What are the stages of diffusion restriction and apparent diffusion coefficient (ADC) changes in acute ischemic stroke versus hemorrhagic stroke?

Stages of Diffusion Restriction and ADC Changes in Acute Ischemic Stroke vs Hemorrhagic Stroke

Acute Ischemic Stroke: Temporal Evolution of DWI and ADC

In acute ischemic stroke, diffusion restriction appears within minutes of arterial occlusion and follows a predictable biphasic pattern: ADC values decrease significantly for the first 96 hours (to approximately 58% of normal), then pseudonormalize around 7-10 days, and finally elevate in the chronic phase due to increased extracellular water from tissue breakdown. 1

Hyperacute Phase (0-6 hours)

• DWI shows hyperintense signal within minutes of symptom onset, detecting ischemia with 88-100% sensitivity compared to only 16% for CT in the first 3 hours 2, 3
• ADC values drop immediately to approximately 58% of contralateral normal tissue due to cytotoxic edema and restricted water diffusion in the intracellular compartment 1
• The severity of ADC decrease correlates directly with perfusion deficit severity, with the lowest ADC values in the ischemic core and progressively higher values toward the periphery 4
• Tissue imaged within 3 hours may show ADC normalization after reperfusion in up to 35.5% of cases, indicating potentially reversible injury, compared to only 7.5% normalization in tissue imaged 3-6 hours after onset 5

Acute Phase (6-96 hours)

• ADC values remain significantly reduced (mean 58.3% of control) throughout the first 96 hours, reflecting ongoing cytotoxic edema 1
• The persistent ADC reduction during this period suggests progressive cytotoxic edema predominates over extracellular edema and cell lysis 1
• DWI lesion volumes correlate with final infarct size and clinical severity 6
• ADC maps are essential to eliminate T2 "shine-through" effect, greatly increasing specificity for acute infarction 3

Subacute Phase (7-14 days)

• ADC values begin pseudonormalization around 7-10 days, transitioning from decreased to normal values 1
• This pseudonormalization represents a critical diagnostic pitfall where DWI may appear falsely normal despite ongoing subacute infarction 1
• Standard T2-weighted and FLAIR sequences become more conspicuous during this phase as vasogenic edema develops 6

Chronic Phase (>14 days)

• ADC values become elevated above normal due to increased extracellular water content from tissue necrosis, gliosis, and cystic encephalomalacia 1
• DWI signal returns to hypointense or isointense relative to normal brain 1
• T2/FLAIR sequences show persistent hyperintensity with tissue loss 6

Hemorrhagic Stroke: DWI and ADC Patterns

Hemorrhagic stroke demonstrates variable and complex DWI/ADC patterns that differ fundamentally from ischemic stroke, with signal characteristics depending on blood product stage, hematoma location, and presence of surrounding ischemia.

Hyperacute Hemorrhage (<24 hours)

• Gradient-echo (GRE) and susceptibility-weighted imaging (SWI) are superior to DWI for detecting acute hemorrhage, showing marked hypointensity due to deoxyhemoglobin 6, 2
• The hematoma center may show variable ADC values depending on protein concentration and blood product evolution, not following the predictable pattern of ischemic stroke 6
• Perihematomal edema may show restricted diffusion if there is associated ischemia from mass effect or vascular compression 7

Acute to Subacute Hemorrhage (1-14 days)

• SWI/GRE sequences remain the primary diagnostic tool, detecting blood products with higher sensitivity than DWI 3
• The hematoma itself does not show the progressive ADC normalization pattern seen in ischemic stroke 1
• Surrounding vasogenic edema shows elevated ADC values (not restricted diffusion), distinguishing it from cytotoxic edema of ischemic stroke 1

Chronic Hemorrhage (>14 days)

• Hemosiderin deposition causes persistent "blooming artifact" on SWI/GRE sequences, allowing detection of remote hemorrhages 3
• ADC values in the residual cavity are markedly elevated due to CSF-like fluid content 1
• Unlike chronic ischemic stroke, the hemosiderin ring remains visible indefinitely on susceptibility sequences 3

Critical Diagnostic Algorithm

For Suspected Acute Stroke (<6 hours)

1. Obtain DWI, ADC maps, FLAIR, and GRE/SWI sequences in a 10-minute protocol 2
2. DWI hyperintensity with corresponding ADC hypointensity confirms acute ischemia 3
3. GRE/SWI hypointensity ("blooming") indicates hemorrhage, which takes precedence in treatment decisions 2
4. Assess ADC severity: tissue with ADC <50% of normal is less likely to be salvageable even with reperfusion 5

For Patients 6-96 Hours from Onset

1. Persistent ADC reduction confirms acute ischemia throughout this window 1
2. Add perfusion imaging to identify penumbra (perfusion-diffusion mismatch) for late intervention decisions 6
3. Beware of ADC normalization in reperfused tissue, which may represent salvaged penumbra rather than chronic infarction 5

For Subacute Presentations (7-14 days)

1. ADC pseudonormalization creates diagnostic uncertainty—rely on FLAIR hyperintensity and clinical timeline 1
2. GRE/SWI remains diagnostic for hemorrhage regardless of timing 3
3. Do not mistake pseudonormalized ADC for absence of infarction in this critical window 1

Key Clinical Pitfalls

• ADC normalization after reperfusion (especially <3 hours) does not indicate tissue viability—19.7% of patients show this phenomenon, predominantly in basal ganglia and white matter 5
• Pseudonormalization at 7-10 days can cause false-negative DWI studies—always correlate with FLAIR and clinical timeline 1
• Hemorrhagic transformation shows early parenchymal enhancement on post-contrast imaging, which is 100% specific for subsequent hemorrhage 7
• T2 "shine-through" on DWI without corresponding ADC hypointensity indicates subacute/chronic infarction, not acute ischemia 3
• The severity of initial ADC decrease predicts tissue fate—more severe decreases are less likely to normalize even with reperfusion 5