MRI Sequences in Neuroradiology

1. C.N.S.
MRI Sequences in Neuroradiology

2. Mohamed Zaitoun
Assistant Lecturer-Diagnostic Radiology
Department , Zagazig University Hospitals
Egypt
FINR (Fellowship of Interventional
Neuroradiology)-Switzerland
zaitoun82@gmail.com

5. Knowing as much as
possible about your enemy
precedes successful battle
and learning about the
disease process precedes
successful management

6. MRI Sequences in Neuroradiology
1-T1
2-T2
3-FLAIR
4-PD
5-DWI & ADC
6-GRE
7-MRS
8-Perfusion

7. 1-Conventional Spin-echo T1 :
-T1 prolongation is hypointense (dark), T1
shortening is hyperintense (bright)
-Most brain tissue are hypointense on T1
-The presence of hyperintensity on T1
(caused by T1 shortening) can be an
important clue leading to a specific
diagnosis

8. Normal T1

9. -Causes of T1 shortening (hyperintensity) include :
1-Gadolinium-based contrast agents
2-Hemoglobin degradation products (intra- and extra-
cellular methemoglobin)
3-Lipid-containing lesions (lipoma, dermoid cyst, implanted
fatty materials, laminar cortical necrosis)
4-Substances with high concentration of proteins (colloid
cyst, craniopharyngioma, Rathke’s cleft cyst, ectopic
posterior pituitary gland)
5-Melanin (metastatic melanoma)
6-Lesions containing mineral substances such as: calcium
(calcifications, Fahr’s disease), copper (Wilson’s
disease) and manganese (hepatic encephalopathy,
manganese intoxication in intravenous drug abusers)

10. Phase Time Hemoglobin ,
Location
T1 T2
1-Hyperacute >6hrs Oxyhemoglobin,
intracellular
Isointense
or
hypointense
Hyperintense
2-Acute 6-72hours Deoxyhemoglobi
n, intracellular
Hypointens
e
Hypointense
3-Early
subacute
3-7days Methemoglobin,
intracellular
Hyperintens
e
Hypointense
4-Late
subacute
1week-month Methemoglobin,
extracellular
Hyperintens
e
Hyperintense
5-Chronic <1month Ferritin and
hemosiderin,
extracellular
Hypointens
e
Hypointense

11. Solid/cystic pituitary macroadenoma of prolactinoma type with hemorrhage
during therapy with bromocriptine, (A&B) axial unenhanced T1-weighted
images show high signal corresponding to methemoglobin, (C) coronal T2
allows for differentiation of methemoglobin types, the lower part of the tumor
contains hypointense intracellular methemoglobin and the upper part of a
lesion contains hyperintense extracellular methemoglobin

12. Left parietal epidural hematoma, (A) T1, (B) T2, hematoma shows high
signal on both images, which is consistent with extracellular
methemoglobin

13. Cerebral venous thrombosis, axial T1, (A) left sigmoid sinus thrombosis, (B)
superior sagittal sinus thrombosis in the inferior-posterior portion (arrow),
(C) superior sagittal sinus thrombosis at the convexity with a thrombosed
draining cortical vein, (D) thrombosis of the right vein of Labbe (arrow)

14. Quadrigeminal plate cistern lipoma (fat)

15. Intracranial lipoma, axial T1 shows small hyperintense lipoma located
near the midline in the quadrigeminal cistern on the left side

16. Non-enhanced CT shows a low-density mass with mural calcifications in the
juxtasellar region (A), T1 without contrast reveals high signal of the lesion
representing its fatty content (B) and hyperintense droplets in the
interpeduncular cistern (B), the frontal horns and sulci (C) after
subarachnoid rupture

17. Lipid-containing filling material in the sphenoid sinus, sagittal T1 shows
iatrogenic hyperintense lipid-containing filling material in the
sphenoid sinus in a patient after transsphenoidal resection of a
pituitary tumor

18. Cortical laminar necrosis, axial T1 demonstrates segmental necrosis of
cerebral cortex visible as linear bands of high signal intensity in the
right temporal cortex at the periphery of a chronic ischemic lesion

