What does increased cord signal intensity on MRI mean?

What Does Increased Cord Signal Intensity on MRI Mean?

Increased T2 signal intensity in the spinal cord on MRI indicates intramedullary pathology that can result from compression, inflammation, ischemia, demyelination, or trauma, and requires systematic evaluation to determine the underlying etiology and guide management.

Clinical Significance and Differential Diagnosis

The presence of increased T2 signal intensity (also called hyperintensity or ISI) within the spinal cord is a nonspecific finding that requires integration of clinical context, timing of onset, pattern of involvement, and associated imaging features to narrow the differential diagnosis 1, 2.

Key Etiologic Categories

Compressive Myelopathy:

• In cervical spondylotic myelopathy, T2 hyperintensity reflects cord injury from chronic compression and appears in 65-80% of patients with moderate to severe disease 1, 3
• The signal change represents edema, gliosis, myelomalacia, or ischemic injury depending on chronicity 1
• Prognostic significance: Multisegmental T2 hyperintensity predicts worse surgical outcomes compared to focal changes or no signal abnormality 1, 3
• When T1 hypointensity accompanies T2 hyperintensity, this indicates more severe irreversible cord damage (myelomalacia or necrosis) and portends particularly poor surgical prognosis 1

Inflammatory/Demyelinating Conditions:

• Multiple sclerosis lesions appear as focal T2 hyperintensities, typically occupying less than half the cross-sectional cord area and extending less than 2 vertebral segments 1
• Neuromyelitis optica produces longitudinally extensive lesions (≥3 vertebral segments) with central cord predilection 1
• Acute disseminated encephalomyelitis involves the cord in 25% of cases 1
• Contrast enhancement suggests active inflammation and is commonly associated with new clinical symptoms 1

Ischemic Myelopathy:

• Acute spinal cord ischemia shows T2 hyperintensity in a characteristic vascular distribution (anterior spinal artery territory most common) 1
• Contrast enhancement is typically absent in early acute ischemia; if present, it suggests alternative inflammatory or infectious etiology 1
• Diffusion-weighted imaging shows restricted diffusion earlier than T2 changes and should be included when ischemia is suspected 1

Traumatic Cord Injury:

• T2 hyperintensity with cord expansion indicates acute edema and hemorrhage 1
• Signal changes from C4-C7 spanning multiple levels suggest more severe injury with worse prognosis 1

Imaging Protocol Recommendations

Essential MRI Sequences:

• Minimum two sagittal sequences with different contrasts (T2-weighted and proton density or STIR) at ≥1.5T field strength with 3mm slice thickness 1
• Axial T2-weighted images to verify sagittal findings and assess cross-sectional cord involvement 1
• Contrast administration for initial evaluation of suspected inflammatory/demyelinating disease 1

Technical Considerations:

• Proper echo time selection renders cord isointense to CSF, facilitating detection of signal abnormalities 1
• High-resolution imaging is critical given the small cross-sectional area of the cord 1

Prognostic Implications in Compressive Myelopathy

Favorable Prognostic Indicators:

• Absence of T2 hyperintensity predicts best surgical recovery 1, 3
• Focal (single segment) hyperintensity allows modest neurological improvement 1
• Resolution of T2 signal after surgery correlates with improved neurological recovery 1

Unfavorable Prognostic Indicators:

• Multisegmental (≥2 segments) T2 hyperintensity predicts poor surgical prognosis 1, 3
• "Snake eyes" appearance (bilateral symmetric T2 hyperintensity in anterior horn cells) indicates particularly poor outcomes 1
• Combined T1 hypointensity with T2 hyperintensity suggests irreversible myelomalacia 1
• Transverse cord area <30-40 mm² indicates severe atrophy with worse outcomes 1

Important Caveat: In patients with mild cervical myelopathy treated conservatively, T2 hyperintensity does not reliably predict poor outcomes, and some patients improve despite persistent signal changes 4. However, for moderate to severe myelopathy requiring surgery, the prognostic value is more established 3, 5.

Clinical Algorithm for Evaluation

Step 1 - Assess Timing:

• Acute onset (<24-48 hours): Consider ischemia, trauma, or acute inflammatory process 1
• Subacute/chronic: Consider compression, demyelination, or chronic inflammatory conditions 1, 2

Step 2 - Evaluate Cord Expansion:

• Expanded cord: Suggests acute edema, inflammation, tumor, or hemorrhage 1, 2
• Normal/atrophic cord: Suggests chronic compression, chronic ischemia, or remote injury 1, 2

Step 3 - Characterize Signal Pattern:

• Focal (<2 segments): MS, focal compression, small infarct 1
• Longitudinally extensive (≥3 segments): NMO, ADEM, extensive compression 1
• Central cord: Ischemia, syringomyelia, NMO 1, 2
• Peripheral cord: MS, extrinsic compression 1, 2

Step 4 - Assess Enhancement:

• Enhancement present: Active inflammation, infection, tumor 1
• No enhancement: Chronic compression, ischemia (acute phase), gliosis 1

Step 5 - Correlate with Clinical Presentation:

• Match signal location with clinical level of dysfunction 1
• Assess for dissemination in space/time if demyelination suspected 1