Introduction

Magnetic resonance spectroscopy (MRS) is used to measure the levels of different metabolites in body tissues. The MR signal produces a spectrum of resonances that correspond to different molecular arrangements of the isotope being "excited". This signature is used to diagnose certain metabolic disorders, especially those affecting the brain, and to provide information on tumor metabolism.
Magnetic resonance spectroscopic imaging (MRSI) combines both spectroscopic and imaging methods to produce spatially localized spectra from within the sample or patient. The spatial resolution is much lower (limited by the available SNR), but the spectra in each voxel contains information about many metabolites. Because the available signal is used to encode spatial and spectral information, MRSI requires high SNR achievable only at higher field strengths (3 T and above).

What we see in spectroscopy

Because of the relatively low sensitivity of in vivo MRS, in order for a compound to be detectable, generally its concentration must be in the millimolar range, and it must be a small, mobile molecule. Large and/or membrane-associated molecules are not usually detected, although they may exhibit broad resonances that contribute to the baseline of the spectrum. The information content of a proton brain spectrum depends on quite a few factors, such as the field strength used, echo time, and type of pulse sequence. At the commonly used 1.5 T field strength, at long echo times (e.g. 140 or 280 ms are often used;) only signals from Cho, Cr, and NAA are observed in normal brain, while compounds such as lactate, alanine, or others may be detectable if their concentrations are elevated above normal levels due to pathological processes.
At short echo times (e.g. 35ms or less) compounds with shorter T2 relaxation times (or multiplet resonances which become dephased at longer echo times) also become detectable. These include resonances from glutamate, glutamine, and GABA, which are not resolved from each other at 1.5 T, myo-inositol, as well as lipids and macromolecular resonances.
Spectral appearance at 3.0T is generally similar to that at 1.5T, although the coupling patterns of the multiplet resonances are somewhat different. Most of the multiplets (e.g. Glu, Gln, mI, taurine) are strongly coupled at these field strengths, and Glu and Gln overlap slightly less at 3 T than at 1.5 T. As field strengths increase further, to 4.0 and 7.0 T, spectral resolution progressively increases (provided that magnetic field homogeneity can be maintained) and more compounds can be assigned with confidence, including separating N-acetyl aspartyl glutamate (NAAG) from NAA, separation of Glu from Gln, and the detection of up to 14 different compounds at short echo times at 7T. A complete list of metabolite structures, chemical shift, coupling constants, and a summary of all compounds that have been detected in the human brain by proton MRS is given in Table 1. For more details about metabolite map in the brain, click here!
NAA
The largest signal in the normal adult brain spectrum, the acetyl group of N-acetyl aspartate resonates at 2.01 ppm, with a usually unresolved (except at very high fields) contribution from N-acetyl aspartyl glutamate (NAAG) at 2.04 ppm. The aspartyl group also exhibits a pH-sensitive, strongly coupled resonance at approximately 2.6 ppm. Despite being one of the most abundant amino acids in the central nervous system, NAA was not discovered until 1956, and its function has been the subject of considerable debate. It has been speculated to be a source of acetyl groups for lipid synthesis, a regulator of protein synthesis, a storage form of acetyl-CoA or aspartate, a breakdown product of NAAG (which, unlike NAA, is a neurotransmitter), or an osmolyte. NAA is believed to be synthesized in neuronal mitochondria, from aspartate and acetyl-CoA. NAA is often referred to as a neuronal marker, based on several lines of evidence. For instance, immunocytochemical staining techniques have indicated that NAA is predominantly restricted to neurons, axons, and dendrites within the central nervous system; and studies of diseases known to involve neuronal and/or axonal loss (for instance, infarcts, brain tumors, or multiple sclerosis (MS) plaques) have without exception found NAA to be decreased. In pathologies such as MS, good correlations between brain NAA levels and clinical measures of disability have been found, suggesting that higher NAA levels may be associated with better neuronal function. Animal models of chronic neuronal injury have also been shown to give good correlations between NAA levels (as measured by MRS) and in vitro measures of neuronal survival. All of these studies therefore suggest that MRS measurements of NAA may be useful for assessment of neuronal health or integrity in the central nervous system.
However, other experiments suggest that caution should be used in interpreting NAA solely as a neuronal marker. For instance, it has also been reported that NAA may be found in non-neuronal cells, such as mast cells or isolated oligodendrocyte preparations, suggesting that NAA may not be specific for neuronal processes. It is unclear if these cells are present at high enough concentrations in the normal human brain to contribute significantly to the NAA signal, however. There are also some rare cases where NAA metabolism is perturbed, almost certainly independently of neuronal density or function. One example is the leukodystrophy, Canavan’s disease, which is associated with a large elevation of intracellular NAA, owing to deficiency of aspartoacylase, the enzyme that degrades NAA to acetate and aspartate.
