DM RESIDENT DEPARTMENT OF NEUROLOGY GOVT MEDICAL COLLEGE KOTA History MRI Paul Lauterbur and Peter Mansfield won the Nobel Prize in PhysiologyMedicine 2003 for their pioneering work in MRI ID: 935121
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Slide1
NORMAL MRI BRAIN
DR. PIYUSH OJHA
DM RESIDENT
DEPARTMENT OF NEUROLOGY
GOVT MEDICAL COLLEGE, KOTA
Slide2History: 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
Slide3The first Human MRI scan was performed on 3rd
july
1977 by Raymond
Damadian, Minkoff and Goldsmith.
Slide4MAGNETIC FIELD STRENGTH
S.I. unit of Magnetic Field is Tesla.
Old unit was Gauss.
1 Tesla = 10,000 GaussEarth’s Magnetic Field ~ 0.7 x 10(-4) TeslaRefrigerator Magnet ~ 5 x 10(-3) Tesla
Slide5MRI 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.
MRI
Slide6Hydrogen nucleus has an unpaired proton which is positively chargedHydrogen 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
Slide7TE (echo time) : time interval in which signals are measured after RF excitationTR (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
Slide8BASIC MR BRAIN SEQUENCES
T1
T2
FLAIRDWIADPMRAMRVMRS
Slide9SHORT TESHORT TR BETTER ANATOMICAL DETAILS
FLUID DARK
GRAY MATTER GRAY
WHITE MATTER WHITE T1 W IMAGES
Slide10MOST PATHOLOGIES DARK ON T1
BRIGHT ON T1
Fat
HaemorrhageMelaninEarly CalcificationProtein Contents (Colloid cyst/ Rathke cyst)Posterior Pituitary appears BRIGHT ON T1
Gadolinium
Slide11T1 W IMAGES
Slide12LONG TELONG TR BETTER PATHOLOGICAL DETAILSFLUID BRIGHT
GRAY MATTER RELATIVELY BRIGHT
WHITE MATTER DARK
T2 W IMAGES
Slide13T1W AND T2 W IMAGES
Slide14LONG TELONG 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
Slide15CT
FLAIR
T2
T1
Slide16T1W
T2W
FLAIR(T2)
TR
SHORTLONG
LONGTESHORTLONGLONGCSFLOW
HIGHLOWFATHIGHLOW
MEDIUMBRAINLOWHIGHHIGHEDEMA
LOW
HIGH
HIGH
Slide17MRI BRAIN :AXIAL SECTIONS
Slide18Post 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
Slide19Post 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
Slide20ICA
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
Slide21Post 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 Artery
Middle Cerebral Artery
Midbrain
Frontal
Lobe
Temporal Lobe
Occipital Lobe
Slide22Fig. 1.5 Post Contrast Axial MR Image of the brain
Post Contrast sagittal T1 Wtd M.R.I.
Section at the level of the
III Ventricle
Occipital Lobe
III Ventricle
Frontal lobe
Temporal Lobe
Sylvian
Fissure
Slide23Fig. 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
Slide24Post 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
Slide25Post 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
Slide26Post
Contrast Axial MR Image of the brain
Post Contrast sagittal T1 Wtd M.R.I.
Section above the Corpus Callosum
Parietal Lobe
Frontal Lobe
Slide27MRI BRAIN :SAGITTAL SECTIONS
Slide28Grey Matter
White Matter
Slide29White
Matter
Cerebellum
Grey Matter
Frontal
Lobe
Parietal Lobe
Temporal Lobe
Lateral
Sulcus
Occipital
Lobe
Slide30Gyri of cerebral
cortex
Sulci
of cerebral
Cortex
Cerebellum
Frontal Lobe
Temporal
Lobe
Slide31Frontal Lobe
Temporal
Lobe
Parietal Lobe
Occipital
Lobe
Cerebellum
Slide32Frontal
Lobe
Parietal
Lobe
Orbit
Occipital Lobe
Transverse sinus
Cerebellar
Hemisphere
Slide33Optic
Nerve
Precentral
Sulcus
Lateral Ventricle
Occipital Lobe
Maxillary sinus
Slide34Caudate
Nucleus
Corpus
callosum
Thalamus
Tongue
Pons
Tentorium
Cerebell
Slide35Splenium
of Corpus
callosum
Pons
Ethmoid air CellsInferior nasal
Concha
Midbrain
Fourth Ventricle
Genu
of Corpus
Callosum
Hypophysis
Thalamus
Slide36Splenium
of Corpus
callosum
Genu
of corpus
callosum
Pons
Superior
Colliculus
Inferior
Colliculus
Nasal
Nasal
Septuml
Medulla
Body
of corpus
callosum
Thalamus
Slide37Cingulate
Gyrus
