MRI utilizes the magnetic spin property of protons in hydrogen atoms to generate images. It works by aligning hydrogen protons in the body with an external magnetic field, manipulating the alignment with radiofrequency pulses, and detecting signals as the protons relax and return to their original alignment. Different tissues can be distinguished based on their relaxation times, T1 and T2. FLAIR and STIR sequences are used to suppress the signal from cerebrospinal fluid and fat, respectively, improving visualization of lesions near these tissues. FLAIR is particularly useful for evaluating diseases of the brain parenchyma near CSF spaces.

1. GUIDE: Dr Anil Rathva (AP/RD) Presented By: Dr. Bhishm Sevendra(R1/RD)

2. 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.
++
µµ
There is electric chargeThere is electric charge
on the surface of the proton,on the surface of the proton,
thus creating a small currentthus creating a small current
loop and generating magneticloop and generating magnetic
momentmoment µµ..

3.  Body has many such atoms that can act as good MR nuclei (1
H, 13
C, 19
F, 23
Na) .
 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

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

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

6. 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.

7. Precession
 The external magnetic field causes the spinning
proton to ‘wobble’ in a regular manner called
‘PRECESSION.

8. 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.

9. 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 field

10. Manipulating the net
magnetization Magnetization can be manipulated 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.

11. 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

14. 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…

15. 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 to recover
63% of its longitudinal magnetization.

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

18. 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.

19. 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.

20. 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 different proton
densities, we have a so called proton density (or spin density) weighted image.

21. 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

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

23. How do we obtain a T2-weighted
image?

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

28.  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

29. PULSE SEQUENCES

30. spin echo pulse sequence

31. 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).

32.  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).

33. Partial saturation/ Saturation
recovery sequence Pulse sequences

34.  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.

35. Inversion recovery sequence

37.  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

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

39.  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.

40.  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.

41. To be continue…..

42. Types of MRI imagingsTypes of MRI imagings
 T1WIT1WI
 T2WIT2WI
 FLAIRFLAIR
 STIRSTIR
 DWIDWI
 ADCADC
 GREGRE
 MRSMRS
 MTMT
 Post-Gd imagesPost-Gd images

43. T1 & T2 W IMAGING

44. GRADATION OF INTENSITY
IMAGING
CT SCAN CSF Edema White
Matter
Gray
Matter
Blood Bone
MRI T1 CSF Edema Gray
Matter
White
Matter
Cartilage Fat
MRI T2 Cartilage Fat White
Matter
Gray
Matter
Edema CSF
MRI T2 Flair CSF Cartilage Fat White
Matter
Gray
Matter
Edema

45. CT SCAN
MRI T1 Weighted
MRI T2 Weighted
MRI T2 Flair

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

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

48. Bright on T2
 Edema,tumor,infection,inflammation,subdural collection
 Methemoglobin in late subacute hemorrhage

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

50. Which scan best defines the abnormality
T1 W Images:
Subacute Hemorrhage
Fat-containing structures
Anatomical Details
T2 W Images:
Edema
Demyelination
Infarction
Chronic Hemorrhage
FLAIR Images:
Edema,
Demyelination
Infarction esp. in Periventricular location

51. FLAIR & STIR

52. Conventional Inversion Recovery
-180° preparatory pulseis applied to flip the net magnetization vector 180° andnull the
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 transverseplane (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).

53. 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.

54. Short TI inversion-recovery (STIR) sequence
 In STIR sequences, an inversion-recovery pulse is used to nullthe 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 magnetizationis
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 STIRsequences are not affected by
magnetic field inhomogeneities,so they are more efficient for nulling the signal
from fat

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

56. 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.

57.  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

58.  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 sub- arachnoid space disease)
 High SI of hyperacute SAH is caused by T2 prolongation in addition to T1
shortening

59. 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.

60.  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

61.  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.

62. T2 W
FLAIR

63. 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.

64. FLAIR
FLAIR

65. DWI & ADC

66. 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

67. • 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

68. description T1 T2 FLAIR DWI ADC
White matter high low intermediate low low
Grey matter intermediate intermediate high intermediate intermediate
CSF low high low low high

69.  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

70.  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

71. • 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).

