Visualization and MRI Timing
The primary tool in the diagnosis of acute transverse myelitis is magnetic resonance imaging. A typical MRI appearance includes diffuse hyperintensity on T2-weighted images (T2WI), accompanied by marked edema and enlargement of the spinal cord contours. It is important to understand that the inflammatory process can involve multiple segments simultaneously.
In the acute phase of the disease, pathological lesions tend to demonstrate patchy contrast enhancement (patchy enhancement). However, a major diagnostic pitfall exists: at the very earliest stages of symptom development, the scan may remain within normal limits. In such situations, the standard procedure is a repeat contrast-enhanced MRI 2–7 days after the onset of clinical manifestations.
Radiological dynamics are closely linked to the patient's condition. Improvement on MRI or complete resolution of lesions directly correlates with the regression of neurological deficit. Moreover, if the patient has already started receiving specific treatment, scanning may not reveal any pathological changes at all.
Analysis of typical scans
Detailed analysis of images from a patient with acute transverse myelitis reveals the following characteristic features:
- Sagittal projection (T2WI): a diffuse zone of hyperintense signal is visualized, extending not to a single level, but across several adjacent segments of the spinal cord.
- Sagittal projection (T1WI before and after contrast): the study proves an active inflammatory process due to clearly visible contrast agent accumulation directly within the lesion itself.
- Axial projection: on T2WI and post-contrast T1WI, it is clearly visible that the lesion is massive—occupying more than 2/3 of the total cross-sectional area of the spinal cord.
Differential Diagnosis: CNS Sarcoidosis
The main objective when identifying a transverse myelitis pattern is to rule out other diseases. One such pathology is sarcoidosis—a systemic disease of unknown etiology whose morphological substrate is non-caseating granulomatosis (non-caseating granulomatosis).
Although CNS sarcoidosis is found at autopsy in 25% of patients with this diagnosis, clinically significant spinal cord involvement is extremely rare. The clinical presentation is non-specific and depends entirely on the precise localization of the granulomas.
On MRI, neurosarcoidosis manifests as extended T2 hyperintensity and fusiform enlargement of the spinal cord (fusiform cord enlargement). Lesions are divided into two categories:
- Enhancing: associated with acute neurological deficit and respond well to corticosteroid therapy.
- Non-enhancing: resembling multiple sclerosis plaques, representing irreversible consequences of inflammation (sequelae) and causing persistent chronic deficit.
Specific Enhancement Patterns
It is the pattern of contrast enhancement that distinguishes sarcoidosis from other causes of myelitis, such as neuromyelitis optica (NMO). While NMO is typically characterized by patchy incomplete ring enhancement, spinal sarcoidosis features linear and subpial enhancement (linear and subpial enhancement).
Radiologists identify several specific signs of sarcoidosis:
- Sagittal slices frequently reveal dorsal subpial linear enhancement.
- Axial slices may demonstrate the 'trident pattern' ('trident pattern'), which results from enhancement of the central canal.
- Ventral subpial contrast accumulation—the 'braid-like sign' ('braid-like sign')—is also encountered on axial scans.
An important temporal marker is that in sarcoidosis, the ability of lesions to accumulate contrast may persist for more than 3 months even during steroid treatment, which is completely uncharacteristic of ordinary transverse myelitis.
Comprehensive Diagnostic Confirmation
Diagnosing isolated neurosarcoidosis based solely on spinal cord MRI is practically impossible. A comprehensive approach and the search for systemic manifestations are required. The diagnosis is confirmed upon detecting:
- Signs of brain involvement (hypothalamic-pituitary axis involvement, dural masses, or leptomeningeal contrast enhancement).
- Elevated serum angiotensin-converting enzyme (ACE) levels.
- Positive Kviem test results (Kviem test).
- Typical granulomatous changes on chest CT or PET/CT.
Also, when analyzing changes on spinal MRI, one should keep demyelinating polyneuropathies in mind. Although these are peripheral nervous system pathologies, they can affect intradural nerves and cauda equina roots (cauda equina), which will be clearly visualized on lumbosacral scans.
Briefly: answers to topical questions
What anatomical structures are affected in demyelinating polyneuropathies visible on lumbosacral MRI?
In demyelinating polyneuropathies, lumbosacral MRI visualizes nerve involvement and concomitant muscle changes.
- Cauda equina (cauda equina) and other intradural nerves — become thickened and enhance with contrast agent.
- Extradural portions of nerves — also demonstrate diffuse contrast enhancement.
- Lumbar muscles (psoas) and pelvic muscles — exhibit signs of acute denervation: asymmetry, atrophy, T2 hyperintensity, and contrast enhancement.
What are the main histological differences of non-caseating granulomatosis in sarcoidosis?
The main histological distinction of non-caseating granulomatosis in sarcoidosis is the absence of caseous necrosis within the granulomas.
| Sign | Sarcoidosis | Tuberculosis |
|---|---|---|
| Morphological substrate | Granulomas in various organs and tissues | Epithelioid cell granuloma (tubercles) |
| Cellular composition | Epithelioid cells, giant cells, macrophages | Epithelioid cells, lymphocytes, macrophages, Pirogov-Langhans giant cells |
| Necrosis | Caseous necrosis is absent | Caseous necrosis in the center |
The absence of caseous necrosis has differential diagnostic significance and contrasts with tuberculous granulomas.
To remember the specific patterns of neurosarcoidosis on axial MRI, imagine a mermaid: she has a 'trident' (central canal enhancement) and a braided 'braid' (ventral subpial enhancement).
Class and exam questions
How to differentiate a fresh neurosarcoidosis lesion from an old lesion on MRI?
Fresh lesions causing acute deficit actively accumulate contrast and respond to steroids. Old lesions (sequelae of inflammation) do not accumulate contrast and lead to irreversible neurological impairment.
Are residual changes always visible on MRI after a past episode of acute transverse myelitis?
No, not always. Improvement or complete resolution of radiological changes directly correlates with clinical recovery, and against the background of successful treatment, the picture may become completely normal.
What else to study on this topic
- Contrast enhancement patterns in neuromyelitis optica (NMO)
- Pathophysiology of non-caseating granulomatosis and the mechanism of ACE elevation
- The role of the Kviem test in modern diagnostics
- MRI signs of cauda equina involvement in demyelinating polyneuropathies
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