Transverse Myelitis: Difference between revisions
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Lumbar puncture is used to look for surrogate markers for inflammation in the cerebrospinal fluid (CSF).<br> | Lumbar puncture is used to look for surrogate markers for inflammation in the cerebrospinal fluid (CSF).<br> | ||
== Management | == Medical Management<br> == | ||
Treatments are intended to reduce spinal cord inflammation and alleviate symptoms<ref>Scott TF, Frohman EM, De Seze J, Gronseth GS, Weinshenker BG. Evidence-based guideline: clinical evaluation and treatment of transverse myelitis: report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology 77(24):2128-2134, 2011.</ref><ref>Krishnan C, Kaplin AI, Deshpande DM, Pardo CA, Kerr DA. Transverse Myelitis: pathogenesis, diagnosis and treatment. Front Biosci 9:1483-1499, 2004</ref>: | Treatments are intended to reduce spinal cord inflammation and alleviate symptoms<ref>Scott TF, Frohman EM, De Seze J, Gronseth GS, Weinshenker BG. Evidence-based guideline: clinical evaluation and treatment of transverse myelitis: report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology 77(24):2128-2134, 2011.</ref><ref>Krishnan C, Kaplin AI, Deshpande DM, Pardo CA, Kerr DA. Transverse Myelitis: pathogenesis, diagnosis and treatment. Front Biosci 9:1483-1499, 2004</ref>: | ||
Revision as of 23:10, 27 July 2015
Original Editor - Wendy Walker
Lead Editors Wendy Walker
Introduction
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Transverse Myelitis (TM), AKA Acute Transverse Myelitis (ATM) is a rare neurological disorder of the spinal cord, caused by inflammation and occurring across one spinal segment, leading to severe motor, sensory and autonomic dysfunction[1].
The term Transverse Myelitis (TM) was first coined in 1948 by Dr Suchett-Kaye, an English neurologist. He uses this to describe a case of rapidly progressive paraparesis with a thoracic sensory level, occurring as a post-infectious complication of pneumonia.
In the MRI scan opposite, the TM lesion is the lighter, oval shape at center-right.
Epidemiology[edit | edit source]
The incidence of TM is 1 (severe) to 8 (mild) cases/million per year[2].
It occurs in adults and children, in both genders, and in all races.
A peak in incidence rates (the number of new cases per year) appears to occur between 10 and 19 years and 30 and 39 years.
Mechanism of Injury / Pathological Process
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The mechanism of injury is inflammation of the spinal cord causing damage to the myelin sheath of the nerves.
Clinical Presentation[edit | edit source]
- Sensory, motor, or autonomic dysfunction attributable to the spinal cord
- Bilateral signs and/or symptoms
- Clearly defined sensory level
The symptoms of TM include muscle weakness, paralysis, parasthesia, neuropathic pain, spasticity, as well as bladder, bowel and sexual dysfunction.
In some cases, symptoms progress over hours whereas in other instances, the presentation is over days. Neurologic function tends to decline during the 4-21 day acute phase, while eighty-percent of cases reach their maximal deficit within 10 days of symptom onset. At its worst point, 50% of individuals have lost all movements of their legs, 80-94% experience numbness, paresthesias or banding or girdling, and almost all have some degree of bladder dysfunction.
There is tremendous variability in the presentation of symptoms, which are based on the level of the spinal cord affected and on the severity of the damage to the myelin and the neurons in the spinal cord.
Some patients recover from transverse myelitis with minor or no residual problems.
Others suffer permanent impairments that affect their ability to perform ordinary tasks of daily living.
Most people will have only one episode of transversemyelitis.
A small percentage (10-20%) may have a recurrence.
Diagnostic Procedures[edit | edit source]
MRI and/or CT scanning are invariably used in diagnosing TM. Up to 40% of cases have no findings on MRI[3].
Lumbar puncture is used to look for surrogate markers for inflammation in the cerebrospinal fluid (CSF).
Medical Management
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Treatments are intended to reduce spinal cord inflammation and alleviate symptoms[4][5]:
- Corticosteroids given intravenously
- Plasmapheresis[6] - for moderate to severe cases, or those who do not respond to steroids after 3-5 days
- Immunosuppresent medication
Differential Diagnosis
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The most common etiologies to be distinguished from idiopathic acute transverse myelitis are:
Parainfectious myelitis
NMO (Devic's disease)
Myelitis related to systemic disease, such as systemic lupus erythematosis
Compression of spinal cord caused by trauma eg. vertebral fractures
Epidural or subdural hematoma
Epidural and/or paraspinal abscess
Tumour
Prognosis[edit | edit source]
Some case series have estimated that approximately one third of patients recover with few or no lasting effects; another third have a moderate degree of residual disability, and one third remain severely disabled[7][8].
Resources
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add appropriate resources here
Case Studies[edit | edit source]
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Recent Related Research (from Pubmed)[edit | edit source]
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References[edit | edit source]
References will automatically be added here, see adding references tutorial.
- ↑ Proposed diagnostic criteria and nosology of acute transverse myelitis. Neurology. 2002;59 (4): 499-505
- ↑ Berman M, Feldman S, Alter M, Zilber N, Kahana E. Acute transverse myelitis: incidence and etiologic considerations. Neurology 1981;31:966–971
- ↑ 8. Scotti G, Gerevini S. Diagnosis and differential diagnosis of acute transverse myelopathy. The role of neuroradiological investigations and review of the literature. Neurol. Sci. 2001;22 Suppl 2 : S69-73
- ↑ Scott TF, Frohman EM, De Seze J, Gronseth GS, Weinshenker BG. Evidence-based guideline: clinical evaluation and treatment of transverse myelitis: report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology 77(24):2128-2134, 2011.
- ↑ Krishnan C, Kaplin AI, Deshpande DM, Pardo CA, Kerr DA. Transverse Myelitis: pathogenesis, diagnosis and treatment. Front Biosci 9:1483-1499, 2004
- ↑ Llufriu S, Castillo J, Blanco Y, Ramio-Torrenta L, Rio J, Valles M, Lozano M, Castella MD, Calabia J, Horga A, Graus F, Montalban X, Saiz A. Plasma exchange for acute attacks of CNS demyelination: Predictors of improvement at 6 months. Neurology 73(12):949-953, 2009
- ↑ Berman M, Feldman S, Alter M, Zilber N, Kahana E. Acute transverse myelitis: incidence and etiologic considerations. Neurology 31(8):966-971, 1981
- ↑ Transverse Myelitis Consortium Working Group (TMCWG). Proposed diagnostic criteria and nosology of acute transverse myelitis. Neurology 59(4):499-505, 2002