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

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

76.  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

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

78. 65 year male- Rt ACA Infarct

79. 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

81. DW MR imaging characteristics of Various Disease Entities
MR Signal Intensity
Disease DW Image ADC Image ADC Cause
Acute Stroke High Low Restricted 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

82. Clinical Uses of DWI &
ADCStroke:
 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)

83. GRE

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

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

86. GREFLAIR
Hemorrhage in right parietal lobe

87. GRE Sequences contd:
Magnetic susceptibility imaging-
 - Basis of cerebral perfusionstudies, 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 gadopentetatedimeglumine) are sensitively
depicted by GRE sequences.
 - Also used in blood oxygenationlevel–dependent (BOLD) imaging, in which the
relativeamount of deoxyhemoglobin in the cerebral vasculature is measuredas a
reflection of neuronal activity. BOLD MR imaging is widelyused for mapping of
human brain function.

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

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

90. MRS & MT-MRI

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

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

93.  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.

94. Technique:
Single volume and Multivolume MRS.
1) Single volume:
 Stimulated echo acquisition mode (STEAM)
 Point-resolved spectroscopy (PRESS)
 It gives a better signal-to noise ratio
2) Multivolume MRS:
 chemical shift imaging (CSI) or spectroscopic imaging (SI)
 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.
 Time of echo: 35 ms and 144ms.
 Resonance frequencies on the x-axis and amplitude (concentration) on the y-
axis.

95. Effect Of TE on the peaks
__________
TE 35ms
___________
___________
TE 144ms
__________

96. Normal mrS CHOLINE CREATINE
NAA

97. Multi voxel MRS

98. Multivoxel MRS

99. Observable metabolites
Metabolite Location
ppm
Normal function Increased
Lipids 0.9 & 1.3 Cell membrane
component
Hypoxia, trauma, high grade
neoplasia.
Lactate 1.3
TE=272
(upright)
TE=136
(inverted)
Denotes anaerobic
glycolysis
Hypoxia, stroke, necrosis,
mitochondrial diseases,
neoplasia, seizure
Alanine 1.5 Amino acid Meningioma
Acetate 1.9 Anabolic precursor Abscess ,
Neoplasia,

100. Principle metabolites
Metabolite Location
ppm
Normal
function
Increased Decreased
NAA 2 Nonspecific
neuronal
marker
(Reference for
chemical shift)
Canavan’s
disease
Neuronal loss,
stroke, dementia,
AD, hypoxia,
neoplasia, abscess
Glutamate ,
glutamine,
GABA
2.1- 2.4
Neurotransmitte
r
Hypoxia, HE Hyponatremia
Succinate 2.4 Part of TCA
cycle
Brain abscess
Creatine 3.03 Cell energy
marker
(Reference for
metabolite
ratio)
Trauma,
hyperosmolar
state
Stroke, hypoxia,
neoplasia

101. Metabolite Location
ppm
Normal
function
Increased Decreased
Choline 3.2 Marker of cell
memb turnover
Neoplasia,
demyelination
(MS)
Hypomyelinatio
n
Myoinositol 3.5 & 4 Astrocyte
marker
AD
Demyelinating
diseases

102. 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

103. MRS
Dec NAA/Cr
Inc acetate,
succinate, amino
acid, lactate
Neuodegenera
tive
Alzheimer
Dec NAA/Cr
Dec NAA/
Cho
Inc
Myo/NAA
Slightly inc Cho/ Cr
Cho/NAA
Normal Myo/NAA
± lipid/lactate
Inc Cho/Cr
Myo/NAA
Cho/NAA
Dec NAA/Cr
± lipid/lactate
Malignancy
Demyelinating
disease Pyogenic
abscess

104. Clinical Applications of MRS:
 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.
 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

105. Class B MRS Applications: Occasionally Useful in Individual
Patients
1) Ischemia, Hypoxia, and Related Brain Injuries
 Ischemic stroke
 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
 Psychiatric disorders

106. 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.

107. 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.

108. Magnetization transfer (MT) contd:-
 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.

109. Magnetization transfer (MT) contd:-
 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:
Reduces 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)

110. MT Effect

111. CLINICAL
APPLICATION• 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

112. T1 T2
MT
PC
MT

113. 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)

114. Magnetization transfer (MT) contd:-
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.

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

116. Magnetization transfer (MT) contd:-
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

117. 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

118. THANK YOU…