Cord Lesion, T2 Hyperintense, Dorsal

Lubdha M. Shah, MD

DIFFERENTIAL DIAGNOSIS

Common

Multiple Sclerosis, Spinal Cord
Contusion-Hematoma, Spinal Cord

Less Common

Subacute Combined Degeneration
- Copper Deficiency
- Nitrous Oxide Misuse
HIV
Sarcoidosis
Cord Wallerian Degeneration

Rare but Important

Neurosyphilis

ESSENTIAL INFORMATION

Key Differential Diagnosis Issues

Intracranial periventricular, subcallosal, cerebellar & brainstem lesions in MS
GRE sequences helpful to evaluate for hemorrhagic products in cord contusion

Helpful Clues for Common Diagnoses

Multiple Sclerosis, Spinal Cord
- 90% of cases have intracranial lesions
- 10-20% cases have isolated spinal cord disease
- Cervical cord is most commonly affected
  - Acutely, central enhancement of peripheral T2 hyperintense lesion
  - Enhancement duration 1-2 months
  - Cord edema lasts 6-8 weeks
  - Dorsolateral aspect of cord involving both the white matter and adjacent gray matter
  - Cord atrophy in late stage
Contusion-Hematoma, Spinal Cord
- Acute: Cord swelling & T2 hyperintensity
- May see hemorrhagic products within cord, fracture, & soft tissue injury
- May see traumatic disc herniation
- STIR sequence is helpful to assess marrow edema and ligamentous injury

Helpful Clues for Less Common Diagnoses

Subacute Combined Degeneration
- T2 hyperintensity confined to dorsal ± lateral columns
- Lower cervical and upper thoracic cord
- Focal cord swelling of myelin tubes progresses to larger areas of myelin vacuolization
- Mild cord enlargement ± mild dorsal column enhancement
- Occurs in setting of some types of severe anemia (e.g., megaloblastic anemia)
  - Methylmalonic acid accumulation causes myelin toxicity
  - Neurologic findings may precede anemia
  - Treatment may improve symptoms but imaging abnormalities may not completely resolve
- Copper Deficiency
  - Spastic gait and sensory ataxia
  - Etiologies include malabsorption, partial gastrectomy, and hyperzincemia
  - Long segment of symmetric increased T2 signal in the dorsal midline cervical and thoracic cord
  - Imaging findings may be reversible with normalization of serum copper
- Nitrous Oxide Misuse
  - May result in subacute combined degeneration with symptoms ranging from paresthesias to autonomic dysfunction
  - Nitrous oxide inhibits the active form of vitamin B12
  - Toxicity is related to the patient’s levels of vitamin B12
  - Demyelination with T2 hyperintensity in the central posterior columns of the cord
  - Pathologically usually begins in thoracic cord
  - Myelopathy has been reported 2-6 weeks after nitrous oxide anesthesia
HIV
- Most common imaging finding is atrophy (72%)
- T2 hyperintensity involving white matter tracts laterally & symmetrically
- May show patchy enhancement
- Thoracic > cervical cord
  - Rostral extension from mid to lower thoracic cord with disease progression
- Progressive spastic paraparesis with ataxia, urinary symptoms & sensory loss
Sarcoidosis
- Focal or diffuse T2 hyperintensity & fusiform cord enlargement
  - Myelomalacia in late stages
- Leptomeningeal & peripheral intramedullary mass-like enhancement
- Lytic spine lesions
- Male > female in spinal sarcoidosis
Cord Wallerian Degeneration
- Post-traumatic: Increased T2 signal in dorsal columns above injury level & in lateral corticospinal tracts below the injury level
  - In lumbar or thoracic cord injury, the portion of dorsal columns that undergoes wallerian degeneration is smaller than in the case of a cervical injury
  - Size effect is a function of the number of axons damaged by the injury & somatotopic arrangement of ascending fibers in the dorsal column tracts
  - Corticospinal tract contains fewer axons in distal than proximal regions; therefore smaller in the lumbar region
- Four stages of wallerian degeneration
  - 1: Physical degradation of axon with little biochemical change in myelin during first 4 weeks & results in no signal intensity abnormality
  - 2: At 4-14 weeks, myelin protein breakdown with intact myelin lipids (high lipid-protein ratio) results in hypointense T2 signal
  - 3: At > 14 weeks, myelin lipid breakdown, gliosis, and changes in water content and structure results in T2 hyperintense signal
  - 4: Several years after injury, there is volume loss
- Late sequela of acute demyelinating lesions, i.e., MS