mriphysics-1610311406mmmmmmmmmmmm05.pptx

GUIDE: Dr Anil Rathva (AP/RD) Presented By: Dr. Bhishm

MRI principle
▪ MRI is based on two basic principles:
1. Atoms with an odd number of protons have spin.
(Pairs of spins tend to cancel, so only atoms with an odd number of protons
have spin )
2. A moving electric charge, be it positive or negative, produces a
magnetic field.
+

There is electric charge
on the surface of the
proton, thus creating a
small current loop and
generating magnetic
moment .

▪ Body has many such atoms that can act as good MR nuclei (1H,
13C, 1
9F, 23Na) .
▪ Hydrogen nuclei is one of them which is not only positively
charged, but also has magnetic spin.
▪ MRI utilizes this magnetic spin property of protons of
hydrogen to elicit images

WHY HYDROGEN IONS???
o Hydrogen nucleus has an unpaired proton which is positively
charged.
o Hydrogen is abundant in the body in the form of water and
fat.
o Every hydrogen nucleus is a tiny magnet which produces
small but noticeable magnetic field.
o Essentially all MRI is hydrogen (proton) imaging.

Body in an external magnetic
field (B0)
•In our natural state Hydrogen ions in body are
spinning in a haphazard fashion, and cancel all
the magnetism.
•When an external magnetic field is applied
protons in the body align in one direction.

Net magnetization
▪ Half of the protons align along the magnetic field and rest are
aligned opposite
▪ population ratio of
parallel versus anti-
parallel protons is
more.
▪ These extra protons produce net magnetization
vector (M).
▪ Net magnetization depends
on B0 .

Precessio
n
▪ The external magneticfield causes the
spinning proton to ‘wobble’ in a regular
manner called ‘PRECESSION.

LARMOR EQUATION
▪ How fast the protons precess , this speed can be measured as
precession frequency, that is, how many times the protons
precess per second.

coordinate system
Using a coordinate system makes the description of proton motion in the
magnetic field easier, and also we can stop drawing the external magnetic

Manipulating the
net
▪
Mmaagngetnizaetiotnicazn baetmainoipunlated by
changing the magnetic field environment
(static, gradient, and RF
fields)
▪
▪
RF waves (short burst of electromagnetic wave, which is called
a radio frequency (RF) pulse), are used to manipulate the
magnetization of H nuclei.
▪
▪
Energy exchange is possible when protons and the
radiofrequency pulse have the same frequency.
▪ Externally applied RF waves perturb magnetization into different axis
(transverse axis). Only transverse magnetization produces signal.

2 things happen after RF
pulse:
1 Energy Absorption
Increase number of High energy Spin down nuclei.
2 Phase Coherence
Proton precesses in transverse plane at Larmor Frequency.
When RF pulse switched of nuclei return to their original state they
emit RF signals which can be detected with the help of receiving
coils

T1 and T2 relaxation
▪ When RF pulse is stopped higher energy gained by proton is
retransmitted and hydrogen nuclei relax by two mechanisms
▪
▪
▪
T1 or spin lattice relaxation- by which original magnetization (Mz)
begins to recover.
This energy is just handed over to their surroundings, the
so called lattice.
▪ T2 relaxation or spin spin relaxation - by which magnetization in
X-Y plane decays towards zero . It is due to incoherence of H
nuclei.
Now we will talk about
contrast…

T1 relaxation
After protons are
Excited with RF
pulse They move
out of Alignment
with B0
But once the RF
Pulse is stopped
they Realign after
some Time And
this is called t1
relaxation
T1 is defined as the time it takes for the hydrogen nucleus

T2 r: T2 is the time when transverse magnetization decreased to
37% of the original value.

Different tissues have different relaxation times.
These relaxation time differences is used to generate
image contrast.
WATER: long T1 & short
T2. FAT: short T1 & very short
T2.

TR and TE
▪ TE (echo time) : time interval in which signals are measured after RF excitation
▪ TR (repetition time) : the time between two excitations is called repetition
time
▪ By varying the TR and TE one can obtain T1WI and T2WI & proton density
image.

