Interpretation of neonatal MRI is very difficult and different from adult MRI. This presentation tries to explain how to read a neonatal MRI.

1. Understanding The
Neonatal MRI
Dr.Vinayak V Kodur
2nd Yr DM Neonaology Resident
L.T.M.General Hospital,Sion
Mumbai

2. Role Of MRI in Newborn
• Confirm a normally developed brain
• Assess severity and pattern of any injury
• Predict outcome form pattern of injury and
clinical details
• Assess/ monitor the effect of any intervention
• Even with all diagnostic criteria
– The spectrum of injury may be wide
– The evolution of lesions variable

4. Sulci and Gyri

5. Sulci and Gyri

6. Ventricular System

7. Parts of the Brain

9. Coronal section of Brain

10. Myelination
• First myelination
– seen as early as 16th week of gestation,
– in the column of Burdach, but only really takes off from the
24th week.
• It does not reach maturity until 2 years or so.
• It correlates very closely to developmental milestones.
• The progression is predictable
• few simple general rules; myelination progresses from:
1. central to peripheral
2. caudal to rostral
3. dorsal to ventral
4. sensory then motor

11. Myelination milestones
• term birth: brainstem, cerebellum, posterior
limb of the internal capsule, optic tract,
perirolandic region
• 2 months: anterior limb of the internal
capsule
• 3 months: splenium of the corpus callosum
• 6 months: genu of the corpus callosum

12. Myelinated Structures at Birth
• dorsal brainstem
• ventrolateral thalamus
• lentiform nuclei
• central corticospinal tracts
• posterior limb of the internal capsule
• Middle cerebellar peduncle
• Optic nerve, chiasma and tract

13. Progression Of Myelination
• The first change is increase in T1 signal, and later
decrease in T2.
• 2-3 months: anterior limb of IC becomes T1 bright
• 3 months: cerebellar WM tracts becomes T1 bright
• 3-6 months: splenium of corpus callosum
becomes T2 dark
• 6 months: genu of corpus callosum
becomes T1 bright
• 8 months: subcortical white matter
becomes T1 bright
• 8 months: genu of corpus callosum becomes T2 dark

14. • 11 months: anterior limb of internal capsule
becomes T2 dark
• 1 year 2 months: occipital white matter
becomes T2 dark
• 1 year 4 months: frontal white matter
becomes T2 dark
• 1 1/2 years: majority of white matter
becomes T2 dark (except terminal myelination zones
adjacent to frontal horns and periatrial regions)
• 2 years: almost all of white matter becomes T2 dark

15. Normal Myelination Newborn Vs 2year
Brain T1 Images

16. Normal IR and T2 sequences showing
myelination in IC and Thalamus

17. MRI - Introduction

18. How MRI works

19. MRI Principle
• MRI scanner forms a strong magnetic field around
the area to be imaged.
• Protons (hydrogen atoms) in tissues containing water
molecules are used to create a signal that is
processed to form an image of body.
• First, energy from an oscillating magnetic field is
temporarily applied to the patient at the appropriate
resonance frequency.
• The excited hydrogen atoms emit a radio
frequency signal which is measured by a receiving
coil.

20. MRI Principle
• The radio signal can be made to encode position
information by varying the main magnetic field using
gradient coils.
• As these coils are rapidly switched on and off they
create the characteristic repetitive noise of an MRI
scan.
• The contrast between different tissues is determined
by the rate at which excited atoms return to
the equilibrium state.
• MRI requires a magnetic field that is both strong
and uniform. The field strength of the magnet is
measured in ”Tesla.”

21. T1 and T2 Images
• To create a T1-weighted image magnetization is
allowed to recover before measuring the MR signal.
• This image weighting is useful for assessing the
cerebral cortex, identifying fatty tissue.
• To create a T2-weighted image magnetization is
allowed to decay before measuring the MR signal.
• This image weighting is useful for detecting edema and
inflammation, revealing white matter lesions.
• T1 weighted imaging is better at demonstrating
myelination in the 1st 6-8 months after birth and T2
weighting is better between 6 and 18 months.

