Normal mri brain

1. NORMAL MRI BRAIN DR. PIYUSH OJHA DM RESIDENT DEPARTMENT OF NEUROLOGY GOVT MEDICAL COLLEGE, KOTA

2. History: MRI • Paul Lauterbur and Peter Mansfield won the Nobel Prize in Physiology/Medicine (2003) for their pioneering work in MRI • 1940s – Bloch & Purcell: Nuclear Magnetic Resonance (Nobel Prize in 1952) • 1990s - Discovery that MRI can be used to distinguish oxygenated blood from deoxygenated blood. Leads to Functional Magnetic Resonance imaging (fMRI) • 1973 - Lauterbur: gradients for spatial localization of images (ZEUGMATOGRAPHY) • 1977 – Mansfield: first image of human anatomy, first echo planar image

3. The first Human MRI scan was performed on 3rd july 1977 by Raymond Damadian, Minkoff and Goldsmith.

4. MAGNETIC FIELD STRENGTH • S.I. unit of Magnetic Field is Tesla. • Old unit was Gauss. • 1 Tesla = 10,000 Gauss • Earth’s Magnetic Field ~ 0.7 x 10(-4) Tesla • Refrigerator Magnet ~ 5 x 10(-3) Tesla

5. • MRI is based on the principle of nuclear magnetic resonance (NMR) • Two basic principles of NMR 1. Atoms with an odd number of protons 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) • MRI utilizes this magnetic spin property of protons of hydrogen to produce images. MRI

6. • Hydrogen nucleus has an unpaired proton which is positively charged • Hydrogen atom is the only major element 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 1H) imaging

7. • 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. TR & TE

8. BASIC MR BRAIN SEQUENCES • T1 • T2 • FLAIR • DWI • ADP • MRA • MRV • MRS

9. • SHORT TE • SHORT TR • BETTER ANATOMICAL DETAILS • FLUID DARK • GRAY MATTER GRAY • WHITE MATTER WHITE T1 W IMAGES

10. • MOST PATHOLOGIES DARK ON T1 • BRIGHT ON T1 – Fat – Haemorrhage – Melanin – Early Calcification – Protein Contents (Colloid cyst/ Rathke cyst) – Posterior Pituitary appears BRIGHT ON T1 – Gadolinium

11. T1 W IMAGES

12. • LONG TE • LONG TR • BETTER PATHOLOGICAL DETAILS • FLUID BRIGHT • GRAY MATTER RELATIVELY BRIGHT • WHITE MATTER DARK T2 W IMAGES

13. T1W AND T2 W IMAGES

14. • LONG TE • LONG TR • SIMILAR TO T2 EXCEPT FREE WATER SUPRESSION (INVERSION RECOVERY) • Most pathology is BRIGHT • Especially good for lesions near ventricles or sulci (eg Multilpe Sclerosis) FLAIR – Fluid Attenuated Inversion Recovery Sequences

15. CT FLAIRT2 T1

16. T1W T2W FLAIR(T2) TR SHORT LONG LONG TE SHORT LONG LONG CSF LOW HIGH LOW FAT HIGH LOW MEDIUM BRAIN LOW HIGH HIGH EDEMA LOW HIGH HIGH

17. MRI BRAIN :AXIAL SECTIONS

18. Post Contrast Axial MR Image of the brain Post Contrast sagittal T1 Weighted M.R.I. Section at the level of Foramen Magnum Cisterna Magna . Cervical Cord . Nasopharynx . Mandible . Maxillary Sinus

19. Post Contrast Axial MR Image of the brain Post Contrast sagittal T1 Wtd M.R.I. Section at the level of medulla Sigmoid Sinus Medulla Internal Jugular Vein Cerebellar Tonsil Orbits

20. ICA Temporal lobe Post Contrast sagittal T1 Wtd M.R.I. Section at the level of Pons Cerebellar Hemisphere Vermis IV Ventricle Pons Basilar Artery Cavernous Sinus MCP IAC Mastoid Sinus

21. Post Contrast Axial MR Image of the brain Post Contrast sagittal T1 Wtd M.R.I. Section at the level of Mid Brain Aqueduct of Sylvius Orbits Posterior Cerebral ArteryMiddle Cerebral Artery Midbrain Frontal Lobe Temporal Lobe Occipital Lobe

22. Fig. 1.5 Post Contrast Axial MR Image of the brain Post Contrast sagittal T1 Wtd M.R.I. Section at the level of theIII Ventricle Occipital Lobe III Ventricle Frontal lobe Temporal Lobe Sylvian Fissure