In addition, there has been a case report of a child, with mental retardation, with a complete absence of NAA. This case suggests that neurons can exist without the presence of NAA, and indeed that NAA is not necessary for neuronal function. While these observations indicate that there is evidence both for and against NAA as a measure of neuronal density and function, on balance, NAA does appear to be one of the better surrogate neuronal markers that can be measured non-invasively in humans. Like all surrogate markers, there will be occasions when it does not reflect the true neuronal status.
Decreases in NAA in some diseases have been shown to be reversible, suggesting that low NAA does not always indicate permanent neuronal damage. Reversible NAA deficits (either spontaneous, or in response to treatment) have been observed in diseases such as multiple sclerosis, mitochondrial diseases, AIDS, temporal lobe epilepsy, amyotrophic lateral sclerosis, or acute disseminated encephalomyelitis (ADEM). Therefore, in individual patients, while a low NAA signal in some pathologies may indicate irreversible neuroaxonal damage (e.g. strokes, brain tumors), in others it may be due to dysfunction (perturbed NAA synthesis or degradation) that may be reversible with either treatment-related or spontaneous recovery.
Choline
The choline signal (Cho, 3.20 ppm) is a composite peak consisting of contributions from the trimethyl amine (–N(CH3)3) groups of glycerophosphocholine (GPC), phosphocholine (PC), and a small amount of free choline itself. These compounds are involved in membrane synthesis and degradation, and it has often been suggested that they are elevated in disease states where increased membrane turnover is involved (e.g. tumors). Glial cells have also been reported to have high levels of Cho. Other pathological processes which lead to Cho elevation include active demyelination, either resulting from the degradation of myelin phospholipids primarily to GPC, or perhaps due to inflammation. Elevated Cho levels seem to be a characteristic of many types of neoplasms, including high-grade brain tumors (provided that they are not necrotic), prostate, breast, head and neck, and other tumors. In particular, it would appear that malignant transformation of tumors involves an increase in PC relative to GPC.
Low brain Cho has been observed in hepatic encephalopathy, and there is also some evidence to suggest that dietary intake of choline can modulate cerebral Cho levels. In both cases, this may be due to altered (decreased or increased) systemic transport of Cho to the brain. Cho also shows quite strong regional variations in the brain, usually with somewhat higher levels in white matter than gray, although the thalamus, hypothalamus, and insular cortex also show high levels in the normal brain.
Creatine
The creatine methyl resonance (Cr, 3.03 ppm) is a composite peak consisting of both creatine and phosphocreatine, compounds that are involved in energy metabolism via the creatine kinase reaction, generating ATP. In many spectra, a second resonance from the CH2 of creatine is also observed at 3.91 ppm (provided that it is not saturated by the water-suppression pulses). In vitro, glial cells contain a two- to fourfold higher concentration of creatine than do neurons. Creatine also shows quite large regional variations, with lower levels in white matter than gray matter in normal brain, as well as very high levels of Cr in the cerebellum compared to supratentorial regions.
Since creatine is synthesized in the liver and transported to the brain, chronic liver disease leads to lower cerebral creatine concentration. There is also a rare group of diseases which involve total Cr deficiency in the brain, resulting from either a lack of synthesis in the liver (GAMT, guanidinoacetate methyl transferase deficiency) or defective transport to the brain.
Lactate
In the human brain, the lactate methyl resonance (1.31 ppm) is below (or at the very limit of) detectability in most studies, due to the low concentration of lactate within the brain under normal conditions. A small lactate signal may sometimes be observed in ventricular cerebrospinal fluid (CSF), where it is more visible due to either being present in higher concentration (than brain), or because it has a longer T2 relaxation time.
Lactate is often increased and detected by MRS in pathological conditions; lack of oxygen (due to either hypoxia or ischemia) will cause an increase in lactate when metabolism of glucose through the Krebs cycle can no longer be sustained. Therefore, increased levels of brain lactate have been observed using MRS in a variety of conditions, including both acute and chronic ischemia, and hypoxia (where it is a poor prognostic indicator). Also, defects in the Krebs cycle (even in the presence of oxygen) can cause lactate to become elevated. Some examples of pathologies where this may occur include brain tumors, mitochondrial diseases, and other conditions. Small elevations of lactate have also been reported in the visual cortex during photic stimulation, believed to be due to increased non-oxidative glycolysis, but this effect does not appear to be particularly reproducible. Lactate may also be difficult to distinguish from overlapping lipid resonances, either originating from the brain itself, or spatial contamination from the very strong lipid signals in the scalp. Several approaches can be used to distinguish lactate from lipid, including the use of spectral editing techniques, although one of the simplest ways is to use an echo time of approximately 140 ms (1/J, where J ≈ 7 Hz) where the lactate methyl resonance should be inverted.
Myo-inositol
One of the larger signals in short echo time spectra occurs from myo-inositol (mI) at 3.5–3.6 ppm. mI is a pentose sugar, which is part of the inositol triphosphate intracellular second messenger system. Levels have been found to be reduced in hepatic encephalopathy, and increased in Alzheimer’s dementia and demyelinating diseases. The exact pathophysiological significance of alterations in mI is uncertain, but a leading hypothesis is that elevated mI reflects increased populations of glial cell, which are known to express higher levels of mI than neurons; this may be related to differences in myo-inositol/sodium co-transporter activity that appears to play a key role in astrocyte osmoregulation. This would explain chronic disturbance in mI both in degenerative and
