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

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

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 MRI is based on the principle of nuclear magnetic resonance (NMR)
Two basic principles of NMR
Atoms with an odd number of protons have spin
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.

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. TR & 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.

8. BASIC MR BRAIN SEQUENCEST1 T2
FLAIR
DWI
ADP
MRA
MRV
MRS

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

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

13. T1W AND T2 W IMAGES

14. FLAIR – Fluid Attenuated Inversion Recovery Sequences
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)

15. CT T1 T2
FLAIR

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

17. MRI BRAIN :AXIAL SECTIONS

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

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

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

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

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

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

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

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

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

27. MRI BRAIN :SAGITTAL SECTIONS

28. White Matter
Grey Matter

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

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

31. Parietal Lobe
Frontal Lobe
Occipital
Lobe
Temporal
Lobe
Cerebellum

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

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

34. Corpus callosum
Thalamus
Caudate
Nucleus
Tentorium
Cerebell
Pons
Tongue

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

36. Thalamus
Body of corpus callosum
Splenium of Corpus callosum
Genu of corpus callosum
Superior
Colliculus
Inferior
Colliculus
Nasal
Nasal Septuml
Pons
Medulla

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

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

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

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

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

42. MRI BRAIN :CORONAL SECTIONS

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

44. Lateral Ventricle,
Occipital Horn
Straight Sinus
Cerebellum

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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. FLAIR
T2 W

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

67. DIFFUSION WEIGHTED IMAGES (DWI)
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

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

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

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 (GADOLINIUM ENHANCED)
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

79. MR ANGIOGRAPHY / VENOGRAPHY

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

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

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

87. MR VENOGRAPHY

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

90. NORMAL MR VENOGRAPHY (Lateral View)

91. GRE Sequences (GRADIENT RECALLED ECHO)
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

92. Hemorrhage in right parietal lobe
FLAIR
GRE
Hemorrhage in right parietal lobe

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

94. NORMAL MR SPECTRUM

95. Observable metabolites
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,
Lipid increase in high-grade gliomas, meningiomas, demyelination, necrotic foci, and inborn errors of metabolism

96. Glutamate , glutamine, GABA
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
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
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'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

97. Marker of cell memb turnover Neoplasia, demyelination (MS)
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
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'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.

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

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

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

102. APPLICATIONS OF PERFUSION IMAGING
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)

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

107. I AND II N
III N
V N
VI N

108. VII AND VIII N
LOWER CRANIAL N

109. TRIGEMINAL NEURALGIA

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
Cartilage
Fat
MRI T2
MRI T2 Flair