23. Fig. 1.6 Post Contrast Axial MR Image of the brain Post Contrast sagittal T1 Wtd M.R.I. Section at the level of Thalamus Superior Sagittal Sinus Occipital Lobe Choroid Plexus . Internal Cerebral Vein Frontal Horn Thalamus Temp Lobe Internal Capsule . Putamen Caudate Nucleus Frontal Lobe

24. Post Contrast sagittal T1 Wtd M.R.I. Section at the level of Corpus Callosum Genu of corpus callosum Splenium of corpus callosum Choroid plexus within the body of lateral ventricle

25. Post Contrast Axial MR Image of the brain Post Contrast sagittal T1 Wtd M.R.I. Section at the level of Body of Corpus Callosum Parietal Lobe Body of the Corpus Callosum Frontal Lobe

26. Post Contrast Axial MR Image of the brain Post Contrast sagittal T1 Wtd M.R.I. Section above the Corpus Callosum Parietal Lobe Frontal Lobe

27. MRI BRAIN :SAGITTAL SECTIONS

28. Grey Matter White Matter

29. White Matter Cerebellum Grey Matter Frontal Lobe Parietal Lobe Temporal Lobe Lateral Sulcus Occipital Lobe

30. Gyri of cerebral cortex Sulci of cerebral Cortex Cerebellum Frontal Lobe Temporal Lobe

31. Frontal Lobe Temporal Lobe Parietal Lobe Occipital Lobe Cerebellum

32. Frontal Lobe Parietal Lobe Orbit Occipital Lobe Transverse sinus Cerebellar Hemisphere

33. Optic Nerve Precentral Sulcus Lateral Ventricle Occipital Lobe Maxillary sinus

34. Caudate Nucleus Corpus callosum Thalamus Tongue Pons Tentorium Cerebell

35. Splenium of Corpus callosum Pons Ethmoid air Cells Inferior nasal Concha Midbrain Fourth Ventricle Genu of Corpus Callosum Hypophysis Thalamus

36. Splenium of Corpus callosumGenu of corpus callosum Pons Superior Colliculus Inferior Colliculus NasalNasal Septuml Medulla Body of corpus callosum Thalamus

37. Cingulate Gyrus Genu of corpus callosum Ethmoid air cells Oral cavity Splenium of Corpus callosum Fourth Ventricle

38. Frontal Lobe Maxillary Sinus Parietal Lobe Occipital Lobe Corpus Callosum Thalamus Cerebellum

39. Frontal Lobe Temporal Lobe Parietal Lobe Lateral Ventricle Occipital Lobe Cerebellum

40. Frontal Lobe Parietal Lobe Superior Temporal Gyrus Lateral Sulcus Inferior Temporal Gyrus Middle Temporal Gyrus External Auditory Meatus

41. . Bone Inferior sagittal sinus Corpus callosum Internal cerebral vein Vein of Galen Superior sagittal sinus Parietal lobe Occipital lobe Straight sinus . Vermis . IV ventricle Cerebellar tonsil Mass intermedia of thalamus Sphenoid Sinus

42. MRI BRAIN :CORONAL SECTIONS

43. Longitudinal Fissure Straight Sinus Superior Sagittal Sinus Sigmoid Sinus Vermis

44. Straight Sinus Cerebellum Lateral Ventricle, Occipital Horn

45. Arachnoid Villi Great Cerebral Vein Tentorium Cerebelli Falx Cerebri Lateral Ventricle Vermis of Cerebellum Cerebellum

46. Splenium of Corpus callosum Posterior Cerebral Artery Superior Cerebellar Artery Foramen Magnum Lateral Ventricle Internal Cerebral Vein Tentorium Cerebelli Fourth Ventricle

47. Cingulate Gyrus Choroid Plexus Superior Colliculus Cerebral Aqueduct Corpus Callosum Thalamus Pineal Gland Vertebral Artery

48. Insula Lateral Sulcus Cerebral Peduncle Olive Crus of Fornix Middle Cerebellar Peduncle

49. Caudate Nucleus Third Ventricle Hippocampus Pons Corpus Callosum Thalamus Cerebral Peduncle Parahippocampal gyrus

50. Lateral Ventricle Body of Fornix Temporal Horn of Lateral Ventricle Uncus of Temporal Lobe Third Ventricle Hippocampus

