1. MRI SEQUENCES
Tushar Patil, MD
Senior Resident
Department of Neurology
King George’s Medical University
Lucknow, India

2. MRI PRINCIPLE
 MRI is based on the principle of nuclear magnetic resonance
(NMR)
 Two basic principles of NMR
1. Atoms with an odd number of protons or neutrons have spin
2. A moving electric charge, be it positive or negative, produces a
magnetic field
 Body has many such atoms that can act as good MR nuclei ( 1H,
13
C, 19F, 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

3. WHY HYDROGEN IONS ARE USED IN
MRI?
 Hydrogen nucleus has an unpaired proton which is positively charged
 Every hydrogen nucleus is a tiny magnet which produces small but
noticeable magnetic field
 Hydrogen atom is the only major species in the body that is MR
sensitive
 Hydrogen is abundant in the body in the form of water and fat
 Essentially all MRI is hydrogen (proton) imaging

4. 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. (As the compass
aligns in the presence of earth’s
magnetic field)

5. NET MAGNETIZATION
 Half of the protons align along the magnetic field and rest are aligned opposite
.
 At room temperature, the
population ratio of anti-
parallel versus parallel
protons is roughly 100,000
to 100,006 per Tesla of B0
 These extra protons produce net magnetization vector (M)
 Net magnetization depends on B0 and temperature

6. MANIPULATING THE NET
MAGNETIZATION
 Magnetization can be manipulated by changing the magnetic
field environment (static, gradient, and RF fields)
 RF waves are used to manipulate the magnetization of H nuclei
 Externally applied RF waves perturb magnetization into different
axis (transverse axis). Only transverse magnetization produces
signal.
 When perturbed nuclei return to their original state they emit
RF signals which can be detected with the help of receiving coils

7. 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.
 T2 relaxation or spin spin relaxation - by which magnetization in
X-Y plane decays towards zero in an exponential fashion. It is due
to incoherence of H nuclei.
 T2 values of CNS tissues are shorter than T1 values

8. 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

9. T2 relaxation time is the time for 63% of the protons to become dephased
owing to interactions among nearby protons.

10. 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
 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

11. Different tissues have different relaxation times.
These relaxation time differences is used to
generate image contrast.

12. TYPES OF MRI IMAGINGS
 T1WI  MRA
 T2WI  MRV
 FLAIR
 STIR
 DWI
 ADC
 GRE
 MRS
 MT
 Post-Gd images

13. T1 & T2 W IMAGING

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

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

16. DARK ON T1
 Edema,tumor,infection,inflammation,hemorrhage(hyperacute,chronic)
 Low proton density,calcification
 Flow void

17. BRIGHT ON T1
 Fat,subacute hemorrhage,melanin,protein rich fluid.
 Slowly flowing blood
 Paramagnetic substances(gadolinium,copper,manganese)
 9

18. BRIGHT ON T2
 Edema,tumor,infection,inflammation,subdural collection
 Methemoglobin in late subacute hemorrhage

19. DARK ON T2
 Low proton density,calcification,fibrous tissue
 Paramagnetic substances(deoxy
hemoglobin,methemoglobin(intracellular),ferritin,hemosiderin,melanin.
 Protein rich fluid
 Flow void

20. 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

21. FLAIR & STIR

22. CONVENTIONAL INVERSION
RECOVERY
-180° preparatory pulse is applied to flip the net magnetization vector 180° and null 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 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).

23. 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.

24. 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 NMV of fat passes its null point , 90° RF pulse is applied. As little or no
longitudinal magnetization is present and the transverse magnetization is
insignificant.
 It is transverse magnetization that induces an electric current in the receiver coil so
no signal is generated from fat.
 STIR sequences provide excellent depiction of bone marrow edema which may be
the only indication of an occult fracture.
 Unlike conventional fat-saturation sequences STIR sequences are not affected by
magnetic field inhomogeneities, so they are more efficient for nulling the signal from
fat

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

26. 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.

27.  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

28.  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

29. 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.

30.  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

31.  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.

32. FLAIR
T2 W

33. 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.

34. FLAIR
FLAIR

35. DWI & ADC

36. 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

37. • 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

38. descriptio T1 T2 FLAIR DWI ADC
n
White high low intermediat low low
matter e
Grey intermediat intermediat high intermediat intermediat
matter e e e e
CSF low high low low high

39.  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

40.  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

41. • 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).

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

45. 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

46.  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

47. NONISCHEMIC CAUSES FOR
DECREASED ADC
 Abscess
 Lymphoma and other tumors
 Multiple sclerosis
 Seizures
 Metabolic (Canavans )

48. 65 year male- Rt ACA Infarct

49. 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

51. 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 Variable High Elevated Vasogenic edema
encephalopathy
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

52. CLINICAL USES OF DWI &
ADC
Stroke:
 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)

53. GRE

54. GRE
 In a GRE sequence, an RF pulse is applied that partly flips the
NMV into the transverse plane (variable flip angle).
 Gradients, as opposed to RF pulses, are used to dephase (negative
gradient) and rephase (positive gradients) transverse magnetization.
 Because gradients do not refocus field inhomogeneities, GRE
sequences with long TEs are T2* weighted (because of magnetic
susceptibility) rather than T2 weighted like SE sequences

55. 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) and thus
dephases the spinning nuclei.
 The technique is particularly helpful for diagnosing hemorrhagic contusions such as
those in the brain and in pigmented villonodular synovitis.
 SE sequences, on the other hand- relatively immune from magnetic susceptibility
artifacts, and also less sensitive in depicting hemorrhage and calcification.

