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MRI SEQUENCES
Tushar Patil, MD
Senior Resident
Department of Neurology
King George’s 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 (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. (As the compassin the body align in one direction. (As the compass
aligns in the presence of earth’saligns in the presence of earth’s
magnetic field)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 B0
 These extra protons produce net magnetization vector (M)
 Net magnetization depends on B0 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 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
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 IMAGINGSTYPES OF MRI IMAGINGS
 T1WIT1WI
 T2WIT2WI
 FLAIRFLAIR
 STIRSTIR
 DWIDWI
 ADCADC
 GREGRE
 MRSMRS
 MTMT
 Post-Gd imagesPost-Gd images
 MRAMRA
 MRVMRV
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 Cartilag
e
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 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).
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 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
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 Taylor’s balloon cell type- markedly hyperintense funnel-
shaped subcortical zone tapering toward the lateral ventricle is the characteristic
FLAIR imaging finding
 In tuberous sclerosis- detection of hamartomatous lesions, is easier with FLAIR than
with PD or T2-W sequences
 Embolic infarcts- Improved visualization
 Chronic infarctions- typically dark with a rim of high signal. Bright peripheral zone
corresponds to gliosis, which is well seen on FLAIR and may be used to distinguish
old lacunar infarcts from dilated perivascular spaces.
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
mm2
/sec)
 Acute Stage:- Hyperintensity in DWI and ADC value low but after 5-
7days of ictus ADC values increase and return to normal value
(Pseudonormalization)
 Subacute to Chronic Stage:- ADC value are increased (Vasogenic edema)
but hyperintensity still seen on DWI (T2 shine effect)
GRE
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
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.
GREFLAIR
Hemorrhage in right parietal lobe
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.
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 METABOLITESMetabolite 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
Neurotransmit
ter
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)
Hypomyelinat
ion
Myoinositol 3.5 & 4 Astrocyte
marker
AD
Demyelinatin
g 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
Neuodegene
rative
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
Demyelinatin
g 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- 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.
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 CSF–spinal 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
 Alzheimer’s disease
MTR Quantitative applications contd:
 May be used to differentiate between progressive multifocal leukoencephalopathy
and HIV encephalitis
 To detect axonal injury in normal appearing splenium of corpus callosum after head
trauma
 In chronic liver failure, diffuse MTR abnormalities have been found in normal
appearing brain, which return to normal following liver transplantation
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 viewMRA 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
NORMAL MRV OBLIQUE VIEW
NORMAL MRV AP VIEW
THANK YOU

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MRI Sequences Explained: T1, T2, FLAIR & More

  • 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 (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
  • 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 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. (As the compassin the body align in one direction. (As the compass aligns in the presence of earth’saligns in the presence of earth’s magnetic field)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 IMAGINGSTYPES OF MRI IMAGINGS  T1WIT1WI  T2WIT2WI  FLAIRFLAIR  STIRSTIR  DWIDWI  ADCADC  GREGRE  MRSMRS  MTMT  Post-Gd imagesPost-Gd images  MRAMRA  MRVMRV
  • 13. T1 & T2 W IMAGING
  • 14. 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 Cartilag e Fat White Matter Gray Matter Edema CSF MRI T2 Flair CSF Cartilage Fat White Matter Gray Matter Edema
  • 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
  • 22. 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).
  • 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 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
  • 25. Comparison of fast SE and STIR sequences for depiction of bone marrow edema FSE STIR
  • 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.
  • 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.
  • 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 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
  • 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).
  • 42.
  • 43.
  • 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
  • 50.
  • 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 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
  • 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 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
  • 55. 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.
  • 57. 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.
  • 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).
  • 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
  • 69. 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,
  • 70. PRINCIPLE METABOLITESMetabolite 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 Neurotransmit ter 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
  • 71. Metabolite Location ppm Normal function Increased Decreased Choline 3.2 Marker of cell memb turnover Neoplasia, demyelination (MS) Hypomyelinat ion Myoinositol 3.5 & 4 Astrocyte marker AD 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 Dec NAA/Cr Inc acetate, succinate, amino acid, lactate Neuodegene rative 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 Demyelinatin g disease Pyogenic abscess
  • 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)
  • 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
  • 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
  • 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.
  • 92.
  • 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. 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 viewMRA lateral view
  • 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);

Notas do Editor

  1. Lipid increase in high-grade gliomas, meningiomas, demyelination, necrotic foci, and inborn errors of metabolism
  2. NAA is the most prominent one in normal adult brain proton MRS and is used as a reference for determination of chemical shift and nonspecific neuronal marker. Normal absolute concentrations of NAA in the adult brain are generally in the range of 8 to 9 mmol/kg. NAA concentrations are decreased in many brain disorders, resulting in neuronal and axonal loss, such as in neurodegenerative diseases, stroke, brain tumors, epilepsy, and multiple sclerosis, but are increased in Canavan&amp;apos;s disease Cr peak is an indirect indicator of brain intracellular energy stores, tends to be relatively constant in each tissue type in normal brain, mean absolute Cr concentration in normal adult brains of 7.49; reduced in all brain tumors, particularly malignant ones
  3. Cho reflects cell membrane synthesis and Degradation. Processes resulting in hypercellularity (e.g., primary brain neoplasms or gliosis) or myelin breakdown (demyelinating diseases) lead to locally increased Cho concentration, whereas hypomyelinating diseases result in decreased Cho levels. Mean absolute Cho concentration in normal adult brain tissue of 1.32 Ig3 MI is believed to be a glial marker because it is present primarily in glial cells and is absent in neurons; abnormally increased in patients with demyelinating diseases and in those with Alzheimer&amp;apos;s disease Lac levels in normal brain tissue are absent or extremely low (C0.5 Mmol/L), they are essentially undetectable on normal spectra. Found in anaerobic glycolysis, which may be seen with brain neoplasms, infarcts, hypoxia, metabolic disorders or seizure and accumulate within cysts or foci of necrosis.
  4. TOF MRA , in a slab of tissue to be imaged rapid RF pulses are given. Stationary tissue is saturated with rapid RF pulses and loses signal but fresh moving blood entering the slide will retain its signal intensity and will create contrast between flowing blood and background tissue. In PC MRA. The contrast between flowing and stationary tissue is a result of phase difference between protons in two tissues Both POF and PC angiograms can be performed using 2D and 3D techniques
  5. Disadv of MRA high cost , cant identify small vs,susceptibility to complex fow, claustrophobia, not good for root of neck and aortic arch
  6. Submentovertex view
  7. Superior saggital sinus runsalong sup margin of falx cerebri and empty in confluence, recievs sup cerebral vv. Inf sag sinus runs along inf margin falx and continue as straight sinus after merging vein of galen Straigt sinus carried in attachment of falx to tentorium cerebelli, empty in confluence Confluence empty in transeverse sinus which runs along tentorium cerebellito sigmoid sinus and drain in IJV cavernous sinus situated in middle cranial fossa and connected to contralat side by intercavernous sinus Cav sinus drain inferior and superficial cerebr vv, opth vv, sphenoparital sinus and empty via sup and inf petrosal sinus into tr/sigmoid and IJV respectivly
  8. Sup cerebral vv drain in SSS, inf cebral vv drain in cavernous sinus, sup middle cerebral vv empty via trlard in SSS and labbe vv in transvers sinus