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Utility of MRI Enhancement Pattern in Myelopathies With Longitudinally Extensive T2 Lesions
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The authors of this study describe patterns of post–gadolinium spinal cord MRI enhancement that can reliably identify different etiologies of longitudinally extensive transverse myelitis. They identified 74 patients and found that raters consistently made the same diagnosis when utilizing post-gadolinium images (kappa = 0.76) but not T2-weighted patterns (kappa = 0.25); they also found that 74% of the patients in this study were initially misdiagnosed. The authors define enhancement patterns for anterior spinal cord infarction, paraneoplastic myelopathy, spondylotic myelopathy with enhancement, sarcoid myelopathy, anti–aquaporin-4-IgG neuromyelitis optic spectrum disorder, dural arteriovenous fistula, and intramedullary metastases.
- The authors note that misdiagnosis of spinal cord disorders is not benign, as certain treatments can worsen the underlying condition. These definitions are important for neurologists to recognize for accurate diagnosis and treatment.
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Patients with a longitudinally extensive transverse myelitis (LETM), defined as involving three or more vertebral segments of the spinal cord, can present with an acute or subacute onset of para- or tetraparesis, ataxia, sensory disturbance, neuropathic pain, or bowel and bladder dysfunction. For the clinician, there is an urgency to making a diagnosis because the sequelae from delayed or incorrect diagnosis or treatment of spinal cord pathology can lead to profound disability.1
The differential diagnosis of LETM is varied and includes demyelination and other autoimmune conditions, infection, granulomatous disease, spondylotic myelopathy, as well as metabolic, vascular, neoplastic, and paraneoplastic causes. Finding the correct diagnosis among so many potential causes is not always straightforward. The workup of a patient with LETM includes MRI of the brain and whole spine, CSF examination, serological investigations, including aquaporin-4 (AQP4)-IgG, myelin oligodendrocyte glycoprotein (MOG)-IgG, and, in some cases, CT-PET or spinal angiography. Biopsy of the spinal cord is reserved as a last resort because it can lead to permanent disability. For this reason, any clues to the etiology of an LETM that can be acquired without resorting to a tissue diagnosis are important.
Over the last 10 years, improvements in the recognition that different causes of LETM can have characteristic patterns on MRI have led to greater diagnostic certainty. In this paper, Mustafa and colleagues demonstrate that the yield of a correct diagnosis of an LETM by MRI is increased from 76% to 95% among blinded raters by the addition of a post-gadolinium sequence to a T2 sequence. Gadolinium is especially helpful in showing the dorsal subpial enhancement pattern of neurosarcoidosis, the “pancake” pattern seen with compressive myelopathy, and the ring-like enhancement pattern of AQP4-IgG seropositive neuromyelitis optica spectrum disorder. Alarmingly, 74% of patients with hallmark findings on their MRI had been misdiagnosed by their original clinician, a statistic that highlights the clinical relevance of the study.
This paper reinforces the importance of careful interpretation of MRI as the modern cornerstone of LETM diagnosis, and it provides MRI examples to help distinguish between a range of pathologies associated with LETM. Better diagnosis of LETM leads to the timely initiation of appropriate treatment, and, just as importantly, avoids the potentially hazardous complications of inappropriate treatment.
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