ROLE OF DIFFUSION IMAGING IN CEREBRAL
PATHOLOGY
A Santa
Sibiu
WATER MOVEMENT PROPRIETIES EXPLOITED
BY DIFFUSION
• Restriction of water movement (diffusion)
• Direction of water movement (tractography)
DIFFUSION FOR DOCTORS….
• Diffusion – brownian movement!
• In MRI – diffusion=water molecules movement
• Isotropic vs anisotroppic
• Cellular packing vs cellular laxity
DIFF, ADC, ACI…
• Diff – water movement restriction – hypersignal
• ADC – relative water movement restriction- hyposignal
• ACI – Attenuation Coefficient or Exponential Coefficient – restriction– hypersignal
• ALL THREE ARE NEEDED FOR A CORRECT DEFINITION OF THE PRESENCE AND
INTENSITY OF RESTRICTION!
DIFFUSION IMAGES
• Multiple examinations with different b values
• b = 0 image – T2
• b = 50-80 – reducing of T2 effect in favor of Diff
• b = 800-1000 – “effacing” of T2 effect
ADC MAP
• Apparent Diffusion Coefficient – calculated
• Minimum two b values necessary for calculation.
• Diffusion images depend on b values, structures that have long T2 exhibiting
hypersignal even without much restriction, their attenuation in high b values being
incomplete – low T2 shine through
• In Diff images, the hypersignal is both T2 effect and restriction
• In ADC Map hyposignal is not both T2 and restriction – ADC is more sensitive in
detection of restriction!
ACI
• Atenuation Coefficient (exponential coefficient)
• Calculation that results from dividing the Diff values S i by the T2 values at b=0 .
The result is the complete elimination of T2 influence, the calculated result being
exclusively based on structure diffusion values
• The most sensitive in detection of REAL diffusion proprieties of substance
TRACTOGRAPHY
• Water movement in CNS – along the axons
• Evaluating of water direction of movement – reproduction of the white matter
tracts path
• Color Mapping representing the movement path of water along axonal
shafts, color-coded and 3D recostructed
Anisotropic restriction
Isotropic
Anisotropic NON-restriction
EQUATIONS….
• r2=6Dt (Einstein)
• Diffusion sequences = T2, with two extra gradient impulses, one before and one after a 180
rephasing – motion sensing gradients .
• Stejskall-Tanner diffusion encoding – the more immobile water molecules are between the two
motion sensing gradients, the higher the signal – restriction of water movement. If water molecules
are moving faster, the initial position of the excited molecule is taken by a non-excited one, thus
produceng a drop in the DIFF signal – low restriction structure.
• Si = S0-e –bADC - (Si – signal intensity after the gradient, S 0 – signal intensity before gradient, ADC –
Apparent Diffusion Coefficient on direction “i”, all in the same voxel
• b – factor established by the examiner
• b = g2G2d2(D-d/e) (b depends on the intensity of gradients – G and on the time gradients are
applied – d g being the gyromagnetic constant)
• b0 – T2
• The longer b is, the more diffusion is responsible for the signal, instead of T2
HOW DIFFUSION IMAGES ARE PRODUCED
THE ROLE OF DIFFUSION IN CNS PATHOLOGY
DIFFUSION:
• Detection of edema
• Characterisation of edema (cytotoxic vs vasogenic)
• Detection of other restrictive elements (tightly packed masses,
pathologic content – epidermoid, puss, blood)
TRACTOGRAPHY
• Showing white matter tracts
• The influence of pathology upon white matter tracts (distruction,
infiltration, deviation)
CYTOTOXIC VERSUS VASOGENIC EDEMA
• T2 and FLAIR – both types of edema are shown as hypersignal (cannot be
diferetiated by conventional sequences)
• DIFF –cytotoxic edema = high signal, vasogenic edema = low signal
• ADC –cytotoxic edema = low signal, vasogenic edema = high signal
CYTOTOXIC VASOGENIC
CYTOTOXIC EDEMA
• Various mechanisms (mainly ischemia) lead to accumulation of water
INSIDE of the cell, in axons, mielin shafts and neurons
• Complex mechanism, of hypoenergetic type, with intracellular ATP decrease,
inefficient Na-K pump, resulting in osmotic gradient that transports the water
inside the cell
• Accumulation of water inside the cell, with swallowing of neurons and glial
cells, resulting in less space for extracellulary water movement – restricted
water.
VASOGENIC EDEMA
• Brain-blood barrier defficiency (locally disrupted by various pathological
conditions)
• Abnormal protein, electrolytes and water passage in EXTRACELULAR space
• The intracellular space is not modified signifficantly
• Extracellular water is not restricted in movement, so vasogenic edema is
NON-RESTRICTIVE (T2 shine-through- progressive decrease of signal with
the b value increase, associated with high ADC signal
BRAIN ISCHEMIA
• Cytotoxic edema
• Early positive images, under 6 hours post start of event
• Evaluation of ischemic process extension and site
• Combined with Perfusion imaging (rCVB) – establishment of penumbra
(reperfuzable cerebral tissue)
STAGES
• Supraacute (under 6 hours) – hiperdiff and hipoADC, 3 hours window for
reperfussion
• Acute (6 hours-3 days) – hiperdiff in attenuation, with low signal in ADC Map
• Subacute (3 days– 3 weeks) – progressive decrease of diff withADC
increase – “Normalising” of aspect
• Chronic (3 weeks-3 months) – “progressiv inversion”, with low signal diff and
high ADC
HYPOXIA
• Not necesarilly ishemic!
• Diff sometimes normal
• ADC most sensitive!
Preop
Postop
PRIMARY AND SECONDARY BRAIN MASSES
• High cellular packed masses – restrictive
• Periferal oedema – NON restrictive
• The combination of restrictive mass-vasogenic edema is highly evocative for expanding
brain mass
• Some BENIGN tumors present with restriction! – epidermoid
• Some malignant secondary deposits DO NOT present with restriction!
Art Portal Late
SVS in centre of lesion SVS periferal
ABSCESS
• Restrictive content (hypercellular puss)
• Periferal vasogenic edema (non-restrictive)
• Variable degree of internal restriction, depending on the necrotic and
inflamatory content
• Abscess wall – contrast uptake!
MENINGITIS-MENINGO-ENCEPHALITIS
• Restrictive content
• Restrictive affected meningeal structures
• Restrictive affected encephalus
HEMORRAGE
• Vasogenic edema
• Non-restrictive in acute phase
• Restrictive in chronic phase
• “Black out” phenomenon due to hemosiderin (low diff and low ADC)
• SWI or T2 star GRE much better in detection and characterisation of blood in
all stages of evolution
Jan 2013
Mar 2016
TRACTO
• Cerebral
• Spinal
• Larger cranial nerves
• Intra or extranevraxial
• Edema versus infiltration versus disruption versus deviation
DTI (TRACTOGRAPHY)
OTHER PATOLOGIES
• Vasculitis (consequences of small infarcts)
• Multiple sclerosis (edema in acute phase - active) – FLAIR and T1 C much
better
• Parasitoses (perilezional vasogen edema, parasitic wall, content)
• Epileptic seissures (ischemia due to hypermetabolism)
• Wallerian degenerescence (post infarct, cortico-spinal tract distruction)
• Creutzfeld-Jakobs (bazal ggl, talamus and cortex, hiperdiff-hipoADC)
• Toxic and metabolic leucodistrophy including drug induced (methotrexate)
