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MRS
Introduction
• There are numerous metabolites found in the human
brain.
• Fortunately, only several of them occur in signi...
• Most of the metabolites
are involved in energy
metabolism.
• Presented here is a
diagram of the major
biochemical pathwa...
MR SPECTROSCOPY
• Detection of frequency dependent signals from
individual metabolites
• Interpretation is based on identi...
METABOLITES
• Cho - Cell membrane turn over
• Cr - Energy marker -Reference
• NAA - Neuronal cell marker
• mI - Osmolyte
•...
NAA Regional Variations
• NAA peak – Highest due to N acetyl group
• Marker of neuronal / axonal viability and
density
• E...
Creatine
• Energy stores.
• Cr 1 - 3.0 ppm
• Cr 2 - 3.9 ppm
• Marker of intact brain Energy Metabolism.
• Reference for in...
Choline
• Cho - 3.2 ppm
• Present in Cell membrane
• Cell membrane turnover
• Choline released during disease from pool
• ...
Choline Regional Variations
• Slightly higher in white matter than gray
• Higher in thalamus and cerebellum
• More choline...
Myo-Inositol
• Cell Volume Regulator - Osmolyte
• mI - 3.5 ppm ; 4.0 ppm.
• Present in astrocytes
• Astrocyte /glial marke...
Lactate
• Accelerated glycolysis /Anaerobic glycolysis
• Lac - 1.3 ppm – Doublet
• Inverts with TE 144 or 135 ms
• Normal ...
Lipids
• Lip 1 - 0.9 ppm; Lip 2 - 1.3 - 1.4 ppm
• Broad based
• Sign of brain injury
• Normally Bound - Not seen
• Seen wh...
Glutamate & Glutamine (Glx)
• Neurotransmitters
• Beta, Gamma Glx - 2.0 - 2.5 ppm
• Alfa Glx - 3.6 - 3.8 ppm
NORMAL H BRAIN SPECTRA
• A spectrum of the metabolites is plotted on a two
dimensional graph.
– The horizontal axis repres...
• This approach allows for consistent spectra
regardless of the field strength.
• It also provides a standardization of th...
• The 1H-MRS spectrum of major metabolites in a
normal brain is shown in Fig 1 below:
Major Metabolites in the Brain
• NAA
• Choline
• Creatine
• Lactate
• Glutamine
• Lipid
• Myo-Inositol
N-ACETYLASPARTATE (NAA)
• NAA is the marker of neuronal density and viability.
– It is present in both gray and white matt...
Choline
• The choline peak receives contribution from
glycerophosphocholine, phosphocholine, and
phosphatidylcholine.
– It...
Creatine (Cr)
• The Cr peak receives contribution mainly from creatine, and creatine
phosphate.
– Note that phospocreatine...
Lactate
• Lactate has a molecular structure of CH3-COH2-CO2.
• Lactate levels in the brain are normally are very low or
ab...
Lactate
• Resonance of lactate consists of two distinct peak (doublet)
due to J-J coupling.
• Lactate peak also occurs at ...
Myo-Inositol (mI)
• Myo-Inositol is a glucose-like metabolite and it
involves primarily in hormone-sensitive
neuroreceptio...
Lipids
• Lipids are often in composition of triglycerides, phospholipids,
and fatty acids.
• These substances are incorpor...
Glutamate and Glutamine (Glx)
• Glutamate is an excitatory neurotransmitter in
mitochondrial metabolism.
• Glutamine and g...
• Glutamine is astrocyte marker
• Glutamate – Neurotransmiter - neurotoxin in
excess amount.
• Main ammonia intake route
•...
T2/FLAIR For ROI
MRS acquisition modes
• STEAM -Stimulated echo acquisition mode
• Single voxel
• Short TE
• PRESS -Point resolved spectros...
PROBE - Single voxel proton MRS
• Fully automated prescan, scan
• shimming
• water suppression
• 2 -6 minutes Complete acq...
Single voxel proton MRS
Multi voxel MRS
• Variable voxel sizes
• More than one lesion
• Control from normal
Acquisition Parameters
TR - 1500 ms
TE - 35 ms
NAV - 64
Voxel Size - 2 x 2 x 2 cm
Voxel Location:-
Cingulate gyrus -GM
Par...