inflammatory disease, and transiently in hypo- and hyperosmolar states.
Myo-inositol resonates at almost the same frequency in the spectrum as glycine; however, glycine is a singlet, while mI is a strongly coupled multiplet, so the two can usually be distinguished by using different echo times (glycine should be the predominant signal at long echo times), or field strengths. Glycine is usually at low concentration in the normal brain, but can increase to detectable levels in some diseases, such as nonketotic hyperglycinemia.
Glutamate and glutamine
Glutamate (Glu) and glutamine (Gln) are key compounds in brain metabolism. Glutamate is the most abundant amino acid in the brain, and is the dominant neurotransmitter. During neuronal excitation, glutamate is released and diffuses across the synapse, where it is rapidly taken up by astrocytes (along with sodium ions (Na+)). The astrocyte converts the glutamate to glutamine, which is then released and reuptaken by neurons. In the neuron, glutamine is converted back to glutamate, and the process repeated. This glutamate–glutamine cycling is an energy-demanding process, which has been speculated to consume as much as 80–90% of the total cortical glucose usage.
Since at a field strength of 1.5 T there is almost complete overlap of Glu and Gln, they are usually labeled as a composite peak Glx, and are very difficult to separate, although some authors have attempted to distinguish them. The 2CH protons of both Glu and Gln resonate around 3.7 ppm, while the 3CH2 and 4CH2 multiplets occur between 2.1 and 2.4 ppm. At 3 T, Glu and Gln may be determined quite reliably with an appropriate pulse sequence and/or curve fitting methods. At higher fields (at 4 T or above), the 4CH2 resonances of Glu and Gln start to become well resolved, and hence more reliably determined.
Because of the difficulty of measuring Glu and Gln at 1.5 T, relatively few studies have looked at pathology-related changes in these compounds. However, recently Glu was found to be elevated in MS plaques at 3 T, and previous studies at 1.5 T found elevated cerebral Gln in patients with liver failure (for example, hepatic encephalopathy and Reye’s syndrome, most likely as the result of increased blood ammonia levels, which increases glutamine synthesis.
Less commonly detected compounds
A survey of the literature reveals more than 25 additional compounds that have been assigned in proton spectra of the human brain. Some of these compounds are present in the normal human brain, but are difficult to detect routinely because they are very small and/or have overlapping peaks. Some examples of these compounds include NAAG, aspartate, taurine, scyllo-inositol, betaine, ethanolamine, purine nucleotides, histidine, glucose and glycogen. Other compounds are yet more difficult to detect, and require the use of spectral editing pulse sequences in order to be detected, because their resonances overlap almost completely with those of other, more abundant, compounds. Examples of these include γ-amino-butyric acid (GABA) and glutathione.
Under disease conditions, certain compounds may become visible as their concentration increases sufficiently high to be detected. Examples of compounds that have been detected under pathological conditions include the ketone bodies β-hydroxybutyrate and acetone, and other compounds such as phenylalanine (in phenylketonurea), galactitol, ribitol, arabitol in polyol disease, and succinate, pyruvate, alanine, glycine, and threonine in various disorders.
Exogenous compounds which are able to cross the blood brain barrier may also reach sufficiently high concentrations to be detected by proton MRS. Examples of exogenous compounds, sometimes termed “xenobiotics”, include the drug delivery vehicle propan-1,2-diol, mannitol (used to reduce swelling and edema in neurosurgical procedures and intensive care), ethanol, and the health food supplement methyl-sulfonyl-methane (MSM).
In addition to metabolite concentrations, other information may also be measured from brain proton spectra. For instance, measurements of absolute (as opposed to relative, as can be measured by MRI) brain temperature have been made using the water–NAA chemical shift difference (the water chemical shift has a 0.01 ppm/°C temperature dependence, whereas that of NAA is temperature-independent).
In addition, the exchangeable protons of metabolites resonating downfield of water may be used to estimate brain pH. These compounds (histidine, homocarnosine, and the amide resonance of NAA) generally have low signal intensity, but are detectable by the use of short echo times, appropriate water suppression methods, and high magnetic field strengths. Using oral loading of histidine (to increase its detectability), Vermathen et al. were able to estimate brain pH from the chemical shift difference of the C2 and C4 resonances of the imidazole ring; similarly, Rothman et al. were able to use the same resonances of homocarnosine to estimate brain pH in epilepsy patients who were receiving therapy which caused increased brain homocarnosine concentrations. The rate of exchange of the NAA amide protons with water is also pH sensitive, and can be used to estimate brain pH.
Compounds detected by proton MRS outside the CNS
The discussion so far has focused entirely on the information content of proton spectra of the human brain; however, when going to other organ systems, different compounds are detected in the spectra – for instance, in normal prostate tissue, a signal from citrate at 2.6 ppm is typically detected, while normal breast tissue usually only contains visible water and fat signals. In muscle, signals may be detected from intra- and extramyocellular lipids, acetylcarnotine, creatines, cholines, taurine and carnosine.
 

