Table of Contents
- Introduction
- Epidemiology
- Etiology
- Clinical Presentation
- History
- Examination
- Table 1: Clinical Signs and Reflexes
- Investigations
- Radiological Investigations
- Laboratory Investigations
- Conduction Studies
- Differential Diagnoses
- Table 1: Differential Diagnosis
- Diagnostic criterion
- Inclusion Criterion
- Exclusion Criterion
- Prognostic factors
- Management
- Pharmacological Management
- Rehabilitation
- Disease Complications
- Conclusion
- Further Reading
- Bibliography
Primary Category
Neuroimmunology
P-Category
Secondary Category
S-Category
Authors:
Introduction
- Inflammatory disorder in which injury to spinal cord results in rapid onset of neurological symptoms such as weakness, sensory loss and autonomic dysfunction.
Epidemiology
- The annual incidence of transverse myelitis ranges from 1.34 to 4.60 cases per million.
- Transverse myelitis has bimodal peak at:
- 10-19 years of age
- More predominant in female
- 30-39 years of age
- Older patients(more than 50) are more prone to develop spinal cord infarction.
It is associated with:
- Spinal cord infarct
Etiology
- Trauma to spinal cord
- Vaccinations in children
- Viral Infections
- Immunocompromised State
- Carcinoma
- Autoimmune disease
- Systemic Lupus Erytheromatosis
- Sjogren Syndrome
- Anti phospholipid Syndrome
- Sarcoidosis
- Bechet Disease
- Multiple Sclerosis
- Devic Syndrome
- Idiopathic(15-30%)
Clinical Presentation
- It has insidious progressive course. It depends upon area of spinal cord involvement.
- Detailed in the following chapter
History
- Development of sensory, motor, or autonomic dysfunction attributable to spinal cord
- Bilateral signs and/or symptoms
- Weakness of the limbs
- Stiffness of the limbs
- Sensory Impairments
- Numbness of limb
- Tingling of limb
- Bowel dysfunction (constipation)
- Bladder Dysfunction (urinary incontinence)
- Pain
Examination
- Clearly defined sensory level
- Increased reflexes
- Decrease muscle strength
- Spastic gait
Hypo-reflexia can occur with transverse myelitis in the setting of spinal shock; can be easily confused with peripheral disorders. Hence acute presentations should follow spine imaging to rule out acute myelopathy like transverse myelitis.
Table 1: Clinical Signs and Reflexes
Table 1: Clinical Signs and Reflexes
Reflexes / sign
Lesion Level of Spinal Cord
Description
C7, C8, T1)
Flexion and adduction of the thumb and flexion of the index finger with snapping of middle finger; usually more specific if unilateral or bilateral with hyperreflexia
Investigations
Radiological Investigations
- Magnetic Resonance Imaging(MRI) is investigation of choice.
- Gadolinium enhancement
- If none of the inflammatory criteria is met at symptom onset (including CSF finding and MRI finding), repeat MRI and LP evaluation between 2-7 days following symptom onset
Laboratory Investigations
- Usual blood Counts( CBC, ESR, LFT, RFT, Serum Electrolytes)
- CSF pleocytosis or elevated IgG index
- Anti nuclear antibodies
- Anti double stranded DNA antibodies
- Anti Sm antibodies
- Serum B12, methylmalonic acid
- VDRL
Conduction Studies
They are used to differentiate transverse myelitis from nervous pathology like Guillain-Barre Syndrome.
- EMG/NCS: absent H-reflex and prolonged latency or absent F-waves in early GBS
Differential Diagnoses
Table 1: Differential Diagnosis
Table 1: Differential Diagnosis
Diseases
Typical Location
Length of segments involved
Onset
MRI features
Other Comments
Cervical or thoracic spine along with lesions in brain
Short peripheral lesions in dorsal/lateral columns
Acute/subacute with contrast enhancement and chronic/progressive/fluctuating with T2 and T1 changes
Post contrast pattern: Ring like, homogeneous. T2 white matter hyperintensity <2 segments and <50% diameter.
