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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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