Fig. 3: Whole brain NAA MRS study of a patient with MS and a healthy control.
a: Axial T1-weighted MRI of a 28 year old female MS patient.
b: Corresponding slice from a 31 year old female healthy control.
a’, b’: The whole-head 1H spectra, on the same chemical-shift and intensity scales. The hatched regions indicate the signal area used to evaluate the amount of NAA from the entire brain. Note increased brain atrophy and decreased NAA peak in the patient compared to the control. From Neuroimage 21: 1825-1829; 2004
A recently introduced 1H-MRS sequence, whole-brain NAA (WBNAA) quantification, can provide a measure of neuronal and axonal losses in the entire brain (Fig. 3). Based on intrinsic, more than five-fold, T1 differences between lipids and NAA in neuronal tissue, appropriate inversion recovery timing can yield equilibrium lipid signals when the NAA is just crossing the null plane. Subtraction of such signals from fully thermal lipids -NAA spectrum yields the spectrum of ONLY the NAA (Fig. 3). The entire procedure, including loading, shimming, tuning, and 1H-MRS takes 15 minutes. The NAA signal is quantified with phantom replacement and the brain’s absolute NAA concentration is obtained. WBNAA is then calculated by dividing the amount of NAA by the brain volume.
Combining Conventional MRI with Perfusion MR and MRS Optimizes Brain Tumor Diagnosis
The MR and MRS findings in a number of different intracranial masses are sometimes non-specific. There is overlap in the spectroscopic appearance of many ring-enhancing lesions such as gliomas, metastases, inflammatory lesions, demyelinating lesions and some AIDS related lesions. However, the combination of clinical findings, conventional MRI, MVS, and DSC perfusion MRI can increase our diagnostic accuracy and confidence. Furthermore, a number of advanced techniques can be employed in specific clinical settings to improve diagnostic specificity. First, comparing metabolite values from the lesion to contralateral normal (n) appearing brain and obtaining choline (Cho)/Cho(n) and Cho/Creatine (Cr)(n) ratios, rather than the conventional Cho/Cr or Cho/NAA ratios, provides a more specific internal standard for semi-quantification of metabolites. Second, obtaining MRSI and DSC MRI data from not only the tumor but also the peritumoral region can help differentiate between infiltrating edema around a primary glioma versus pure vasogenic edema around metastases and other non-infiltrating lesions. Third, there are some pathologies where finding resonances such as leucine, isoleucine, valine, alanine, acetate, succinate and glycine help establish the diagnosis of a bacterial abscess. Lastly, additional perfusion parameters such as finding increased mean transit time (MTT) within a region of ischemia or finding increased vascular permeability in atypical meningiomas may increase diagnostic specificity.
3D 1H-MRS and WBNAA spectroscopy in multiple sclerosis: a global approach
MR imaging is the most sensitive tool for confirming the diagnosis of MS, the most common cause of non-traumatic disability in young adults. 1H-MRS can complement MR findings by providing biochemical information related to the different pathological substrates of the disease, especially with regard to neuronal/axonal injury which leads to clinical disability. Currently funded research projects directed by Dr. Robert Grossman at NYU include the quantification of the neuronal/axonal damage by means of 1H-MRS and the study of its impact on neurological disability. The rationale for 3D 1H-MRS and WBNAA, developed by Dr. Gonen, is in the diffuse nature of MS pathology which requires methods capable of investigating the entire brain. The 3D 1H-MRS technique enables us to focus on a large volume of normal-appearing tissue and on several lesions spatially separated and in different stages of evolution (Fig. 2). We have investigated 66 hypo- and iso-intense lesions and 31 areas of normal appearing white matter with 3D 1H-MRS and reported that metabolic abnormalities persist in lesions and in normal-appearing tissue even during periods of clinical quiescence and when current MRI markers of activity are lacking. Using the new WBNAA quantification method we have demonstrated how consistent NAA deficits indicate global neuronal/axonal losses sustained throughout the brain of MS patients as a function of age and, therefore, disease duration. In a study of 71 early relapsing-remitting MS patients whose typical lesion burden does not exceed 50 cm3, we have found that a WBNAA loss greater than 10–20% cannot be explained by changes within the lesions alone. Such extensive deficits can only be accounted for in terms of significant involvement of normal-appearing white and gray matter supporting the neurodegenerative hypothesis of MS. WBNAA is a metric for measuring neuronal damage and may be important for monitoring the efficacy of neuroprotective strategies in the context of both routine clinical management and in treatment trials. This technique can also be applied to quantifying the degree of brain dysfunction in diseases such as Alzheimer’s disease, traumatic brain injury, radiation induced brain injury, and HIV related encephalopathy.
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