Dissemination in space and time; meeting McDonald Criteria
Thoracic
Long cord lesion
Chronic/progressive
Symmetric T2 hyperintensity in the posterior and lateral columns; no contrast enhancement
Gastric bypass, malabsorption
Cervical or thoracic
Long segment
Hyperacute/acute
Linear strip, owl eye
Vascular Risk Factors
Cervical or thoracic
Variable
Variable
Almost Universal: Linear dorsal subpial/trident enhancement
Lung/eyes/skin involvement; biopsy to confirm
Cervical or thoracic
tract-specific lesion, especially gadolinium enhancing
Variable
usually lateral tracts
Antineuronal antibody testing
Cervical more common
Long or short T2 lesion
Faint or no enhancement; conus involvement may suggest MOG-Ab T1 hypo- and T2 hyperintense
Optic neuritis; brainstem symptoms
Thoracic level more common
Longitudinally extensive T2 lesion (≥3 vertebral segments)
Variable (hyperacute in AQP4-Ig positive cases only)
Central lesion with grey matter or holocord involvement
optic neuritis and area postrema involvement
*
Coexisting deep gray brain lesions
Commonly diffuse lesions
Altered mental status, more common in children
Variable
Variable
Acute
Leptomeningeal enhancement
Recent tick bite/rash; IV drug use
Variable
Variable
Acute/subacute
Predominantly central grey matter
Zoster rash, genital herpes, endemic region for enterovirus
*
*
Acute/subacute
White matter nodules or target lesions on axial cuts
Marked pleocytosis and raised protein on CSF
Diagnostic criterion
Inclusion Criterion
- Neurologic impairment attributable to the spinal cord
- Bilateral symptoms
- Clearly defined sensory level
- Exclusion of extra-axial compressive etiology by neuroimaging(MRI)
- Evidence of inflammation in the spinal cord (CSF cells or IgG index, or MRI gadolinium enhancement) seen at onset or within 7 day
- Progression to nadir between 4 hour and 21 day following the onset of symptoms (if patient awakens with symptoms, symptoms must become more pronounced from point of awakening)
Exclusion Criterion
- History of radiation to the spine within 10 year
- Clear arterial distribution clinical deficit consistent with thrombosis of the anterior spinal artery
- Abnormal flow voids on the spinal cord
- Serologic or clinical evidence of systemic autoimmune disease
- CNS manifestations of infectious etiology (eg, syphilis, Lyme, HIV, HTLV-1, Mycoplasma)
- Brain MRI lesions suggestive of multiple scleroma
- History of Optic Neuritis
Prognostic factors
1/3 of patients recover with little to no sequelae, 1/3 are left with moderate degree of permanent disability, and 1/3 have severe disabilities
Following are poor prognostic Factors:
- Time to maximal deficit of <24 h
- Back pain
- Requirement of respiratory Support
- Spinal shock
- A higher anatomical spinal lesion
- Complete paraplegia
Management
First monitoring of vital signs, respiratory rate is done then we can use following:
Pharmacological Management
- High dose IV methyl prednisolone 2.5–3g for 3-5 days
- Followed by oral prednisolone starting at 1 mg/kg/day.
- Taper steroid over 1-3 months
- Plasmapheresis for severe attack
- IV cyclophosphamide
- Azathioprine prevent relapses
Rehabilitation
Physical, mental, and vocational rehabilitation can be achieved through multi-disciplinary approach:
- Strengthening muscle technique
- Ankle foot orthoses
- Functional Electrical Stimulator device
Disease Complications
Following are complications due to spinal cord dysfunction:
- Spasticity
- Constipation
- Ileus
- Impaired thermoregulation
- Gaseous Distension
- Neuropathic pain
- Bladder Dysfunction
- Sexual Dysfunction
- Anxiety and Depression
Conclusion
- It needs immediate treatment.