Sequences

(MRS / MRSI - Magnetic Resonance Spectroscopic Imaging) A method using the NMR phenomenon to identify the chemical state of various elements without destroying the sample. MRS therefore provides information about the chemical composition of the tissues and the changes in chemical composition, which may occur with disease processes.
Although MRS is primarily employed as a research tool and has yet to achieve widespread acceptance in routine clinical practice, there is a growing realization that a noninvasive technique, which monitors disease biochemistry can provide important new information for the clinician.
The underlying principle of MRS is that atomic nuclei are surrounded by a cloud of electrons, which very slightly shield the nucleus from any external magnetic field. As the structure of the electron cloud is specific to an individual molecule or compound, then the magnitude of this screening effect is also a characteristic of the chemical environment of individual nuclei.
In view of the fact that the resonant frequency is proportional to the magnetic field that it experiences, it follows that the resonant frequency will be determined not only by the external applied field, but also by the small field shift generated by the electron cloud. This shift in frequency is called the chemical shift (see also Chemical Shift). It should be noted that chemical shift is a very small effect, usually expressed in ppm of the main frequency. In order to resolve the different chemical species, it is therefore necessary to achieve very high levels of homogeneity of the main magnetic field B0. Spectra from humans usually require shimming the magnet to approximately one part in 100. High resolution spectra of liquid samples demand a homogeneity of about one part in 1000.
In addition to the effects of factors such as relaxation times that can affect the NMR signal, as seen in magnetic resonance imaging, effects such as J-modulation or the transfer of magnetization after selective excitation of particular spectral lines can affect the relative strengths of spectral lines.
In the context of human MRS, two nuclei are of particular interest - H-1 and P-31. (PMRS - Proton Magnetic Resonance Spectroscopy) PMRS is mainly employed in studies of the brain where prominent peaks arise from NAA, choline containing compounds, creatine and creatine phosphate, myo-inositol and, if present, lactate; phosphorus 31 MR spectroscopy detects compounds involved in energy metabolism (creatine phosphate, adenosine triphosphate and inorganic phosphate) and certain compounds related to membrane synthesis and degradation. The frequencies of certain lines may also be affected by factors such as the local pH. It is also possible to determine intracellular pH because the inorganic phosphate peak position is pH sensitive.
If the field is uniform over the volume of the sample, "similar" nuclei will contribute a particular frequency component to the detected response signal irrespective of their individual positions in the sample. Since nuclei of different elements resonate at different frequencies, each element in the sample contributes a different frequency component. A chemical analysis can then be conducted by analyzing the MR response signal into its frequency components.
 