Chemical Shift Imaging in Tumors
Spatial distribution of metabolites
METABOLITES
SHORT TE 35
• mI
• LACTATE
• LIPIDS
• GLUTAMATE /
GLUTAMINE
BOTH SHORT 35 AND
LONG TE 144
• NAA
• CREATINE
• C...
Lactate Vs Lipid
• Lactate is doublet
• Inversion below the
baseline at 144 ms
• Persists at TE 270 ms.
• Lipid peak is br...
Lactate
TE 35 TE 144
TE 270
LIP-LACTATE
Tumor Biochemistry
• Understood by identifying important
metabolites and quantifying them.
• Comparing with normal and ben...
Alteration of metabolites in Brain Tumors
• Decreased or absence of N – Acetyl Aspartate (NAA) (Non-
neuronal and NAA is o...
FAQ
• Is it a tumour
• GBM/ Metz/ Abscess?
• Grade?
• Survival?
• ? Oligodentroglioma?
Tumour?
• D/D -Stroke, Focal cortical dysplasia,
Herpes and Neoplasm
• ^ Cho – Neoplasm
• Always exclude Demylination - ^ ...
GBM/Metz/Abscess
• Multivoxel PRESS sequence with intermediate
TE -for elevation of Cho in enhancing rim and
in peri-lesio...
Grade
• Cho/NAA ratio - Most sensitive
index for tumor cell density and
proliferation.
• Marker of tumor infiltration
• Hi...
Prognosis
• High Creatine levels in grade II
gliomas- malignant transformation
and poor survival
• High Cho -Pediatric bra...
Oligo dentro glioma
Sky-rocketing Choline - high cellular density
MR perfusion:Increased- rCBV- high capillary density
low...
Low-grade astrocytoma with elevated
lactate
High grade
glial tumors
TE 35
TE 135
57 yr M + LOC
After 20 days
Key points
• High Cho - High tumor cell density & high vascular
proliferation.
• Low Cho and elevation of lipids - Necrosi...
Spectra of active demyelination indistinguishable from
gliomas.
MR perfusion may be helpful.
41y focal seizure
Tumefactive...
• Alanine (Ala) doublet at 1.4 ppm
• Elevation of Cho
• Presence of Lac at 1.3 ppm.
• Absent NAA - Non-neural origin.
• Al...
Recurrent astrocytoma
24 y post Rx
Recurrent astrocytoma
• Normal -1 Infiltrative -2
• Solid -3 Early necrotic -4
• All with high Cho/ Cr >1.7
• High Cho, ve...
• 51y M, GBM Rx RT.
• Reduced Cho, NAA and
Cr relative to normal brain
indicates necrosis.
Stroke
• Localized decreased NAA - few hours of ischemia.
• Very low or absent – chronic infarcts.
• Lac is elevated in ac...
Occlusion of the left ICA /MCA @ 24 h
Left - Elevated Lac and near absent NAA
Occlusion of Right ICA
With in 24 hr
Lac- Elevated
NAA- Preserved
Follow-up @ 1 wk
absence of NAA
Lac in infarct region.
High Cho in peri
infarct...
Pyogenic meningitis
large amount of amino acids -1, lactate -2, alanine -3, acetate -4,acetoacetate -5
Pyogenic abscess
135 TE
Inv Of AA,0.9 ppm, Lac, 1.33 ppm, and Ala, 1.47 ppm peaks
TUBERCULOMA
• Similar on MRI.
• Tuberculous abscesses - only Lac and lipid signals @
0.9 and 1.3 ppm; No amino acids
• Lipid peaks –In...
Tuberculous abscesses
STEAM
TE 35, only Lip and Lac at 1.3 ppm.
TE 135 spectrum, phase reversal & reduction in signal
HSE
Findings are due to interstitial edema; MRS - Non-specific.
Fungal abscess
• TE 135 proton MR spectrum
from core of abscess - inverted
AA and Lac peaks.
• Multiple signal (*) @ 3.6–3...
Hydatid cyst:
MRS with TE 35 - Lac at 1.33 ppm,
acetate at 1.92 ppm, and succinate at 2.4
ppm;
@TE 135 - Lac and Ala at 1....
Neurocysticercosis
• Spectroscopy may be of value in the large
cysticercus cyst without visible scolex, where
differential...
HIV encephalopathy
• Reductions in NAA and increases in Cho, mI
in both lesional and normal appearing brain
tissues.
• Tox...