51. Internal Capsule Caudate Nucleus Optic Tract Insula Lentiform Nucleus Parotid Gland Amygdala Hypothalamus

52. Internal Capsule Cingulate Gyrus Optic Nerve Nasopharynx Internal Carottid Artery Lentiform Nucleus Caudate Nucleusa

53. Longitudinal Fissure Superior Sagittal Sinus Lateral Sulcus Parotid Gland Genu Of Corpus Callosum Temporal Lobe

54. Ethmoid Sinus Frontal Lobe Nasal Turbinate Massetor Nasal Septum Nasal Cavity Tongue

55. Medial Rectus Frontal Lobe Lateral Rectus Inferior Turbinate Superior Rectus Inferior Rectus Maxillary Sinus Tooth

56. Grey Matter Superior Sagittal Sinus White Matter Eye Ball Maxillary Sinus Tongue

57. Coronal Section of the Brain at the level of Pituitary gland Post Contrast Coronal T1 Weighted MRI sp np Frontal lobe Corpus callosum Frontal horn Caudate nucleus III Pituitary stalk Pituitary gland Optic nerve Internal carotid artery Cavernous sinus

58. FLAIR & STIR SEQUENCES

59. Short TI inversion-recovery (STIR) sequence • In STIR sequences, an inversion-recovery pulse is used to null the signal from fat (180° RF Pulse). • STIR sequences provide excellent depiction of bone marrow edema which may be the only indication of an occult fracture.

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

61. 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 • Nulled tissue remains dark and all other tissues have higher signal intensities.

62. • 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 T2-WI sequences. • FLAIR images are heavily T2-weighted with CSF signal suppression, highlights hyper-intense lesions and improves their conspicuity and detection, especially when located adjacent to CSF containing spaces

63. Clinical Applications of FLAIR sequences: • 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 • Mesial temporal sclerosis (MTS) (thin section coronal FLAIR) • Tuberous Sclerosis – for detection of Hamartomatous lesions. • Helpful in evaluation of neonates with perinatal HIE.

64. • 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.

65. T2 W FLAIR

66. T1 W Images: Subacute Hemorrhage Fat-containing structures Anatomical Details T2 W Images: Edema Tumor Infarction Hemorrhage FLAIR Images: Edema, Tumor Periventricular lesion WHICH SCAN BEST DEFINES THE ABNORMALITY

67. • Free water diffusion in the images is Dark (Normal) • Acute stroke, cytotoxic edema causes decreased rate of water diffusion within the tissue i.e. Restricted Diffusion (due to inactivation of Na K Pump ) • Increased intracellular water causes cell swelling DIFFUSION WEIGHTED IMAGES (DWI)

68. • Areas of restricted diffusion are BRIGHT. • Restricted diffusion occurs in – Cytotoxic edema – Ischemia (within minutes) – Abscess

69. Other Causes of Positive DWI • Bacterial abscess, Epidermoid Tumor • Acute demyelination • Acute Encephalitis • CJD • T2 shine through ( High ADC)

70. T2 SHINE THROUGH • Refers to high signal on DWI images that is not due to restricted diffusion, but rather to high T2 signal which 'shines through' to the DWI image. • T2 shine through occurs because of long T2 decay time in some normal tissue. • Most often seen with sub-acute infarctions, due to Vasogenic edema but can be seen in other pathologic abnormalities i.e epidermoid cyst.

71. • To confirm true restricted diffusion - compare the DWI image to the ADC. • In cases of true restricted diffusion, the region of increased DWI signal will demonstrate low signal on ADC. • In contrast, in cases of T2 shine-through, the ADC will be normal or high signal.

72. • Calculated by the software. • Areas of restricted diffusion are dark • Negative of DWI – i.e. Restricted diffusion is bright on DWI, dark on ADC APPARENT DIFFUSION COEFFICIENT Sequences (ADC MAP)

73. • 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.

74. Nonischemic causes for decreased ADC • Abscess • Lymphoma and other tumors • Multiple sclerosis • Seizures • Metabolic (Canavans Disease)

75. 65 year male-Acute Rt ACA Infarct DWI Sequence ADC Sequence

76. Clinical Uses of DWI & ADC in Ischemic 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 episode ADC values increase and return to normal value (Pseudonormalization) • Subacute to Chronic Stage:- ADC value are increased but hyperintensity still seen on DWI (T2 shine effect)

77. • Post contrast images are always T1 W images • Sensitive to presence of vascular or extravascular Gd • Useful for visualization of: – Normal vessels – Vascular changes – Disruption of blood-brain barrier POST CONTRAST (GADOLINIUM ENHANCED)

79. MR ANGIOGRAPHY / VENOGRAPHY

80. • TWO TYPES OF MR ANGIOGRAPHY – CE (contrast-enhanced) MRA – Non-Contrast Enhanced MRA • TOF (time-of-flight) MRA • PC (phase contrast) MRA MR ANGIOGRAPHY

81. CE (CONTRAST ENHANCED) 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  CAN BE USED FOR MRA, MRV  FASTER (WITHIN SECONDS)