Binomial Pulses
A sequence of two or more pulses with a null response at a particular frequency used to suppress the water signal in localized proton spectroscopy.

Chemical Shift Imaging
(CSI) Chemical shift imaging is an extension of MR spectroscopy, allowing metabolite information to be measured in an extended region and to add the chemical analysis of body tissues to the potential clinical utility of Magnetic Resonance. The spatial location is phase encoded and a spectrum is recorded at each phase encoding step to allow the spectra acquisition in a number of volumes covering the whole sample. CSI provides mapping of chemical shifts, analog to individual spectral lines or groups of lines.
Spatial resolution can be in one, two or three dimensions, but with long acquisition times od full 3D CSI. Commonly a slice-selected 2D acquisition is used. The chemical composition of each voxel is represented by spectra, or as an image in which the signal intensity depends on the concentration of an individual metabolite. Alternatively frequency-selective pulses exite only a single spectral component.
There are several methods of performing chemical shift imaging, e.g. the inversion recovery method, chemical shift selective imaging sequence, chemical shift insensitive slice selective RF pulse, the saturation method, spatial and chemical shift encoded excitation and quantitative chemical shift imaging.

Chemical Shift Selective Imaging Sequence
(CHESS) A sequence for water suppression in proton MR spectroscopy and for water or fat suppression in MR imaging. This technique uses a frequency-selective 90° pulse to selectively excite the water signal, followed by a spoiler gradient to dephase the resulting magnetization. The gradients may be repeated several times in different directions to increase its effectiveness.

Depth Resolved Spectroscopy
(DRESS) Depth resolved surface spectroscopy is a localization method that employ gradients to select the region from which spectra are acquired.

Point Resolved Spectroscopy
(PRESS) Point resolved spectroscopy is a multi echo single shot technique to obtain spectral data. PRESS is a 90°-180°-180° (slice selective pulses) sequence. The 90° radio frequency pulse rotates the spins in the yx-plane, followed by the first 180° pulse (spin rotation in the xz-plane) and the second 180° pulse (spin rotation in the xy-plane), which gives the signal.
With the long echo times used in PRESS, there is a better visualization of metabolites with longer relaxation times. Many of the metabolites depicted by stimulated echo technique are not seen on point resolved spectroscopy, but PRESS is less susceptible to motion, diffusion, and quantum effects and has a better SNR than stimulated echo acquisition mode (STEAM).

Long TE 136 msec spectroscopy	Short TE 30 msec spectroscopy

Spectroscopy Evaluation
Integrated software package with extensive graphical display functionality to evaluate and post-process spectroscopy acquisition data.
Features
Display of CSI data as colored metabolite images or spectral overview maps, overlaid on anatomical image
Export of spectroscopy data to a user-accessible file format
Relative quantification of spectra, compilation of the data to result table
Automated peak normalization tissue, water or reference
New dedicated SVS breast evaluation protocols

Step by step for basic functionality (SVS)

1. Load the SVS data set into the Spectroscopy application. The metabolite spectrum will automatically be shown in the first segment.
2. Select single data set mode. This will allow for creation of tables in the empty segments.
3. View the localizer. Double clicking on a localizer image puts this image in the large segment.
4. Activate an empty segment and right click select results table. This table will give you a ratio of metabolite integrals, where you select the denominator.
5. Save the results. Activate a segment and select save as, choose "selected results". This can be viewed or sent to PACs from the patient browser.