Genu
of corpus
callosum
Ethmoid
air cells
Oral cavity
Splenium
of Corpus
callosum
Fourth Ventricle
Slide38Frontal
Lobe
Maxillary
Sinus
Parietal Lobe
Occipital Lobe
Corpus
Callosum
Thalamus
Cerebellum
Slide39Frontal Lobe
Temporal
Lobe
Parietal Lobe
Lateral Ventricle
Occipital Lobe
Cerebellum
Slide40Frontal
Lobe
Parietal
Lobe
Superior Temporal
Gyrus
Lateral
Sulcus
Inferior Temporal
Gyrus
Middle Temporal
Gyrus
External Auditory
Meatus
Slide41. 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
Slide42MRI BRAIN :CORONAL SECTIONS
Slide43Longitudinal
Fissure
Straight
Sinus
Superior
Sagittal
Sinus
Sigmoid Sinus
Vermis
Slide44Straight Sinus
Cerebellum
Lateral Ventricle,
Occipital Horn
Slide45Arachnoid
Villi
Great Cerebral
Vein
Tentorium
Cerebelli
Falx
Cerebri
Lateral Ventricle
Vermis
of
Cerebellum
Cerebellum
Slide46Splenium
of
Corpus
callosum
Posterior
Cerebral
Artery
Superior
Cerebellar
Artery
Foramen
Magnum
Lateral Ventricle
Internal Cerebral
Vein
Tentorium
Cerebelli
Fourth Ventricle
Slide47Cingulate
Gyrus
Choroid Plexus
Superior
Colliculus
Cerebral Aqueduct
Corpus
Callosum
Thalamus
Pineal Gland
Vertebral Artery
Slide48Insula
Lateral
Sulcus
Cerebral Peduncle
Olive
Crus
of Fornix
Middle
Cerebellar
Peduncle
Slide49Caudate Nucleus
Third Ventricle
Hippocampus
Pons
Corpus
Callosum
Thalamus
Cerebral
Peduncle
Parahippocampal
gyrus
Slide50Lateral
Ventricle
Body of
Fornix
Temporal Horn of Lateral Ventricle
Uncus
of Temporal Lobe
Third Ventricle
Hippocampus
Slide51Internal
Capsule
Caudate
Nucleus
Optic Tract
Insula
Lentiform
Nucleus
Parotid Gland
Amygdala
Hypothalamus
Slide52Internal
Capsule
Cingulate
Gyrus
Optic Nerve
Nasopharynx
Internal
Carottid
Artery
Lentiform
Nucleus
Caudate
Nucleusa
Slide53Longitudinal
Fissure
Superior
Sagittal
Sinus
Lateral
Sulcus
Parotid Gland
Genu
Of Corpus
Callosum
Temporal Lobe
Slide54Ethmoid
Sinus
Frontal
Lobe
Nasal Turbinate
Massetor
Nasal Septum
Nasal Cavity
Tongue
Slide55Medial Rectus
Frontal
Lobe
Lateral Rectus
Inferior Turbinate
Superior Rectus
Inferior Rectus
Maxillary Sinus
Tooth
Slide56Grey Matter
Superior
Sagittal
Sinus
White
Matter
Eye Ball
Maxillary Sinus
Tongue
Slide57Coronal 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
Slide58FLAIR & STIR SEQUENCES
Slide59Short 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.
Slide60Comparison of fast SE and STIR sequences
for depiction of bone marrow edema
FSE
STIR
Slide61Fluid-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.
Slide62Most 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
Slide63Clinical 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 artifactsMesial temporal sclerosis (MTS) (
thin section coronal FLAIR)Tuberous Sclerosis – for detection of Hamartomatous
lesions.Helpful in evaluation of neonates with perinatal HIE.
Slide64Embolic 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.
Slide65T2 W
FLAIR
Slide66T1 W Images:
Subacute
Hemorrhage
Fat-containing structuresAnatomical Details T2 W Images:
EdemaTumorInfarction
HemorrhageFLAIR Images:Edema, TumorPeriventricular lesionWHICH SCAN BEST DEFINES THE ABNORMALITY
Slide67Free 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)
Slide68Areas of restricted diffusion are
BRIGHT
.
Restricted diffusion occurs in Cytotoxic edemaIschemia (within minutes) Abscess
Slide69Other Causes of Positive DWI
Bacterial abscess,
Epidermoid
TumorAcute demyelinationAcute EncephalitisCJDT2 shine through ( High ADC)
Slide70T2 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.
Slide71To 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.
Slide72Calculated 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)
Slide73The 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.
