Intracerebral Hemorrhage: Overview & Pathophysiology

Intracerebral hemorrhage (ICH) is bleeding directly into the brain parenchyma. Though it accounts for only about 10–15% of all strokes, it is the deadliest and most disabling subtype. Understanding why a hemorrhage occurs — and how it injures the brain — frames every downstream decision, from the imaging workup to blood-pressure targets. This overview covers epidemiology, classification, the major causes and risk factors, and the pathophysiology of primary and secondary brain injury. For imaging and scoring, see Diagnosis & Grading.

1. Epidemiology & Burden

ICH represents roughly 10–15% of strokes in Western populations and a higher proportion (up to ~20–30%) in East Asian, Black, and Hispanic populations, paralleling the prevalence and control of hypertension. Outcomes remain poor despite decades of research: 30-day mortality is approximately 40% (reported 35–52%), roughly half of deaths occur within the first 48 hours, and only about one in five survivors is functionally independent at 6 months. This burden — and the fact that its principal drivers are modifiable or treatable — is why ICH is a central target of acute stroke care.

2. Classification

ICH is first divided by mechanism:

• Primary ICH (~80–85%) — rupture of small vessels chronically damaged by hypertension or cerebral amyloid angiopathy.
• Secondary ICH (~15–20%) — an underlying structural lesion (vascular malformation, aneurysm, tumor), coagulopathy/medication, venous thrombosis, or another identifiable cause.

It is also classified by location — deep (basal ganglia, thalamus, brainstem, cerebellum), lobar (cortical–subcortical), or infratentorial — which strongly shapes the likely cause (Section 6).

3. Primary Causes (Small-Vessel Disease)

Hypertensive arteriopathy

Chronic hypertension drives lipohyalinosis and the formation of Charcot–Bouchard microaneurysms on the small, deep penetrating arteries (lenticulostriate, thalamoperforator, paramedian pontine, cerebellar). Rupture produces the characteristic deep hemorrhages of the basal ganglia (especially the putamen — the single most common site), thalamus, pons, and cerebellum.

Cerebral amyloid angiopathy (CAA)

CAA is the progressive deposition of β-amyloid in the walls of cortical and leptomeningeal small vessels, predominantly in the elderly. It causes lobar (cortical–subcortical) hemorrhages that are often recurrent, along with lobar microbleeds and cortical superficial siderosis. Diagnosis uses the Boston criteria v2.0 (2022), which incorporate these MRI markers. APOE genotype modifies risk — ε4 promotes amyloid deposition, while ε2 is associated with the vasculopathic changes that predispose to rupture.

4. Secondary Causes

A secondary cause should be actively sought when the clinical or imaging picture is atypical (young, normotensive, lobar, or no small-vessel disease) — see the macrovascular-screening scores (DIAGRAM, MACRO) in Diagnosis & Grading.

• Vascular malformations — arteriovenous malformation, cavernous malformation, dural arteriovenous fistula, ruptured saccular aneurysm.
• Anticoagulant / coagulopathy-related — vitamin-K antagonists, DOACs, thrombocytopenia, hepatic or hematologic disease.
• Hemorrhagic transformation of an ischemic infarct (spontaneous or post-reperfusion).
• Tumor — hemorrhagic primary or metastatic neoplasm.
• Cerebral venous thrombosis — often lobar/parasagittal with surrounding edema.
• Drugs / toxins — sympathomimetics (cocaine, amphetamines).
• Vasculopathies — CNS vasculitis, reversible cerebral vasoconstriction syndrome (RCVS), infective (mycotic) aneurysm from endocarditis.

5. Risk Factors

6. Location → Likely Etiology

7. Pathophysiology of Brain Injury

Brain injury in ICH unfolds in two overlapping phases — an immediate mechanical insult, then a cascade of secondary processes that evolve over hours to days and are the main targets of acute treatment.

Primary injury

The extravasating blood mechanically disrupts and displaces brain tissue and raises local pressure. The resulting mass effect can cause midline shift, raised intracranial pressure, and herniation — the proximate cause of early death in large hemorrhages.

Hematoma expansion

Bleeding is frequently not a single event: ongoing hemorrhage and mechanical shearing of surrounding vessels ("avalanche" model) cause the hematoma to enlarge in roughly a third of patients, mostly within the first few hours. Expansion is the strongest modifiable predictor of poor outcome and the rationale for early blood-pressure control and reversal of coagulopathy (see Blood Pressure Management; expansion-prediction scores are in Diagnosis & Grading).

Secondary injury & perihematomal edema

Around the clot, a zone of perihematomal edema (PHE) develops in temporally distinct phases:

Together these produce blood–brain-barrier breakdown, cytotoxic and vasogenic edema, oxidative injury, and inflammatory cell death — extending damage beyond the original hematoma.

Intraventricular extension & hydrocephalus

Extension of blood into the ventricles (IVH) occurs in a large minority of cases and independently worsens prognosis, both directly and by causing obstructive hydrocephalus and raised intracranial pressure.

References

1. Greenberg SM, et al. 2022 Guideline for the Management of Patients With Spontaneous Intracerebral Hemorrhage. Stroke. 2022;53(7):e282–e361.
2. Sheth KN. Spontaneous Intracerebral Hemorrhage. N Engl J Med. 2022;387(17):1589–1596.
3. Charidimou A, et al. The Boston criteria version 2.0 for cerebral amyloid angiopathy. Lancet Neurol. 2022;21(8):714–725.
4. Wilkinson DA, et al. Injury mechanisms in acute intracerebral hemorrhage. Neuropharmacology. 2018;134(Pt B):240–248.
5. Hostettler IC, Seiffge DJ, Werring DJ. Intracerebral hemorrhage: an update on diagnosis and treatment. Expert Rev Neurother. 2019;19(7):679–694.