22. CT BRAIN MRI T1 MRI T2
GREY Parenchyma
Tumor
Edema
Edema
Tumor
Inflammation
Adult GM
Neonate WM
Adult: WM
Neonate: GM, PLIC
and Thalamus
BLACK CSF
Air
Fat
CSF
Air
Bone(skull)
Calcification
Flow void
Air
Dense Bone
Calcification
WHITE Bone
Blood
Calcification
Tumor
Fat
Blood
Adult: WM
Neonate: GM,PLIC
and Thalamus
CSF
Blood
Edema
Tumor
Most brain lesions
Adult: GM
Neonate: WM

23. Hemorrhage on MRI
• Change with the age of the blood.
• In general, five stages of haematoma evolution:
• hyperacute
– intracellular oxyhaemoglobin
– isointense on both T1 and T2
• acute (1 to 2 days)
– intracellular deoxyhaemoglobin
– T2 signal intensity drops (T2 shortening)
– T1 remains intermediate-to-long
• early subacute (2 to 7 days)
– intracellular methaemoglobin
– T1 signal gradually increases to become hyperintense

24. • late subacute (7 to 14-28 days)
– extracellular methaemoglobin: over the next few
weeks, as cells break down, extracellular
methaemoglobin leads to an increase in T2 signal also
• chronic (>14-28 days)
– periphery
• intracellular haemosiderin
• low on both T1 and T2
– center
• extracellular hemichromes
• isointense on T1, hyperintense on T2

26. Diffusion Images
• Diffusion MRI measures the diffusion of water
molecules in biological tissues.
• The extent of tissue cellularity and the presence
of intact cell membrane help determine the
impedance of water molecule diffusion.
• In an isotropic medium (inside a glass of water
for example), water molecules naturally move
randomly according to turbulence and Brownian
motion.
• In biological tissues however, where the Reynolds
number is low enough for flows to be laminar, the
diffusion may be anisotropic.

27. Diffusion Images
• For example, a molecule inside the axon of a neuron has a
low probability of crossing the myelin membrane.
• Therefore the molecule moves principally along the axis of
the neural fiber.
• If it is known that molecules in a particular voxel diffuse
principally in one direction, the assumption can be made
that the majority of the fibers in this area are parallel to
that direction.
• “Diffusion demonstrates greater restriction than one would
expect for this tissue”- This is how it should be reported.
• DWI (Diffusion Weighted Imaging)
• ADC (Apparent Diffusion Coefficient)
• DTI (Diffusion Tensor Imaging)

28. DWI
• Following an infarct , DWI is highly sensitive to the
changes occurring in the lesion.
• Increases in restriction (barriers) to water diffusion, as
a result of cytotoxic edema (cellular swelling), is
responsible for the increase in signal on a DWI scan.
• The DWI enhancement appears within 5–10 minutes of
the onset of stroke symptoms (CT which often does not
detect changes of acute infarct for up to 4–6 hours)
and remains for up to 2 weeks.
• Coupled with imaging of cerebral perfusion,
"perfusion/diffusion mismatch” may indicate regions
capable of salvage by reperfusion therapy.

29. DWI
• Areas of restricted diffusion are bright on DWI and
dark on ADC.
• Restricted diffusion occurs in cytotoxic edema:
– Ischemia (possibly within minutes)
– Seizures
• DWI detects infarction within 24hrs.
• Rapidly increases and peak at 3-5 days.
• Then gradually fades away called as
“pseudonormalization”

30. ADC
• The extent of tissue cellularity and the presence
of intact cell membrane help determine the
impedance of water molecule diffusion.
• The impedance of water molecules diffusion can
be quantitatively assessed using the apparent
diffusion coefficient (ADC) value.
• An ADC of a tissue is expressed in units of
mm2/s.
– white matter: 670 - 800
– cortical grey matter: 800 - 1000
– deep grey matter: 700 - 850
– CSF: 3000 - 3400

31. FLAIR
• Fluid Attenuated Inversion Recovery (FLAIR) is
an inversion-recovery pulse sequence used to
nullify the signal from fluids.
• High weighted T1 images.
• Used to asses the myelination in newborns
and infants.
• Used in brain imaging to suppress CSF so as to
bring out periventricular hyperintense lesions,
such as PVL.
• Most pathology is BRIGHT.

