar intracerebral hemorrhages. Later publications of Jellinger and Zenkevich, in 1977 and 1978, respectively, firmly established congophilic or cerebral amyloid angiopathy as a cause of lobar intracerebral hemorrhage (Smith and Eichler 2006). In 1980, Ropper and Davis suggested that hypertension is not an etiologic factor in most lobar hemorrhages (Ropper and Davis 1980).

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