Step by step for basic functionality (CSI)

1. Load the CSI data set into the Spectroscopy Application.
2. Select Spectral Map on an empty segment. This will provide spectral graphs for all voxel within the Vol.
3. Zoom and pan the image to the desired size.
4. Select the last empty segment and select metabolite map. Create a ratio map to show levels of a desired metabolite compared to another.
5. Zoom and pan this image to the desired size.
6. Select the Save Data icon, Selected Results, to save maps.
7. Individual voxel graphs can be viewed by selecting a voxel on the localizer

 

Single Voxel Spectroscopy
Software package with sequences and protocols for single voxel proton spectroscopy.
Features
Streamlined for easy push-button operation
Matrix Spectroscopy – phase-coherent signal combination from several coil elements for maximum SNR based on the head matrix coil
Spectral suppression (user definable parameter) to avoid lipid superposition in order to reliably detect e.g. choline in the breast
Up to 8 regional saturation (RSat) bands for outer volume suppression can be defined by the user
Physiological triggering (ECG, pulse, respiratory or external trigger) in order to avoid e.g. CSF pulsation artifacts

	SVS shows increased Choline signal in the lesion of the right parietal lobe, proving malignancy

Step by step:

1. Run localizers, and open the svs_se_135 sequence. This is found in the exam explorer, under; Spectroscopy, Head, SVS.
2. Position the VOI on one image and go to scroll, nearest. This will align the VOI in plane for all orientations.
3. Notice that the VOI has solid borders. This means that the VOI intersects in all three planes.
4. Select "Reference Lines". This will show where the slices intersect the VOI.
5. Apply the sequence.
6. Notice in this example that the sequence name has been changed from the factory default nomenclature.
This will disable the automatic postprocessing protocol when loaded into Spectroscopy Evaluation. To correct this ensure the scanned sequence stays the same as the factory default.

GRACE: GeneRAlized breast speCtroscopy Exam- Choline level follow up to evaluate Ca breast: (GeneRAlized breast speCtroscopy Exam)
SVS technique (spin echo sequence) optimized for breast spectroscopy.
The technique contains a special spectral lipid suppression pulse (user definable) for lipid signal reduction. Siemens unique water reference detection to visualize the normalized choline ratio.
Online frequency shift correction for reduction of breathing related artifacts, Inline implementation – no additional user interaction is required.
Clinical applications:
• Differentiating benign from malignant breast lesions
• Predicting clinical response to neoadjuvant chemotherapy in an early stage (24hours after receiving the first dose)
 

3D CSI (Chemical Shift Imaging):
Integrated multivoxel spectroscopy software package with sequences and protocols for 3D Chemical Shift Imaging (CSI).
Features
Matrix Spectroscopy – phase-coherent signal combination from several coil elements for maximum SNR with configurable prescan-based normalization for optimal homogeneity
3D Chemical Shift Imaging
Hybrid CSI with combined Volume selection and Field of View (FoV) encoding
Short TEs available (30 ms for SE, 20 ms for STEAM)
Automized shimming of the higher order shimming channels for optimal homogeneity of the larger CSI volumes
Weighted acquisition, leading to a reduced examination time compared to full k-space coverage while keeping SNR and spatial resolution
Outer Volume Suppression
Spectral Suppression
Protocols for prostate spectroscopy
Clinical Applications
Prostate Spectroscopy for diagnosis, localization of prostate cancer
Improved spatial localization of metabolic changes in biopsy or radiotherapy planning
 

Cho/Cr ratio map generated from 3D CSI measurement	Spectral nap generated from 3D CSI measurement	Increased Cho-signal in a medulloblastoma case

Step by step:
1. Perform imaging in all three planes to include the entire brain. Open the csi 3D se 135 sequence. Located in the exam explorer in the Spectroscopy, CSI, head region.
2. Scroll thru the transversal images for area of interest.
3. Copy image position. Right click on the selected transverse image, from the menu select copy image position.
4. Go to the scroll drop down menu and select scroll nearest. This will align the 3D VOI in all three orientations.
5. Rotate the VOI inplane on the transversal image to cover the area of interest.
6. Open toolbar, and and select create sat bands. Draw saturation bands around all sides of the 3D VOI to remove lipid signal from calvarium.
7. Select fully excited VOI, on the Geometry card.
Apply the sequence.