19. Hemorrhagic necrosis of the cortex and basal ganglia, axial T1,
hyperintense basal ganglia (A) and cortex along both central sulci
(B) consistent with necrosis with petechial hemorrhage in a patient 3
days after cardiopulmonary resuscitation following cardiac arrest

20. Colloid cyst, T1 shows an ovoid hyperintense lesion in the typical
location near foramina of Monro diagnostic of a colloid cyst (protein)

21. A 21-year-old patient with a solid/cystic craniopharyngioma, located in the
sellar-suprasellar region, sagittal T1 shows high signal intensity of the cystic
portion of the tumor as well as a significant enlargement of sella turcica and
compression of the optic chiasm

22. Rathke’s cleft cyst, sagittal T1-weighted image demonstrates a
hyperintense intrasellar cyst located between anterior and posterior
pituitary lobes

23. Ectopic posterior pituitary lobe, sagittal (A) and coronal (B) T1 show
hyperintense posterior pituitary lobe in the ectopic location within
hypothalamus (arrows)

24. Metastatic melanoma to the right eyeball, axial unenhanced
T1

25. Calcifications within oligodendroglioma, unenhanced T1 (A)
demonstrates hyperintense foci within the tumor in the right frontal
area (arrows) requiring differentiation between hemorrhage and
calcifications, unenhanced CT image (B) confirms presence of
calcifications (arrows)

26. Fahr’s disease, unenhanced T1 (A) reveals high signal intensity of the
heads of both caudate nuclei and putamina. Unenhanced CT (B)
confirms presence of calcification in the region of basal ganglia

27. Wilson’s disease, axial T1 shows bilateral regions of increased signal
intensity within globi pallidi (arrows) due to pathological copper
accumulation

28. Hepatic encephalopathy in a 66-years-old man, axial T1 show bilateral
symmetrical regions of hyperintensity within globi pallidi (arrows) (A)
and substantia nigra in the midbrain (arrows) (B)

29. Manganese intoxication in a 32-year-old intravenous drug abuser. Axial T1
reveal diffuse brain injury due to abnormal manganese accumulation after
15 years of addiction, significantly increased signal can be noted within the
anterior lobe of the pituitary gland (white arrow), superior cerebellar
peduncles (black arrows) (A) as well as basal ganglia and hemispheric white
matter (B)

30. 2-Conventional Spin-echo T2 :
-T2 prolongation is hyperintense, T2 shortening is
hypointense
-Most brain lesions are hyperintense on T2
-Water has a very long T2 relaxation constant
(water is very bright on T2), edema is a hallmark
of many pathologic processes & causes T2
prolongation
-Since most pathologic lesions are hyperintense
on T2, the clue to a specific diagnosis may be
obtained when a lesion is hypointense

31. Normal T2

32. -Causes of hypointensity on T2 :
1-Gadolinium-based contrast materials
2-Hemoglobin degradation products
3-Melanin
4-Mucous or protein-containing lesions
5-Highly cellular lesions (Due to their high
cellularity, malignant tumors such as
medulloblastomas and lymphomas or high-
grade gliomas may appear as T2 hypointense
lesions, Medulloblastomas and lymphomas are
also known as tumors with a very high nuclear to
cytoplasmatic ratio)
6-Lesions containing mineral substances such as:
calcium, copper and iron
7-Turbulent and rapid blood or CSF flow
8-Air-containing spaces

33. Midline glioblastoma multiforme, DSC perfusion weighted imaging, (A)
Cerebral Blood Volume Map showing malignant hyperperfusion
within the tumor core, (B) source T2 image showing hypointense
tumor after contrast injection

34. Phase Time Hemoglobin ,
Location
T1 T2
1-Hyperacute >6hrs Oxyhemoglobin,
intracellular
Isointense
or
hypointense
Hyperintense
2-Acute 6-72hours Deoxyhemoglobi
n, intracellular
Hypointens
e
Hypointense
3-Early
subacute
3-7days Methemoglobin,
intracellular
Hyperintens
e
Hypointense
4-Late
subacute
1week-month Methemoglobin,
extracellular
Hyperintens
e
Hyperintense
5-Chronic <1month Ferritin and
hemosiderin,
extracellular
Hypointens
e
Hypointense

