Transverse myelitis (TM) is a rare neurological disorder defined as acute inflammation affecting the spinal cord. This inflammation damages the myelin, the protective covering around nerve fibers, disrupting the flow of electrical signals between the brain and the rest of the body. Symptoms, which often include weakness, sensory changes, and bladder dysfunction, develop rapidly over hours or days. Due to the nonspecific nature of these symptoms, Magnetic Resonance Imaging (MRI) of the spine is the primary diagnostic tool used in the initial evaluation.
The Necessity of Spinal MRI
Immediate imaging of the entire spine is required for any patient presenting with acute myelopathy. The primary purpose of the MRI is to urgently exclude mechanical compression of the spinal cord. Conditions such as a herniated disc, spinal tumor, or an epidural abscess can mimic TM symptoms but require immediate surgical intervention to prevent permanent paralysis.
The high-resolution images produced by the MRI allow physicians to clearly visualize the spinal cord parenchyma and surrounding structures. By using T1- and T2-weighted sequences, with and without an injected contrast agent, the MRI can distinguish between a non-compressive inflammatory lesion and a surgical emergency. Once a compressive cause is ruled out, the imaging confirms inflammation and characterizes the lesion.
Key Radiological Features of Transverse Myelitis
The characteristic finding of TM on MRI is a bright signal, known as T2 hyperintensity, within the spinal cord. This bright signal represents increased water content, indicating edema and inflammation within the affected segment. These lesions typically involve a large portion of the spinal cord’s cross-sectional area, often spanning more than two-thirds of its width.
A significant feature guiding diagnosis is the length of the inflammation along the spinal cord. TM is frequently characterized by Longitudinally Extensive Transverse Myelitis (LETM), defined as a lesion spanning three or more vertebral segments. While not exclusive to TM, this extensive length indicates a severe inflammatory process.
On axial images, the inflammation often shows a preference for the central gray matter. This pattern can sometimes produce a visual feature known as the “H-sign,” reflecting the shape of the gray matter on the scan. When an intravenous contrast agent like gadolinium is administered, the area of active inflammation may show enhancement. This enhancement occurs because inflammation temporarily breaks down the blood-brain barrier, allowing contrast material to leak into the tissue.
Differentiating TM from Related Conditions
Once a spinal cord lesion is confirmed, specific radiological patterns help differentiate TM from other demyelinating diseases. Multiple Sclerosis (MS) lesions tend to be shorter, spanning only one or two vertebral segments. MS lesions are also typically smaller and located peripherally, often along the surface of the spinal cord.
In contrast, Neuromyelitis Optica Spectrum Disorder (NMOSD) and Myelin Oligodendrocyte Glycoprotein Antibody Disease (MOGAD) frequently cause LETM, similar to idiopathic TM. NMOSD lesions, which are associated with the AQP4 antibody, often involve the entire cross-section of the cord and can be associated with more severe atrophy over time.
MOGAD lesions show a distinct tendency to involve the central gray matter, producing the axial H-sign more prominently than in NMOSD or MS. These lesions are also more likely to involve the conus medullaris (the bottom tip of the spinal cord). MOGAD lesions have a higher likelihood of resolving completely on subsequent follow-up MRIs compared to those seen in NMOSD.
Subsequent Diagnostic Testing
The spinal MRI confirms the presence, location, and characteristics of the myelitis, but it cannot identify the underlying cause of the inflammation. Therefore, additional non-imaging tests are necessary to classify the transverse myelitis as idiopathic, infectious, or associated with a specific autoimmune disorder.
A lumbar puncture (spinal tap) is performed to collect and analyze the Cerebrospinal Fluid (CSF) that surrounds the brain and spinal cord. CSF analysis can reveal an elevated white blood cell count (pleocytosis) or an increased IgG index, which are markers of inflammation within the central nervous system. The fluid is also tested to rule out infectious agents, such as viruses or bacteria, that could be causing the myelitis.
Blood tests are performed to search for specific antibodies that link the myelitis to a defined autoimmune condition. Testing for the Aquaporin-4 (AQP4) antibody and the Myelin Oligodendrocyte Glycoprotein (MOG) antibody is standard practice. The presence of these antibodies shifts the diagnosis from idiopathic TM to NMOSD or MOGAD, which significantly impacts long-term treatment and prognosis.