Diagnosis & Grading of Intracerebral Hemorrhage
The diagnostic workup of intracerebral hemorrhage (ICH) answers three sequential questions: Is it hemorrhage? (non-contrast CT), Why did it bleed? (CTA and MRI screening for a macrovascular or secondary cause), and What is the prognosis and who is at risk of deterioration? (grading and expansion-prediction scores). This topic walks through imaging β NCCT, CTA, and MRI β and then the validated scores used for prognostication, secondary-cause screening, and hematoma-expansion risk.
Bottom Line: Diagnosis & Grading
- Non-contrast CT is first-line: confirms hemorrhage, localizes it, estimates volume (ABC/2), and detects IVH, mass effect, and hydrocephalus.
- CTA serves two roles β the spot sign (active extravasation) flags hematoma-expansion risk, and CTA screens for a macrovascular cause (AVM, aneurysm, dural fistula, cavernoma) or an enhancing tumor.
- MRI stages blood by age on T1/T2 and β via blood-sensitive sequences (GRE/T2*/SWI) β reveals microbleed patterns that distinguish CAA (lobar) from hypertensive (deep) etiology.
- Prognosis: the ICH Score grades 30-day mortality; the FUNC score predicts functional independence. Use them to inform, not to justify early withdrawal of care.
- Secondary-cause screening: the DIAGRAM (CT/CTA) and MACRO (MRI) scores quantify the probability of a macrovascular cause and push toward angiography in higher-risk patients.
- Expansion risk: the BAT and HEP scores estimate hematoma growth from non-contrast CT alone, identifying patients who warrant closer monitoring and aggressive early management.
1. Clinical Picture
ICH classically presents with a sudden focal neurological deficit that progresses over minutes to hours, frequently accompanied by headache, vomiting, depressed level of consciousness, and markedly elevated blood pressure β features that, together, favor hemorrhage over ischemia but are not specific enough to defer imaging. The deficit reflects hematoma location:
- Putaminal / basal ganglia (most common, hypertensive): contralateral hemiparesis, gaze deviation toward the lesion.
- Thalamic: contralateral sensorimotor loss, downward/medial gaze, miosis; IVH and hydrocephalus common.
- Lobar: deficits by lobe (aphasia, neglect, hemianopia, seizures); raises suspicion for CAA or a secondary cause.
- Cerebellar: ataxia, vomiting, headache β a neurosurgical emergency given risk of brainstem compression and hydrocephalus.
- Pontine: coma, pinpoint pupils, quadriparesis β typically devastating.
2. Non-Contrast CT (NCCT)
NCCT is the universal first-line study: it is fast, available, and highly sensitive for acute blood, which appears hyperdense (β 50β70 Hounsfield units) against lower-density brain. Beyond simple detection, the initial scan defines the parameters that drive grading and management:
- Volume by the bedside ABC/2 method (A = greatest diameter, B = diameter perpendicular to A, C = number of slices with hemorrhage Γ slice thickness, divided by 2) β the volume term used in nearly every ICH score.
- Intraventricular extension (IVH) and hydrocephalus β independent predictors of poor outcome.
- Mass effect, midline shift, and herniation.
- Early NCCT markers of expansion (blend, swirl, black-hole, island, satellite signs) β detailed in Section 8.
3. CT Angiography (CTA)
CTA is increasingly obtained acutely because it answers two distinct questions at once β will it grow? and why did it bleed?
The spot sign β predicting expansion
The spot sign is one or more foci of contrast enhancement within the hematoma on CTA, representing active contrast extravasation from ongoing bleeding. It is the strongest imaging predictor of hematoma expansion and of in-hospital mortality, and it underlies CTA-based expansion scores. (Despite its predictive power, spot-signβtargeted hemostatic therapy has not improved outcomes in trials such as SPOTLIGHT/STOP-IT.)
Screening for a secondary cause
CTA also screens for a macrovascular or structural cause, which changes management entirely:
- Vascular malformations β arteriovenous malformation (AVM), saccular aneurysm, dural arteriovenous fistula, developmental venous anomaly, or cavernoma.
- Enhancing tumor β a hemorrhagic neoplasm (primary or metastatic), suggested by disproportionate edema, an enhancing nodule, or atypical location.
- Cerebral venous thrombosis β particularly with lobar/parasagittal hemorrhage and a non-arterial pattern.
Suspicion for a secondary cause rises with younger age, lobar or intraventricular location, absence of hypertension or small-vessel disease, and atypical imaging features. The DIAGRAM and MACRO scores (Sections 6β7) formalize this judgment.