82. TOF (TIME OF FLIGHT) MRA  Signal from movement of unsaturated blood converted into image  No contrast agent injected  Motion artifact  Non-uniform blood signal  2D TOF- SENSITIVE TO SLOW FLOW – VENOGRAPHY  3D TOF- SENSITIVE TO HIGH FLOW – MR ANGIOGRAPHY

83. PHASE CONTRAST (PC) MRA  Phase shifts in moving spins (i.e. blood) are measured  Phase is proportional to velocity  Allows quantification of blood flow and velocity  velocity mapping possible  USEFUL FOR – CSF FLOW STUDIES (NPH) – MR VENOGRAPHY

85. Internal Carotid Artery Basilar Artery Vertebral Artery Middle Cerebral Artery Anterior Cerebral Artery Posterior Cerebral Artery Posterior Inferior Cerebellar Artery Superior Cerebellar Artery Anterior Inferior Cerebellar Artery

86. Vertebral Artery Basilar Artery Posterior Cerebral Artery Internal Carotid Artery Anterior Cerebral Artery Middle Cerebral Artery

87. MR VENOGRAPHY

89. NORMAL MR VENOGRAPHY (Lateral View) Superior Sagittal Sinus Internal Jugular Vein Sigmoid Sinus Transverse Sinus Confluence of Sinuses Straight Sinus Vein of Galen Internal Cerebral Vein

90. NORMAL MR VENOGRAPHY (Lateral View)

91. • Form of T2-weighted image which is susceptible to iron, calcium or blood. • Blood, bone, calcium appear dark • Areas of blood often appears much larger than reality (BLOOMING) • Useful for: – Identification of haemorrhage / calcification Look for: DARK only GRE Sequences (GRADIENT RECALLED ECHO)

93. • Non-invasive physiologic imaging of brain that measures relative levels of various tissue metabolites. • Used to complement MRI in characterization of various tissues. MR SPECTROSCOPY

95. Observable metabolites Metabolite Resonating Location ppm Normal function Increased Lipids 0.9 & 1.3 Cell membrane component Hypoxia, trauma, high grade neoplasia. Lactate 1.3 Denotes anaerobic glycolysis Hypoxia, stroke, necrosis, mitochondrial diseases, neoplasia, seizure Alanine 1.5 Amino acid Meningioma Acetate 1.9 Anabolic precursor Abscess , Neoplasia,

96. Metabolite 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 Neurotransmitter 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

97. Metabolite Location ppm Normal function Increased Decreased Choline 3.2 Marker of cell memb turnover Neoplasia, demyelination (MS) Hypomyelination Myoinositol 3.5 & 4 Astrocyte marker AD Demyelinating diseases

98. 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

99. MRS Dec NAA/Cr Inc acetate, succinate, amino acid, lactate Neuodegenerat ive Alzheimer Dec NAA/Cr Dec NAA/ Cho Inc Myo/NAA Slightly inc Cho/ Cr Cho/NAA Normal Myo/NAA ± lipid/lactate Inc Cho/Cr Myo/NAA Cho/NAA Dec NAA/Cr ± lipid/lactate Malignancy Demyelinating disease Pyogenic abscess

100. • ICSOLs • Differentiate Neoplasms from Nonneoplastic Brain Masses • Radiation Necrosis versus Recurrent Tumor • Inborn Errors of Metabolism • RESEARCH PURPOSE FOR NEURODEGENERATIVE DISEASES MRS APPLICATION

101.  Perfusion is the process of nutritive delivery of arterial blood to a capillary bed in the biological tissue means that the tissue is not getting enough blood with oxygen and nutritive elements (ischemia) means neoangiogenesis – increased capillary formation (e.g. tumor activity) PERFUSION STUDIES

102.  Stroke Detection and assessment of ischemic stroke (Lower perfusion )  Tumors Diagnosis, staging, assessment of tumour grade and prognosis Treatment response Post treatment evaluation Prognosis of therapy effectiveness (Higher perfusion) APPLICATIONS OF PERFUSION IMAGING

104. REFERENCES • CT and MRI of the whole body – John R Haaga (5th edition) • Osborne Brain : Imaging, Pathology and Anatomy • Neurologic Clinics (Neuroimaging) : February 2009, volume 27 • Bradley ‘s Neurology in Clinical Practice (6th edition) • Adams and Victor’s: Principles of Neurology (10th edition) • Understanding MRI : basic MR physics : Stuart Currie et al : BMJ 2012 • Harrison’s textbook of Internal Medicine (18th edition)

105. THANK YOU

106. • CISS / 3D FIESTA SEQUENCE • Heavily T2 Wtd Sequences • Allows much higher resolution and clearer imaging of tiny intracranial structures CRANIAL NERVES IMAGING

110. 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.

111. 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

Normal mri brain

Normal mri brain

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