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Multiple Sclerosis, Transverse Myelitis, Tropical Spastic Paraparesis, Progressive Multifocal Leukoencephalopathy, Lyme Disease
Published in Jacques Corcos, Gilles Karsenty, Thomas Kessler, David Ginsberg, Essentials of the Adult Neurogenic Bladder, 2020
Michele Fascelli, Howard B. Goldman
Transverse myelitis (TM) is a clinical syndrome following an immune-mediated process causing neural injury to the spinal cord, and manifests varying degrees of weakness, sensory alterations, and autonomic dysfunction. Acute transverse myelitis (ATM) has an incidence of one to four cases per million people per year with bimodal prevalence between the ages of 10–19 and 30–39 years. ATM is commonly parainfectious. Classification is based on speed of symptom progression (acute, subacute, or chronic) or etiology (viral, bacterial, idiopathic, etc.).2,64–66
Cytomegalovirus
Published in Avindra Nath, Joseph R. Berger, Clinical Neurovirology, 2020
Other potential etiologies of transverse myelitis need to be excluded. While many viruses can cause transverse myelitis, the exact etiology is never established in many of these patients. The differential diagnosis also includes transverse myelitis secondary to multiple sclerosis or spinal cord ischemia. Ideally, CSF PCR for CMV is positive, but CSF viral culture or CSF/blood CMV antibody levels indicating CMV intrathecal antibody synthesis.
The nervous system and the eye
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
James A.R. Nicoll, William Stewart, Fiona Roberts
Transverse myelitis: This is a clinical rather than a pathological term and is used to describe an acute transverse lesion in the spinal cord in the absence of a compressive lesion. Causes include infarction, demyelination, caisson disease (decompression sickness), infection, or haemorrhage
Spinal cord involvement in COVID-19: A review
Published in The Journal of Spinal Cord Medicine, 2023
Ravindra Kumar Garg, Vimal Kumar Paliwal, Ankit Gupta
Acute transverse myelitis is clinically characterized by sensorimotor disturbances, bladder/bowel dysfunction, and/or autonomic dysfunction attributable to the spinal cord. Typically, it manifests as a rapid disease progression within a few hours to up to 21 days, with a sharp sensory affection level, bilateral pyramidal signs, and bladder/bowel dysfunction. While neuroimaging is not usually suggestive of compressive myelopathy, cerebrospinal fluid (CSF) examination may reveal inflammatory changes.1,2 Acute demyelinating diseases of the central nervous system, such as multiple sclerosis, neuromyelitis optica spectrum disorder, and acute disseminated encephalomyelitis are other frequently encountered causes of acute myelitis. Moreover, many viruses can be directly implicated in the etiopathogenesis of acute transverse myelitis, including varicella-zoster, herpes simplex, Epstein–Barr, West Nile, Dengue, Japanese encephalitis, Zika, influenza, echovirus & hepatitis B, mumps, measles, and rubella viruses. However, most often, it is difficult to differentiate between a viral-induced and immune-mediated transverse myelitis.2,3 Furthermore, there is an increasing number of reports that have linked the SARS-CoV-2 virus to the pathogenesis of acute transverse myelitis.4–6 The spinal cord involvement can result either from the direct invasion of the spinal cord, cytokine storm, or an autoimmune response.
Acute onset paraplegia in a case of granulomatosis with polyangitis (GPA) – an unusual complication
Published in Modern Rheumatology Case Reports, 2021
Debashis Maikap, Prasanta Padhan
Longitudinally extensive transverse myelitis (LETM) describes myelitis spanning three or more vertebral segments [5] that can cause quadriplegia, marked sensory dysfunction, autonomic instability, and respiratory failure in severe cases. Transverse myelitis symptoms develop rapidly over several hours to several weeks. When the maximal level of deficit is reached, approximately 50% of patients have lost all movements of their legs, virtually all patients have some degree of bladder dysfunction, and 80–94% of patients have numbness, paraesthesia or band like dysesthesias [6]. Transverse myelitis typically affects the mid-thoracic region in adults or the cervical region in children. A band-like tightening sensation (Girdle-like sensation) around the chest or abdomen usually seen in thoracic transverse myelitis and suggests involvement of the posterior columns of the spinal cord. As is typical of most spinal cord lesions, patients develop a horizontal sensory level that is almost always in the midthoracic region, below which they are numb [7]. Other causes include infection like herpes zoster& simplex, cytomegalovirus, demyelinating disease like multiple sclerosis, systemic disease (e.g. systemic lupus erythematosus [SLE], anti-phospholipid syndrome, Sjögren disease). It may also occur in compressive myelopathy like tumour, tuberculosis, neurosarcoidosis, thoracic discogenic pain syndrome (TDPS).
Transverse myelitis associated with yellow fever vaccination
Published in Baylor University Medical Center Proceedings, 2019
Kyle D. Bartol, Jose L. Aguirre, Salvatore V. Labruzzo, Russ P. Henriet
A 35-year-old active-duty man with no significant past medical history presented to the hospital with a 3-week history of progressively worsening urinary retention, sensory disturbances and weakness in both arms and legs, loss of balance, and difficulty ambulating. Examination revealed moderately decreased strength in the lower extremities, ascending sensory loss up to the level of the elbows and knees, and diffuse hyperreflexia without clonus. Within the last month he had received multiple predeployment vaccines (meningococcal, tetanus-diphtheria-pertussis, typhoid, and YF) and had a mild self-limited upper respiratory tract infection. Magnetic resonance imaging (MRI) of the brain showed nonspecific findings that may have been related to the patient’s clinical presentation (Figure 1). Multiple MRI examinations of the spine revealed longitudinally extensive transverse myelitis (Figure 2). An extensive workup for primary neurologic, infectious, and malignant etiologies was obtained. Pertinent results in cerebrospinal fluid (CSF) were lymphocytic pleocytosis (white blood cells 300 cells/mcL, lymphocytes 82%), elevated protein (147.24 mg/dL), qualitatively positive immunoglobulin M (IgM) antibodies to YF vaccine virus, and negative neuromyelitis optica-immunoglobulin G (NMO-IgG) antibodies (titer <1:1). The patient was started on high-dose intravenous corticosteroid therapy with suboptimal results. His treatment regimen was escalated to 5 days of plasmapheresis, which resulted in adequate improvement in symptoms. He was subsequently discharged to a neurologic rehabilitation center.