Slide74Nonischemic
causes for decreased ADC
Abscess
Lymphoma and other tumors
Multiple sclerosisSeizuresMetabolic (
Canavans Disease)
Slide7565 year
male-Acute
Rt
ACA Infarct
DWI Sequence ADC Sequence
Slide76Clinical 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 mm
2/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
(T
2 shine effect)
Slide77Post contrast images are always T1 W imagesSensitive to presence of vascular or
extravascular
Gd Useful for visualization of: Normal vessels Vascular changes Disruption of blood-brain barrier
POST CONTRAST (GADOLINIUM ENHANCED)
Slide78Slide79MR ANGIOGRAPHY / VENOGRAPHY
Slide80TWO TYPES OF MR ANGIOGRAPHY CE (contrast-enhanced) MRA
Non-Contrast Enhanced MRA
TOF (time-of-flight) MRA
PC (phase contrast) MRA
MR ANGIOGRAPHY
Slide81CE (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)
Slide82TOF (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
Slide83PHASE 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 FORCSF FLOW STUDIES (NPH)MR VENOGRAPHY
Slide84Slide85MR ANGIOGRAPHY
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
Slide86MR ANGIOGRAPHY
Vertebral Artery
Basilar Artery
Posterior Cerebral Artery
Internal Carotid Artery
Anterior Cerebral Artery
Middle Cerebral Artery
Slide87MR VENOGRAPHY
Slide88Slide89NORMAL 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
Slide90NORMAL MR VENOGRAPHY (Lateral
View)
Slide91Form 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 / calcificationLook for: DARK only
GRE Sequences (
GRADIENT RECALLED ECHO)
Slide92GRE
FLAIR
Hemorrhage in right parietal lobe
Slide93Non-invasive physiologic imaging of brain that measures relative levels of various tissue metabolites.
Used to complement MRI in characterization of various tissues.
MR SPECTROSCOPY
Slide94NORMAL MR SPECTRUM
Slide95Observable metabolites
Metabolite
Resonating
Location
ppm
Normal function Increased Lipids 0.9 & 1.3Cell membrane componentHypoxia, trauma, high grade neoplasia.
Lactate 1.3Denotes anaerobic glycolysisHypoxia, stroke,
necrosis, mitochondrial diseases, neoplasia, seizureAlanine 1.5Amino acidMeningiomaAcetate
1.9
Anabolic
precursor
Abscess ,
Neoplasia
,
Slide96Metabolite
Location
ppm
Normal function
Increased Decreased
NAA2Nonspecific neuronal marker(Reference for chemical shift)
Canavan’s diseaseNeuronal loss, stroke, dementia, AD, hypoxia, neoplasia, abscessGlutamate , glutamine, GABA
2.1- 2.4 Neurotransmitter Hypoxia, HEHyponatremia Succinate 2.4Part of TCA
cycle
Brain abscess
Creatine
3.03
Cell energy marker
(Reference for metabolite ratio)
Trauma,
hyperosmolar
state
Stroke, hypoxia,
neoplasia
Slide97Metabolite
Location
ppm
Normal function
Increased
Decreased Choline 3.2Marker of cell memb turnoverNeoplasia
, demyelination (MS)Hypomyelination Myoinositol 3.5 & 4
Astrocyte markerADDemyelinating diseases
Slide98Metabolite ratios:
Normal
abnormal
NAA/ Cr2.0
<1.6NAA/ Cho1.6<1.2Cho/Cr1.2>1.5Cho/NAA
0.8>0.9Myo/NAA0.5>0.8
Slide99MRS
Dec NAA/Cr
Inc acetate,
succinate
, amino acid, lactate
Neuodegenerative
AlzheimerDec NAA/CrDec 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
Slide100ICSOLsDifferentiate Neoplasms from Nonneoplastic
Brain Masses
Radiation Necrosis versus Recurrent
TumorInborn Errors of MetabolismRESEARCH PURPOSE FOR NEURODEGENERATIVE DISEASESMRS APPLICATION
Slide101Perfusion
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) PERFUSION STUDIES
Slide102S
troke
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
Slide103Slide104REFERENCES
CT and MRI of the whole body – John R
Haaga
(5th edition)Osborne Brain : Imaging, Pathology and AnatomyNeurologic Clinics (Neuroimaging
) : February 2009, volume 27Bradley ‘s Neurology in Clinical Practice (6th edition)Adams and Victor’s: Principles of Neurology (10
th edition)Understanding MRI : basic MR physics : Stuart Currie et al : BMJ 2012Harrison’s textbook of Internal Medicine (18th edition)
Slide105THANK YOU
Slide106CISS / 3D FIESTA SEQUENCE Heavily T2
Wtd
Sequences
Allows much higher resolution and clearer imaging of tiny intracranial structuresCRANIAL NERVES IMAGING
Slide107I AND II N
III N
V N
VI N
Slide108VII AND VIII N
LOWER CRANIAL N
Slide109TRIGEMINAL NEURALGIA
Slide110MAGNETIZATION 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.
Slide111GRADATION OF INTENSITY
IMAGING
CT SCAN
CSF
Edema
White Matter
Gray Matter
BloodBoneMRI T1CSF
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