What is the differential diagnosis for a T1 hyperintense cortical lesion on MRI?

Differential Diagnosis for T1 Hyperintense Cortical Lesions

The differential diagnosis for T1 hyperintense cortical lesions includes hemorrhagic metastases (especially melanoma, renal, thyroid, and ovarian primaries), subacute cortical infarction with laminar necrosis, focal cortical dysplasia type IIb, melanin-containing lesions, and proteinaceous lesions, with the specific diagnosis determined by clinical context, lesion morphology, and additional MRI sequences including T2, susceptibility-weighted imaging, and contrast enhancement patterns.* 1, 2

Hemorrhagic Lesions

Brain Metastases

• Hemorrhagic metastases are the most common cause of T1 hyperintense cortical lesions in patients with known malignancy, particularly from melanoma, renal cell carcinoma, thyroid carcinoma, and ovarian cancer 1
• These lesions typically appear at the gray-white junction with surrounding vasogenic edema and demonstrate contrast enhancement 1
• T2* or susceptibility-weighted imaging will show blooming artifact (signal loss) confirming hemorrhagic content, which is critical for distinguishing hemorrhagic from non-hemorrhagic causes 2, 3
• The presence of multiple lesions strongly favors metastatic disease over other etiologies 1

Subacute Infarction with Laminar Necrosis

• Curvilinear T1 hyperintense lesions following cortical contours in a vascular distribution represent laminar cortical necrosis from subacute infarction 4
• These lesions do NOT show blooming on T2*/SWI sequences, distinguishing them from hemorrhagic transformation 3, 4
• The hyperintensity corresponds histologically to complete cortical necrosis involving all cortical layers, not hemorrhage 4
• Clinical history of acute stroke and wedge-shaped distribution involving both cortex and underlying white matter support this diagnosis 1

Developmental and Epileptogenic Lesions

Focal Cortical Dysplasia (FCD)

• FCD type IIb characteristically shows T1 hyperintensity in unmyelinated infant brains, appearing opposite to the expected signal (hypointense T2, hyperintense T1) in the involved cortical region 1
• In myelinated brains, FCD may show focal cortical thickening, blurred gray-white junction, and the pathognomonic "transmantle sign" (radially oriented T2/FLAIR hyperintensity pointing to the ventricle) 1
• Solitary cortical tubers (with or without tuberous sclerosis) can present as T1 hyperintense cortical lesions in seizure patients 5
• Clinical presentation with medically refractory focal seizures strongly suggests FCD 1

Melanin-Containing Lesions

Melanoma Metastases and Melanosis

• Melanin produces characteristic T1 hyperintensity with T2 hypointensity (opposite to most lesions) 2, 6
• Leptomeningeal melanosis shows diffuse cortical involvement rather than focal lesions 6
• History of melanoma or neurocutaneous melanosis is essential for diagnosis 2

Proteinaceous and Lipid-Containing Lesions

• Dermoid cysts and lipomas show T1 hyperintensity but are typically extra-axial or midline, not cortical 6
• Chemical shift artifact on MRI confirms lipid content 2
• These are rarely purely cortical in location 6

Critical Diagnostic Algorithm

Step 1: Obtain T2/SWI sequences*

• Blooming present → hemorrhagic lesion (metastasis, hemorrhagic infarct, vascular malformation) 3
• No blooming → non-hemorrhagic causes (laminar necrosis, FCD, melanin, protein) 3, 4

Step 2: Assess lesion morphology

• Curvilinear following cortical ribbon → laminar necrosis from infarction 4
• Focal mass with enhancement at gray-white junction → metastasis 1
• Cortical thickening with transmantle sign → FCD type IIb 1

Step 3: Evaluate T2-weighted characteristics

• T1 hyperintense + T2 hypointense → melanin-containing lesion 2
• T1 hyperintense + T2 hyperintense → hemorrhage, protein, or fat 2, 6

Step 4: Assess contrast enhancement

• Ring or nodular enhancement with edema → metastasis 1
• No enhancement with vascular distribution → subacute infarction 4
• Variable enhancement with seizure history → FCD or tuber 1, 5

Common Pitfalls

• Do not assume all T1 hyperintense cortical lesions are hemorrhagic—always obtain T2*/SWI to confirm or exclude blood products 3, 4
• Curvilinear cortical T1 hyperintensity in stroke patients represents laminar necrosis, not hemorrhagic transformation, which has important implications for anticoagulation decisions 4
• In infants, FCD shows paradoxical signal (T1 hyperintense, T2 hypointense) that normalizes after myelination, potentially causing false-negative studies if imaged at 2-3 months of age 1
• Multiple sclerosis cortical lesions are typically NOT T1 hyperintense—they appear as T1 hypointense or isointense lesions best seen on DIR sequences 1
• Always correlate with clinical history: known malignancy favors metastases 1, acute stroke favors laminar necrosis 4, and refractory seizures favor FCD 1