35. Intracerebral active bleeding from an arteriovenous malformation located
parasagitally (black arrows) within the left hemisphere, (A) T2 and (B) T1,
central area of low signal on T2 (A) is consistent with acute bleeding and
deoxyhemoglobin (white arrows) which is surrounded by a large hyperacute
hematoma with T2 and T1 signal characteristic of oxyhemoglobin

36. Early subacute hematoma within the right cerebellar hemisphere 72
hours after the onset of bleeding, (A) T1, (B) T2, (C) unenhanced
CT, low signal on T2 and high signal on T1 indicate intracellular
methemoglobin

37. Chronic intracerebral hematomas in both frontal and left temporal
lobes, T2 shows hyperintense hematomas with hypointense margins
indicating hemosiderin

38. Chronic hemorrhagic infarction within the right hemisphere, T2 (A)
shows a diffuse hypointense area indicating hemosiderin which is
better visualized on a susceptibility-weighted image (B)

39. Cavernoma in the left parasagittal location, T2 shows typical salt and
pepper appearance with central high signal and peripheral
hypointense rim

40. Cavernoma and developmental venous anomaly within the left cerebellar
hemisphere, T2 (A) shows hypointense oval cavernoma and bands of
superficial hemosiderosis due to chronic bleeding which are better depicted
on SWI (B), T1+C (C) reveals coexisting developmental venous anomaly

41. Diffuse axonal injury, axial susceptibility weighted images show
multiple small hypointense foci of hemorrhage within the right
temporal lobe and midbrain (A), splenium of the corpus callosum (B)
and right parietal lobe (C), which are usually hardly visible on other
MR sequences

42. Metastatic melanoma to the right eyeball, axial T2 shows low signal
characteristic of melanin

43. Colloid cyst, T2 shows a hypointense ovoid lesion in a typical location
within the third ventricle close to the foramina of Monro (arrow)

44. Rathke’s cleft cyst, sagittal T2 shows low signal within the cyst which is
typically located between the anterior and posterior pituitary lobes

45. Primary central nervous system lymphoma, MRI show two
homogeneously hypointense tumors on T2 (A) with strong contrast
enhancement on T1+C (B), DWI reveals almost homogenous
diffusion restriction with high signal on DW image (C) and low signal
on the ADC map (D)

46. Aging brain, T2 (A) shows low signal of both globi pallidi due to iron
accumulation in a 75-year-old female patient, iron overload may be
better visualized on T2* (B)

47. Fahr’s disease, unenhanced CT image (A) shows typical bilateral calcifications
in the region of basal ganglia, T2 (B) shows hypointense both globi pallidi,
while T2* image (C) reveals larger areas of hypointensity due to a
susceptibility artifact and a “blooming effect”

48. Calcified meningioma in the left frontal location with a very
low signal on T2

49. Vascular malformations, sagittal T2 (A) shows small pericallosal
aneurysm (arrow), axial T2 (B) shows multiple flow voids within a
large arteriovenous malformation in the left hemisphere

50. High-pressure hydrocephalus due to a tumor located at the cranio-
cervical junction, sagittal T2 shows enlarged ventricles and a
hypointense jet through an aqueduct indicating very fast flow of the
CSF

51. T2 shows a large amount of hypointense air within the
lateral ventricles after a neurosurgical procedure

52. 3-Fluid Attenuation Inversion Recovery
(FLAIR):
-FLAIR sequence is a T2 with suppression of
water signal based on water’s T1 characteristics
-A normal FLAIR image may appear similar to T1
since the CSF is dark on both, however, the
signal intensities of the gray & white matter are
different :
*T1 : normal white matter is brighter than gray
matter
*FLAIR : white matter is darker than gray matter

54. 4-Conventional Spin-echo Proton Density
(PD):
-PD images aren’t used in many
Neuroradiology MRI protocols, but they do
have the highest signal to noise ratio of
any MRI sequence
-PD sequences are useful in the evaluation
of multiple sclerosis (MS), especially for
visualization of demyelinating plaques in
the posterior fossa

55. Axial brain MR images of a patient with MS, obtained before the onset
of clinical symptoms, on the proton density-weighted image (A),
many periventricular and discrete white matter lesions are visible.
Two of them enhance on T1+C (B)

