By Dr Piyush Ojha , DM Resident, GMC Kota under guidance of Prof. Dr Vijay Sardana (HOD,Neurology)

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