D/D
Demyelination
Multiple sclerosis - Axonal damage - Decreased NAA
Demyelination - Increased mI, Cho.
Acute MS plaques - Dec...
Multiple sclerosis
• Long TE spectra in acute and chronic MS
lesions.
– Both - Elevated Cho and reduced NAA
– Only acute l...
Acute Vs Chronic Plaque
• During acute phase- focal increases in Cho and Lac
and decreases in NAA, Cr.
• 15 m later - Redu...
Seizure disorders
• Help in localize and characterize epileptogenic
foci.
• Helps in lateralizing in temporal lobe epileps...
TLE
Ipsilat MRS:
Reduced NAA signal and increased Cho
and mI signals- Gliosis
Helpful in identification of seizure focus i...
Aging and dementia
• Aging - Cho and Cr increase and NAA stable
• AD – Reduced NAA and High mI
• NAA/Cr and mI/Cr ratios c...
• Progression of AD - Regional
elevation of mI/Cr levels in
prodromal AD
• mI/Cr and NAA/Cr - useful for
predicting and mo...
Neurodegenerative diseases
• Neuronal dysfunction & cell death.
• Metabolite changes in idiopathic Parkinson’s
disease are...
Traumatic brain injury
• Conventional CT and MR – major role
• High lactate levels - Poor outcome.
• Visible Lac in normal...
3 Mon
after
injury
Hypoxic brain injury
• Loss of NAA, increase in Lac and
glutamine and decrease in Cr
• High Lac; low NAA and Cr -Bad
progn...
In severe HIE distinction
between poor prognosis
and good prognosis is
made on basis of:
(1) excess Lac
(2) decreased NAA
...
Pediatric white matter disease
• Reduced axonal integrity - Reduced
NAA
• Demyelination -High cho and mI
• Hypomyelination...
M
L
D
Loss of NAA and elevation of mI
Adrenoleukodystrophy
• Most common leukodystrophy in children
• Zones- demylination, inflamm, gliosis
• MRI often precede ...
Inborn errors of metabolism
• Canavan and Salla disease show an elevated NAA
• Maple syrup urine disease -Branched-chain a...
Canavan’s disease- AR
• Deficiency of aspartoacylase an enzyme that
deacetylates NAA, Increased free acetate
• Hypotonia a...
NAA is elevated in posterior
sub cortical WM (1) that is
hyper intense on T2 image;
NAA is near normal levels in
(2) is re...
Maple syrup urine disease
• Deficiency of branched-chain -keto acid dehydrogenase,
catalyzing essential branched-chain ami...
Elevation of Lac (1.3 ppm) and of the methyl group of BCAA/BCKA (0.9
ppm).
After therapy at day 12 the two abnormal peaks ...
Phenylketonuria
• Phe hydroxylase def
• Periatrial and periventricular WM symmetrical
hyperintensities.
• Calcifications b...
Phe signal at 7.36 ppm
Non-ketotic hyperglycinemia
• Highly elevated glycine in the CSF and
absence of ketoacidosis
• Large glycine peak at 3.55 ...
abnormal elevation of Gly at 3.55 ppm with a Gly/Cr ~ 1.
Progressive decrease of Gly during treatment with a protein restr...
Mitochondrial encephalopathy
• Diffuse symmetrical hyperintensity and
volume loss in WM
• mild Lac accumulation in WM, wit...
Multivoxel TE 136 ms at centrum semiovale level
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  1. 1. MRS
  2. 2. Introduction • There are numerous metabolites found in the human brain. • Fortunately, only several of them occur in significant quantities and are useful in proton spectroscopic studies. • There is evidence that the normal metabolites in the brain vary with according to the patient's age. • The changes are most noticeable during the first three years of life.
  3. 3. • Most of the metabolites are involved in energy metabolism. • Presented here is a diagram of the major biochemical pathways in the energy production.
  4. 4. MR SPECTROSCOPY • Detection of frequency dependent signals from individual metabolites • Interpretation is based on identity of chemical and concentration • Baseline normal spectra - constant • Concentration of each metabolites alter in a reproducible pattern - Abnormal spectra = DISEASE PATTERN
  5. 5. METABOLITES • Cho - Cell membrane turn over • Cr - Energy marker -Reference • NAA - Neuronal cell marker • mI - Osmolyte • Lactate - Anerobic state - NOT SEEN IN NORMAL BRAIN
  6. 6. NAA Regional Variations • NAA peak – Highest due to N acetyl group • Marker of neuronal / axonal viability and density • Evenly distributed in Cerebral hemisphere • Less in hippocampus and cerebellum • NAA - Neuronal marker • Decreases with loss of neuronal integrity.