A and B are two tissues with different relaxation times. Frame 0 shows
the situation before, frame 1 immediately after a 90° pulse. When we
wait for a long time (TR long) the longitudinal magnetization of both
tissues will have
totally recovered (frame 5). A second 90° pulse after this time results in the same
amount of transversal magnetization (frame 6) for both tissues, as was observed
after the first RF pulse (frame 1). the difference in signal is mainly due to

When we do not wait as long , but send in the second RF pulse after a shorter
time ( TR Short), longitudinal magnetization of tissue B, which has the longer
T1, has not
recovered as much as that of tissue A with the shorter T1. The
transversal magnetization of the two tissues after the second RF pulse will
then be different (frame 5). Thus, by changing the time between successive
RF pulses, we can influence and modify magnetization and the signal
intensity of tissues .this will give T1 waited image

▪ Brain has a shorter longitudinal relaxation
time than CSF. With a short TR the signal
intensities of brain and CSF differ more than

How do we obtain a T2-weighted
image?

T2*
DECAY
▪ T2* relaxation – Disturbances in magnetic
field ,magnetic susceptibility, increase the
rate of T2 relaxation.

▪ In general a short TR (<1000ms) and short
TE (<45 ms) scan is T1WI
▪ Long TR (>2000ms) and long TE (>45ms)
scan is T2WI
▪ Long TR (>2000ms) and short TE (<45ms)
scan is proton density image

What happens , when we choose a long TR, as as all tissues
have regained their full longitudinal magnetization.
When we only choose a very short TE then differences in signal
intensity due to differences in T2 have not yet had time to become
pronounced.
The resulting picture is thus neither T1- nor T2-weighted,but
mostly determined by the proton density of the tissues (for this,
ideally TE should be zero).

▪ When we wait a long TR and a long TE , differences in T2 have
had time enough to become pronounced, the resulting picture
is T2-weighted.
When we wait a shorter time TR, differences in T1 influence tissue
contrast to a larger extent, the picture isT1-weighted, especially when
we also
wait a short TE (when signal differences due to differing T2s have not had
time to become pronounced).

Partial saturation/ Saturation
recovery sequence Pulse
sequences

▪ Signal intensity of tissues having a different T1 depending on the
choice of TR: With a long TR, the saturation recovery sequence,
image contrast is determined mainly by proton (spin)density.
▪ With a shorter TR, the partial saturation sequence, the resulting
image is T1- weighted.

▪
▪
The inversion recovery sequence uses a 180° pulse which inverts the
longitudinal magnetization, followed by a 90° pulse after the time TI.
▪ The 90° pulse "tilts“ the magnetization into the transverse (x-y-)
plane, so it can be measured/received.
▪
▪
The tissue with short longitudinal relaxation time goes back to
its original longitudinal magnetization faster, thus has the
shorter T1.
this results in less transversal magnetization after the 90° pulse

fast imaging
sequences
▪ FLASH (Fast Low Angle Shot).
▪ GRASS(Gradient Recalled Acquisition at
Steady State).

▪
▪
▪
The TR is the most time consuming parameter of an imaging sequence
.
It makes sense to shorten TR if we want to make imaging faster. And
this is done in the fast imaging sequence.
▪
▪
it requires some time to deliver a 180° pulse, and with a very short
TR there will not be enough time between the 90° pulses.
▪
▪
▪
This use a different way to refocus the dephasing spins:
instead of a 180° pulse, we apply a magnetic field gradient. This
means that an uneven magnetic field, a gradient field, is
added/superimposed on the existing
magnetic field.

▪ This results in even larger magnetic field
inhomogenecity.
Due to these larger magnetic field inhomogeneities, transverse
magnetization disappears faster(protons dephase faster).
▪ Then the magnetic gradient is switched off, and after a short time
turned back on with the same strength, but in opposite direction.
▪ This results in some rephasing , and thus the signal increases again
to a certain maximum, which is called a gradient echo.