4. MRI: Staging Blood by Age
MRI signal of hemorrhage evolves predictably as hemoglobin degrades from oxyhemoglobin β deoxyhemoglobin β intracellular methemoglobin β extracellular methemoglobin β hemosiderin. Recognizing the stage helps date the bleed and is central to detecting old or multiple hemorrhages.
| Stage | Approx. age | Hemoglobin form | T1 | T2 |
|---|---|---|---|---|
| Hyperacute | < 24 h | Oxyhemoglobin (intracellular) | Iso / dark | Bright |
| Acute | 1β3 days | Deoxyhemoglobin (intracellular) | Iso / dark | Dark |
| Early subacute | 3β7 days | Methemoglobin (intracellular) | Bright | Dark |
| Late subacute | 1 week β 1 month | Methemoglobin (extracellular) | Bright | Bright |
| Chronic | > 1 month | Hemosiderin / ferritin | Dark | Dark |
Memory aid (T1, T2 signal by stage): IB β ID β BD β BB β DD ("Iso-Bright, Iso-Dark, Bright-Dark, Bright-Bright, Dark-Dark"), where I = isointense, B = bright, D = dark. A useful clinical anchor: the late subacute stage is bright on both T1 and T2, and the chronic stage is dark on both.
5. Blood-Sensitive MRI Sequences
Beyond conventional T1/T2, susceptibility-based sequences exploit the paramagnetic effect of blood-breakdown products and are essential for detecting acute blood, chronic microbleeds, and cortical superficial siderosis.
| Sequence | What it detects | Notes |
|---|---|---|
| GRE (gradient echo) | "Blooming" of deoxyhemoglobin, methemoglobin, and hemosiderin | Detects acute hemorrhage and chronic microbleeds; widely available |
| T2* | Same susceptibility effect as GRE | Older susceptibility technique; superseded by SWI where available |
| SWI (susceptibility-weighted) | Most sensitive to blood products, microbleeds, and superficial siderosis | More sensitive than GRE/T2*; can overestimate hematoma size due to blooming |
| DWI | Co-existing acute ischemia; variable signal within clot | Useful when an underlying infarct or tumor is suspected |
| FLAIR / T2 | Perihematomal edema, chronic cavity, cortical superficial siderosis | Supports CAA diagnosis and dating |
Microbleed distribution is an etiologic clue: a strictly lobar / cortical pattern (Β± cortical superficial siderosis) supports cerebral amyloid angiopathy, whereas a deep / basal-ganglia / brainstem pattern supports hypertensive arteriopathy. This same small-vessel-disease burden is what the MACRO score uses to estimate how likely a macrovascular cause is.
6. Prognostic Grading Scores
ICH Score (Hemphill, 2001)
The original and most widely used grading scale, designed for rapid bedside risk stratification and standardized communication. It sums five variables (0β6 points) and correlates strongly with 30-day mortality.
| Component | Finding | Points |
|---|---|---|
| GCS | 3β4 | 2 |
| 5β12 | 1 | |
| 13β15 | 0 | |
| ICH volume | β₯ 30 mL | 1 |
| Intraventricular hemorrhage | Present | 1 |
| Infratentorial origin | Yes | 1 |
| Age | β₯ 80 years | 1 |
| ICH Score | 0 | 1 | 2 | 3 | 4 | 5 |
|---|---|---|---|---|---|---|
| 30-day mortality | 0% | 13% | 26% | 72% | 97% | 100% |
(No patients scored 6 in the original cohort; a score of 6 is presumed near-uniformly fatal.) Subsequent validations reproduce this near-linear mortality gradient.
Important caveat: these mortality figures derive from eras with frequent early withdrawal of life-sustaining treatment, creating a self-fulfilling prophecy. Current AHA/ASA guidance recommends against using early prognostic scores to justify limiting care in the first 24β48 hours; default to full aggressive treatment.
FUNC Score (Rost, 2008)
Where the ICH Score predicts death, the FUNC score predicts functional independence at 90 days (0β11 points; higher = better outcome).
| Component | Finding | Points |
|---|---|---|
| ICH volume | < 30 mL | 4 |
| 30β60 mL | 2 | |
| > 60 mL | 0 | |
| Age | < 70 | 2 |
| 70β79 | 1 | |
| β₯ 80 | 0 | |
| Location | Lobar | 2 |
| Deep | 1 | |
| Infratentorial | 0 | |
| GCS | β₯ 9 | 2 |
| Pre-ICH cognitive impairment | Absent | 1 |
Functional independence (GOS β₯ 4) at 90 days rises steeply with score: roughly 0% at β€ 4 points up to ~80% at 11 points, supporting goals-of-care discussions once the acute phase has stabilized.
7. Screening for a Macrovascular / Secondary Cause
A macrovascular cause is found in roughly 7β15% of spontaneous ICH and is far more common in younger, normotensive patients with lobar or posterior-fossa bleeds. Missing one (e.g., an AVM or aneurysm) risks catastrophic rebleeding, so structured scores help decide who needs vascular imaging up to digital subtraction angiography (DSA).
DIAGRAM score (Hilkens, 2018) β CT/CTA-based
Combines age (18β50, 51β70, >70), ICH location (lobar or posterior-fossa vs. deep), and small-vessel-disease markers on CT, with an optional CTA term. Predicted probability of a macrovascular cause ranges from ~1% (older patient, deep ICH, with SVD) to > 50% (young patient, lobar/posterior-fossa ICH, no SVD). Discrimination: c-statistic 0.83 with clinical + CT variables, rising to 0.91 when CTA is added (DIAGRAM-plus). It flags patients in whom a negative CTA should still prompt MRI/MRA or DSA.
