Pathophysiology and Common Locations of Hypertensive Intracerebral Hemorrhage
Hypertensive intracerebral hemorrhage results from arteriolosclerosis (lipohyalinosis) causing rupture of penetrating arterioles in deep brain territories, most commonly the basal ganglia, thalamus, brainstem, and deep cerebellar nuclei. 1
Underlying Vascular Pathology
The fundamental pathophysiology involves arteriolosclerosis, a chronic hypertensive small vessel disease characterized by: 1
- Concentric hyalinized vascular wall thickening affecting penetrating arterioles 1
- Early proliferation of arteriolar smooth muscle, followed by apoptotic smooth muscle cell death and collagen deposition 2
- Eventually, excessive or deficient collagen deposition leads to arteriolar occlusion, ectasia, or both 2
- Collagen lacks contractile capability and is brittle, unable to withstand pulse pressure forces 2
- Formation of Charcot-Bouchard aneurysms (fusiform, not saccular structures) from excessive arteriolar dilatation 2, 3
Risk Factors
The major associated risk factors are: 1
Common Anatomical Locations
The distribution of hypertensive hemorrhage reflects the high pulse pressure of arterioles immediately downstream from major end arteries with minimal intervening branching. 2 The typical locations in order of frequency are:
- Basal ganglia (55%) - most common site 5
- Thalamus (26%) 5
- Brainstem (8%) 5
- Deep cerebellar nuclei (7%) 5
- Deep white matter 1
These are collectively referred to as "deep territories" to distinguish them from lobar locations associated with cerebral amyloid angiopathy. 1 Deep/mixed cerebellar hemorrhages are strongly associated with hypertensive arteriopathy, with patients showing higher admission systolic blood pressure (172 vs 146 mmHg) and more frequent deep cerebral microbleeds. 6
Mechanisms of Brain Injury
ICH causes injury through two primary pathways: 1
Direct Pressure Effects
- Local compression of immediately surrounding brain tissue 1
- Increased intracranial pressure (ICP) 1
- Hydrocephalus 1
- Herniation 1
- Early hematoma expansion (HE), possibly driven by mechanical shearing of surrounding vessels, which is a consistent predictor of worse outcomes 1
Secondary Injury Mechanisms
- Cerebral edema 1
- Inflammation 1
- Biochemical toxicity from blood products including hemoglobin, iron, and thrombin 1
The brittle arterioles with poor contractile capability from hypertensive vasculopathy likely account for early hematoma growth when they rupture. 2 Fibrin globes form in concentric spheres attempting to seal off the bleeding site, but the impaired contractile capability inhibits effective hemostasis. 2, 3
Clinical Implications
Since arteriolar bleeding is slower than arterial bleeding, several hours exist where intervention may be useful - this is the rationale for early intensive blood pressure lowering and hemostatic therapies aimed at limiting hematoma expansion. 2, 3 The size of the final sphere of blood at cessation of bleeding determines the clinical spectrum, from asymptomatic to fatal. 2
Major medical therapies such as blood pressure lowering and reversal of anticoagulation are aimed at limiting hematoma expansion, though the search for effective neuroprotectants has been unsuccessful to date. 1