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Abstract Details

Imaging analysis differentiates vascular versus inflammatory myelopathies in children
Child Neurology and Developmental Neurology
P6 - Poster Session 6 (11:30 AM-1:00 PM)
15-001

Vascular myelopathy in children is a rare condition that may be difficult to distinguish clinically from inflammatory myelopathy.Identification of features to distinguish these two conditions may help guide appropriate diagnosis and treatment and lead to better outcomes. 

To compare MRI imaging features in children with acute vascular myelopathies (VM) to children with acute inflammatory myelopathies (IM).

We included patients with myelopathy under 21 years of age referred to the Johns Hopkins Transverse myelitis center between 2010-2017. After detailed review, the treating neurologists classified the suspected etiology of each case as VM, IM or other. MRI images of brain and spine obtained at initial presentation and follow-up were then reviewed by a neuroradiologist who was blinded to the diagnosis. The analysis examined number of spinal cord levels and axial topography (white matter tracts and gray matter) affected at each level. Brain MRIs were analyzed qualitatively.

43 children with acute myelopathies were identified. 9 of 43 were classified as vascular etiology(mean age at onset was 14 years [IQR 13-16 ]) while 34 were classified as inflammatory (mean age 8 ys [ IQR 4-13 ]).  At initial presentation, involvement of cord segments T6- T10 was most common in the VM. Lack of enhancement was a prominent feature in VM. IM did not have regional predilection. Brain MRI involvement was an important feature in cases of IM.  LETM lesions were more common in the inflammatory group compared with vascular group. In the inflammatory group involvement of both gray and white matter in the same level was more common compared to vascular group.

Comparison of the images between VM with other etiologies showed significant differences as there was prominent gray matter and thoracic cord involvement.  Identification of T2 hyperintensities at the T6-T10 levels at initial presentation may point toward vascular etiology. 

Authors/Disclosures
Maria A. Garcia-Dominguez, MD (UMass Memorial Medical Center)
PRESENTER
Dr. Garcia-Dominguez has nothing to disclose.
Laura S. Munoz-Arcos, MD (Johns Hopkins Hospital) No disclosure on file
Eliza M. Gordon-Lipkin, MD (Kennedy Krieger Institute) No disclosure on file
Paula Barreras, MD (Cedars-Sinai Medical Center) The institution of Dr. Barreras has received research support from Foundation for Sarcoidosis Research. The institution of Dr. Barreras has received research support from 好色先生.
Olwen Murphy, MD (Johns Hopkins Hospital) Dr. Murphy has nothing to disclose.
No disclosure on file
No disclosure on file
Luisa A. Diaz-Arias, MD (Luisa Diaz Arias) Dr. Diaz-Arias has nothing to disclose.
Carlos A. Pardo-Villamizar, MD (Johns Hopkins U, Med Dept of Neurology) The institution of Dr. Pardo-Villamizar has received research support from National Institutes of Health. The institution of Dr. Pardo-Villamizar has received research support from Bart McLean Fund for Neuroimmunology Research .