  7. 7. Creatine • Energy stores. • Cr 1 - 3.0 ppm • Cr 2 - 3.9 ppm • Marker of intact brain Energy Metabolism. • Reference for interpretation of ratio. • Higher in grey matter than white matter • Higher in thalamus and cerebellum
  8. 8. Choline • Cho - 3.2 ppm • Present in Cell membrane • Cell membrane turnover • Choline released during disease from pool • Choline - Increased with increased cellular turnover • Elevated in tumors and inflammation
  9. 9. Choline Regional Variations • Slightly higher in white matter than gray • Higher in thalamus and cerebellum • More choline in pons and terminal zones of myelination
  10. 10. Myo-Inositol • Cell Volume Regulator - Osmolyte • mI - 3.5 ppm ; 4.0 ppm. • Present in astrocytes • Astrocyte /glial marker - Product of myelin degradation
  11. 11. Lactate • Accelerated glycolysis /Anaerobic glycolysis • Lac - 1.3 ppm – Doublet • Inverts with TE 144 or 135 ms • Normal in preterm / term infants & CSF contamination
  12. 12. Lipids • Lip 1 - 0.9 ppm; Lip 2 - 1.3 - 1.4 ppm • Broad based • Sign of brain injury • Normally Bound - Not seen • Seen when there is cell death and cell membrane destruction • Indicates necrosis and / or disruption of myelin • Difficult to differentiate from macromolecules • Non significant lipid – from scalp contamination
  13. 13. Glutamate & Glutamine (Glx) • Neurotransmitters • Beta, Gamma Glx - 2.0 - 2.5 ppm • Alfa Glx - 3.6 - 3.8 ppm
  14. 14. NORMAL H BRAIN SPECTRA • A spectrum of the metabolites is plotted on a two dimensional graph. – The horizontal axis represents the frequencies (chemical shifts) and the vertical axis represents the concentration of the metabolites. • The frequencies are plotted with reference to a stable compound. – The reference compound most often used is tetramethylsilane (TMS). The chemical shifts are now expressed as parts per million (ppm).
  15. 15. • This approach allows for consistent spectra regardless of the field strength. • It also provides a standardization of the spectrum . – TMS is assigned a chemical shift of zero ppm and it lies to the far most right hand . – The far left end is occupied by water approximately 4.7 ppm. – The area under a peak is contributed by the concentration of that metabolites. – Therefore, higher or wider peak results from higher concentration.
  16. 16. • The 1H-MRS spectrum of major metabolites in a normal brain is shown in Fig 1 below:
  17. 17. Major Metabolites in the Brain • NAA • Choline • Creatine • Lactate • Glutamine • Lipid • Myo-Inositol
  18. 18. N-ACETYLASPARTATE (NAA) • NAA is the marker of neuronal density and viability. – It is present in both gray and white matter and the difference in concentration is not clinically significant. – NAA is detected by the its N-acetyl methyl group. – Its concentration appears to decrease with any brain insults such as infection, ischemic injury, neoplasm, and demyelination process. • NAA is not in found in tumors outside the central nervous system (CNS) such as meningioma. • NAA is the tallest peak in the proton MR spectrum and it is assigned at 2.0ppm. Additional smaller peaks may be seen at 2.6 and 2.5 ppm. • Elevation of NAA is rare and may be found in hyperosmolar state and axonal recovery.
  19. 19. Choline • The choline peak receives contribution from glycerophosphocholine, phosphocholine, and phosphatidylcholine. – It is the precursor of acetyl choline and phosphatidylcholine. – Acetylcholine is an important neurotransmitter and the latter is an integral part of cell membrane synthesis. • Disease processes affecting the cell membrane and myelin can lead to the release of phosphatidylcholine. • Thus, elevation of choline can be seen during ischemic injury, neoplasm or acute demyelination diseases. • Many brain tumors will lead to elevated choline peak, presumably associated with their increased cellularity and compression of surrounding brain tissue. • Choline is the second largest peak and assigned to 3.2 ppm.