32. T1 T2 and FLAIR

34. How Neonatal MR Different Than Adult
• The term neonatal brain contains approximately 92-
95% water and this decreases over the 1st 2 years of
life to adult values of 80-85%.
• The high water content of the neonatal brain is
associated with a marked increase in T1
(longitudinal) and T2 (transverse) relaxation times in
comparison to adults.
• The pulse sequences need to be adjusted to allow for
the different MR properties of the immature brain.

35. • In the neonatal brain, unmyelinated
whitematter (WM) has a low signal intensity
(SI) onT1weighted images and high SI onT2
weighted images, opposite of adult brain.

36. Patient Preparation
• Sedate baby, rarely complete anesthesia.
• MR compatible monitoring
• Metal check
• Ear protection of patient and accompanying
relative
• Swaddle babies (decreases effects of motion)
• Staff and equipment for neonatal
resuscitation.

37. How to read a MRI
• We should know what structures are seen in which
sections of brain so that we can identify the
abnormality.
• Showing you sections of adult brain and structures
seen in them.
• For neonatologists dealing with asphyxial injuries we
should focus on sections involving basal ganglia and
thalami as they are primarily involved in HIE.
• You can only interpret MRI if you what structure to see
in which disorders and which sections to see it in.
• One can read MRI from top i.e. parietal region to base
of skull or in reverse direction but maintain a flow and
don`t jump sections.

38. MRI T2 Sectional Anatomy 1st Section

39. MRI T2 2nd Section

40. MRI T2 Sections 1,2,3

41. MRI T2 Sections 4,5,6
Central Sulcus
Post-Central Sulcus
Parieto-occipital Sulcus
Marginal Sulcus
Lat.Ventri

42. MRI T2 Sections 7,8

43. MRI T2 Sections 9 to 12

44. MRI T2 Sections 13,14

45. MRI T2 Sections 15,16

46. Case 1
• Case: Mother complained decreased fetal
movements for 48 hours.
• Unreactive NST
• Emergency LSCS performed.
• Born at 37+3 weeks GA .
• Required resuscitation and encephalopathic baby
• Had seizures within 6 hours of life.
• Imaged day 2

47. MRI Brain on DOL 2

48. • Diffusion imaging excellent for early detection
of WM injury.
• Note abnormal high signal throughout the
white matter on DWI and corresponding low
signal in the ADC map.
• Decreased fetal movements associated with
WM injury.

49. Case 2
• Primigravida mother,registered in other hospital.
• Mother referred for MSAF.
• 40weeks baby 2.9kg
• Baby required resuscitation and was
encephalopathic and needed ventilatory
assistance.
• Put on therapeutic hypothermia.
• Scan done on DOL 5

53. Description of MRI
• T1 and T2 images showed increased and
decreased signal intensities in the lentiform
nuclei and the ventero-lateral part of
thalamus but PLIC signals are intact.
• DWI shows diffusion restriction in same areas.
• As the baby received therapeutic hypothermia
the mild basal ganglia affection without
involving PLIC is seen.

54. Therapeutic Hypothermia
• Not associated with atypical injury
• Does not alter ability to predict outcome
• Therapeutic hypothermia was associated with a
reduction in:
– Basal ganglia or thalamus lesions (P=0.02)
– White matter lesions (P=0.01)
– Abnormal posterior limb of the internal capsule
(P=0.02).
• Cooled infants:
– Had fewer scans predictive of later neuromotor
abnormalities (P=0.03)
– Were more likely to have normal scans ( P=0.03).
• Ref: Rutherford et al Lancet Neurol 2010

55. CASE 3
• 2nd gravida mother referred for MSAF
• Baby non-vigorous required resuscitation as
bag and mask for 2 mins.
• Cord pH 6.9 with BE -18
• Convulsions within 2 hours of life and required
3 anticonvulsants to control seizures.
• MRI done on DOL 6.

