MRI SEQUENCES

Tushar Patil, MD

Senior Resident
Department of Neurology
King Georges Medical University
Lucknow, India
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 (
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
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



BODY IN AN EXTERNAL MAGNETIC FIELD (B
0
)
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 earths
magnetic field)


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 B
0



These extra protons produce net magnetization vector (M)

Net magnetization depends on B
0
and temperature
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



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

T1 RELAXATION
After protons are
Excited with RF pulse
They move out of
Alignment with B
0
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
T2 relaxation time is the time for 63% of the protons to become dephased
owing to interactions among nearby protons.
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



Different tissues have different relaxation times.
These relaxation time differences is used to
generate image contrast.
TYPES OF MRI IMAGINGS
T1WI
T2WI
FLAIR
STIR
DWI
ADC
GRE
MRS
MT
Post-Gd images

MRA
MRV


T1 & T2 W IMAGING

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

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
Fat,subacute hemorrhage,melanin,protein rich fluid.
Slowly flowing blood
Paramagnetic substances(gadolinium,copper,manganese)









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(deoxy
hemoglobin,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
Demyelination
Infarction
Chronic Hemorrhage

FLAIR Images:
Edema,
Demyelination
Infarction esp. in Periventricular location

FLAIR & STIR

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).


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 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
Comparison of fast SE and STIR sequences
for depiction of bone marrow edema
FSE STIR
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 sub-arachnoid 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 Taylors 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.
T2 W
FLAIR

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.

FLAIR
FLAIR
DWI & ADC

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


descriptio
n
T1 T2 FLAIR DWI ADC
White
matter
high low intermediat
e
low

low

Grey
matter
intermediat
e

intermediat
e

high

intermediat
e

intermediat
e

CSF low

high

low

low

high

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
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

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 )
65 year male- Rt ACA Infarct
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 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
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

mm
2
/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

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
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.

GRE
FLAIR
Hemorrhage in right parietal lobe
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

leveldependent (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.

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).
MRS & MT-MRI
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.

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).


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)
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.

EFFECT OF TE ON THE PEAKS
__________
TE 35ms
___________



___________
TE 144ms
__________
NORMAL MRS CHOLINE CREATINE
NAA
MULTI VOXEL MRS
MULTIVOXEL MRS
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,
PRINCIPLE METABOLITES
Metabolite

Location
ppm

Normal
function

Increased

Decreased
NAA 2 Nonspecific
neuronal
marker
(Reference for
chemical shift)

Canavans
disease
Neuronal loss,
stroke,
dementia, AD,
hypoxia,
neoplasia,
abscess
Glutamate ,
glutamine,
GABA
2.1- 2.4
Neurotransmitt
er
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

Metabolite

Location
ppm

Normal
function

Increased

Decreased
Choline 3.2 Marker of cell
memb turnover
Neoplasia,
demyelination
(MS)
Hypomyelinati
on
Myoinositol 3.5 & 4 Astrocyte
marker
AD
Demyelinating
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

MRS
Dec NAA/Cr
Inc acetate,
succinate,
amino acid,
lactate
Neuodegener
ative
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
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
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
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- H
1
proton spins in water molecules can exchange magnetization
with H
1
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.
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.
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)
MT Effect
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


T1 T2
MT
PC
MT
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)
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.
GRE images of the cervical spine without (A) and with (B) MT
show improved CSFspinal cord contrast
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
Alzheimers 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



MRA & MRV
MR ANGIOGRAPHY


TECHNIQUES



1.TIME OF FLIGHT (TOF)

2.PHASE CONTRAST (PC)

3.CONTRAST ENHANCED MRA (CE MRA)






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
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.


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
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

MRA lateral view


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);




NORMAL MRV LATERAL VIEW
Cavernous sinus
Clivalvenousplexus/inferior
petrosal sinus
NORMAL MRV OBLIQUE VIEW
NORMAL MRV AP VIEW
Ext. jug. vein
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