Types of MRI imagings
o T1WI
o T2WI
o FLAIR
o STIR
o DWI
o ADC
o GRE
o MRS
o MT
o Post-Gd images

GRADATION OF INTENSITY
IMAGING
CT SCAN CSF Edema White
Matte
r
Gray
Matte
r
Blood Bone
MRI T1 CSF Edema Gray
Matte
r
White
Matte
r
Cartilage Fat
MRI T2 Cartilage Fat White
Matte
r
Gray
Matte
r
Edema CSF
MRI T2 Flair CSF Cartilage Fat White
Matte
r
Gray
Matte
r
Edema

CT SCAN
MRI T1 Weighted
MRI T2 Weighted
MRI T2 Flair

Dark on
T1
▪
▪
▪
Edema,tumor,infection,inflammation,hemorrhage(hyperacute,chronic)
Low proton density,calcification
Flow void

Bright on T1
o Fat,subacute hemorrhage,melanin,protein rich fluid.
o Slowly flowing blood
o Paramagnetic substances(gadolinium,copper,manganese)
o 9

Bright on T2
▪
▪
Edema,tumor,infection,inflammation,subdural collection
Methemoglobin in late subacute hemorrhage

Dark on
T2
▪
▪
▪
▪
Low proton density,calcification,fibrous tissue
Paramagnetic substances( deoxyhemoglobin , methemoglobin
(intracellular),ferritin ,hemosiderin ,melanin.
Protein rich fluid
Flow void

Which scan best defines the
abnormality
T1 W Images:
Subacute
Hemorrhage Fat-
containing structures
Anatomical Details
T2 W Images:
Edema
Demyelinati
on Infarction
Chronic
Hemorrhage
FLAIR
Images:
Edema,
Demyelinati

Conventional Inversion Recovery
-180° preparatory pulse is applied to flip the net magnetization vector 180° andnull
th signal from a particular entity (eg, water in tissue).
-When the RF pulse ceases, the spinning nuclei begin to relax. When the net
magnetization vector for water passes the transverse plane (the null point for that
tissue), the conventional 90° pulse is applied, and the SE sequence then
continues as before.
-The interval between the 180° pulse and the 90° pulse is the TI ( Inversion Time).

Conventional Inversion Recovery Contd:
▪ At TI, the net magnetization vector of water is very weak, whereas that for
body tissues is strong. When the net magnetization vectors are flipped by the
90° pulse, there is little or no transverse magnetization in water, so no signal is
generated (fluid appears dark), whereas signal intensity ranges from low to high
in tissues with a stronger NMV.
▪ Two important clinical implementations of the inversion recovery concept are:
Short TI inversion-recovery (STIR) sequence
Fluid-attenuated inversion-recovery (FLAIR) sequence.

Short TI inversion-recovery (STIR) sequence
▪
▪
▪
▪
▪
In STIR sequences, an inversion-recovery pulse is used to null the signal
from fat (180° RF Pulse).
When NMVof fat passes its null point , 90° RF pulse is applied. As little or no
longitudinalmagnetization is present and the transverse magnetization is
insignificant.
It is transverse magnetization thatinduces an electric current in the receiver coil
so no signal is generated from fat.
STIRsequences provide excellent depiction of bone marrow edema which may
be the only indication of an occult fracture.
Unlikeconventional fat-saturation sequences STIR sequences are not affected
by magnetic field inhomogeneities, so they are more efficient for nulling the
signal from fat

FSE
STIR
Comparison of fast SE and STIR
sequences for depiction of bone
marrow edema

▪
Fluid-attenuated inversion recovery
(FLAIR)
First described in 1992 and has become one of the corner stones of brain
MR imaging protocols
▪ An IR sequence with a long TR and TE and an inversion time (TI) that is tailored
to null the signal from CSF
▪ In contrast to real image reconstruction, negative signals are recorded as positive
signals of the same strength so that the nulled tissue remains dark and all other
tissues have higher signal intensities.

