normal mri brain

NORMAL MRI BRAIN

DR. PIYUSH OJHADM RESIDENT

DEPARTMENT OF NEUROLOGYGOVT MEDICAL COLLEGE, KOTA

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

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

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

• MRI is based on the principle of nuclear magnetic resonance (NMR)

• Two basic principles of NMR1. 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

• 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

• 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

BASIC MR BRAIN SEQUENCES

• T1• T2• FLAIR• DWI• ADP• MRA• MRV• MRS

• SHORT TE• SHORT TR

• BETTER ANATOMICAL DETAILS• FLUID DARK• GRAY MATTER GRAY• WHITE MATTER WHITE

T1 W IMAGES

• 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

T1 W IMAGES

• LONG TE• LONG TR

• BETTER PATHOLOGICAL DETAILS• FLUID BRIGHT • GRAY MATTER RELATIVELY BRIGHT• WHITE MATTER DARK

T2 W IMAGES

T1W AND T2 W IMAGES

• 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

CT

FLAIRT2

T1

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

MRI BRAIN :AXIAL SECTIONS

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


Post Contrast sagittal T1 Wtd M.R.I.

Section at the level of medulla

Sigmoid Sinus Medulla

Internal Jugular Vein

Cerebellar Tonsil

Orbits

ICA

Temporallobe


Section at the level of Pons

Cerebellar Hemisphere

Vermis

IV Ventricle

Pons

Basilar Artery

Cavernous Sinus

MCPIAC

Mastoid Sinus



Section at the level of Mid Brain

Aqueduct of Sylvius

Orbits

Posterior Cerebral Artery Middle Cerebral Artery

Midbrain

FrontalLobe

Temporal Lobe

Occipital Lobe

Fig. 1.5 Post Contrast Axial MR Image of the brain


Section at the level of theIII Ventricle

Occipital Lobe

III Ventricle

Frontal lobe

Temporal Lobe

Sylvian Fissure

Fig. 1.6 Post Contrast Axial MR Image of the brain


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


Section at the level of Corpus Callosum

Genu of corpus callosum

Splenium of corpus callosum

Choroid plexus within the body of lateral ventricle



Section at the level of Body of Corpus Callosum

Parietal Lobe

Body of the Corpus Callosum

Frontal Lobe



Section above the Corpus Callosum

Parietal Lobe

Frontal Lobe

MRI BRAIN :SAGITTAL SECTIONS

Grey Matter

White Matter

White Matter

Cerebellum

Grey Matter

Frontal Lobe

Parietal Lobe

Temporal Lobe

Lateral Sulcus Occipital Lobe

Gyri of cerebral cortex

Sulci of cerebral Cortex

Cerebellum

Frontal LobeTemporalLobe

Frontal Lobe

Temporal Lobe

Parietal Lobe

OccipitalLobe

Cerebellum

Frontal Lobe

Parietal Lobe

Orbit

Occipital Lobe

Transverse sinus

Cerebellar Hemisphere

Optic Nerve

Precentral Sulcus

Lateral Ventricle

Occipital Lobe

Maxillary sinus

Caudate Nucleus

Corpus callosum

Thalamus

Tongue

Pons

Tentorium Cerebell

Splenium of Corpus callosum

Pons

Ethmoid air Cells

Inferior nasalConcha

Midbrain

Fourth Ventricle

Genu of CorpusCallosum

Hypophysis

Thalamus

Splenium of Corpus callosumGenu of corpus

callosum

Pons

SuperiorColliculus

Inferior Colliculus

NasalNasal Septuml

Medulla

Body of corpus callosum

Thalamus

Cingulate Gyrus

Genu of corpuscallosum

Ethmoid air cells

Oral cavity

Splenium of Corpus callosum

Fourth Ventricle

FrontalLobe

MaxillarySinus

Parietal Lobe

Occipital Lobe

Corpus CallosumThalamus

Cerebellum

Frontal Lobe

TemporalLobe

Parietal Lobe

Lateral Ventricle

Occipital Lobe

Cerebellum

Frontal Lobe

Parietal Lobe

Superior Temporal Gyrus

Lateral Sulcus

Inferior Temporal Gyrus

Middle Temporal Gyrus

External Auditory Meatus

. 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

MRI BRAIN :CORONAL SECTIONS

LongitudinalFissure

Straight Sinus


Sigmoid Sinus

Vermis

Straight Sinus

Cerebellum

Lateral Ventricle,Occipital Horn

Arachnoid Villi

Great CerebralVein

TentoriumCerebelli

Falx Cerebri

Lateral Ventricle

Vermis ofCerebellum

Cerebellum

Splenium ofCorpus callosum

Posterior CerebralArterySuperior CerebellarArtery

Foramen Magnum

Lateral Ventricle

Internal CerebralVein

Tentorium Cerebelli

Fourth Ventricle

Cingulate Gyrus

Choroid Plexus

Superior Colliculus

Cerebral Aqueduct

Corpus Callosum

Thalamus

Pineal Gland

Vertebral Artery

Insula

Lateral Sulcus

Cerebral Peduncle

Olive

Crus of Fornix

Middle CerebellarPeduncle

Caudate Nucleus

Third Ventricle

Hippocampus

Pons

Corpus Callosum

Thalamus

CerebralPeduncle

Parahippocampalgyrus

Lateral VentricleBody of Fornix

Temporal Horn of Lateral Ventricle

Uncus of Temporal Lobe

Third Ventricle

Hippocampus

Internal CapsuleCaudate Nucleus

Optic Tract

InsulaLentiform Nucleus

Parotid Gland

Amygdala

Hypothalamus

Internal Capsule

Cingulate Gyrus

Optic Nerve

Nasopharynx

Internal Carottid Artery

Lentiform Nucleus

Caudate Nucleusa