58. Identify Sequence and Defect

59. Extent of damage???

60. Description of MRI
• T1 and T2 images show loss of PLIC signal and
increased and decreased intensity (in T1 and T2
respectively) involving the entire basal ganglia
and thalamus.
• Also the frontal lobe shows loss of normal sulci
and gyri pattern (compare with occipital and
parietal lobe)
• In DWI there is restricted diffusion in the fronto-
parieto-temporal region, thalami and lentiform
nuclei with low ADC values in the same region.
• Suggests Severe HIE and as the area of affection is
extensive mostly had severe and acute asphyxia
but not sever enough to involve brainstem which
was preserved because of diving reflex.

61. Case 4
• Full term baby delivered by trained dai at a
village.
• Baby didn`t cry immediately after birth
• Was not feeding well for initial 24 hours of life
and referred to LTMGH at 30hrs of life i/v/o
convulsions.
• Baby had prolonged NICU stay of 3 weeks.
• MRI done at 3 months of life.

68. Description Of MRI
• In such cases when there is >2weeks gap between the
asphyxial episode and MRI (here 3 months) DWI and
ADC sequences are of no use due to pseudo-
normalization.
• T1 and T2 images show cystic encephalomalacia more
on right side than left in the parietal, temporal and
some part of occipital lobes with secondary
ventriculomegaly and thinning of corpus callosum.
• Increased and decreased signal intensity on T1 an T2
respectively in the some areas basal ganglia and
thalami.
• Such extensive involvement but no need for respiratory
support in initial 30 hrs of life suggest chronic and
persistent asphyxia as brainstem was preserved.

69. Case 5
• FT baby 3.5 kg
• Born with macrocephlay
• MRI done on DOL 3

75. Description of MRI
• Case of hydrencephaly showing huge ventricular
dilatation.
• Communicating hydrocephalus.
• Underlying pathology being IVH as blood clot is
seen in the left ventricle.
• In such cases inherited bleeding disorders should
be ruled out.
• Patient required operative intervention as NS
washes of the ventricular cavity to remove the
blood clot followed by VP shunt.

76. Areas involved in HIE
• basal ganglia and thalami
• internal capsule
• cortex
• subcortical white matter
• medial temporal lobe
• Brainstem
• These are susceptible b`coz,
– Increased metabolic rate
– Actively myelinating
– Increased glutamate receptors

78. • BGT lesions give rise to cerebral palsy
• BGT lesions can be graded as mild, moderate
and severe
• The severity of neonatal BGT lesion dictates
severity of impairment

80. Brainstem Injury

81. Brainstem Injury
• In surviving infants with BGT lesions:
• mesencephalic injury was associated with
prolonged feeding difficulties (p<0.001)
• pontine injury was associated with
gastrostomy (p<0.001).
• Ref: Martinez Biarge Neurology 2011

82. Isolated White Matter Injury
• Uncommon in HIE
• More common if history of decreased fetal
• movements
• More common if infection
• Associated with hypoglycaemia

84. TIMING OF THE MRI
• The ideal time to image depends on the information
required.
• Conventional scans performed within the 1st 24 hrs
may appear normal even when there has been severe
perinatal injury to the brain.
• Early imaging will help to differentiate antenatal from
perinatal lesions. Perinatally acquired abnormalities
‘mature’ and become easier to identify by the end of
the 1st week.
• For information on the exact pattern of injury a scan
between1and 2weeks of age is usually ideal.
• After 2weeks there may be signs of cystic breakdown
and atrophy, which may make the initial pattern of
injury more difficult to detect.