31 P Spectroscopy: Optimized for liver and heart applications.
Integrated package with RF coil, sequences and protocols for 31P spectroscopy.
Offering the same level of user friendliness and automation as 1H spectroscopy.
1H/31P transmit/ receive Heart Liver coil for 31P spectroscopy
Short TE CSI sequence and protocols optimized for heart and liver applications
NOE (Nuclear Overhauser Effect) and 1H decoupling available
ECG triggering available
Weighted acquisition available
 

 

 

Prostate Package #T+D

The prostate spectroscopy package is an comprehensive software package which bundles:
- Single Voxel Spectroscopy
- 2D Chemical shift Imaging
- 3D Chemical Shift Imaging
- Spectroscopy Evaluation syngo
- syngo Tissue 4D Evaluation
Sequences and protocols for proton spectroscopy, 2D and 3D proton chemical shift imaging (2D CSI and 3D CSI) to examine metabolic changes in the prostate are included. Furthermore included is the comprehensive Spectroscopy evaluation software which enables fast evaluation of spectroscopy data on the syngo Acquisition Workplace.
Tissue 4D is an application for visualizing and post-processing dynamic contrast-enhanced 3D datasets.
Tissue 4D provides two evaluation options:
- Standard curve evaluation
- Curve evaluation according to a pharmacokinetic model.

The spectroscopy evaluation software is fully integrated in syngo MR.
Evaluation protocols adapted to the scan protocols carry out a complete and automatic evaluation of the measured data.
Optimized protocols for 3D CSI in the prostate are included.

The following functions are included:
- Subsequent water suppression with optional phase correction
- Apodization
- Zero filling
- Fourier transformation
- Base line correction
- Automatic or manual phase correction
- Curve fitting and peak labeling
- Summaries in tabular form of the essential results specifying the metabolites, their position, integrals and signal ratios in relation to a selectable reference.

Tissue 4D provides the tissue visualization features:
- 4D visualization (3D and over time)
- Color display of parametric cards (Ktrans, Kep, Ve, Vp, iAUC)
- Additional visualization of 2D or 3D morphological dataset

Post-processing features:
- Elastic 3D motion correction
- Fully automatic calculation of subtracted images

Standard curve evaluation:
- Calculation and display of enrichment curves

Pharmacokinetic model:
- Pharmacokinetic calculation on a pixel-by-pixel basis using a 2-compartment model
- Calculation is based on the Toft model. Various model functions are available.
- Manual segmentation and calculation on the result images.

The following result images can be saved as DICOM images:
- 3D motion-corrected, dynamic images
- Colored images
- Possibility for exporting results in the relevant layout format.

