Fetzer Daniel,  Aaen Gregory,  Udochukwu Oyoyo,  Achiriloaie Adina

Final Pr. ID: Paper #: 164

Pediatric multiple sclerosis (MS) is difficult to diagnose at presentation, and the clinical features often overlap those of acute disseminated encephalomyelitis (ADEM), neuromyelitis optica or clinically isolated syndrome. Established criteria for diagnosing MS are less reliable in pre-pubescent children. We seek to qualitatively and quantitatively define the MRI features of pediatric MS compared to ADEM at initial presentation. Read More

Authors:  Fetzer Daniel , Aaen Gregory , Udochukwu Oyoyo , Achiriloaie Adina

Keywords:  Multiple sclerosis, ADEM, white matter disease

Lorentz Liam

Final Pr. ID: Poster #: CR-020

Introduction

Leukodystrophy with vanishing white matter (VWM), previously known as childhood ataxia with central hypomyelination (CACH) is considered one of the most prevalent inherited white matter disorders.<span style="font-size:11px"> </span>The incidence of VWM is not well defined, however, there appears to be a predilection for Caucasians.

Clinical history

We report a 20 month old male with a two week history of right hemiplegia and ataxic gait. Infant is well grown with no previous medical or familial history of note. Normal development and unremarkable birth history.

MRI findings

Brain MRI demonstrates multiple T2 hyperintense periventricular deep white matter cavitating lesions with cortical sparing (fig 2, top arrow). These lesions were of CSF signal intensity on FLAIR and demonstrated differential water content; central hypointensity with peripheral hyperintesity (fig 3). There is no restricted diffusion centrally, however, the peripheral areas that are hyperintense on FLAIR were restricting. The temporal lobes are unaffected. Single, non-enhancing cerebellar white matter hyperintensity (non-cystic) within right hemisphere (fig 2, bottom arrow); no cerebellar or brainstem atrophy. White matter involvement of the corpus callosum with outer rim sparing (fig 1). There is no hydrocephalus and no basal ganglia involvement. Read More

Authors:  Lorentz Liam

Keywords:  Leukodystrophy, Vanishing White Matter

Guillen Gutierrez Cinthia,  Rodriguez Garza Claudia,  Elizondo Riojas Guillermo,  Hernández Grimaldo Edgar,  Garza Acosta Andrea

Final Pr. ID: Poster #: EDU-018 (S)

Myelination it's a dynamic process through which a lipoprotein sheath that covers the axons develops. It begins at the 4th month of gestation and reaches its maximum at 24 months and occurs from caudal to rostral, from dorsal to ventral, from central to peripheral

Normal myelination by MRI

Sequences
T1 key sequence to evaluate myelination <1 year. The signal reflects the presence of proteins
T2 key sequence to evaluate myelination 1 and 2 years As the myelin sheaths thicken the surrounding interstitial water moves
FLAIR, DP, DTI complementary sequences

T1WI
RN Brain stem, optical tracts, anterior commissure, ventral thalamus, posterior limb of the internal capsule, rolandic and perirolandic gyrus
2 months deep white matter and anterior limb of internal capsule
4 months Splenium, optical radiations become more evident, cerebellar white matter
6 months Genu, body and splenus of the corpus callosum
8 months U fibers in occipital lobes progressing slowly to frontal and temporal at one year of age.
10-12 months Appearance of myelination with adult pattern in T1WI

T2WI
RN Dorsal brain stem, posterior limb of the internal capsule, ventral thalamus, perirolandic gyrus
2 months Posterior internal capsule arm, semiovale centrum and optical tracts
4 months Optical radiation and subcortical white matter
6 months Splenium
8 months Genu, body and splenic corpus callosum, anterior arm of the internal capsule
12 months cerebellar white matter and occipital subcortical U fibers
18 months Frontal white matter. Some residual hyperintense signals around the trigons of the lateral ventricles
36 months Myelination appearance with adult pattern in T2WI

Myelination Terminal Zones
Normal variant of development
Zones of incomplete myelination
Hyperintense, bilateral and symmetric foci in dorsolateral WM to the atrium of the lateral ventricle

Abnormal Patterns
Delayed myelination Situations in which myelination is slow but present.Usually bilateral and symmetric

Hypermyelination Rare pathology, it can be local or generalized. Sturge Webber, epilepsy and late sequelae of perinatal hypoxia.

Hypomyelinization Permanent deficit of the myelin deposit. Unlike the delay of myelination these do not present myelination over time
It can be seen as normal myelination in T1 but with deficit in T2

White matter diseases
Demyelinating diseases They are acquired and have destruction of normal myelin
Demyelinating diseases Hereditary enzyme deficiency that causes abnormal myelin formation, destruction or turnover Read More

Authors:  Guillen Gutierrez Cinthia , Rodriguez Garza Claudia , Elizondo Riojas Guillermo , Hernández Grimaldo Edgar , Garza Acosta Andrea

Keywords:  Development, white matter

Vasung Lana,  Borradori Tolsa Cristina,  Hanquinet Sylviane,  Huppi Petra,  Merlini Laura

Final Pr. ID: Poster #: SCI-004

A spatio-temporal delay in maturation and reorganization of transient fetal compartements, such as subplate zone, Von Monakow segments of white matter, crossroad areas and migrating cell bands, seems to be linked to abnormal brain growth and radial vulnerability(Kostovic et al. 2014) in preterm born infants (PT). The aim of our study was to test the MRI visibility of these transient fetal structures and eventually to compare their appearance patterns in two group of infants: term borns and PT at term equivalent age. Read More

Authors:  Vasung Lana , Borradori Tolsa Cristina , Hanquinet Sylviane , Huppi Petra , Merlini Laura

Keywords:  Transient fetal zones, Subplate zone, Scoring, Prematurity, Fetal white matter