56. FLAIR GRE
Hemorrhage in right parietal lobe

57. GRE Sequences contd:
Magnetic susceptibility imaging-
 - Basis of cerebral perfusion studies, in which the T2* effects (ie, signal decrease)
created by gadolinium (a metal injected intravenously as a chelated ion 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
relative amount of deoxyhemoglobin in the cerebral vasculature is measured as a
reflection of neuronal activity. BOLD MR imaging is widely used for mapping of
human brain function.

58. GRADIENT ECHO
Pros:
 fast technique
Cons:
 More sensitive to magnetic susceptibility artifacts
 Clinical use:
 eg. Hemorrhage , calcification

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

60. MRS & MT-MRI

61. 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.

62. 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).

63.  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.

64. 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.

65. EFFECT OF TE ON THE PEAKS
__________
TE 35ms
___________
___________
TE 144ms
__________

66. NORMAL MRS CHOLINE CREATINE
NAA

67. MULTI VOXEL MRS

68. MULTIVOXEL MRS

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

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

71. Metabolite Location Normal Increased Decreased
ppm function
Choline 3.2 Marker of Neoplasia, Hypomyelinat
cell memb demyelination ion
turnover (MS)
Myoinositol 3.5 & 4 Astrocyte AD
marker Demyelinatin
g diseases

72. 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

73. MRS
Inc Cho/Cr Dec NAA/Cr Dec
Myo/NAA Slightly inc Cho/ Cr Inc acetate, NAA/Cr
Cho/NAA Cho/NAA succinate, Dec NAA/
Dec NAA/Cr Normal Myo/NAA amino acid, Cho
± lipid/lactate ± lipid/lactate lactate Inc
Myo/NAA
Demyelinatin
Malignancy Neuodegene
g disease Pyogenic
abscess rative
Alzheimer

74. 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

75. 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

76. 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.

77. 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 .

78. 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.

79. 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)

80. MT Effect

81. 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

82. T1 T2
PC
MT MT

83. 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)

84. 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.

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

86. 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

87. 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

88. MRA & MRV

89. MR ANGIOGRAPHY
TECHNIQUES
1.TIME OF FLIGHT (TOF)
2.PHASE CONTRAST (PC)
3.CONTRAST ENHANCED MRA (CE MRA)

90. TOF MRA
Signal from “flight” of unsaturated blood into image
No contrast agent injected
Motion artifact
Non-uniform blood signal
PC MRA
Phase shifts in moving spins (i.e. blood) are measured
Phase is proportional to velocity
Allows quantification of blood flow and velocity
CE MRA
T1-shortening agent, Gadolinium, injected iv as contrast
Gadolinium reduces T1 relaxation time
When TR<<T1, minimal signal from background tissues
Result is increased signal from Gd containing structures
Faster gradients allow imaging in a single breathhold

91. 2D AND 3D FOURIER TRASFORM
 In 2DFT technique, multiple thin sections of body are studied individually and even
slow flow is identified
 In 3DFT technique , a large volume of tissue is studied ,which can be subsequently
partitioned into individual slices, hence high resolution can be obtained and flow
artifacts are minimised, and less likely to be affected by loops and tortusity of
vessels
 MOTSA(multiple overlapping thin slab acquisition): prevents proton saturation
across the slab. This technique have advantage of both 2D and 3D studies. It is better
than 3D TOF MRA in correctly identifying vascular loops and tortusity,and have
lesser chances of overestimating carotid stenosis.

93. MRA CRANIAL VIEW
1. Anterior cerebral artery
2. Anterior communicating artery
3. Basilar artery
4. branches (in insula) of middle
cerebral artery
5. Cavernous portion of internal
carotid artery
6. Cervical portion of internal
carotid artery
7. Genu of middle cerebral
artery
8. Intracranial (supraclinoid)
internal carotid artery
9. Middle cerebral artery
10. Ophthalmic artery
11. Petrous portion of internal
carotid artery
12. Posterior cerebral artery
13. Posterior cerebral artery in
ambient cistern
14. posterior cerebral artery in
interpeduncular cistern
15. Posterior communicating artery
16. Posterior inf cerebellar
artery.
17. Quadrigeminal portion of
posterior cerebral artery
18. Superior cerebellar artery
19. Vertebral artery

94. MRA lateral view
1. Anterior cerebral artery
2. Anterior communicating artery
3. Basilar artery
4. branches (in insula) of middle cerebral
artery
5. Cavernous portion of internal carotid
artery
6. Cervical portion of internal carotid
artery
7. Genu of middle cerebral artery
8. Intracranial (supraclinoid) internal
carotid artery
9. Middle cerebral artery
10. Ophthalmic artery
11. Petrous portion of internal carotid artery
12. Posterior cerebral artery
13. Posterior cerebral artery in ambient
cistern
14. posterior cerebral artery in
interpeduncular cistern
15. Posterior communicating artery
16. Posterior inf cerebellar artery.
17. Quadrigeminal portion of posterior
cerebral artery
18. Superior cerebellar artery
19. Vertebral artery

95. Magnetic Resonance Venography (MRV)
Indications
For evaluation of thrombosis or compression by tumor of the cerebral venous sinus
in members who are at risk
(e.g., otitis media, meningitis, sinusitis, oral contraceptive use, underlying malignant
process,hypercoagulable disorders)
or have signs or symptoms
(e.g., papilledema, focal motor or sensory deficits, seizures, or drowsiness and
confusion accompanying a headache);

96. NORMAL MRV LATERAL VIEW

97. NORMAL MRV OBLIQUE VIEW

98. NORMAL MRV AP VIEW

99. THANK YOU