MACRO score (Fandler-HΓΆfler, 2024) β MRI-based
A newer, MRI-based complement (MRI Assessment of the Causes of intRacerebral haemOrrhage) that leverages small-vessel-disease burden β the opposite of macrovascular disease. It combines age (0β39 / 40β69 / β₯70), ICH location (lobar / deep / infratentorial), and MRI SVD markers (cerebral microbleeds, lacunes, cortical superficial siderosis, white-matter hyperintensities by Fazekas).
| Total score (0β7) | Estimated macrovascular probability | Implication |
|---|---|---|
| β₯ 6 (high SVD burden) | β 0.2% | Very low β extensive angiographic workup rarely needed |
| β€ 2 (little/no SVD) | β 48.9% | High β pursue DSA / dedicated vascular imaging |
Note the direction: higher MACRO score = lower macrovascular risk (more small-vessel disease makes a "primary" cause likelier). In derivation (1,043 patients, 7.5% with a macrovascular cause) the c-statistic was 0.90 (95% CI 0.88β0.93) and 0.87 on external validation β outperforming CT-based scores. MACRO and DIAGRAM are complementary: DIAGRAM triages at the CT/CTA stage, MACRO refines the decision once MRI is available.
8. Hematoma-Expansion Prediction
Hematoma expansion β growth of β₯ 6 mL or β₯ 33% β occurs in roughly a third of patients, mostly within the first few hours, and is the strongest modifiable predictor of poor outcome. Identifying high-risk patients early targets monitoring and aggressive blood-pressure and reversal strategies (see INTERACT2 and the Acute Management β Blood Pressure topic).
Non-contrast CT markers of expansion
| Marker | Description |
|---|---|
| Blend sign | Hypoattenuating region blended with adjacent hyperattenuating hematoma, with a clear demarcation |
| Black-hole sign | Encapsulated hypoattenuating area within the hyperdense hematoma, distinct densities |
| Swirl sign | Region of hypo- or isodensity within a hyperdense hematoma (active bleeding) |
| Island sign | β₯ 3 scattered small hematomas separate from the main bleed, or β₯ 4 bubble-/budding-shaped foci |
| Satellite sign | Small hemorrhage separate from but within 20 mm of the main hematoma |
BAT score (Morotti, 2019)
A simple 0β5 non-contrast score combining one imaging sign, one density feature, and timing:
| Component (BAT) | Finding | Points |
|---|---|---|
| Blend sign | Present | 1 |
| Any hypodensity | Present | 2 |
| Timing (onset β NCCT) | < 2.5 hours | 2 |
Higher scores predict greater expansion risk; a score β₯ 3 identifies a high-risk group. The BAT score requires only the initial non-contrast scan and the time of onset.
HEP score (Hematoma Expansion Prediction)
A more granular 0β18 nomogram-derived scale that integrates several NCCT features (hypodensities, blend sign, hematoma shape and density, fluid level) with clinical variables (including a history of dementia and smoking). It predicts substantial expansion (β₯ 6 mL or β₯ 33%) with accuracy comparable to the CTA spot sign β a useful advantage where CTA is unavailable or contraindicated.
9. Putting It Together
- Everyone: NCCT β confirm, localize, volume (ABC/2), IVH, hydrocephalus; compute the ICH Score.
- Expansion risk: assess NCCT markers + BAT/HEP; add CTA for the spot sign when early intervention is being considered.
- Secondary cause: in younger, lobar, or normotensive patients, use DIAGRAM (CT/CTA) and, once MRI is done, MACRO to decide on DSA.
- Prognosis: ICH Score (mortality) and FUNC (function) inform β but do not dictate β goals of care; avoid early nihilism.
References
- Hemphill JC 3rd, et al. The ICH Score: a simple, reliable grading scale for intracerebral hemorrhage. Stroke. 2001;32(4):891β897.
- Rost NS, et al. Prediction of functional outcome in patients with primary intracerebral hemorrhage: the FUNC score. Stroke. 2008;39(8):2304β2309.
- Hilkens NA, et al. Predicting the presence of macrovascular causes in non-traumatic intracerebral haemorrhage: the DIAGRAM prediction score. J Neurol Neurosurg Psychiatry. 2018;89(7):674β679.
- Fandler-HΓΆfler S, et al. MRI-based prediction of macrovascular causes of intracerebral hemorrhage: the MACRO score. Neurology. 2024;103(10):e209950.
- Morotti A, et al. Predicting intracerebral hemorrhage expansion with noncontrast computed tomography: the BAT score. Stroke. 2018;49(5):1163β1169.
- Yao X, et al. The HEP score: a nomogram-derived hematoma expansion prediction scale. Neurocrit Care. 2015;23(2):179β187.
- Greenberg SM, et al. 2022 Guideline for the Management of Patients With Spontaneous Intracerebral Hemorrhage. Stroke. 2022;53(7):e282βe361.