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Aug 23, 2014
MRI SEQUENCES
Tushar Patil, MD
Senior ResidentDepartment of Neurology
King George’s Medical UniversityLucknow, India
MRI PRINCIPLE MRI is based on the principle of nuclear magnetic resonance
(NMR) Two basic principles of NMR1. Atoms with an odd number of protons or neutrons have spin 2. A moving electric charge, be it positive or negative,
produces a magnetic field Body has many such atoms that can act as good MR nuclei
(1H, 13C, 19F, 23Na) Hydrogen nuclei is one of them which is not only positively
charged, but also has magnetic spin MRI utilizes this magnetic spin property of protons of
hydrogen to elicit images
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 are Hydrogen ions in body are spinning in a haphazard fashion, and cancel all spinning in a haphazard fashion, and cancel all the magnetism.the magnetism.
•When an external magnetic field is applied protons When an external magnetic field is applied protons in the body align in one direction. (As the compass in the body align in one direction. (As the compass aligns in the presence of earth’s aligns 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 RELAXATIONAfter protons are Excited with RF pulse They move out of Alignment with B0
But once the RF Pulseis stopped they Realign after some Time And this is called t1 relaxationT1 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 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 HemorrhageFat-containing structuresAnatomical Details
T2 W Images:EdemaDemyelinationInfarctionChronic 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 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 WFLAIR
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
description
T1 T2 FLAIR DWI ADC
White matter
high low intermediate
low low
Grey matter
intermediate
intermediate
high intermediate
intermediate
CSF low high low low high
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 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.
GREFLAIR
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 level–dependent (BOLD) imaging, in which the relative amount of deoxyhemoglobin in the cerebral vasculature is measured as a reflection of neuronal activity. BOLD MR imaging is widely used for mapping of human brain function.
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 METABOLITESMetabolite Location
ppmNormal function
Increased
Lipids 0.9 & 1.3 Cell membrane component
Hypoxia, trauma, high grade neoplasia.
Lactate 1.3TE=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 Neurotransmi
tter
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, demyelinatio
n (MS)
Hypomyelination
Myoinositol 3.5 & 4 Astrocyte marker
ADDemyelinatin
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/CrInc acetate, succinate,
amino acid, lactate
Neuodegenerative
Alzheimer
Dec NAA/Cr
Dec NAA/ ChoInc
Myo/NAA
Slightly inc Cho/ CrCho/NAA
Normal Myo/NAA± lipid/lactate
Inc Cho/CrMyo/NAACho/NAA
Dec NAA/Cr± lipid/lactate
Malignancy Demyelinating disease Pyogenic
abscess
CLINICAL APPLICATIONS OF MRS: Class A MRS Applications: Useful in Individual Patients1) 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
MTPCMT
NEUROCYSTICERCOSISFindings 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 imageNo contrast agent injectedMotion artifactNon-uniform blood signal
PC MRA
Phase shifts in moving spins (i.e. blood) are measuredPhase is proportional to velocityAllows 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 tissuesResult 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 artery2. Anterior communicating
artery3. Basilar artery4. branches (in insula) of
middle cerebral artery5. Cavernous portion of
internal carotid artery6. Cervical portion of
internal carotid artery7. Genu of middle cerebral
artery8. Intracranial (supraclinoid)
internal carotid artery9. Middle cerebral artery10. Ophthalmic artery11. Petrous portion of internal
carotid artery12. Posterior cerebral artery13. Posterior cerebral artery
in ambient cistern14. posterior cerebral artery
in interpeduncular cistern15. Posterior communicating
artery16. Posterior inf cerebellar
artery.17. Quadrigeminal portion of
posterior cerebral artery18. Superior cerebellar artery19. Vertebral artery
1. Anterior cerebral artery2. Anterior communicating artery3. Basilar artery4. branches (in insula) of middle
cerebral artery5. Cavernous portion of internal
carotid artery6. Cervical portion of internal carotid
artery7. Genu of middle cerebral artery8. Intracranial (supraclinoid) internal
carotid artery9. Middle cerebral artery10. Ophthalmic artery11. Petrous portion of internal carotid
artery12. Posterior cerebral artery13. Posterior cerebral artery in
ambient cistern14. posterior cerebral artery in
interpeduncular cistern15. Posterior communicating artery16. Posterior inf cerebellar artery.17. Quadrigeminal portion of posterior
cerebral artery18. Superior cerebellar artery19. 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
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