What are the potential causes of C1-2 cord signal changes on a T2 weighted MRI?

C1-2 Cord Signal Changes on T2-Weighted MRI

C1-2 cord signal changes on T2-weighted MRI arise from both compressive and non-compressive etiologies, with spondylotic myelopathy being the most common compressive cause and demyelinating diseases (particularly multiple sclerosis affecting 80-90% of cervical cords) representing the most frequent non-compressive etiology. 1

Compressive Etiologies

Mechanical compression at the C1-2 level produces T2 hyperintensity through chronic cord injury and edema:

• Spondylotic myelopathy from degenerative changes, disc herniations, epidural lipomatosis, and malalignment represents the primary compressive cause at this level 1
• Congenitally short pedicles can accentuate compression specifically at C1-2 1
• Postoperative hematomas in the early surgical period can cause extrinsic cord compression 2
• Intramedullary signal changes in spondylotic myelopathy serve as prognostic factors for neurosurgical outcomes, with T2-only changes indicating better prognosis than combined T1/T2 changes 2, 3

Non-Compressive Etiologies

Demyelinating Diseases

• Multiple sclerosis affects the cervical cord in 80-90% of cases, most commonly at the cervical level, with lesions disseminated in space and time fulfilling 2016 MAGNIMS criteria 2, 1
• Primary progressive MS demonstrates more extensive spinal cord involvement than relapsing-remitting MS 2
• Neuromyelitis optica (NMO) presents with longitudinally extensive transverse myelitis, characteristically longer than MS lesions 2
• Acute disseminated encephalomyelitis (ADEM) involves the spinal cord in approximately 25% of cases 2

Vascular Etiologies

• Spinal cord ischemia from atheromatous disease, aortic surgery complications, systemic hypotension, thoracoabdominal aneurysms, or sickle cell disease produces T2 hyperintensity 2
• Diffusion-weighted imaging demonstrates signal changes earlier than T2-weighted sequences in cord ischemia and should be included whenever ischemia is suspected 2, 1
• Contrast enhancement is typically absent in early acute ischemia; if present, it suggests inflammatory or infectious etiology rather than vascular 2
• Hematomyelia from intramedullary AVM or spinal artery aneurysm rupture rarely causes acute myelopathy 2
• Fibrocartilaginous embolic disease can produce acute ischemic myelopathy 2

Inflammatory and Infectious Etiologies

• Systemic inflammatory conditions including systemic lupus erythematosus, Sjögren syndrome, mixed connective tissue disorder, Behçet disease, and sarcoidosis can cause myelopathy 2
• Infectious diseases produce cord signal changes, with contrast-enhanced imaging recommended for initial diagnostic evaluation 2, 1
• Transverse myelitis presents with T2 hyperintensities in cortical white and gray matter extending into the spinal cord 2

Other Causes

• Trauma produces cord signal changes reflecting edema, contusion, or hemorrhage 4
• Radiation myelitis following therapeutic radiation 4
• Subacute combined degeneration from vitamin B12 deficiency 4
• AIDS-associated vacuolar myelopathy 4
• Syringohydromyelia 4

Diagnostic Approach

MRI with and without IV contrast is the definitive imaging modality, providing superior soft-tissue resolution and multiplanar capability essential for identifying both compressive and non-compressive etiologies 1

Key Imaging Protocols

• Contrast-enhanced imaging is recommended for initial diagnostic evaluation of all demyelinating conditions 2, 1
• Diffusion-weighted imaging should be included whenever spinal cord ischemia is suspected 2, 1
• IV contrast is typically not required for spondylotic myelopathy diagnosis, though characteristic enhancement patterns appear immediately at and below stenosis levels 2

Clinical Correlation Requirements

Comprehensive neurological examination must systematically assess:

• All upper extremity myotomes to detect bilateral weakness patterns 1
• Reflexes for hyperreflexia or pathologic responses 1
• Gait assessment for spasticity or ataxia 1
• Lower extremity function for pyramidal tract involvement 1
• Sensory distribution to establish a sensory level 1

Prognostic Significance

Signal changes on T2-weighted imaging predict clinical outcomes and guide management decisions:

• Patients with T2-only signal changes demonstrate better surgical outcomes than those with combined T1/T2 changes 3, 5
• Regression of T2 hyperintensity postoperatively correlates with significantly better clinical outcomes 3, 5
• T1 hypointensity represents irreversible cord damage and predicts worse prognosis 5
• Patients with intrinsic cord signal changes experience more adverse events (65.0% vs 44.8%), longer hospital stays, and worse baseline and final AIS scores 6

Critical Pitfalls

• Do not assume isolated finger weakness correlates with C1-2 cord edema—cord pathology at this level produces bilateral upper extremity dysfunction, not isolated findings 7
• Contrast enhancement in suspected ischemia suggests alternative inflammatory or infectious etiology, not vascular pathology 2
• Low CSF JC virus copy numbers may represent incidental findings in suspected progressive multifocal leukoencephalopathy, requiring clinical and radiographic correlation 2