  20. 20. Creatine (Cr) • The Cr peak receives contribution mainly from creatine, and creatine phosphate. – Note that phospocreatine supplies phosphate to adenosine diphosphate (ADP) to form adenosine triphosphate (ATP) with the release of creatine. • The overall level of total creatine in normal brain is fairly constant. – Reduced Cr level may be seen in pathologic processes such as neoplasm, ischemic injury, infection or some systemic diseases. – Most metastatic tumors to the brain do not produce creatine since they do not possess creatine kinase. – Therefore, metastatic tumors should be suspected if there is an absence of a Cr peak in the proton spectrum. • Cr is the third highest peak and is assigned to 3.03 ppm. It is usually seen next to the right of choline. An additional peak occurs near 4 ppm but is usually suppressed with water.
  21. 21. Lactate • Lactate has a molecular structure of CH3-COH2-CO2. • Lactate levels in the brain are normally are very low or absent. When oxygen supply is depleted, the brain switches to anaerobic respiration for which one end product is lactate. • Therefore, elevated lactate peak is a sign of hypoxic tissue. – Low oxygen supply can result from decreased oxygen supply or increased oxygen requirement. – The former may be seen in vascular insults, or hypoventilation and the latter may be seen in neoplastic tissue.
  22. 22. Lactate • Resonance of lactate consists of two distinct peak (doublet) due to J-J coupling. • Lactate peak also occurs at two different locations. – The lower field peak (a doublet) occurs at approximately 1.32 ppm. – The other peak (a quartet) is seen at 4.1 ppm and this is very close to the water peak. • usually suppressed during data processing. • The lactate peak at lower frequency field show a peak inversion for different TE's. – This property serves as an excellent confirmation for the presence of lactate. The lactate peak is above the baseline at TE of 270 ms and below the baseline at TE of 136 ms. The inversion arises from the weak J-J coupling from the CH3 and CH protons. The coupling constant J is 7Hz.
  23. 23. Myo-Inositol (mI) • Myo-Inositol is a glucose-like metabolite and it involves primarily in hormone-sensitive neuroreception. It is found mainly in astrocytes and helps to regulate cell volume. • Elevated level of mI would be seen where there is glial cell proliferation as in gliosis. – Depressed level of mI would be seen processes causing glial cell destruction , as in neoplasm, infection or ischemic injury. The main mI peak is assigned to 3.56 ppm and additional peak may be seen at 4.06 ppm.
  24. 24. Lipids • Lipids are often in composition of triglycerides, phospholipids, and fatty acids. • These substances are incorporated into cell membranes and myelin. – Lipid peak should not be seen unless there is destructive process of the brain including necrosis, inflammation or infection. – Lipids have a very short T1 relaxation time and are normally not seen unless short TEs are utilized. • The proton lipid peaks occur at several frequencies including 0.8, 1.2, 1.5 and 6.0 ppm. • Lipid resonance at 1.2 ppm can sometimes obscure the lactate peak at 1.32 ppm. • Fat in the cranium can contaminate the true disease process if the voxels are placed too close the cranium.
  25. 25. Glutamate and Glutamine (Glx) • Glutamate is an excitatory neurotransmitter in mitochondrial metabolism. • Glutamine and glutamate resonate closely together. • Their sum is often designated as Glx and is assigned between 2.1 and 2.5 ppm.
  26. 26. • Glutamine is astrocyte marker • Glutamate – Neurotransmiter - neurotoxin in excess amount. • Main ammonia intake route • Elevated - In hypoxia, ischemia, recovering brain. • Its not a grave prognostic finding like lactate
  27. 27. T2/FLAIR For ROI
  28. 28. MRS acquisition modes • STEAM -Stimulated echo acquisition mode • Single voxel • Short TE • PRESS -Point resolved spectroscopy • Twice the SNR of STEAM • Short and long TE - single voxel possible
  29. 29. PROBE - Single voxel proton MRS • Fully automated prescan, scan • shimming • water suppression • 2 -6 minutes Complete acquisition • Short TE (PRESS, STEAM) and • long TE (PRESS)
  30. 30. Single voxel proton MRS
  31. 31. Multi voxel MRS • Variable voxel sizes • More than one lesion • Control from normal
  32. 32. Acquisition Parameters TR - 1500 ms TE - 35 ms NAV - 64 Voxel Size - 2 x 2 x 2 cm Voxel Location:- Cingulate gyrus -GM Parietal -WM
  33. 33. Chemical Shift Imaging in Tumors Spatial distribution of metabolites
  34. 34. METABOLITES SHORT TE 35 • mI • LACTATE • LIPIDS • GLUTAMATE / GLUTAMINE BOTH SHORT 35 AND LONG TE 144 • NAA • CREATINE • CHOLINE • LACTATE signal lowered
  35. 35. Lactate Vs Lipid • Lactate is doublet • Inversion below the baseline at 144 ms • Persists at TE 270 ms. • Lipid peak is broad • Has a shoulder to left • Suppressed at TE 270 ms
  36. 36. Lactate TE 35 TE 144 TE 270
  37. 37. LIP-LACTATE
  38. 38. Tumor Biochemistry • Understood by identifying important metabolites and quantifying them. • Comparing with normal and benign tissues, we can understand metabolite markers and grade them.
