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MRI sequences

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MRI sequences

  1. 1. MRI SEQUENCES Tushar Patil, MD Senior Resident Department of NeurologyKing George’s Medical University Lucknow, India
  2. 2. 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 spin2. A moving electric charge, be it positive or negative, produces a magnetic field Body has many such atoms that can act as good MR nuclei ( 1H, 13 C, 19F, 23Na) Hydrogen nuclei is one of them which is not only positively charged, but also has magnetic spin MRI utilizes this magnetic spin property of protons of hydrogen to elicit images
  3. 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. 4. BODY IN AN EXTERNALMAGNETIC FIELD (B0)•In our natural state Hydrogen ions in body are spinning in a haphazard fashion, and cancel allthe magnetism.•When an external magnetic field is applied protonsin the body align in one direction. (As the compassaligns in the presence of earth’s magnetic field)
  5. 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. 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. 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. 8. T1 RELAXATIONAfter protons areExcited with RF pulseThey move out ofAlignment with B0But once the RF Pulseis stopped they Realignafter some Time Andthis is called t1 relaxationT1 is defined as the time it takes for the hydrogen nucleus to recover 63% of its longitudinal magnetization
  9. 9. T2 relaxation time is the time for 63% of the protons to become dephasedowing to interactions among nearby protons.
  10. 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. 11. Different tissues have different relaxation times.These relaxation time differences is used togenerate image contrast.
  13. 13. T1 & T2 W IMAGING
  14. 14. GRADATION OF INTENSITYIMAGINGCT SCAN CSF Edema White Gray Blood Bone Matter MatterMRI T1 CSF Edema Gray White Cartilage Fat Matter MatterMRI T2 Cartilag Fat White Gray Edema CSF e Matter MatterMRI T2 CSF Cartilage Fat White Gray EdemaFlair Matter Matter
  15. 15. CT SCAN MRI T1 WeightedMRI T2 WeightedMRI T2 Flair
  16. 16. DARK ON T1 Edema,tumor,infection,inflammation,hemorrhage(hyperacute,chronic) Low proton density,calcification Flow void
  17. 17. BRIGHT ON T1 Fat,subacute hemorrhage,melanin,protein rich fluid. Slowly flowing blood Paramagnetic substances(gadolinium,copper,manganese) 9
  18. 18. BRIGHT ON T2 Edema,tumor,infection,inflammation,subdural collection Methemoglobin in late subacute hemorrhage
  19. 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. 20. WHICH SCAN BEST DEFINES THEABNORMALITYT1 W Images:Subacute HemorrhageFat-containing structuresAnatomical DetailsT2 W Images:EdemaDemyelinationInfarctionChronic HemorrhageFLAIR Images:Edema,DemyelinationInfarction esp. in Periventricular location
  21. 21. FLAIR & STIR
  22. 22. CONVENTIONAL INVERSION RECOVERY-180° preparatory pulse is applied to flip the net magnetization vector 180° and null the signal from a particular entity (eg, water in tissue).-When the RF pulse ceases, the spinning nuclei begin to relax. When the net magnetization vector for water passes the transverse plane (the null point for that tissue), the conventional 90° pulse is applied, and the SE sequence then continues as before.-The interval between the 180° pulse and the 90° pulse is the TI ( Inversion Time).
  23. 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) sequenceFluid-attenuated inversion-recovery (FLAIR) sequence.
  24. 24. SHORT TI INVERSION-RECOVERY (STIR)SEQUENCE In STIR sequences, an inversion-recovery pulse is used to null the signal from fat (180° RF Pulse). When NMV of fat passes its null point , 90° RF pulse is applied. As little or no longitudinal magnetization is present and the transverse magnetization is insignificant. It is transverse magnetization that induces an electric current in the receiver coil so no signal is generated from fat. STIR sequences provide excellent depiction of bone marrow edema which may be the only indication of an occult fracture. Unlike conventional fat-saturation sequences STIR sequences are not affected by magnetic field inhomogeneities, so they are more efficient for nulling the signal from fat
  25. 25. FSE STIRComparison of fast SE and STIR sequences for depiction of bone marrow edema
  26. 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. 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. 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. 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. 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. 31.  Embolic infarcts- Improved visualization Chronic infarctions- typically dark with a rim of high signal. Bright peripheral zone corresponds to gliosis, which is well seen on FLAIR and may be used to distinguish old lacunar infarcts from dilated perivascular spaces.