Applications of Spectroscopy

In (1H) Magnetic Resonance Spectroscopy each proton can be visualized at a specific chemical shift (peak position along x-axis) depending on its chemical environment. This chemical shift is dictated by neighboring protons within the molecule. Therefore, metabolites can be characterized by their unique set of 1H chemical shifts. The metabolites that MRS probes for have known (1H) chemical shifts that have previously been identified in NMR spectra. These metabolites include:
1.) N-acetyl Aspartate (NAA): with its major resonance peak at 2.02ppm, is a neuronal marker and decrease in levels of NAA indicate loss or damage to neuronal tissue, which results from many types of insults to the brain. Its presence in normal conditions indicates neuronal and axonal integrity.
2.) Choline: with its major peak at 3.2ppm, choline is known to be associated with membrane turnover, or increase in cell division. Increased choline indicates increase in cell production or membrane breakdown, which can suggest demyelination or presence of malignant tumors or inflammatory processes.
3.) Creatine & phosphocreatine: with its major peak at 3.0ppm, creatine marks metabolism of brain energy. Gradual loss of creatine in conjunction with other major metabolites indicates tissue death or major cell death resulting from disease, injury or lack of blood supply. Increase in creatine concentration could be a response to cerebral trauma. Absence of creatine may be indicative of a rare congenital disease.
4.) Lipids: with their major aliphatic peaks located in the 0.9-1.5ppm range, increase in lipids is seen is also indicative of necrosis. These spectra are easily contaminated, as lipids are not only present in the brain, but also in other biological tissue such as the fat in the scalp and area between the scalp and skull.
5.) Lactate: is a market of oxygen deficiency, reveals itself as a doublet (two symmetric peaks in one) at 1.33ppm. Normally lactate is not visible, for its concentration is lower that the detection limit of MRS, however presence of this peak indicates glycolysis has been initiated in an oxygen deficient environment. Several causes of this include ischemia, hypoxia, mitochondrial disorders, and some types of tumors.
6.) Myo-inositol: with its major peak at 3.56ppm, an increase in Myo-inositol has been seen in granulation and gliosis and patients with Alzheimer’s, dementia, and HIV patients.
7.) Glutamate and Glutamine: these amino acids are marked by a series of resonance peaks between 2.2 and 2.4ppm. Hyperammonemia, hepatic encephalopathy are two major conditions that result in elevated levels of glutamine and glutamate. MRS, used in conjunction with MRI or some other imaging technique, can be used to detect changes in the concentrations of these metabolites, or significantly abnormal concentrations of these metabolites.

Indication for Spectroscopy

Differential diagnosis of low-grade and high=grade tumors.

Monitoring under radio-chemotherapy.

differentiation of recurrent tumor from secondary necrosis due to therapy.

Spectroscopy In Case of PNET

 



These pictures showing the case of 17 years age boy with highly malignant tumor PNET (Primitive neuroectodermal tumor). Notice the very malignant area where the Ch:Cr ratio reaching 63:1 and the rapid slope at the nearby boundaries and the relatively high NAA, indicating the presence of rapid cell proliferation.

 

Spectroscopy In Case of Pilocytic astrocytoma

The patient came to the clinic 03-June-2014 with the family, telling that the patient the last month got headache with vomiting and fainting attacks, ataxia and blurred vision. CT-scan done today showing a mass with the diagnosis of medulloblastoma.
On examination at the patient has no meningism, nor nystagmus. The patient except for the above mentioned complains was neurologically free.
The patient was sent for MR investigations with MRS and DTI. The conventional MRI data and the spectroscopy were in favor of policytic astrocytoma.
In setting position, midline posterior approach with reflection of the bone flap to the neck was done. The dura was opened to expose both cerebellar hemisphere more to the left. The nidus of the tumor was fleshy violate and it was possible to resect all of it and sent for fresh frozen sections which confirmed the presence of pilocytic astrocytoma. Total resection of the cystic mass with its fleshy contents was achieved. The vermian and the tonsilar parts of the tumor were also included in the resection. After strict hemostasis, the wound was closed temporarily and the patient sent to the MRI. There is air over the left cerebral hemisphere and a suspected remnant near the removed left tonsil. The patient sent back to the operating table and in supine position, the surgery was continued. The suspected mass in the new MRI data was resected. Routine closure of the wound.
Smooth postoperative recovery. The patient sent to ICU for observation.

Normal brain MR Spectroscopy.

Spectroscopy of the intracyst material

Spectroscopy of the nidus material.

Cystic wall spectroscopy

Choline distribution.

Creatine distribution

Lactate distribution

Choline/Lactate ratio.

The medulloblastoma shows low levels of NAA, as well as elevated levels of Cho, lactate, and lipids, and peaks assigned to taurine (Tau) and guanadinoacetate (Gua). Pilocytic astrocytomas typically have low levels of Cr, as well as elevated lactate in this example. As in adults, high-grade astrocytomas show increased Cho compared to low grade, while NAA is absent in both examples.
 

Comments

MRS is a helpful tool to diagnose the tumor before surgery.
Intraoperative MRI can confirm the radical resection before closure and can show if there are any other events in the brain nearby or remote from the site of surgery. It can predict the postoperative care system of the patient.