  39. 39. Alteration of metabolites in Brain Tumors • Decreased or absence of N – Acetyl Aspartate (NAA) (Non- neuronal and NAA is only found in neurons) • Decreased Creatine • Increased Choline • Appearance of Lactate (Anaerobic glycolysis) • Myo-Inositol may distinguish hemangiopericytomas from meningiomas • Glutamine and Glutamate are prominent in meningiomas
  40. 40. FAQ • Is it a tumour • GBM/ Metz/ Abscess? • Grade? • Survival? • ? Oligodentroglioma?
  41. 41. Tumour? • D/D -Stroke, Focal cortical dysplasia, Herpes and Neoplasm • ^ Cho – Neoplasm • Always exclude Demylination - ^ Cho
  42. 42. GBM/Metz/Abscess • Multivoxel PRESS sequence with intermediate TE -for elevation of Cho in enhancing rim and in peri-lesional T2 hyperintensity • If Cho is elevated in both areas - GBM • Elevated in rim; N –Around - Metz • Detection of peptides and amino acids in Short TE - Pyogenic abscess
  43. 43. Grade • Cho/NAA ratio - Most sensitive index for tumor cell density and proliferation. • Marker of tumor infiltration • High Cho/NAA and Cho/Cr - Fast growing and high grade neoplasm
  44. 44. Prognosis • High Creatine levels in grade II gliomas- malignant transformation and poor survival • High Cho -Pediatric brain tumors
  45. 45. Oligo dentro glioma Sky-rocketing Choline - high cellular density MR perfusion:Increased- rCBV- high capillary density low level of angiogenesis
  46. 46. Low-grade astrocytoma with elevated lactate
  47. 47. High grade glial tumors
  48. 48. TE 35
  49. 49. TE 135
  50. 50. 57 yr M + LOC After 20 days
  51. 51. Key points • High Cho - High tumor cell density & high vascular proliferation. • Low Cho and elevation of lipids - Necrosis. • Cho higher enhancing rim -may be the faster growing side of the tumor. • Vasogenic edema -Normal Cho and slightly decreased NAA.
  52. 52. Spectra of active demyelination indistinguishable from gliomas. MR perfusion may be helpful. 41y focal seizure Tumefactive multiple sclerosis
  53. 53. • Alanine (Ala) doublet at 1.4 ppm • Elevation of Cho • Presence of Lac at 1.3 ppm. • Absent NAA - Non-neural origin. • Ala -30–40% of Meningioma • Mobile lipid and high Cho - aggressive lesions 43 y Focal deficit
  54. 54. Recurrent astrocytoma 24 y post Rx
  55. 55. Recurrent astrocytoma • Normal -1 Infiltrative -2 • Solid -3 Early necrotic -4 • All with high Cho/ Cr >1.7 • High Cho, very low NAA and no lipid -Solid tumor. • Small Lac without lipid may be early indicator of transformation to high grade.
  56. 56. • 51y M, GBM Rx RT. • Reduced Cho, NAA and Cr relative to normal brain indicates necrosis.
  57. 57. Stroke • Localized decreased NAA - few hours of ischemia. • Very low or absent – chronic infarcts. • Lac is elevated in acute stroke due to anaerobic glycolysis in ischemic brain. • Creatine and Choline may change in acute and chronic stroke. • Lipid - Reflect necrosis. • MRS is added value to diffusion and perfusion
  58. 58. Occlusion of the left ICA /MCA @ 24 h Left - Elevated Lac and near absent NAA
  59. 59. Occlusion of Right ICA
  60. 60. With in 24 hr Lac- Elevated NAA- Preserved Follow-up @ 1 wk absence of NAA Lac in infarct region. High Cho in peri infarct WM Follow-up @ 5 m Reduced NAA high Cho in WM No Lac Lipid + in infarcted right basal ganglia.
