4. How does it work?
The human body is mostly water. Water
molecules (H2O) contain hydrogen nuclei
(protons), which become aligned in a magnetic
field. An MRI scanner applies a very strong
magnetic field (about 0.2 to 3 teslas, or roughly a
thousand times the strength of a typical fridge
magnet), which aligns the proton "spins."
5.
6.
7.
8. Protons align themselves parallel to the MRI device's
magnetic field; the Z axis, also termed B0).
9. Excitation. A 90° rotation of the net magnetization to the
transversal plane. The red arrow indicates the direction of
the net magnetization. RF pulse = radiofrequent pulse.
10. When the radiofrequent (RF) pulse is switched off, T1
relaxation occurs; longitudinal magnetization increases.
11.
12. When transmitting a radiofrequent (RF) pulse,
the protons in the transversal plane (XY axis) will
be in-phase.
16. TR & TE
TE (Echo Time): This is the time between an RF
excitation pulse and the collection of the signal.
TR (Repetition Time): is the length of time from
one 90° RF pulse to the next 90° RF pulse.
17. TE and TR
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
18.
19. General MRI Terms
Signal intensity (SI) :
In MRI the terms low, intermediate and high signal
intensity are used.
Depending on the scan protocol, tissue is imaged as
white (= high signal intensity), as a
gray tone (= intermediate signal intensity) or as
dark gray/black (= low signal intensity).
20. Short TR+ short TE= T 1
weighted image
In general a short TR (<1000ms) and short TE
(<45 ms) scan is T1WI.
21. Long TR+ Long TE= T 2
weighted image
Long TR (>2000ms) and long TE (>45ms)
scan is T2WI.
22.
23.
24. Indications:
- Neurological deficit,
- Evidence of radiculopathy,
- Cauda equina compression
- Primary tumors or drop metastases
- Infection/inflammatory disease,
- Multiple sclerosis
- Localized back pain with no radiculopathy (leg pain)
- Postoperative evaluation of lumbar spine: disk vs. scar
27. Water and pathology:
Dark on T1.
White on T2,
Pathology stays white on FLAIR, water doesn't
TISSUE COLOURS
28. TISSUE COLOURS
Bone Marrow: normally fatty
- White on T1
- White on T2
Bone cortex, stones, and ligaments and rapidly flowing
blood
- Dark on everything
29. T1 weighted images
Best demonstrate anatomy
but also show pathology if used after contrast
enhancement.
Typical parameters
TR 300–600 ms (shorter in gradient echo sequences)
TE 10–30 ms (shorter in gradient echo sequences)
30.
31. Signal intensities in T1 weighted image.
Depending on protein content, the tissue may
have an intermediate or high signal intensity (SI).
32. T2 weighted images
• Best demonstrate pathology as most
pathology has an increased water content and
is therefore bright on T2 weighted images.
• Typical parameters
• TR 2000 ms +
• TE 70 ms +
33.
34. Signal intensities in T2 weighted image. Liver, pancreas
and adrenals may have low or intermediate signal
intensity (SI) caused by variation in individual fluid
contents.
35.
36. Brain tumor with surrounding (reactive) edema frontoparietal left.
Both the tumor and the edema have high signal intensity on T2
37.
38. FLAIR
Fluid attenuated inversion recovery.
A type of T2-weighted with suppressed
CSF signal in brain.
The vast majority of intracranial lesions exhibit long
T2 values. FLAIR is a similar sequence to STIR.
39. STIR
Short Time Inversion Recovery (TR 3500,
TE 74)
A type of T2-weighted with Fat
suppressed sequence
40.
41.
42.
43.
44. Axial T2 FLAIR MRI Minimal mass effect and
fluid-attenuated inversion recovery (FLAIR)
45. Gradient-echo Imaging
Used :
- In cases of trauma or
- where hemorrhage is suspected.
The iron content causes dephasing and
signal loss due to susceptibility effects on
T2*–W sequence.
46.
47.
48. Spin Echo:
T1 and T2 and Flair
Hemorrhage Sequence :
T2* or Gradient Echo
Stroke Sequence :
DWI and ADC map
50. In an infarction, the ion pump of the cell membrane will
break down and ions & water will stay in the cell (=
cytotoxic edema). This will increase intracellular
pressure, leading to reduced intracellular diffusion.
Blockage of fluid ,Tissues with large molecules have
relatively lower diffusion.
51. there is limited movement of protons, shown as a
high signal intensity on DWI. This can been
seen in disorders including cytotoxic edema and
inflammation.
