Frequency ,Etiology and Prognostic Factors of Acute Transverse Myelitis

Transverse Myelitis Clinical Trial

Official title:

Frequency ,Etiology and Prognostic Factors of Acute Transverse Myelitis in Neurology and Psychiatry Department, Assiut University

Clinical Trial Details — Status: Not yet recruiting

Administrative data

• NCT number: NCT06055998
• Other study ID #: acute transverse myelitis
• Status: Not yet recruiting
• Start date: December 2023
• Est. completion date: February 2026

Study information

• Verified date: September 2023
• Source: Assiut University
• Contact: Fouad E Fawaz, Resident
• Phone: +201030698686
• Email: fouadabdelrahman55[@]gmail.com
• Is FDA regulated: No
• Study type: Observational

Clinical Trial Summary

To identify the frequency of ATM and its different aetiologies, alongside the different clinical and radiological patterns and prognostic factors .

Description:

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

Recruitment information / eligibility

• Status: Not yet recruiting
• Enrollment: 50
• Est. completion date: February 2026
• Est. primary completion date: December 2024
• Accepts healthy volunteers: No
• Gender: All
• Age group: N/A and older

Eligibility

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

Related Conditions & MeSH terms

• Myelitis
• Myelitis, Transverse
• Transverse Myelitis

Intervention

Device:
• MRI
MRI SPINE

Locations

Country	Name	City	State
n/a

Sponsors (1)

Lead Sponsor	Collaborator
Assiut University

References & Publications (13)

Beh SC, Greenberg BM, Frohman T, Frohman EM. Transverse myelitis. Neurol Clin. 2013 Feb;31(1):79-138. doi: 10.1016/j.ncl.2012.09.008. — View Citation

Berman M, Feldman S, Alter M, Zilber N, Kahana E. Acute transverse myelitis: incidence and etiologic considerations. Neurology. 1981 Aug;31(8):966-71. doi: 10.1212/wnl.31.8.966. — View Citation

Bhat A, Naguwa S, Cheema G, Gershwin ME. The epidemiology of transverse myelitis. Autoimmun Rev. 2010 Mar;9(5):A395-9. doi: 10.1016/j.autrev.2009.12.007. Epub 2009 Dec 24. — View Citation

Christensen PB, Wermuth L, Hinge HH, Bomers K. Clinical course and long-term prognosis of acute transverse myelopathy. Acta Neurol Scand. 1990 May;81(5):431-5. doi: 10.1111/j.1600-0404.1990.tb00990.x. — View Citation

de Seze J, Stojkovic T, Breteau G, Lucas C, Michon-Pasturel U, Gauvrit JY, Hachulla E, Mounier-Vehier F, Pruvo JP, Leys D, Destee A, Hatron PY, Vermersch P. Acute myelopathies: Clinical, laboratory and outcome profiles in 79 cases. Brain. 2001 Aug;124(Pt — View Citation

Debette S, de Seze J, Pruvo JP, Zephir H, Pasquier F, Leys D, Vermersch P. Long-term outcome of acute and subacute myelopathies. J Neurol. 2009 Jun;256(6):980-8. doi: 10.1007/s00415-009-5058-x. Epub 2009 Feb 28. — View Citation

Dumic I, Vitorovic D, Spritzer S, Sviggum E, Patel J, Ramanan P. Acute transverse myelitis - A rare clinical manifestation of Lyme neuroborreliosis. IDCases. 2018 Dec 29;15:e00479. doi: 10.1016/j.idcr.2018.e00479. eCollection 2019. — View Citation

Frohman EM, Wingerchuk DM. Clinical practice. Transverse myelitis. N Engl J Med. 2010 Aug 5;363(6):564-72. doi: 10.1056/NEJMcp1001112. No abstract available. — View Citation

Harizi E, Shemsi K, Kola E, Hyseni F, Kola I, Siddique MA, Sadeque J, Decka A, Dervishi M, Nasir F, Capi L, Ayala I, Ghosh AS, Swarna SS, Musa J, Ahmetgjekaj I. Transverse myelitis in a 26-year-old male with tuberculosis. Radiol Case Rep. 2022 Aug 1;17(10 — View Citation

Jacob A, Weinshenker BG. An approach to the diagnosis of acute transverse myelitis. Semin Neurol. 2008 Feb;28(1):105-20. doi: 10.1055/s-2007-1019132. — View Citation

Murthy JM, Reddy JJ, Meena AK, Kaul S. Acute transverse myelitis: MR characteristics. Neurol India. 1999 Dec;47(4):290-3. — View Citation

Transverse Myelitis Consortium Working Group. Proposed diagnostic criteria and nosology of acute transverse myelitis. Neurology. 2002 Aug 27;59(4):499-505. doi: 10.1212/wnl.59.4.499. — View Citation

Wingerchuk DM. Postinfectious encephalomyelitis. Curr Neurol Neurosci Rep. 2003 May;3(3):256-64. doi: 10.1007/s11910-003-0086-x. — View Citation

* Note: There are 13 references in all — Click here to view all references

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	Determine the relative frequency of different aetiologies of ATM among Southern Egyptian patients attending Assiut University Hospital	All cases of all ages and both sex attending the neurology and psychiatry department at Assiut University Hospital during one year period who meet the diagnostic criteria of ATM according to the TM; Consortium Working Group (TMCWG) in 2002 will be recriuted.1 Diagnostic criteria include: Sensory, motor, or autonomic dysfunction originating from the spinal cord; T2 hyperintense signal changes on MRI; No evidence of a compressive lesion; Bilateral signs/symptoms.; Clearly defined sensory level.; Evidence of inflammatory process demonstrated by gadolinium enhancement on MRI, cerebrospinal fluid (CSF) analysis showing pleocytosis, or elevated immunoglobulin G (IgG) index.; Progression to nadir between 4 hours and 21days.	1 year