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 received honorariums from Genentech for service on a scientific advisory committee and a research grant from Genentech as a principal investigator.)
Originally released September 15, 1994; last updated May 14, 2017; expires May 14, 2020

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.

Overview

Lobar intracerebral hemorrhage is the major clinical manifestation of cerebral amyloid angiopathy. Hematoma expansion is an accurate predictor of poor outcome of intracerebral hemorrhage. Hematoma volumes are substantially larger in patients who are older than 70 years. Hypertension continues to be an important risk factor for lobar intracerebral hemorrhage. However, hypertension is about twice as less frequent a risk factor in lobar than in deep intracerebral hemorrhage. Patients treated with oral anticoagulants have an increased risk of intracerebral lobar hemorrhage. Carriers of apolipoprotein E2 and E4 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. There is evidence that cerebral amyloid angiopathy may be a risk factor for thrombolysis and anticoagulant-related intracerebral hemorrhage as well. In cerebral amyloid angiopathy-related lobar hemorrhage the parietal lobes are the most frequently affected site. Leukoaraiosis has been found to be an independent risk factor for warfarin-related intracerebral hemorrhage. 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. 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. The presence of cerebral microbleeds may be an independent risk factor for warfarin-related intracerebral hemorrhage. Inadequate blood pressure control during follow-up are associated with higher risk of hemorrhage recurrence. Findings of the STICH II trial suggest that early surgery may have a small survival benefit for patients with superficial lobar intracerebral hemorrhage. 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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