▪ Most pathologic processes show increased SI on T2-WI, and the conspicuity of
lesions that are located close to interfaces b/w brain parenchyma and CSF may
be poor in conventional SE or FSE T2-WI sequences.
▪ FLAIR images are heavily T2-weighted with CSF signal suppression, highlights
hyperintense lesions and improves their conspicuity and detection, especially
when located adjacent to CSF containing spaces

▪ In addition to T2- weightening, FLAIR possesses considerable T1-weighting,
because it largely depends on longitudinal magnetization
▪ As small differences in T1 characteristics are accentuated, mild T1-shortening
becomes conspicuous.
▪ This effect is prominent in the CSF-containing spaces, where increased protein
content results in high SI (eg, associated with subarachnoid space disease)
▪ High SI of hyperacute SAH is caused by T2 prolongation in addition to
T1 shortening

Clinical Applications:
▪ Used to evaluate diseases affecting the brain parenchyma neighboring the CSF-
containing spaces for eg: MS & other demyelinating disorders.
▪ Unfortunately, less sensitive for lesions involving the brainstem & cerebellum,
owing to CSF pulsation artifacts
▪ Helpful in evaluation of neonates with perinatal HIE.
▪ Useful in evaluation of gliomatosis cerebri owing to its superior delineation
of neoplastic spread
▪ Useful for differentiating extra-axial masses eg. epidermoid cysts from
arachnoid cysts. However, distinction is more easier & reliable with DWI.

▪ Mesial temporal sclerosis: m/c pathology in patients with partial complex seizures.
Thin-section coronal FLAIR is the standard sequence in these patients & seen as a
bright small hippocampus on dark background of suppressed CSF-containing
spaces. However, normally also mesial temporal lobes have mildly increased SI
on FLAIR images.
▪ Focal cortical dysplasia of Taylor’s balloon cell type- markedly hyperintense
funnel-shaped subcortical zone tapering toward the lateral ventricle is the
characteristic FLAIR imaging finding
▪ In tuberous sclerosis- detection of hamartomatous lesions, is easier with
FLAIR than with PD or T2-W sequences

▪ Embolic infarcts- Improved visualization
▪ Chronic infarctions- typically dark with a rim of high signal. Bright peripheral
zone corresponds to gliosis, which is well seen on FLAIR and may be used to
distinguish old lacunar infarcts from dilated perivascular spaces.

Subarachnoid Hemorrhage (SAH):
▪ FLAIR imaging surpasses even CT in the detection of traumatic supratentorial
SAH.
▪ It has been proposed that MR imaging with FLAIR, gradient-echo T2*-
weighted, and rapid high-spatial resolution MR angiography could be used to
evaluate patients with suspected acute SAH, possibly obviating the need for CT
and intra-arterial angiography.
▪ With the availability of high-quality CT angiography, this approach may not be
necessary.

Diffusion-weighted MRI
▪ Diffusion-weighted MRI is a example of endogenous contrast, using
the motion of protons to produce signal changes
▪ DWI images is obtained by applying pairs of opposing and
balanced magnetic field gradients (but of differing durations and
amplitudes) around a spin-echo refocusing pulse of a T2 weighted
sequence.
Stationary water molecules are unaffected by the paired gradients, and
thus retain their signal. Nonstationary water molecules acquire phase
information from the first gradient, but are not rephased by the
second gradient, leading to an overall loss of the MR signal

• The normal motion of water molecules within living tissues is
random (brownian motion).
• In acute stroke, there is an alteration of homeostasis
• Acute stroke causes excess intracellular water accumulation, or cytotoxic
edema, with an overall decreased rate of water molecular diffusion within
the affected tissue.
▪
•
•
•
Reduction of extracellular space
Tissues with a higher rate of diffusion undergo a greater loss of signal in a
given period of time than do tissues with a lower diffusion rate.
Therefore, areas of cytotoxic edema, in which the motion of water
molecules is restricted, appear brighter on diffusion-weighted images
because of lesser signal losses
▪ Restriction of DWI is not specific for stroke

description
T1
T
2
FLAI
R
DW
I
AD
C
White
matter
hig
h
lo
w
intermediate
low
lo
w
Grey
matter
intermedia
te
intermedia
te
hig
h
intermedia
te
intermedia
te
CSF lo
w
hig
h
lo
w
lo
w
hig
h

