What is a burst lobe, specifically in the context of intracranial hemorrhage in older adults with a history of hypertension (high blood pressure), atherosclerosis (hardening of the arteries), or amyloid angiopathy (a condition affecting the blood vessels in the brain)?

Burst Lobe: Definition and Clinical Context

A "burst lobe" refers to a large lobar intracerebral hemorrhage (ICH) that causes significant mass effect and often ruptures through the cortical surface into the subarachnoid space, typically occurring in older adults with cerebral amyloid angiopathy (CAA) or hypertensive small vessel disease. 1

Anatomical Location and Characteristics

Lobar hemorrhages originate in the cerebral cortex and subcortical white matter of the brain lobes (frontal, parietal, temporal, or occipital), as opposed to deep hemorrhages in the basal ganglia or brainstem. 1

Key features distinguishing lobar ICH include:

• Superficial location affecting the cortical and subcortical regions rather than deep penetrating vessels 1
• Larger hematoma volumes (≥30 ml in 85.3% of CAA cases) compared to deep hemorrhages 2
• Lobulated appearance on neuroimaging 2
• Frequent rupture into subarachnoid space (63.4% in CAA-related ICH versus 26.2% in hypertensive ICH) 2
• Secondary intraventricular extension from the lobar hemorrhage site 2

Underlying Pathophysiology

Cerebral Amyloid Angiopathy (CAA)

CAA is the most common cause of lobar hemorrhage in elderly patients, characterized by amyloid Aβ peptide deposition in small cerebral arteries and arterioles. 1, 3

• Weakens vessel walls leading to microleaks and larger hemorrhages 1
• Preferentially affects cortical and leptomeningeal vessels rather than deep penetrating arteries 3
• Associated with multiple microhemorrhages visible on MRI gradient echo sequences 1, 3
• Higher recurrence risk compared to deep hemorrhages (annual recurrence 1.8-7.4%) 1

Hypertensive Arteriopathy

Chronic hypertension causes small vessel disease affecting deep penetrating arteries, but can also produce lobar hemorrhages. 1

• Deep hemorrhages (basal ganglia, thalamus, brainstem) more typical of hypertensive etiology 1
• Lobar hypertensive hemorrhages occur but less commonly than CAA-related 2
• Associated with age and vascular risk factors 1

Clinical Presentation

Patients present with sudden onset focal neurological deficits corresponding to the affected lobe, often with decreased level of consciousness due to mass effect. 1, 4

Specific deficits by location:

• Frontal lobe: Motor weakness, personality changes, Broca's aphasia (left hemisphere) 4
• Parietal lobe: Sensory deficits, neglect, apraxia 4
• Temporal lobe: Wernicke's aphasia (left hemisphere), memory impairment 4
• Occipital lobe: Visual field deficits 4

Diagnostic Approach

Non-contrast head CT is the gold standard for acute hemorrhage detection and should be performed emergently. 1, 4

Initial Imaging

• CT demonstrates acute blood as hyperdense signal within brain parenchyma 1, 5
• Identifies hematoma location, size, and mass effect 1, 5
• Detects subarachnoid or intraventricular extension 1, 2

Advanced Imaging for Etiology

In patients with lobar ICH and age <70 years, or without hypertension history, CTA should be performed to exclude vascular malformations. 1

MRI with gradient echo (GRE) or susceptibility-weighted imaging (SWI) identifies microhemorrhages suggesting CAA. 1, 4

• Multiple lobar microhemorrhages strongly suggest CAA 1
• Deep/brainstem microhemorrhages suggest hypertensive angiopathy 1
• Superficial siderosis (0.7% prevalence) indicates CAA 1

Distinguishing CAA from Hypertensive ICH

Features Favoring CAA:

• Older age (mean 74 years versus 66.5 years) 2
• Strictly lobar location (no basal ganglia involvement) 2
• Subarachnoid hemorrhage (63.4% versus 26.2%) 2
• Multiple hemorrhages in different lobes (17.1% of cases) 2
• Bilateral hemorrhages 2
• Recurrent episodes 2

Features Favoring Hypertension:

• Deep location (basal ganglia in 40.5% of hypertensive ICH) 2
• History of hypertension 2
• Younger age 2

Clinical Significance and Prognosis

Lobar ICH has 30-day mortality of 35-52%, with only 20% of patients functionally independent at 6 months. 1

CAA-related ICH has lower mortality than deep hemorrhages but higher recurrence risk. 3

Poor prognostic factors include:

• Larger hematoma volume 3
• Intraventricular extension 3
• Lower Glasgow Coma Scale score 3
• Advanced age 3
• Dementia 3

Management Implications

Patients with lobar ICH and suspected CAA should avoid anticoagulation and antiplatelet therapy when possible due to high rebleeding risk. 1, 6

If anticoagulation is necessary (e.g., atrial fibrillation), delay at least 4 weeks and consider left atrial appendage occlusion for high-risk patients. 6

Blood pressure control is essential, with target <130/80 mmHg before considering any antithrombotic therapy. 6