What are the causes of posterior putaminal hyperintensity on imaging studies?

Posterior Putaminal Hyperintensity: Causes

Posterior putaminal hyperintensity on MRI most commonly indicates hypertensive hemorrhage, but can also represent ischemic stroke, manganese deposition in chronic liver disease, or rarely CSF1R-related leukoencephalopathy depending on the clinical context and imaging characteristics.

Primary Causes by Imaging Sequence

T2/FLAIR Hyperintensity

Hypertensive Intracerebral Hemorrhage (Most Common)

• The putamen is the most frequent site of hypertensive cerebral hemorrhage, presenting with T2 hyperintensity in the acute-to-subacute phase 1
• Putaminal hemorrhages show a wide range of presentations, from massive hemorrhages extending into white matter and ventricles to small asymptomatic bleeds 1
• Approximately 45% of spontaneous intracerebral hemorrhages involve the basal ganglia (including putamen) and extend into the ventricular system 2
• Look for associated findings: mass effect, surrounding edema, and potential intraventricular extension 3

Ischemic Stroke

• Putaminal infarction presents as T2/FLAIR hyperintensity, typically involving the lenticulostriate artery territory 4
• May show restricted diffusion on DWI in acute phase (first 7-10 days) 5
• Associated with poor clinical outcome when involving the corpus striatum (putamen, caudate, pallidum) 4

CSF1R-Related Leukoencephalopathy (Rare)

• Can show putaminal iron deposition on susceptibility-weighted imaging, though white matter lesions predominate 3
• Typically presents with frontoparietal white matter lesions as the primary finding, with putaminal changes being secondary 3

T1 Hyperintensity

Chronic Liver Disease/Portosystemic Shunting

• Bilateral symmetric pallidal (and putaminal) T1 hyperintensity results from manganese accumulation 3
• Related to portal hypertension and portosystemic shunting rather than hepatic encephalopathy itself 3
• T2-weighted images remain normal despite T1 hyperintensity 3
• May increase after TIPS placement and can reverse following liver transplantation or shunt occlusion 3

Subacute Hemorrhage

• Methemoglobin in subacute hemorrhage (typically 3-21 days post-ictus) causes T1 hyperintensity 5
• Should have corresponding signal void on T2* GRE or SWI sequences to confirm hemorrhagic etiology 5

Non-Hemorrhagic Ischemic Stroke (Uncommon)

• T1 hyperintensity can occur in ischemic stroke without hemorrhage, likely due to partial tissue infarction or selective neuronal necrosis 5
• Appears 1-21 days after onset, either homogeneously throughout the lesion or with rim-like peripheral distribution 5
• Distinguished from hemorrhage by absence of signal void on GRE/SWI sequences 5

Critical Diagnostic Algorithm

Step 1: Determine the MRI sequence showing hyperintensity

• T2/FLAIR hyperintensity → Consider hemorrhage (acute-subacute), ischemia, or inflammatory process
• T1 hyperintensity → Consider chronic liver disease (if bilateral and symmetric), subacute hemorrhage, or non-hemorrhagic infarction

Step 2: Assess for hemorrhage markers

• Check T2* GRE or SWI sequences for signal void (blooming artifact) 5
• Signal void present → Confirms hemorrhagic component 5
• No signal void → Consider non-hemorrhagic ischemia or manganese deposition 3, 5

Step 3: Evaluate distribution pattern

• Unilateral putaminal involvement → Strongly suggests vascular etiology (hemorrhage or ischemia) 1, 6
• Bilateral symmetric involvement → Consider manganese deposition from liver disease 3
• Associated white matter changes → Consider CSF1R-related leukoencephalopathy or small vessel disease 3, 4

Step 4: Correlate with clinical presentation

• Acute onset with hypertension → Hypertensive hemorrhage most likely 1, 6
• Liver disease history → Manganese deposition 3
• Progressive cognitive decline with white matter disease → CSF1R-related disorder 3

Common Pitfalls and Caveats

Do not assume all T1 hyperintensity represents hemorrhage - Non-hemorrhagic ischemic stroke can show T1 hyperintensity without GRE/SWI signal void, particularly in the subacute phase (1-21 days) 5

Timing matters for hemorrhage detection - Most putaminal hemorrhages complete within 6 hours of onset, so early imaging may underestimate final hemorrhage size 6

Bilateral putaminal T1 hyperintensity requires liver function assessment - This finding is highly specific for manganese deposition in chronic liver disease and portosystemic shunting 3

Pontine hyperintensity as a prognostic marker - When posterior putaminal changes are associated with pontine T2 hyperintensity, this combination relates to poor clinical outcome after supratentorial stroke 4

Contrast enhancement is rarely needed - Gadolinium enhancement is not typical for putaminal hemorrhage or ischemia; if present, consider alternative diagnoses such as tumor, infection, or inflammatory conditions 3