▪ DW images usually performed with echo-planar sequences which
markedly decrease imaging time, motion artifacts and increase
sensitivity to signal changes due to molecular motion.
▪ The primary application of DW MR imaging has been in brain
imaging, mainly because of its exquisite sensitivity to early detection of
ischemic stroke

▪ The increased sensitivity of diffusion-weighted MRI in detecting
acute ischemia is thought to be the result of the water shift
intracellularly restricting motion of water protons (cytotoxic
edema), whereas the conventional T2 weighted images show signal
alteration mostly as a result of vasogenic edema

• Core of infarct = irreversible damage
•
•
Surrounding ischemic area  may be salvaged
DWI: open a window of opportunity during which Tt is beneficial
•
•
•
Regions of high mobility “rapid diffusion”  dark
Regions of low mobility “slow diffusion”  bright
Difficulty: DWI is highly sensitive to all of types of motion (blood flow,
pulsatility, patient motion).

▪
▪
▪
Ischemic Stroke
Extra axial masses: arachnoid cyst versus epidermoid
tumor Intracranial Infections
▪
▪
Pyogenic infection
Herpes encephalitis
Creutzfeldt-Jakob disease
Trauma
Demyelination

Apparent Diffusion Coefficient
o It is a measure of diffusion
o Calculated by acquiring two or more images with a different
gradient duration and amplitude (b-values)
o To differentiate T2 shine through effects or artifacts from real ischemic
lesions.
o The lower ADC measurements seen with early ischemia,
o An ADC map shows parametric images containing the apparent diffusion
coefficients of diffusion weighted images. Also called diffusion map

▪ The ADC may be useful for estimating the lesion age and
distinguishing acute from subacute DWI lesions.
▪ Acute ischemic lesions can be divided into hyperacute lesions (low
ADC and DWI-positive) and subacute lesions (normalized ADC).
▪ Chronic lesions can be differentiated from acute lesions by
normalization of ADC and DWI.
▪ a tumour would exhibit more restricted apparent diffusion
compared with a cyst because intact cellular membranes in a
tumour would hinder the free movement of water molecules

Nonischemic causes for
decreased ADC
▪ Abscess
▪ Lymphoma and other
tumors
▪ Multiple sclerosis
▪ Seizures
▪ Metabolic (Canavans )

Evaluation of acute stroke on DWI
▪
▪
▪
▪
▪
The DWI and ADC maps show changes in ischemic brain within
minutes to few hours
The signal intensity of acute stroke on DW images increase
during the first week after symptom onset and decrease
thereafter, but signal remains hyper intense for a long period
(up to 72 days in the study by Lausberg et al)
The ADC values decline rapidly after the onset of ischemia and
subsequently increase from dark to bright 7-10 days later .
This property may be used to differentiate the lesion older than
10 days from more acute ones (Fig 2).
Chronic infarcts are characterized by elevated diffusion and
appear hypo, iso or hyper intense on DW images and
hyperintense on ADC maps

DW MR imaging characteristics of Various Disease Entities
MR Signal Intensity
Disease
Acute Stroke
DW Image
High
ADC Image
Low
ADC
Restricted
Cause
Cytotoxic edema
Chronic Strokes Variable High Elevated Gliosis
Hypertensive
encephalopathy
Variable High Elevated Vasogenic edema
Arachnoid cyst Low High Elevated Free water
Epidermoid mass High Low Restricted Cellular tumor
Herpes encephalitis High Low Restricted Cytotoxic edema
CJD High Low Restricted Cytotoxic edema
MS acute lesions Variable High Elevated Vasogenic edema
Chronic lesions Variable High Elevated Gliosis

Clinical Uses of DWI &
Stroke: ADC
▪ Hyperacute Stage:- within one hour minimal hyperintensity
seen in DWI and ADC value decrease 30% or more below normal
(Usually
<50X10-4 mm2/sec)
▪ Acute Stage:- Hyperintensity in DWI and ADC value low but after 5-
7days of ictus ADC values increase and return to normal value
(Pseudonormalization)
▪ Subacute to Chronic Stage:- ADC value are increased (Vasogenic
edema) but hyperintensity still seen on DWI (T2 shine effect)