To be sure that tissue diffusion has been
reduced, we need to filter the T2 effect out. To
this end a quantitative calculation of diffusion is
made; the so-called ADC map (apparent
diffusion coefficient). The ADC map filters
out the T2 effect and produces inverse images.
Diffusion is reduced when the tissue has high
signal intensity on DWI and low signal intensity
on ADC
52. Quantitative Diffusion:ADC
• If images with different b-values are acquired,a
parameter map of the apparent diffusion
coefficient or ADC can be determined.
• This overcomes “T2 shine-through”, or the
appearance of high DWI signal in areas of long
T2. ADC measurement has been used both in
stroke and tumor studies.
53. Remember: when evaluating diffusion, also look at
the ADC. We do not use the term diffusion
restriction until the tissue has high signal intensity on
DWI and low signal intensity on ADC.
When both DWI and ADC have high signal
intensity, we have a T2 effect without diffusion
component.
Better known as the T2 shine-through. An example
is (reactive) vasogenic edema. In vasogenic edema
there is more free moving water in the extracellular
space. This may develop in response to a tumor.
54. Signal intensity of DWI and ADC in diffusion
restriction, increased diffusion and T2 shine-through.
55.
56.
57.
58.
59. Diffusion restriction secondary to cytotoxic edema in
an infarction in the left hemisphere (middle cerebral
artery territory).
69. We will discuss the following
subjects:
- Role of MR in patients with stroke
- Early MR signs of infarction
- How to identify patients with tissue at risk for
guidance in selecting the appropriate therapy
71. Knowledge of the vascular territories is
important, because it enables you to recognize
infarctions in arterial territories, in watershed
regions and also venous infarctions. It also helps
you to differentiate infarction from other
pathology.
73. The goal of imaging in a patient with acute stroke is: Exclude hemorrhage
Differentiate between irreversibly affected brain tissue and reversibly impaired
tissue (dead tissue versus tissue at risk)
Identify stenosis or occlusion of major extra- and intracranial arteries .
In this way we can select patients who are candidates for thrombolytic therapy.
74.
75.
76.
77. Posterior Inferior Cerebellar Artery (PICA in blue)
The PICA territory is on the inferior occipital surface of the cerebellum
and is in equilibrium with the territory of the AICA in purple, which is on
the lateral side .
Superior Cerebellar Artery (SCA in grey)
The SCA territory is in the superior and tentorial surface of the
cerebellum.
Branches from vertebral and basilar artery
These branches supply the medulla oblongata (in blue) and the pons (in
green).
Anterior Choroideal artery (AchA in blue))
The territory of the AChA is part of the hippocampus, the posterior
limb of the internal capsule and extends upwards to an area lateral to the
posterior part of the cella media.
78. Anterior cerebral artery
(ACA in red)
The ACA supplies :
1-the medial part of the frontal and
2-the parietal lobe and
3- the anterior portion of the corpus callosum,
4-basal ganglia and
5-internal capsule
79. Middle cerebral artery
(MCA in yellow)
The cortical branches of the MCA supply
1-the lateral surface of the hemisphere, except for
the medial part of the frontal and
2-the parietal lobe (anterior cerebral artery), and
3- the inferior part of the temporal lobe (posterior
cerebral artery).
80. Lenticulo-striate arteries
The lateral LSA' s (in orange) are deep
penetrating arteries of the middle cerebral artery
(MCA).
Their territory includes most of the basal ganglia.
The medial LSA' s (indicated in dark red) arise
from the anterior cerebral artery (usually the A1-
segment).
81. Posterior cerebral artery
(PCA in green)
P1 extends from origin of the PCA to the
posterior communicating artery, contributing to
the circle of Willis.
Posterior thalamoperforating arteries branch off
the P1 segment and supply blood to the midbrain
and thalamus.
Cortical branches of the PCA supply the
inferomedial part of the temporal lobe, occipital
pole, visual cortex, and splenium of the corpus
callosum.
82.
83. A detail to illustrate the vascular supply to the basal ganglia.
84.
85.
86.
87.
88.
89.
90.
91.
92. When we look at the DWI-images it is very easy and you
don't have to be an expert radiologist to notice the
infarction.
This is why DWI is called 'the stroke sequence'.
93. On T2WI and FLAIR infarction is seen as high SI.
These sequences detect 80% of infarctions before 24
hours. They may be negative up to 2-4 hours post-ictus!
It is the result of irreversible injury with cell death.