  61. 61. Pyogenic meningitis large amount of amino acids -1, lactate -2, alanine -3, acetate -4,acetoacetate -5
  62. 62. Pyogenic abscess 135 TE Inv Of AA,0.9 ppm, Lac, 1.33 ppm, and Ala, 1.47 ppm peaks
  63. 63. TUBERCULOMA
  64. 64. • Similar on MRI. • Tuberculous abscesses - only Lac and lipid signals @ 0.9 and 1.3 ppm; No amino acids • Lipid peaks –In Both tuberculoma and pyogenic abscess. • Amino acid signals helps to discriminate pyogenic from tuberculous abscess • @ 135 TE Inv of AA- 0.9 ppm Tuberculous vs Pyogenic abscesses
  65. 65. Tuberculous abscesses STEAM TE 35, only Lip and Lac at 1.3 ppm. TE 135 spectrum, phase reversal & reduction in signal
  66. 66. HSE Findings are due to interstitial edema; MRS - Non-specific.
  67. 67. Fungal abscess • TE 135 proton MR spectrum from core of abscess - inverted AA and Lac peaks. • Multiple signal (*) @ 3.6–3.8 ppm- trehalose
  68. 68. Hydatid cyst: MRS with TE 35 - Lac at 1.33 ppm, acetate at 1.92 ppm, and succinate at 2.4 ppm; @TE 135 - Lac and Ala at 1.5 ppm show phase reversal while Ace and Suc show normal phase.
  69. 69. Neurocysticercosis • Spectroscopy may be of value in the large cysticercus cyst without visible scolex, where differential diagnosis includes brain abscess and cystic metastases. • In vivo MRS shows acetate, succinate and Lac. • Presence of Cr depending on whether the lesion is in the vesicular or colloid stage
  70. 70. HIV encephalopathy • Reductions in NAA and increases in Cho, mI in both lesional and normal appearing brain tissues. • Toxoplasmosis Vs lymphoma – Toxoplasmosis -Very large lipid signals – Lymphoma -Large lipid (smaller than toxo) -High Cho (not seen in toxo).
  71. 71. D/D
  72. 72. Demyelination Multiple sclerosis - Axonal damage - Decreased NAA Demyelination - Increased mI, Cho. Acute MS plaques - Decreased NAA and Cr in large plaques Increased mI, Cho and Lac Chronic plaque - Cr and Lac return quickly to normal, Cho - months to return to normal NAA -may or may not recover to normal. Tumefactive demyelination may be similar to neoplasm (elevated Cho, Lac, decreased NAA) –Perfusion useful. Monophasic Acute Disseminated Encephalo Myelitis - Mild, reversible NAA reductions without changes in other metabolites - Good prognosis.
  73. 73. Multiple sclerosis • Long TE spectra in acute and chronic MS lesions. – Both - Elevated Cho and reduced NAA – Only acute lesion - Elevated lactate • Short TE spectra from acute lesion and normal brain for comparison – Increased mI, choline, and lipids, slightly decreased Cr and NAA.
  74. 74. Acute Vs Chronic Plaque • During acute phase- focal increases in Cho and Lac and decreases in NAA, Cr. • 15 m later - Reduction of lesion and normalization of Cho, Cr, and Lactate. NAA- partial recovery.
  75. 75. Seizure disorders • Help in localize and characterize epileptogenic foci. • Helps in lateralizing in temporal lobe epilepsy • @35TE: Decreased NAA, Increased Cho and mI - Gliosis • MRS may help to characterize epileptogenic lesions visible on MRI (aggressive vs. indolent neoplasia, dysplasia)
  76. 76. TLE Ipsilat MRS: Reduced NAA signal and increased Cho and mI signals- Gliosis Helpful in identification of seizure focus in refractory pts with normal MR Contralateral MRS: Reversible with time - transient neuronal dysfunction. Bilateral metabolic changes, associated with poor post-op seizure outcome
  77. 77. Aging and dementia • Aging - Cho and Cr increase and NAA stable • AD – Reduced NAA and High mI • NAA/Cr and mI/Cr ratios correlate with cognitive function in AD, and this correlation is more significant with NAA/mI ratios. • WM NAA/Cr is lower in VaD –than AD
  78. 78. • Progression of AD - Regional elevation of mI/Cr levels in prodromal AD • mI/Cr and NAA/Cr - useful for predicting and monitoring prodromal AD. AD
  79. 79. Neurodegenerative diseases • Neuronal dysfunction & cell death. • Metabolite changes in idiopathic Parkinson’s disease are inconsistent. • Multiple system atrophy -reduction in NAA and NAA/Cr ratio when compared with IPD. • Lactate increased in Huntington’s disease.