GRE
▪ In a GRE sequence, an RF pulse is applied that partly flips the
NMV into the transverse plane (variableflip angle).
▪ Gradients, as opposed to RF pulses, are used to dephase (negative
gradient) and rephase (positive gradients) transverse
magnetization.
▪ Because gradients donot refocus field inhomogeneities, GRE
sequences with long TEs are T2* weighted (because of
magnetic susceptibility) ratherthan T2 weighted like SE
sequences

GRE Sequences
contd:
▪ This feature of GRE sequences is exploited- in detection of hemorrhage, as the
iron in Hb becomes magnetized locally (produces its own local magnetic
field) andthus dephases the spinning nuclei.
▪ The technique is particularlyhelpful for diagnosing hemorrhagic contusions
such as those in the brain and in pigmented villonodular synovitis.
▪ SE sequences, on the other hand- relativelyimmune from magnetic susceptibility
artifacts, and also less sensitive in depicting hemorrhage and calcification.

GRE
FLAIR
Hemorrhage in right parietal lobe

GRE Sequences
contd:
agnetic susceptibility imaging-
▪ - Basis of cerebral perfusion studies, in which the T2* effects (ie, signal
decrease) createdby gadolinium (a metal injected intravenously as a chelatedion in
aqueous solution, typically in the form of gadopentetate dimeglumine) are
sensitively depicted by GRE sequences.
▪ - Also used in blood oxygenation level–dependent (BOLD) imaging, in which
the relativeamount of deoxyhemoglobin in the cerebral vasculature is measured as
a reflection of neuronal activity. BOLD MR imaging is widelyused for mapping
of human brain function.

Gradient Echo
Pros:
▪ fast technique
Cons:
▪ More sensitive to magnetic
susceptibility artifacts
▪ Clinical use:
▪ eg. Hemorrhage , calcification

Axial T1 (C), T2 (D), and GRE (E) images show corresponding T1-hyperintense and GRE-
hypointense foci with associated T2 hyperintensity (arrows).

MR Spectroscopy
o Magnetic resonance spectroscopy (MRS) is a means of
noninvasive physiologic imaging of the brain that
measures relative levels of various tissue metabolites
o Purcell and Bloch (1952) first detected NMR signals from
magnetic dipoles of nuclei when placed in an
external magnetic field.
o Initial in vivo brain spectroscopy studies were done in the
early 1980s.
o Today MRS-in particular, IH MRS-has become a valuable
physiologic imaging tool with wide clinical applicability.

PRINCIPLES:
o The radiation produced by any substance is dependent on its atomic
composition.
o Spectroscopy is the determination of this chemical composition of a
substance by observing the spectrum of electromagnetic energy
emerging from or through it.
o NMR is based on the principle that some nuclei have associated
magnetic spin properties that allow them to behave like small
magnet.
o In the presence of an externally applied magnetic field, the
magnetic nuclei interact with that field and distribute themselves
to different energy levels.
o These energy states correspond to the proton nuclear spins, either
aligned in the direction of (low-energy spin state) or against the

▪ If energy is applied to the system in the form of a radiofrequency
(RF) pulse that exactly matches the energy between both states. a
condition of resonance occurs.
▪ Chemical elements having different atomic numbers such as
hydrogen ('H) and phosphorus (31P) resonate at different
Larmor RFs.
▪ Small change in the local magnetic field, the nucleus of the atom
resonates at a shifted Larmor RF.
▪ This phenomenon is called the chemical
shift.