  32. 32. FLAIRT2 W
  33. 33. Subarachnoid Hemorrhage (SAH): FLAIR imaging surpasses even CT in the detection of traumatic supratentorial SAH. It has been proposed that MR imaging with FLAIR, gradient-echo T2*-weighted, and rapid high-spatial resolution MR angiography could be used to evaluate patients with suspected acute SAH, possibly obviating the need for CT and intra-arterial angiography. With the availability of high-quality CT angiography, this approach may not be necessary.
  34. 34. FLAIRFLAIR
  35. 35. DWI & ADC
  36. 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. 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. 38. descriptio T1 T2 FLAIR DWI ADCnWhite high low intermediat low lowmatter eGrey intermediat intermediat high intermediat intermediatmatter e e e eCSF low high low low high
  39. 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. 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. 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. 42.  Ischemic Stroke Extra axial masses: arachnoid cyst versus epidermoid tumor Intracranial Infections Pyogenic infection Herpes encephalitis Creutzfeldt-Jakob disease Trauma Demyelination
  43. 43. 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
  44. 44.  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
  45. 45. NONISCHEMIC CAUSES FORDECREASED ADC Abscess Lymphoma and other tumors Multiple sclerosis Seizures Metabolic (Canavans )
  46. 46. 65 year male- Rt ACA Infarct
  47. 47. 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
  48. 48. DW MR imaging characteristics of Various Disease Entities MR Signal IntensityDisease DW Image ADC Image ADC CauseAcute Stroke High Low Restricted Cytotoxic edemaChronic Strokes Variable High Elevated GliosisHypertensive Variable High Elevated Vasogenic edemaencephalopathyArachnoid cyst Low High Elevated Free waterEpidermoid mass High Low Restricted Cellular tumorHerpes encephalitis High Low Restricted Cytotoxic edemaCJD High Low Restricted Cytotoxic edemaMS acute lesions Variable High Elevated Vasogenic edemaChronic lesions Variable High Elevated Gliosis
  49. 49. CLINICAL USES OF DWI & ADCStroke: Hyperacute Stage:- within one hour minimal hyperintensity seen in DWI and ADC value decrease 30% or more below normal (Usually <50X10-4 mm2/sec) Acute Stage:- Hyperintensity in DWI and ADC value low but after 5- 7days of ictus ADC values increase and return to normal value (Pseudonormalization) Subacute to Chronic Stage:- ADC value are increased (Vasogenic edema) but hyperintensity still seen on DWI (T2 shine effect)
  50. 50. GRE
  51. 51. 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
  52. 52. 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.
  53. 53. FLAIR GRE Hemorrhage in right parietal lobe
  54. 54. 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.
  55. 55. GRADIENT ECHOPros: fast techniqueCons: More sensitive to magnetic susceptibility artifacts Clinical use: eg. Hemorrhage , calcification
  56. 56. Axial T1 (C), T2 (D), and GRE (E) images show corresponding T1-hyperintense and GRE-hypointense foci with associated T2 hyperintensity (arrows).
  57. 57. MRS & MT-MRI
  58. 58. 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.
  59. 59. 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).
  60. 60.  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.
  61. 61. 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 ratio2) 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.