87. Why we need early DI ??
• Early conventional imaging may
underestimate extent of injury
• Need to use diffusion imaging
• Excellent for white matter infarction
• Less predictable in serial early imaging of BGT
injury

90. MR of Preterm Newborn
• The very premature brain has little sulcation and
gyration at 24 weeks GA but this rapidly evolves.
• The cerebral cortex(GM) is demonstrated as high SI on
T1 weighted imaging and low SI onT2 weighted
imaging.
• On T2 weighted imaging prior to 30 weeks GA, bands
of low SI are visible within the cerebral WM, around
the lateral ventricles, representing glia migrating from
the germinal matrix to the developing cerebral cortex.
• The germinal matrix is visible up to around 32 weeks
GA as a prominent structure at the margins of the
lateral ventricles.
• Germinal matrix is demonstrated as high SI
onT1weighted imaging and low SI onT2 weighted
imaging.

91. Preterm Brain MRI
• Myelin has been demonstrated in numerous
central structures in the very preterm brain
such as the brainstem, cerebellum and
thalami.
• Myelin is not seen in the whitematter of the
cerebral hemispheres until 35weeks GA.
• There is a steady increase in brain surface area
and cortical folding and a reduction in T2
values in the cerebral WM with increasing GA.

92. 26 weeks Preterm Brain MRI
Germinal matrix at
anterior horn
Over Caudate
Head
Roof of
Temporal horn

93. MRS
• At birth, term baby has higer myoinositol(ml), creatine
plus phosphocreatine (Cr). and choline(Cho) and low N-
acetyl aspartate(NAA) than an adult.
• Then progressive decrease in lactate and increase in
NAA occurs normally.
• In HIE there are high lactate and glutamine/glutamate
levels on MRS
• Early abnormal Lac/NAA ratio poor outcome at 2 year
of age.
• Low NAA/Cho and elevated Lac/NAA in 1st month of
life is marker of poor outcome in case of HIE.
• Best site is GP/Thalami.

94. MRS
• MR spectra from an 8
cm3 voxel within the basal
ganglia of (a) a normal
preterm infant (b) a normal
term infant, (c) an infant
aged 6 months with normal
neurodevelopmental
outcome, and (d) an adult
control.
• By 6 months NAA has
become the dominant peak
in the spectrum, the Cho/Cr
ratio decreases with
maturation and that lactate
is only easily visible in the
preterm infant.

95. MR in HIE- Pattern and Site
Severity and
duration of
hypoperfusion
Mild to
Moderate
Severe
Level of brain
Maturation
Preterm Full Term

96. Mild to moderate injury
• Prolonged partial insult.
• e.g. cord around the neck
• Time for redistribution of cerebral blood flow.
• Ensures perfusion to metabolically active
areas of grey matter (BGT, brainstem,
cerebellum)
• Injury to watershed (inter-vascular) area of
cerebrum.
• Injury is different in PT and Term.

97. Mild to Mod Injury
• Preterm
• Periventricular white
matter
1. PVL
I. Initially Hyperintense on
T1 and T2 with restricted
diffusion on DWI
II. After 4-6weeks: Cysts
III. End stage:
Ventriculomegaly, loss of
periventricular white
matter with increased
signal on T2 and thinning
of corpus callosum.
2. IVH due to reperfusion
injury
• Term
• Parasagittal cortical and
subcortical injury.
• Watershed area between
ACA, MCA, PCA.
• T1 Hypointense T2
Hyperintense lesion with
restricted diffusion on
DWI.

98. Severe Injury
• Acute insult such as, cord prolapse or uterine rupture
or abruptio placentae
• No time for redistribution
• Injury in metabolically active areas of brain
Preterm
Grey matter
especially Thalami
and Brainstem
Term
Brainstem
Lat Thalami
Globus Pallidus
Putamen
Hippocamus
Perirolandic
(Sensorymotor) cortex

99. THANK YOU