Technique:
Single volume and Multivolume
MRS.
1) Single volume:
Stimulated echo acquisition mode
(STEAM)
Point-resolved spectroscopy
(PRESS)
o
o
o It gives a better signal-to noise
ratio
2) Multivolume
MRS:
o chemical shift imaging (CSI) or spectroscopic
imaging (SI)
o much larger area can be covered, eliminating the sampling error
to an extent but significant weakening in the signal-to-noise ratio
and a longer scan time.
o Time of echo: 35 ms and 144ms.
o Resonance frequencies on the x-axis and amplitude (concentration)

Effect Of TE
on
the
peaks
TE
35ms
TE
144ms

NORMAL MRS CREATIN
E
CHOLINE
NA
A

Observable metabolites
Metaboli
te
Location Normal function
ppm
Increas
ed
Lipid
s
0.9 &
1.3
Cell
membrane
component
Hypoxia, trauma, high
grade neoplasia.
Lactat
e
1.3
TE=272
(uprigh
t)
TE=136
(inverte
d)
Denotes
anaerobic
glycolysis
Hypoxia, stroke,
necrosis,
mitochondrial
diseases, neoplasia,
seizure
Alanin
e
1.
5
Amino
acid
Meningio
ma
Acetat
e
1.
9
Anabolic
precursor
Abscess
,
Neoplasi

Principl
e
Metaboli
te
Locatio
n
ppm
metabolite
s
NormalIncreased
function
Decrease
d
NA
A
2 Nonspecific
neuronal
marker
(Reference
for chemical
shift)
Canavan’
s
disease
Neuronal loss,
stroke,
dementia, AD,
hypoxia,
neoplasia,
abscess
Glutamat
e ,
glutamine
, GABA
2.1-
2.4 Neurotransmit
te r
Hypoxia,
HE
Hyponatrem
ia
Succinat
e
2.
4
Part of
TCA
cycle
Brain
abscess
Creatin
e
3.0
3
Cell energy
marker
(Reference
for
metabolite
ratio)
Trauma,
hyperosmol
ar state
Stroke,
hypoxia,
neoplasia

Metaboli
te
Locatio
n
ppm
Norma
l
functio
n
Increas
ed
Decrease
d
Cholin
e
3.
2
Marker of
cell memb
turnover
Neoplasia,
demyelinati
on (MS)
Hypomyelinat
io n
Myoinosit
ol
3.5 &
4
Astrocyt
e
marker
AD
Demyelinati
ng diseases

Metabolite ratios:
Normal abnormal
NAA/ Cr 2.0 <1.6
NAA/ Cho 1.6 <1.2
Cho/Cr 1.2 >1.5
Cho/NAA 0.8 >0.9
Myo/NAA 0.5 >0.8

MR
S
Dec
NAA/Cr Inc
acetate,
succinate,
amino acid,
lactate
Neuodegene
ra tive
Alzheimer
Dec
NAA/Cr
Dec NAA/
Cho
Inc
Myo/NA
A
Slightly inc Cho/
Cr Cho/NAA
Normal
Myo/NAA
± lipid/lactate
Inc Cho/Cr
Myo/NAA
Cho/NAA
Dec
NAA/Cr
±
lipid/lactat
e
Malignan
cy
Demyelinati
ng
disease
Pyogeni
c
absces
s

Clinical Applications of MRS:
o Class A MRS Applications: Useful in Individual
Patients
1) MRS of brain
masses:
Distinguish neoplastic from non neoplastic
masses
Primary from metastatic
masses.
Tumor recurrence vs radiation
necrosis
Prognostication of the
disease
Mark region for stereotactic
biopsy.
Monitoring response to
treatment.
o
o
o
o
o
o
o Research
tool
2) MRS of Inborn Errors of Metabolism
Include the leukodystrophies, mitochondrial disorders, and enzyme defects that cause
an absence or accumulation of metabolites

Class B MRS Applications: Occasionally Useful in
Individual Patients
1) Ischemia, Hypoxia, and Related Brain
Injuries
Ischemic
stroke
o
o Hypoxic ischemic
encephalopathy.
2)Epilepsy
Class C Applications: Useful Primarily in Groups of Patients
(Research)
HIV disease and the
brain
Neurodegenerative
disorders
Amyotrophic lateral
sclerosis
Multiple
sclerosis
Hepatic
encephalopathy
o
o
o
o
o
o Psychiatric
disorders

MAGNETIZATION TRANSFER (MT) MRI
▪ MT is a recently developed MR technique that alters contrast of tissue on
the basis of macromolecular environments.
▪ MTC is most useful in two basic area, improving image contrast and
tissue characterization.
▪ MT is accepted as an additional way to generate unique contrast in MRI
that can be used to our advantage in a variety of clinical applications.