LongitudinalFissure

Superior SagittalSinus

Lateral Sulcus

Parotid Gland

Genu Of Corpus Callosum

Temporal Lobe

Ethmoid Sinus

Frontal Lobe

Nasal Turbinate

Massetor

Nasal Septum

Nasal Cavity

Tongue

Medial Rectus

Frontal Lobe

Lateral Rectus

Inferior Turbinate

Superior Rectus

Inferior Rectus

Maxillary Sinus

Tooth

Grey Matter


White Matter

Eye Ball

Maxillary Sinus

Tongue

Coronal Section of the Brain at the level of Pituitary glandPost Contrast Coronal T1 Weighted MRI

sp

np

Frontal lobe

Corpus callosum

Frontal horn

Caudate nucleus

III

Pituitary stalk

Pituitary glandOptic nerve

Internal carotid artery

Cavernous sinus

FLAIR & STIR SEQUENCES

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.

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

FSE STIR

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.

• 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

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.

• 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.

T2 WFLAIR

T1 W Images:Subacute HemorrhageFat-containing structuresAnatomical Details

T2 W Images:EdemaTumorInfarctionHemorrhage

FLAIR Images:Edema, TumorPeriventricular lesion

WHICH SCAN BEST DEFINES THE ABNORMALITY

• 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)

• Areas of restricted diffusion are BRIGHT.

• Restricted diffusion occurs in – Cytotoxic edema– Ischemia (within minutes) – Abscess

Other Causes of Positive DWI

• Bacterial abscess, Epidermoid Tumor• Acute demyelination• Acute Encephalitis• CJD• T2 shine through ( High ADC)

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.

• 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.

• 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)

• 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.

Nonischemic causes for decreased ADC• Abscess

• Lymphoma and other tumors

• Multiple sclerosis

• Seizures

• Metabolic (Canavans Disease)

65 year male-Acute Rt ACA Infarct

DWI Sequence ADC Sequence

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)

• 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)

MR ANGIOGRAPHY / VENOGRAPHY

• TWO TYPES OF MR ANGIOGRAPHY

– CE (contrast-enhanced) MRA

– Non-Contrast Enhanced MRA• TOF (time-of-flight) MRA• PC (phase contrast) MRA

MR ANGIOGRAPHY

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)

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

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

MR 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

MR ANGIOGRAPHY

Vertebral Artery

Basilar Artery

Posterior Cerebral Artery

Internal Carotid Artery

Anterior Cerebral Artery

Middle Cerebral Artery

MR VENOGRAPHY

NORMAL MR VENOGRAPHY (Lateral View)


Internal Jugular Vein

Sigmoid Sinus

Transverse Sinus

Confluence of Sinuses

Straight Sinus

Vein of Galen

Internal Cerebral Vein

NORMAL MR VENOGRAPHY (Lateral View)

• 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 / calcificationLook for: DARK only

GRE Sequences (GRADIENT RECALLED ECHO)

GREFLAIR

Hemorrhage in right parietal lobe

• 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

NORMAL MR SPECTRUM

Observable metabolitesMetabolite Resonating

Locationppm

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,

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

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

ADDemyelinating

diseases

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

MRS

Dec NAA/CrInc acetate,

succinate, amino acid, lactate

Neuodegenerative

Alzheimer

Dec NAA/CrDec NAA/

ChoInc

Myo/NAA

Slightly inc Cho/ CrCho/NAA

Normal Myo/NAA± lipid/lactate

Inc Cho/CrMyo/NAACho/NAA

Dec NAA/Cr± lipid/lactate

Malignancy Demyelinating disease Pyogenic

abscess

• ICSOLs• Differentiate Neoplasms from Nonneoplastic

Brain Masses• Radiation Necrosis versus Recurrent Tumor• Inborn Errors of Metabolism• RESEARCH PURPOSE FOR

NEURODEGENERATIVE DISEASES

MRS APPLICATION

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)

PERFUSION STUDIES

Stroke Detection and

assessment of ischemic stroke

(Lower perfusion )

Tumors Diagnosis, staging, assessment of tumour grade and prognosisTreatment responsePost treatment evaluationPrognosis of therapy effectiveness (Higher perfusion)

APPLICATIONS OF PERFUSION IMAGING

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)

THANK YOU

• CISS / 3D FIESTA SEQUENCE

• Heavily T2 Wtd Sequences

• Allows much higher resolution and clearer imaging of tiny intracranial structures

CRANIAL NERVES IMAGING

I AND II N III N

V N VI N

VII AND VIII N

LOWER CRANIAL N

TRIGEMINAL NEURALGIA

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.

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

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