56. 5-Diffusion Weighted Images (DWI) & Apparent
Diffusion Coefficient (ADC) :
-Diffusion MRI is based on the principal that the
Brownian motion of water protons can be
imaged
-Signal is lost with increasing Brownian motion
-Free water (CSF) experiences the most signal
attenuation, while many pathologic processes
(primarily ischemia) cause reduced diffusivity &
less signal loss

57. -Diffusion MRI consists of two separate
sequences, DWI & ADC, which are interpreted
together to evaluate the diffusion characteristics
of tissue
-Diffusion is 95 % sensitive & specific for infarct
within minutes of symptom onset
-DWI is an inherently T2 weighted sequence
(obtained with an echo-planar technique), on
DWI, reduced or restricted diffusivity will be
hyperintense (less Brownian motion >> less loss
of signal) & lesions are very conspicuous

58. -The ADC map shows pure diffusion information
without any T2 weighting, in contrast to DWI,
reduced diffusivity is hypointense on the ADC
map
-An important pitfall to be aware of it is the
phenomenon of T2 shine through, because DWI
images are T2 weighted, lesions that are
inherently hyperintense on T2 may also be
hyperintense on DWI even without diffusion
restriction, this phenomenon is called T2 shine
through, correlation with ADC map for a
corresponding dark spot is essential before
concluding that diffusion is restricted

59. -In the brain, diffusion images are obtained in three
orthogonal gradient planes to account for the
inherent anisotropy of large white matter tracts,
anisotropy is the tendency of water molecules to
diffuse directionally along white matter tracts
-The b-value is an important concept that affects
the sensitivity for detecting diffusion
abnormalities, the higher the b-value, the more
contrast the image will provide for detecting
reduced diffusivity

60. -Although diffusion MRI is most commonly used to
evaluate for infarct, the differential diagnosis
for reduced diffusion includes :
1-Acute Stroke
2-Bacterial Abscess
3-Cellular Tumors (Lymphoma &
Medulloblastoma)
4-Epidermoid Cyst
5-Herpes Encephalitis
6-Creutzfeldt-Jakob Disease

61. Acute Stroke

62. Acute Stroke

63. Bacterial Abscess

64. Bacterial Abscess

65. CNS Lymphoma

66. CNS Lymphoma

67. CNS Lymphoma

68. Medulloblastoma

69. Medulloblastoma

70. Epidermoid Cyst

71. Epidermoid Cyst

72. Herpes Encephalitis

73. Herpes Encephalitis

74. Creutzfeldt-Jakob Disease

75. Creutzfeldt-Jakob Disease

76. 6-Gradient Recall Echo (GRE) :
-GRE captures the T2* signal, because the 180-degree
rephasing pulse is omitted, GRE images are susceptible
to signal loss from magnetic field inhomogeneites
-Hemosiderin & calcium produce inhomogeneites in the
magnetic field, which creates blooming artifacts on GRE
& makes even small lesions conspicuous
-Susceptibility-weighted imaging (SWI) is a rapidly evolving
technique that utilizes both the magnitude and phase
information to obtain valuable information about
susceptibility changes between tissues
-SWI is very sensitive to the paramagnetic effects of
deoxyhemoglobin

77. -The D.D. of multiple dark spots on GRE
includes :
1-Hypertensive microbleeds (dark spots are
primarily in the basal ganglia, thalami,
cerebellum & pons)
2-Cerebral amyloid angiopathy (dark spots are in
the subcortical white matter, most commonly the
parietal & occipital lobes)
3-Familial cerebral cavernous malformations (an
inherited form of multiple cavernous
malformations)
4-Axonal shear injury
5-Multiple hemorrhagic metastases

