Normal

developmental
milestones

Introduction
T1WIs and T2WIs allow evaluation and staging of
the myelination process.
Neonatal brain- higher water content, lower
protein and lipid contents. Longer T1 and T2
relaxation times.
To optimize SNR and contrast, TR must be
increased.
T1 WI, TR of 400500 msec increased to 800
850 msec.
T2 WI, TR of 35005000 msec increased to
900010,000 msec.

General myelination
patterns
Myelination causes shortening of T1
relaxation time in white matter
structures T1 high, T2 low signal.
Unmyelinated white matter- T1
hypointense and T2 hyperintense
relative to cortex.
Myelination proceeds from dorsal to
ventral, from caudad to cephalad,
from central to peripheral.

T1 vs T2 sequences
T2 changes occur days to months
after white matter has become
hyperintense on the complimentary
T1-weighted images.
T1-WI most useful in earlier stages of
myelination, T2-WI superior in later
stages.

At birth - newborn
T1 Hyperintense

T2 Hypointense

Medulla
Dorsal pons
Brachium pontis
Cerebellar peduncles
Midbrain
VL Thalamus
Posterior limb IC
Perirolandic centrum
semiovale and gyri
Optic nerves, tracts,
radiations

Medulla
Dorsal pons
Midbrain
Cerebellar peduncles
VL Thalamus
Perirolandic gyri

Newborn T1, T2 WI

Brainstem, PLIC, VL Thalami

2 months
T1 Hyperintense

T2 Hypointense

Deep cerebellar WM
Anterior limb IC

Brachium pontis
Posterior limb IC
Perirolandic centrum
semiovale
Optic tracts

2 months

IC , VL Thalami, brachium pontis deep cerebellar WM

T1
Hyperintense

T2
Hypointense

4 months

Entire
cerebellum
CC (splenium)

Optic radiations
Calcarine
fissure

6 months

CC (entire)

CC (splenium)
Ventral pons

8 months

Subcortical Ufibers
occipital

Anterior limb IC
CC (entire)
Occipital
central WM

6 months

CC, Ventral pons

T1
Hyperintense

T2
Hypointense
Deep WM
cerebellum
Early occipital
subcortical Ufibers
Frontal, Temporal
central WM

18 months

Subcortical Ufibers
frontal and
temporal
Brain achieves
adult
appearance on
T1.
Minimal change

24 months

Minimal change

12 months

Subcortical Ufibers
occipital poles
Entire posterior
fossa
Subcortical Ufibers frontal and

12 months

Subcortical U fibres, deep Cbll WM, central WM

18 months

Subcortical WM, Cbll WM

Terminal myelination
zones
Region of persistent T2 hyperintensity within
peritrigonal area.
Small bands of low signal, normally myelinated
brain separate high signal region from the
ventricles in terminal zones of myelination.
In periventricular leukomalacia, high signal
intensity extends all the way to ventricular
ependyma.
Fronto-temporal subcortical white matter may
also persist as regions of signal hyperintensity
beyond 2 years.

 Terminal myelination zone vs PVL

Myelination in preterm infant

Age adjusted to account for
prematurity.
Rapid acceleration of brain growth
occurs during first 2 postnatal
months due to endogenous steroid
secretion.
Adjustment may not be needed after
2months of age.

HIE PATTERNS

Introduction
HIE - common cause of cerebral
palsy.
Depends on severity of insult, degree
of brain maturation.

Causes

Patterns of brain injury

Mild to moderate hypotension in
preterm infants
Severe hypotension in preterm
infants
Mild to moderate hypotension in
term infants
Severe hypotension in term infants.

Vascular supply and brain

maturation
Hypoxic-anoxic event lasting
> 10 minutes - induce
parenchymal changes.
Premature neonatal brain ventriculopetal vascular
pattern. Border zone periventricular white matter.
Term neonate ventriculofugal vascular
pattern. Border zone subcortical white matter and
parasagittal cortex.

Hypoperfusion Injury in
Preterm Infants

Mild to Moderate Hypotension

Periventricular white matter, PVL.
USG: Hyperechogenic globular
change in periventricular regions
cavitation - cyst formation.

PVL grading

 MR: areas of T1 hyperintensity within

larger areas of T2 hyperintensity.

ICH
Reperfusion injury - germinal matrix
hemorrhage.

ICH grading

End
stag
e
Ventriculomegaly
with irregular
margins
Loss of
periventricular WM
with increased T2
signal
Thinning of corpus

Severe Hypotension
Thalami, brainstem, and cerebellum
more susceptible.
Hyperechogenicity on US.
Hypoattenuation on CT.
Restricted diffusion, variable T2
signal on MR.

Deep gray matter injury in

preterm

Hypoperfusion Injury in
Term Infants

Mild to Moderate
Hypotension
Watershed zones
between anterior and
middle cerebral arteries
and between middle
and posterior cerebral
arteries.
Cortex and underlying
subcortical white matter
in parasagittal locations.

 Hyperintense T2
signal, hypointense
T1 signal.
Restricted diffusion.
MR spectroscopyincreased lactate.

Severe Hypotension
Lateral thalami, posterior putamina,
hippocampi, brainstem, corticospinal tracts,
sensorimotor cortex Most susceptible.
USG: Hyperechogenicity of involved
structures.
CT: Hypoattenuation of thalami and basal
ganglia.
MR: T1 hyperintensity, T2 hyper-or
hypointensity. Restricted diffusion. MR
spectroscopy- elevation of lactate.

Overlap
exists

DWI more sensitive

HIE signs
1-2-3-4 sign: Severe total
hypoxia
Increased T1 signal intensity in
basal ganglia
Increased T1 signal intensity in
thalamus
Absent or decreased T1 signal
intensity in the posterior limb of
internal capsule (absent
posterior limb sign)
Restricted water diffusion on DWI.

Relative increase in signal intensity in posterior

putamen relative to
posterior limb of internal capsule.
White cerebellum sign, Reversal sign.

Summary
HIE

Mild to moderate
hypotension =
Watershed area

Severe
hypotension =
Most
metabolically
active area

PRETERM

Periventricular
white matter

Thalami, brainstem,
and cerebellum

TERM

Subcortical white
matter and
parasagittal cortex

Lateral thalami,
posterior putamina,
hippocampi,
brainstem,
corticospinal tracts,
sensorimotor
cortex

Conclusion
Imaging excludes other causes of
encephalopathy.
Helps to determine prognosis and
treatment.
Short therapeutic window; early
identification of hypoxic-ischemic
insult is of paramountimportance.