  80. 80. Traumatic brain injury • Conventional CT and MR – major role • High lactate levels - Poor outcome. • Visible Lac in normal appearing brain soon after injury - Poor outcome • Fall in NAA - Continue for months after the initial insult.
  81. 81. 3 Mon after injury
  82. 82. Hypoxic brain injury • Loss of NAA, increase in Lac and glutamine and decrease in Cr • High Lac; low NAA and Cr -Bad prognosis.
  83. 83. In severe HIE distinction between poor prognosis and good prognosis is made on basis of: (1) excess Lac (2) decreased NAA (3) loss of Cr
  84. 84. Pediatric white matter disease • Reduced axonal integrity - Reduced NAA • Demyelination -High cho and mI • Hypomyelination or Gliosis -low Cho, normal NAA
  85. 85. M L D Loss of NAA and elevation of mI
  86. 86. Adrenoleukodystrophy • Most common leukodystrophy in children • Zones- demylination, inflamm, gliosis • MRI often precede clinical symptoms showing symmetrical WM lesions in parietal and occipital regions. • MRS - Onset of demyelination and extent of WM damage, information for Hemo Stem Cell Transplant.
  87. 87. Inborn errors of metabolism • Canavan and Salla disease show an elevated NAA • Maple syrup urine disease -Branched-chain amino acids at 0.9 ppm. • Phenylketonuria -Small phenylalanine signal at 7.36ppm (i.e. downfield of water) • Non-ketotic hyperglycinemia -Glycine at 3.55 ppm (use long TE to distinguish from mI)
  88. 88. Canavan’s disease- AR • Deficiency of aspartoacylase an enzyme that deacetylates NAA, Increased free acetate • Hypotonia and macrocephaly • Symmetrical confluent subcortical WM T2 prolongation & Centripetal spread • Bilateral involvement of globi pallidi, thalami, cerebellum and brainstem
  89. 89. NAA is elevated in posterior sub cortical WM (1) that is hyper intense on T2 image; NAA is near normal levels in (2) is relatively spared by signal abnormality
  90. 90. Maple syrup urine disease • Deficiency of branched-chain -keto acid dehydrogenase, catalyzing essential branched-chain amino acids (BCAA) isoleucine, leucine and valine. • Hypertonia and hypotonia, irregular respiration and apnea • Diffusion restriction compatible with cytotoxic edema in pons, midbrain, pallidi, thalami, cerebellar, and periventricular WM • Abnormal peak at 0.9 ppm due to accumulation of lactate (Lac) and loss of NAA • Prognostic value & monitor response to Rx / diet • TE 136 ms- avoids lipids
  91. 91. Elevation of Lac (1.3 ppm) and of the methyl group of BCAA/BCKA (0.9 ppm). After therapy at day 12 the two abnormal peaks have disappeared.
  92. 92. Phenylketonuria • Phe hydroxylase def • Periatrial and periventricular WM symmetrical hyperintensities. • Calcifications bilaterally in the globi pallidi and frontal subcortical regions • Elevated Phe signal at 7.36 ppm
  93. 93. Phe signal at 7.36 ppm
  94. 94. Non-ketotic hyperglycinemia • Highly elevated glycine in the CSF and absence of ketoacidosis • Large glycine peak at 3.55 ppm • Long TE is necessary to distinguish glycine resonance from that of mI at 3.56 ppm which is normally high in neonates
  95. 95. abnormal elevation of Gly at 3.55 ppm with a Gly/Cr ~ 1. Progressive decrease of Gly during treatment with a protein restriction diet
  96. 96. Mitochondrial encephalopathy • Diffuse symmetrical hyperintensity and volume loss in WM • mild Lac accumulation in WM, with moderate NAA and mild Cho and Cr signal losses
  97. 97. Multivoxel TE 136 ms at centrum semiovale level
  98. 98. Thank You

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