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7/25/2019 Myelination milestones on MRI and HIE patterns
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Normal
developmentalmilestones
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Introduction
T1WIs and T2WIs allow evaluation and staging ofthe myelination process.
Neonatal brain- higher water content, lower
protein and lipid contents. onger T1 and T2rela!ation times.
To optimi"e #N$ and contrast, T$ must beincreased.
T1 WI, T$ of %&&'(&& msec increased to )&&')(& msec.
T2 WI, T$ of *(&&'(&&& msec increased to+&&&'1&,&&& msec.
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General myelinationpatterns yelination causes shortening of T1
rela!ation time in white matterstructures ' T1 high, T2 low signal.
nmyelinated white matter- T1hypointense and T2 hyperintenserelative to corte!.
yelination proceeds from dorsal toventral, from caudad to cephalad,from central to peripheral.
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T1 vs T2 sequences
T2 changes occur days to monthsafter white matter has becomehyperintense on the complimentary
T1-weighted images.
T1-WI most useful in earlier stages ofmyelination, T2-WI superior in later
stages.
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At birth - newborn
T1 Hyperintense
edulla
orsal pons
/rachium pontis 0erebellar peduncles
idbrain
Thalamus
osterior limb I0
erirolandic centrumsemiovale and gyri
3ptic nerves, tracts,radiations
T2 Hypointense
edulla
orsal pons
idbrain
0erebellar peduncles
Thalamus
erirolandic gyri
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Newborn T1, T2 I
Brainstem, PLIC, VL Thalami
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2 months
T1 Hyperintense
eep cerebellar W
4nterior limb I0
T2 Hypointense
/rachium pontis
osterior limb I0
erirolandic centrumsemiovale
3ptic tracts
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2 months
IC , VL Thalami, brachium pontis deep cerebellar WM
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T1Hyperintense
T2Hypointense
% months 5ntirecerebellum00 6splenium7
3ptic radiations0alcarine8ssure
9 months 00 6entire7 00 6splenium7entral pons
) months #ubcortical -
8bersoccipital
4nterior limb I0
00 6entire73ccipitalcentral W
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! months
CC, Ventral pons
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T1Hyperintense
T2Hypointense
12 months #ubcortical -8bersfrontal andtemporal/rain achievesadultappearance on
T1.
eep Wcerebellum5arly occipitalsubcortical -8bers:rontal, Temporalcentral W
1) months inimal change #ubcortical -
8bersoccipital poles5ntire posteriorfossa
2% months inimal change #ubcortical -
8bers frontal and
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12 months
Subcortical U fbres, deep Cbll WM, central WM
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1" months
Subcortical WM, Cbll WM
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Terminal myelination#ones $egion of persistent T2 hyperintensity within
peritrigonal area.
#mall bands of low signal, normally myelinatedbrain separate high signal region from theventricles in terminal "ones of myelination.
In periventricular leu;omalacia, high signalintensity e!tends all the way to ventricularependyma.
:ronto-temporal subcortical white matter mayalso persist as regions of signal hyperintensitybeyond 2 years.
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Terminal myelination "one vs
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$yelination in preterm in%ant
4ge ad
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HIE PATTERNS
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Introduction
=I5 - common cause of cerebralpalsy.
epends on severity of insult, degreeof brain maturation.
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&auses
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'atterns o% brain in(ury
ild to moderate hypotension inpreterm infants
#evere hypotension in preterminfants
ild to moderate hypotension interm infants
#evere hypotension in term infants.
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*ascular supply and brainmaturation
=ypo!ic-ano!ic event lasting> 1& minutes - induceparenchymal changes.
remature neonatal brain -ventriculopetal vascularpattern. /order "one -periventricular white matter.
Term neonate -
ventriculofugal vascularpattern. /order "one -subcortical white matter andparasagittal corte!.
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Hypoperfusion Injury inPreterm Infants
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$ild to $oderate Hypotension
eriventricular white matter, .
#?@ =yperechogenic globularchange in periventricular regions 'cavitation - cyst formation.
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'*+ radin
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$@ areas of T1 hyperintensity withinlarger areas of T2 hyperintensity.
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I&H
$eperfusion in
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I&H radin
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nd
stae
entriculomegalywith irregularmargins
oss ofperiventricular Wwith increased T2signal
Thinning of corpus
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.evere Hypotension
Thalami, brainstem, and cerebellummore susceptible.
=yperechogenicity on #.
=ypoattenuation on 0T.
$estricted diBusion, variable T2signal on $.
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/eep ray matter in(ury inpreterm
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Hypoperfusion Injury inTerm Infants
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$ild to $oderateHypotension Watershed "ones
between anterior andmiddle cerebral arteries
and between middleand posterior cerebralarteries.
0orte! and underlying
subcortical white matterin parasagittal locations.
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=yperintense T2signal, hypointense
T1 signal.
$estricted diBusion.
$ spectroscopy-increased lactate.
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.evere Hypotension
ateral thalami, posterior putamina,hippocampi, brainstem, corticospinal tracts,sensorimotor corte! ' ost susceptible.
#?@ =yperechogenicity of involvedstructures.
0T@ =ypoattenuation of thalami and basalganglia.
$@ T1 hyperintensity, T2 hyper-orhypointensity. $estricted diBusion. $spectroscopy- elevation of lactate.
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0verlap
eists
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/I more sensitive
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HI sins
C1-2-*-% signD@ #evere total
hypo!ia Increased T1 signal intensity in
basal ganglia
Increased T1 signal intensity inthalamus
4bsent or decreased T1 signalintensity in the posterior limb ofinternal capsule 6Cabsentposterior limb signD7
$estricted water diBusion on WI.
$elative increase in signal intensity in posteriorputamen relative to posterior limb of internal capsule. White cerebellum sign, $eversal sign.
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.ummary
HI Mild to moderatehypotension =Watershed area
.everehypotension $ostmetabolicallyactive area
'3T3$ eriventricularwhite matter
Thalami, brainstem,and cerebellum
T3$ #ubcortical whitematter andparasagittal corte!
ateral thalami,
posterior putamina,hippocampi,brainstem,corticospinal tracts,sensorimotorcorte!
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&onclusion
Imaging e!cludes other causes ofencephalopathy.
=elps to determine prognosis andtreatment.
#hort therapeutic windowE earlyidenti8cation of hypo!ic-ischemic
insult is of paramount importance.
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