  62. 62. EFFECT OF TE ON THE PEAKS__________TE 35ms______________________TE 144ms__________
  66. 66. OBSERVABLE METABOLITESMetabolite Location Normal function Increased ppm Lipids 0.9 & 1.3 Cell membrane Hypoxia, trauma, high component grade neoplasia.Lactate 1.3 Denotes anaerobic Hypoxia, stroke, necrosis, TE=272 glycolysis mitochondrial diseases, (upright) neoplasia, seizure TE=136 (inverted) Alanine 1.5 Amino acid Meningioma Acetate 1.9 Anabolic Abscess , precursor Neoplasia,
  67. 67. PRINCIPLE METABOLITESMetaboliteLocation Normal Increased Decreased ppm function NAA 2 Nonspecific Canavan’s Neuronal loss, neuronal disease stroke, marker dementia, AD, (Reference for hypoxia, chemical shift) neoplasia, abscessGlutamate , 2.1- 2.4 Hypoxia, HE Hyponatremiaglutamine, Neurotransmit GABA terSuccinate 2.4 Part of TCA Brain abscess cycle Creatine 3.03 Cell energy Trauma, Stroke, hypoxia, marker hyperosmolar neoplasia (Reference for state metabolite ratio)
  68. 68. Metabolite Location Normal Increased Decreased ppm function Choline 3.2 Marker of Neoplasia, Hypomyelinat cell memb demyelination ion turnover (MS)Myoinositol 3.5 & 4 Astrocyte AD marker Demyelinatin g diseases
  69. 69. METABOLITE RATIOS: Normal abnormalNAA/ Cr 2.0 <1.6NAA/ Cho 1.6 <1.2Cho/Cr 1.2 >1.5Cho/NAA 0.8 >0.9Myo/NAA 0.5 >0.8
  70. 70. MRS Inc Cho/Cr Dec NAA/Cr Dec Myo/NAA Slightly inc Cho/ Cr Inc acetate, NAA/Cr Cho/NAA Cho/NAA succinate, Dec NAA/ Dec NAA/Cr Normal Myo/NAA amino acid, Cho ± lipid/lactate ± lipid/lactate lactate Inc Myo/NAA DemyelinatinMalignancy Neuodegene g disease Pyogenic abscess rative Alzheimer
  71. 71. 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 tool2) MRS of Inborn Errors of Metabolism Include the leukodystrophies, mitochondrial disorders, and enzyme defects that cause an absence or accumulation of metabolites
  72. 72. CLASS B MRS APPLICATIONS: OCCASIONALLY USEFUL ININDIVIDUAL PATIENTS1) Ischemia, Hypoxia, and Related Brain Injuries Ischemic stroke Hypoxic ischemic encephalopathy.2)EpilepsyClass 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
  73. 73. 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.
  74. 74. 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 .
  75. 75. 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.
  76. 76. 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 cordDoes not influence liquid like tissues significantly, such as the cerebrospinal fluid (CSF)
  77. 77. MT Effect
  78. 78. 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
  79. 79. T1 T2 PCMT MT
  80. 80. 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)
  81. 81. 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.
  82. 82. GRE images of the cervical spine without (A) and with (B) MT show improved CSF–spinal cord contrast
  83. 83. 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
  84. 84. 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
  85. 85. MRA & MRV
  87. 87. TOF MRASignal from “flight” of unsaturated blood into imageNo contrast agent injectedMotion artifactNon-uniform blood signal PC MRAPhase shifts in moving spins (i.e. blood) are measuredPhase is proportional to velocityAllows quantification of blood flow and velocityCE 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
  88. 88. 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.
  89. 89. 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
  90. 90. MRA lateral view 1. Anterior cerebral artery 2. Anterior communicating artery 3. Basilar artery 4. branches (in insula) of middle cerebral artery 5. Cavernous portion of internal carotid artery 6. Cervical portion of internal carotid artery 7. Genu of middle cerebral artery 8. Intracranial (supraclinoid) internal carotid artery 9. Middle cerebral artery 10. Ophthalmic artery 11. Petrous portion of internal carotid artery 12. Posterior cerebral artery 13. Posterior cerebral artery in ambient cistern 14. posterior cerebral artery in interpeduncular cistern 15. Posterior communicating artery 16. Posterior inf cerebellar artery. 17. Quadrigeminal portion of posterior cerebral artery 18. Superior cerebellar artery 19. Vertebral artery
  91. 91. Magnetic Resonance Venography (MRV) IndicationsFor evaluation of thrombosis or compression by tumor of the cerebral venous sinusin members who are at risk(e.g., otitis media, meningitis, sinusitis, oral contraceptive use, underlying malignantprocess,hypercoagulable disorders)or have signs or symptoms(e.g., papilledema, focal motor or sensory deficits, seizures, or drowsiness andconfusion accompanying a headache);
  95. 95. THANK YOU

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