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 <b>Normal myelination by MRI </b> Sequences <b>T1 </b>key sequence to evaluate myelination <1 year. The signal reflects the presence of proteins <b>T2 </b>key sequence to evaluate myelination 1 and 2 years As the myelin sheaths thicken the surrounding interstitial water moves <b>FLAIR, DP, DTI </b>complementary sequences <b>T1WI</b> <b>RN </b>Brain stem, optical tracts, anterior commissure, ventral thalamus, posterior limb of the internal capsule, rolandic and perirolandic gyrus <b>2 months </b>deep white matter and anterior limb of internal capsule <b>4 months</b> Splenium, optical radiations become more evident, cerebellar white matter <b>6 months</b> Genu, body and splenus of the corpus callosum <b>8 months </b>U fibers in occipital lobes progressing slowly to frontal and temporal at one year of age. <b>10-12 months </b>Appearance of myelination with adult pattern in T1WI <b>T2WI RN </b>Dorsal brain stem, posterior limb of the internal capsule, ventral thalamus, perirolandic gyrus <b>2 months </b>Posterior internal capsule arm, semiovale centrum and optical tracts <b>4 months </b>Optical radiation and subcortical white matter <b>6 months </b>Splenium <b>8 months </b>Genu, body and splenic corpus callosum, anterior arm of the internal capsule <b>12 months </b>cerebellar white matter and occipital subcortical U fibers <b>18 months </b>Frontal white matter. Some residual hyperintense signals around the trigons of the lateral ventricles <b>36 months </b>Myelination appearance with adult pattern in T2WI <b>Myelination Terminal Zones</b> Normal variant of development Zones of incomplete myelination Hyperintense, bilateral and symmetric foci in dorsolateral WM to the atrium of the lateral ventricle <b>Abnormal Patterns</b> <b>Delayed myelination </b>Situations in which myelination is slow but present.Usually bilateral and symmetric <b>Hypermyelination </b>Rare pathology, it can be local or generalized. Sturge Webber, epilepsy and late sequelae of perinatal hypoxia. <b>Hypomyelinization </b>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 <b>White matter diseases</b> <b>Demyelinating diseases</b> They are acquired and have destruction of normal myelin <b>Demyelinating diseases </b>Hereditary enzyme deficiency that causes abnormal myelin formation, destruction or turnover
Read More
Meeting name:
SPR 2020 Annual Meeting & Postgraduate Course
, 2020
Authors:
Guillen Gutierrez Cinthia,
Rodriguez Garza Claudia,
Elizondo Riojas Guillermo,
Hernández Grimaldo Edgar,
Garza Acosta Andrea
Keywords:
Development,
white matter