So hyperintensity means BAD news: dead brain.
94.
95. When we compare the findings on T2WI and DWI in time we will
notice the following:
In the acute phase : T2WI will be normal, but in time the
infarcted area will become hyperintense.
The hyperintensity on T2WI reaches its maximum between 7 and
30 days. After this it starts to fade.
DWI : is already positive in the acute phase and then becomes
more bright with a maximum at 7 days.
DWI : in brain infarction will be positive for approximately for 3
weeks after onset (in spinal cord infarction DWI is only positive
for one week!).
ADC : will be of low signal intensity with a maximum at 24 hours
and then will increase in signal intensity and finally becomes bright
in the chronic stage.
96.
97.
98. Acute phase (1-7 d)
Edema increases, maximizing at 48-72 hours, and
MRI signals become more prominent and well
demarcated.
The ischemic area continues to appear as an area of
hypointensity on T1-WI and as a hyperintense area
on T2-WI.
The mass effect can be appreciated in this phase.
99. Subacute phase (7-21 d)
In this phase, the edema resolves and the mass effect
becomes less appreciated; however, the infarcted areas
still appear as a hypointensity on T1-WI and as a
hyperintensity on T2-WI.
100. Chronic phase (>21 d)
In this phase:
the edema completely resolves, and
The infarcted area still appears as a hypointensity on T1-
WI and as a hyperintensity on T2-WI.
Because of tissue loss in the infarcted area by this time,
ex-vacuo ventricular enlargement and widening of the
cortical gyri and fissures take place.
101. PICA
On the CT-images of a left-sided PICA-infarction.
Notice the posterior extention.
102. MR-images of a left-sided PICA-infarction. In unilateral infarcts there is always a sharp delineation in the midline because
the superior vermian branches do not cross the midline, but have a sagittal course.This sharp delineation may not be
evident until the late phase of infarction .In the early phase, edema may cross the midline and create diagnostic difficulties.
Infarctions at pontine level are usually paramedian and sharply defined because the branches of the basilar arery have a
sagittal course and do not cross the midline.Bilateral infarcts are rarely observed because these patients do not survive long
enough to be studied, but sometimes small bilateral infarcts can be seen.
103. SCA : On the MR-image of a cerebellar infarction in the region of the superior
cerebellar artery and also in the brainstem in the territory of the PCA.
Notice the limitation to the midline.
104.
105. On the left images of a hemorrhagic infarction in the area of the deep
perforating lenticulostriate branches of the MCA.
106.
107. Lacunar infarcts
Lacunar infarcts are small infarcts (<15 mm) in
the deeper parts of the brain (basal ganglia,
thalamus, white matter) and in the brain stem.
Lacunar infarcts are caused by occlusion of a
single deep penetrating artery.
Lacunar infarcts account for 25% of all ischemic
strokes.
Atherosclerosis is the most common cause of
lacunar infarcts followed by emboli.
25% of patients with clinical and radiologically
defined lacunes had a potential cardiac cause
for their strokes.
108.
109.
110.
111.
112.
113.
114. Watershed cerebral infarctions,
- also known as border zone infarcts,
occur at the border between cerebral vascular territories where
the tissue is furthest from arterial supply and thus most vulnerable
to reductions in perfusion.
Watershed infarction has been classified to:
- cortical (external) border zones infarct
between ACA, MCA, and PCA territories
-deep (internal) border zones infarct:
between ACA, MCA, and PCA territorie
115.
116. The hypoperfusion in the hemispheres resulted
in multiple internal border zone infarctions.
This pattern of deep watershed infarction is
quite common and should urge you to examine
the carotids.
Episodes of systemic hypotension particularly
with severe stenosis or occlusion of the feeding
arteries, in particular intra and extracranial
carotid arteries, is the typical scenario in which
watershed infarction is encountered.
117.
118.
119.
120.
121.
122.
123. DW MR imaging characteristics of Various Disease Entitie
MR Signal Intensity
Disease DW Image ADC Image ADC Cause
Acute Stroke High Low Restricted Cytotoxic edema
Chronic Strokes Variable High Elevated Gliosis
Hypertensive
encephalopathy
Variable High Elevated Vasogenic edema
Arachnoid cyst Low High Elevated Free water
Epidermoid mass High Low Restricted Cellular tumor
Herpes encephalitis High Low Restricted Cytotoxic edema
CJD High Low Restricted Cytotoxic edema
MS acute lesions Variable High Elevated Vasogenic edema
Chronic lesions Variable High Elevated Gliosis
