Understanding The Neonatal MRI

Dr.Vinayak V Kodur2nd Yr DM Neonaology Resident

L.T.M.General Hospital,SionMumbai

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

Sulci and Gyri

Sulci and Gyri

Ventricular System

Parts of the Brain

Coronal section of Brain

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 peripheral2. caudal to rostral3. dorsal to ventral4. sensory then motor

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

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

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

• 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

Normal Myelination Newborn Vs 2year Brain T1 Images

Normal IR and T2 sequences showing myelination in IC and Thalamus

MRI - Introduction

How MRI works

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.

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.”

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.

CT BRAIN MRI T1 MRI T2GREY Parenchyma

TumorEdema

Edema TumorInflammationAdult GMNeonate WM

Adult: WMNeonate: GM, PLIC and Thalamus

BLACK CSFAirFat

CSFAir Bone(skull)Calcification

Flow voidAirDense BoneCalcification

WHITE Bone BloodCalcificationTumor

FatBloodAdult: WMNeonate: GM,PLIC and Thalamus

CSFBloodEdemaTumorMost brain lesionsAdult: GMNeonate: WM

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

• 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

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.

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)

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.

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”

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

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.

T1 T2 and FLAIR

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.

• 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.

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.

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.

MRI T2 Sectional Anatomy 1st Section

MRI T2 2nd Section

MRI T2 Sections 1,2,3

MRI T2 Sections 4,5,6

Central SulcusPost-Central Sulcus

Parieto-occipital Sulcus

Marginal Sulcus

Lat.Ventri

MRI T2 Sections 7,8

MRI T2 Sections 9 to 12

MRI T2 Sections 13,14

MRI T2 Sections 15,16

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

MRI Brain on DOL 2

• 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.

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

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.

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

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.

Identify Sequence and Defect

Extent of damage???

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.

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.

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.

Case 5

• FT baby 3.5 kg• Born with macrocephlay• MRI done on DOL 3

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.

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

• 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

Brainstem Injury

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

Isolated White Matter Injury

• Uncommon in HIE• More common if history of decreased fetal• movements• More common if infection• Associated with hypoglycaemia

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.

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

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.

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.

26 weeks Preterm Brain MRI

Germinal matrix at anterior horn

Over Caudate Head

Roof of Temporal horn

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.

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.

MR in HIE- Pattern and Site

Severity and duration of

hypoperfusion

Mild to Moderate Severe

Level of brain Maturation

Preterm Full Term

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.

Mild to Mod Injury• Preterm• Periventricular white matter1. PVL

I. Initially Hyperintense on T1 and T2 with restricted diffusion on DWI

II. After 4-6weeks: CystsIII. 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.

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

PretermGrey matter

especially Thalami and Brainstem

TermBrainstem

Lat ThalamiGlobus Pallidus

PutamenHippocamusPerirolandic

(Sensorymotor) cortex

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