79. Hypertensive Microbleeds

80. Hypertensive Microbleeds

81. Amyloid Angiopathy

82. Amyloid Angiopathy

83. Amyloid Angiopathy Hypertensive Microbleeds

84. Multiple Cavernous Malformations

85. Multiple Cavernous Malformations

86. Multiple Cavernous Malformations

87. Axonal Shear Injury

88. Axonal Shear Injury

89. Multiple hemorrhagic metastases

90. Multiple hemorrhagic metastases

91. 7-Magnetic Resonance Spectroscopy (MRS) :
-MRS describes the chemical composition of a brain region
-The ratio of specific compounds may be altered in various
disease states :
1-Choline : is a marker of cellular membrane turnover and
is therefore elevated in neoplasms , demyelination and
gliosis
2-Creatine : provides information about cellular energy
stores , reduces in high grade gliomas
3-N-acetylaspartate (NAA) : is a normal marker of
neuronal viability , it is therefore reduced in any process
that destroys neurons , such as high grade tumors,
radionecrosis , non-neuronal tumors (e.g. cerebral
metastases and primary CNS lymphoma)
4-Lactate : is a marker of anaerobic metabolism (no peak
is seen in normal spectra) , it is therefore elevated in
necrotic areas (e.g. higher grade tumors) and infections
(cerebral abscess)

93. Patient with glioblastoma with oligodendroglioma component , (a) MRS
spectrum from region of brain not affected by the tumor , (b)
Spectrum from a voxel within the tumor showing elevated choline ,
decreased NAA & Creatine

94. MRS shows decreased NAA peak & elevated lactate in
infarction

95. 5-Lipid : is a marker of severe tissue damage with
liberation of membrane lipids, as is seen in cerebral
infarction or cerebral abscesses
6-Alanine : elevated in meningioma
7-Gamma-aminobutyric acid (GABA) : is the principle
inhibitory neurotransmitter of the central nervous system,
decreases in epilepsy & schizophrenia
8-Glutamate-Glutamine (Glx) peak : It overlaps with the
GABA peak and cannot be routinely separated from
each other
9-Citrate : decreased in prostate cancer
10-Myo-inositol : elevated in low grade astrocytoma, PML,
Alzheimer disease, regions of gliosis & congenital CMV
infection
Decreases hepatic encephalopathy & Glioblastoma

96. -The peaks of the three principle compounds
analyzed occur in alphabetical order :
Choline, Creatine & NAA
-Canavan disease is a dysmyelinating disorder
known for being one of the few disorders with
elevated NAA
-Hunter’s angle is a quick way to see if the
spectrum is close to normal, a line connecting
the tallest peaks should point up like a plane
taking off

97. MRS in Canavan disease , the NAA peak is abnormally
high due to the inability to catabolize NAA

98. (a) Normal spectrum , Hunter’s angle (yellow arrow) is pointing up as a
plane at take off , (b) Abnormal spectrum due to oligoastrocytoma ,
with elevated choline & decreased NAA , a line connecting the
tallest peaks would point down , which is a clue that the spectrum is
abnormal

99. -In some circumstances, Spectroscopy may help
distinguish :
1-Recurrent tumor from Radiation necrosis :
-Recurrent tumor : choline will be elevated
-Radiation change : NAA, Choline and Creatine
will all be low
2-Glioblastoma & Metastases :
-Glioblastoma : is an infiltrative tumor that features
a gradual transition from abnormal to normal
spectroscopy
-Metastases : would be expected to have a more
abrupt transition

100. 3-Lymphoma From Toxoplasmosis in AIDS :
-Lymphoma shows high choline peak
-Toxoplasmosis shows high lipid peak
4-Brain Abscess From Necrotic Brain Tumor :
-Increased lipid/lactate is noted in both tumors and
abscess
-BUT only abscess spectrum shows amino acids,
acetate, aspartate and succinate peaks

101. MRS in brain abscess

102. 8-Perfusion :
-Advanced technique where the brain is imaged
repeatedly as a bolus of gadolinium contrast is
injected
-The principle of perfusion MRI is based on the
theory that gadolinium causes a magnetic field
disturbance which (counterintuitively) transiently
the image intensity
-Perfusion images are echo-planar T2* images
which can be acquired very quickly
-Perfusion MRI may be used for evaluation of
stroke & tumors

103. Acute Stroke

104. Acute Stroke

105. Biopsy-proven glioblastoma multiforme, (A) T1+C shows a
heterogeneous enhancing lesion within the posterior right frontal
and parietal lobes, (B) Increased blood volume in the region of the
tumor is shown on the relative cerebral blood volume map