A 72-year-old woman with a history of hypertension and diabetes mellitus presents with acute onset of severe headache, vomiting, and left-sided weakness. CT head shows a 4 cm hyperdense lesion in the right basal ganglia with 8 mm midline shift and intraventricular extension. MRI performed 6 hours later shows the same lesion with T1 hyperintensity, T2 isointensity, and susceptibility artifact. What is the most likely timing of this hemorrhage, and what does the susceptibility artifact represent?

Explanation

## Clinical Presentation & Imaging Correlation **Key Point:** The patient presents with acute hypertensive hemorrhagic stroke (basal ganglia location is classic for hypertensive ICH). The imaging was performed 6 hours after symptom onset, placing the hemorrhage in the **acute phase** (6 hours to 3 days). ## MRI Signal Evolution in Intracerebral Hemorrhage ```mermaid flowchart TD A["Intracerebral Hemorrhage"]:::outcome --> B["Hyperacute Phase<br/>< 6 hours"]:::outcome B --> B1["Oxyhemoglobin (Hb-O2)<br/>T1: Isointense<br/>T2: Hyperintense<br/>SWI: No artifact"] A --> C["Acute Phase<br/>6 hours - 3 days"]:::outcome C --> C1["Deoxyhemoglobin<br/>T1: Isointense/Hypointense<br/>T2: Hypointense<br/>SWI: Marked artifact ✓"] A --> D["Subacute Phase<br/>3-7 days"]:::outcome D --> D1["Methemoglobin (intracellular)<br/>T1: Hyperintense<br/>T2: Hyperintense<br/>SWI: Artifact"] A --> E["Chronic Phase<br/>> 7 days"]:::outcome E --> E1["Hemosiderin in macrophages<br/>T1: Hypointense<br/>T2: Hypointense<br/>SWI: Persistent artifact"] ``` ## Why Acute Phase (6 hours to 3 days)? **High-Yield:** At 6 hours post-hemorrhage, the red blood cells are intact but oxyhemoglobin has been converted to **deoxyhemoglobin** due to consumption of oxygen and local hypoxia. Deoxyhemoglobin is a **paramagnetic substance** (unpaired electrons in iron), which causes: - **T2 hypointensity** (signal loss on T2/FLAIR) - **Susceptibility artifact** on SWI (gradient echo sequences) — this is the blooming effect seen as a dark halo larger than the actual lesion - **T1 isointensity or mild hypointensity** (not hyperintense, which occurs later) ## Susceptibility Artifact: Mechanism **Clinical Pearl:** Susceptibility artifact (blooming on SWI/GRE) is caused by local magnetic field inhomogeneity created by paramagnetic deoxyhemoglobin. The artifact makes the lesion appear larger than it truly is — clinically important for assessing mass effect and midline shift. This is the most sensitive sequence for detecting microhemorrhages and old bleeding. **Mnemonic:** **DOSH** = Deoxyhemoglobin → Susceptibility artifact → Hypointense on T2 → Artifact on SWI ## Why Not Other Phases? | Phase | Timeline | T1 Signal | T2 Signal | SWI Artifact | Key Hemoglobin Form | |-------|----------|-----------|-----------|--------------|---------------------| | **Hyperacute** | < 6 hrs | Isointense | **Hyperintense** | Minimal | Oxyhemoglobin | | **Acute** | 6 hrs–3 d | Isointense | **Hypointense** | **Marked** | **Deoxyhemoglobin** ✓ | | **Subacute** | 3–7 d | **Hyperintense** | Hyperintense | Present | Methemoglobin (intracellular) | | **Chronic** | > 7 d | Hypointense | Hypointense | Persistent | Hemosiderin | **High-Yield:** The T1 hyperintensity mentioned in the question is NOT consistent with acute phase alone — it suggests early transition to subacute, but the prominent susceptibility artifact and T2 isointensity (not hyperintensity) favor acute phase. The question stem emphasizes the susceptibility artifact, which is the hallmark of deoxyhemoglobin in the acute phase. [cite:Robbins 10e Ch 28; Neuroradiology Board Review (ASNR)]