Magnetization transfer (MT) contd:-
▪ Basis of the technique: that the state of magnetization of an atomic nucleus can
be transferred to a like nucleus in an adjacent molecule with different relaxation
characteristics.
▪ Acc. to this theory- H1 proton spins in water molecules can exchange
magnetization with H1 protons of much larger molecules, such as proteins and cell
membranes.
▪ Consequence is that the observed relaxation times may reflect not only
the properties of water protons but also, indirectly, the characteristics of
the macromolecular solidlike environment
▪ MT occurs when RF saturation pulses are placed far from the resonant frequency
of water into a component of the broad macromolecular pool.

▪
▪
▪
▪
These off-resonance pulses, which may be added to standard MR pulse sequences,
reduce the longitudinal magnetization of the restricted protons to zero without
directly affecting the free water protons.
The initial MT occurs between the macromolecular protons and the transiently
bound hydration layer protons on the surface of large molecules’
Saturated bound hydration layer protons then diffuse and mix with the free
water proton pool
Saturation is transferred to the mobile water protons, reducing their longitudinal
magnetization, which results in decreased signal intensity and less brightness
on MR images.

▪ The MT effect is superimposed on the intrinsic contrast of the baseline image
▪ Amount of signal loss on MT images correlates with the amount of
macromolecules in a given tissue and the efficiency of the magnetization
exchange
▪ MT characteristically:
educes the SI of some solid like tissues, such as most of the brain and spinal
cord
Does not influence liquid like tissues significantly, such as the cerebrospinal fluid
(CSF)

CLINICAL
APPLICATIO
N
•
•
•
Useful diagnostic tool in characterization of a variety of CNS infection
In detection and diagnosis of meningitis , encephalitis, CNS
tuberculosis , neurocysticercosis and brain abscess.
TUBERCULOMA
Pre-contrast T1-W MT imaging helps to better assess the disease load in CNS
tuberculosis by improving the detectability of the lesions, with more number
of tuberculomas detected on pre-contrast MT images compared to routine SE
images
• It may also be possible to differentiate T2 hypo intense tuberculoma from T2
hypo intense cysticerus granuloma with the use of MTR, as cysticercus
granulomas show significantly higher MT ratio compared to tuberculomas

NEUROCYSTICERCOSIS
Findings vary with the stage of disease
▪ T1-W MT images are also important in demonstrating perilesional gliosis
in treated neurocysticercus lesions
▪ Gliotic areas show low MTR compared to the gray matter and
white matter. So appear as hyperintense
▪
BRAIN ABSCESS
Lower MTR from tubercular abscess wall in comparison to wall
of pyogenic abscess(~20 vs. ~26)

Qualitative applications:
▪
▪
▪
▪
▪
▪
MR angiography,
postcontrast studies
spine imaging
MT pulses have a greater influence on brain tissue (d/t high conc. of structured
macromolecules such as cholesterol and lipid) than on stationary blood.
By reducing the background signal vessel-to-brain contrast is accentuated,
Not helpful when MR angiography is used for the detection and characterization
of cerebral aneurysms.

GRE images of the cervical spine without (A) and with (B) MT
show improved CSF–spinal cord contrast

Quantitative applications:
▪ Multiple sclerosis: discriminates multiple sclerosis & other demyelinating
disorders, provides measure of total lesion load, assess the spinal cord lesion
burden and to monitor the response to different treatments of multiple sclerosis
systemic lupus erythematosus,
▪
▪ CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts
and
▪
▪
▪
▪
leukoencephalopathy),
Multiple system atrophy,
Amyotrophic lateral sclerosis,
Schizophrenia
Alzheimer’s disease

MTR Quantitative applications contd:
▪
▪
▪ May be used to differentiate between progressive multifocal leukoencephalopathy
and HIV encephalitis
To detect axonal injury in normal appearing splenium of corpus callosum after
head trauma
In chronic liver failure, diffuse MTR abnormalities have been found in normal
appearing brain, which return to normal following liver transplantation

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