- Transverse Myelitis is a serious spinal cord injury and has catastrophic implications.
- There are multiple triggers of transverse myelitis such as infections, auto-immune Diseases and vaccinations
Further Reading
Frohman, E. M., & Wingerchuk, D. M. (2010). Transverse myelitis. New England Journal of Medicine, 363(6), 564-572.
Bibliography
- Paul, Robert H.; Cohen, Ronald; Ott, Brian R.; Salloway, Stephen (2002). Proposed diagnostic criteria and nosology of acute transverse myelitis. Neurology, 59(4), 499–505. doi:10.1212/wnl.59.4.499
- Beh, S. C., Greenberg, B. M., Frohman, T., & Frohman, E. M. (2013). Transverse myelitis. Neurologic clinics, 31(1), 79–138. https://doi.org/10.1016/j.ncl.2012.09.008
- Lim P. (2020). Transverse Myelitis. Essentials of Physical Medicine and Rehabilitation, 952–959. https://doi.org/10.1016/B978-0-323-54947-9.00162-0
- Frohman, E. M., & Wingerchuk, D. M. (2010). Transverse myelitis. New England Journal of Medicine, 363(6), 564-572.
- Borchers, A. T., & Gershwin, M. E. (2012). Transverse myelitis. Autoimmunity reviews, 11(3), 231-248.
- Krishnan, C., Kaplin, A. I., Deshpande, D. M., Pardo, C. A., & Kerr, D. A. (2004). Transverse myelitis: pathogenesis, diagnosis and treatment. Front Biosci, 9(1483), 99.
- Kitley, J. L., Leite, M. I., George, J. S., & Palace, J. A. (2012). The differential diagnosis of longitudinally extensive transverse myelitis. Multiple Sclerosis Journal, 18(3), 271-285.
- Goh, C., Desmond, P. M., & Phal, P. M. (2014). MRI in transverse myelitis. Journal of Magnetic Resonance Imaging, 40(6), 1267-1279.
- West, T. W. (2013). Transverse myelitis—a review of the presentation, diagnosis, and initial management. Discovery medicine, 16(88), 167-177.
- Sepúlveda, M., Blanco, Y., Rovira, A., Rio, J., Mendibe, M., Llufriu, S., ... & Saiz, A. (2013). Analysis of prognostic factors associated with longitudinally extensive transverse myelitis. Multiple Sclerosis Journal, 19(6), 742-748.Chicago0
- Scott, T. F. (2007). Nosology of idiopathic transverse myelitis syndromes. Acta neurologica scandinavica, 115(6), 371-376.
- Syme Jr, J. A., & Kelly Jr, J. J. (1994). Absent F‐waves early in a of transverse myelitis. Muscle & Nerve: Official Journal of the American Association of Electrodiagnostic Medicine, 17(4), 462-465.
- Inslicht, D. V., Stein, A. B., Pomerantz, F., & Ragnarsson, K. T. (1998). Three women with lupus transverse myelitis: case reports and differential diagnosis. Archives of physical medicine and rehabilitation, 79(4), 456-459.
- Mariano, R., Flanagan, E. P., Weinshenker, B. G., & Palace, J. (2018). A practical approach to the diagnosis of spinal cord lesions. Practical neurology, 18(3), 187-200.
- Jacob, A., & Weinshenker, B. G. (2008, February). An approach to the diagnosis of acute transverse myelitis. In Seminars in neurology (Vol. 28, No. 01, pp. 105-120). © Thieme Medical Publishers.
- (2005). AUTOIMMUNE TRANSVERSE MYELITIS. CONTINUUM: Lifelong Learning in Neurology, 11 (3, Spinal Cord Disorders), 25-45. doi: 10.1212/01.CON.0000293719.78615.94.
- Chiriboga, S. L., & Flanagan, E. P. (2021). Myelitis and other autoimmune Myelopathies. CONTINUUM: Lifelong Learning in Neurology, 27(1), 62-92.
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