Clinical Trial Finder

Inclusion Criteria:

Diagnostic criteria include: 1. Sensory, motor, or autonomic dysfunction originating from the spinal cord. 2. T2 hyperintense signal changes on MRI. 3. No evidence of a compressive lesion. 4. Bilateral signs/symptoms. 5. Clearly defined sensory level. 6. Evidence of inflammatory process demonstrated by gadolinium enhancement on MRI, cerebrospinal fluid (CSF) analysis showing pleocytosis, or elevated immunoglobulin G (IgG) index. 7. Progression to nadir between 4 hours and 21 days.

Exclusion Criteria:

1. An alternative diagnosis became apparent any time along the study period including evidence of compressive lesion in MRI, history of previous radiation to the spine within the past 10 years, clinical deficit consistent with thrombosis of the anterior spinal artery or Abnormal flow voids on the surface of the spinal cord consistent with AVFs. 2. Incomplete clinical, laboratory or radiographic data. 3. Patients refused to sign the informed consent

Acute transverse myelitis (ATM) is an inflammatory condition of the spinal cord, covering the entire cross section and spreading on two or more vertebral segments, without evidence of a compressive lesion.1 This shows clinically as acute or subacute spinal cord dysfunction resulting in paresis, sensory level, and autonomic (bladder, bowel, and sexual) impairment below the level of the lesion.2 ATM is typically classified as either idiopathic ATM where no causative factor found or disease- associated transverse myelitis.3 Disease- associated transverse myelitis results from heterogenous pathophysiologic causes including infectious, parainfectious, paraneoplastic, drug/toxin-induced, systemic autoimmune disorders (SAIDs), Neurosarcoidosis and acquired demyelinating diseases like multiple sclerosis (MS) or neuromyelitis optica (NMO).4 5 6 The annual incidence of ATM ranges from 1.34 to 4.60 cases per million,7 8 but increases to 24.6 cases per million if acquired demyelinating diseases like MS are included.9 TM can occur at any age, although a bimodal peak in incidence occurs in the second and fourth decades of life.7 8 10 This broad differential can overlap with noninflammatory myelopathies and can be very challenging for clinicians to navigate, causing delays in diagnosis or treatment.11 MRI is essential to rule out compressive causes of these neurologic manifestations, such as tumour, epidural abscess, herniated disc, stenosis of the medullary canal or hematoma. It is also used to show the extension of the lesion and for follow-up progress of these lesions after treatment.12 The lack of large-scale and longitudinal studies has hindered the understanding of this complex disorder. Approximately 33% of patients recover with little to no lasting deficits, 33% have a moderate degree of permanent disability, and 33% are permanently disabled.13 The disease is often a monophasic illness and will only not recur unless it is secondary to a chronic comorbid condition, highlight the need for early and prompt recognition of aetiology. Steroids and immunosuppression are the only potential treatments for ATM at this time, but there is potential for monoclonal antibody drugs that might alter the disease course if an autoinflammatory process was identified. Although individuals affected by ATM show residual neurologic deficits if they have not recovered to normal within 3-6 months, no report has considered earlier factors that might determine the prognosis of the illness. The objective of this study was to determine frequency of ATM and its different etiologies, clinical and radiological patterns, and the different prognostic factors associated in a large tertiary center in the south of Egypt with a goal to improve awareness of ATM to ensure prompt recognition and treatment