Purpose or Case Report: 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
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