Frequency and phase drift correction of magnetic resonance spectroscopy data by spectral registration in the time domain

Abstract

Purpose Frequency and phase drifts are a common problem in the acquisition of in vivo magnetic resonance spectroscopy (MRS) data. If not accounted for, frequency and phase drifts will result in artifactual broadening of spectral peaks, distortion of spectral lineshapes, and a reduction in signal-to-noise ratio (SNR). We present herein a new method for estimating and correcting frequency and phase drifts in in vivo MRS data. Methods We used a simple method of fitting each spectral average to a reference scan (often the first average in the series) in the time domain through adjustment of frequency and phase terms. Due to the similarity with image registration, this method is referred to as “spectral registration.” Using simulated data with known frequency and phase drifts, the performance of spectral registration was compared with two existing methods at various SNR levels. Results Spectral registration performed well in comparison with the other methods tested in terms of both frequency and phase drift estimation. Conclusions Spectral registration provides an effective method for frequency and phase drift correction. It does not involve the collection of navigator echoes, and does not rely on any specific resonances, such as residual water or creatine, making it highly versatile.

Human Auditory Cortex Neurochemistry Reflects the Presence and Severity of Tinnitus

“…GABA has three distinct peaks in its magnetic resonance spectrum, but each of these coincides in frequency with the peak of a more abundant metabolite, necessitating the use of a specific GABA measurement technique to quantify its concentration Mullins et al, 2014). We used the Mescher-Garwood proton resolved spectroscopy (MEGA-PRESS) technique (Mescher et al, 1998), in which alternate acquisitions are applied an editing pulse at 1.9 ppm, which modulates all three of the GABA peaks attributable to J coupling. Subtraction of the EDIT-OFF from EDIT-ON spectra thus allows separation of the GABA signal at 3 ppm from the overlying creatine signal.…”

“…The final measurement of interest, GABA concentration, was estimated relative to water amplitude, accounting for metabolite relaxation times and tissue fractions, as discussed by Gao et al (2015). Choline, creatine, and NAA amplitudes were quantified from non-edited spectra only using the AMARES (Advanced Method for Accurate, Robust, and Efficient Spectral fitting of MRS data with use of prior knowledge) algorithm from jMRUI (Naressi et al, 2001), and similarly to GABA were converted to tissue concentrations by taking account of water level, tissue fractions, and known tissue metabolite relaxation times from the literature (Mlynárik et al, 2001;Ethofer et al, 2003). As part of the quality assurance routine, MRS fit quality was assessed by an experienced physicist; the spectra were rejected if the Gannet fit error was Ͼ10% (GABA measurements) or metabolite line width was Ͼ12 Hz (NAA, creatine, and choline).…”

“…However, increased synchrony between neurons has been observed, in certain studies, to begin immediately after noise trauma (thus mirroring tinnitus onset; Noreña and Eggermont, 2003) and in the tonotopic region of noise trauma (Seki and Eggermont, 2003). Human tinnitus patients exhibit excessive neural synchrony, in the form of abnormal spontaneous electromagnetic field/potential oscillations in auditory cortex (Weisz et al, 2007;Adjamian et al, 2012;Tass et al, 2012) and increased responses to sound at various levels of the central auditory pathway (Lanting et al, 2008;Melcher et al, 2009;Gu et al, 2010). Although the exact role of these different types of activity in tinnitus pathogenesis is still debated (Sedley and Cummingham, 2013;De Ridder et al, 2015), they appear important and might plausibly be produced or enhanced by deficient inhibition in the central auditory pathway.…”

“…Significant differences were found only at the level of the auditory thalamus, contralateral to the exposed ear, with exposed rats showing lower GABA concentrations. Studies using flavoprotein autofluorescence to measure the spatial spread of neural responses have found evidence of reduced GABAergic inhibition, associated with noise trauma animal tinnitus models, in the dorsal cochlear nucleus (Middleton et al, 2011) and auditory cortex (Llano et al, 2012). Chronic salicylate exposure (which causes tinnitus) has been found to result in reduced expression of glutamic acid decarboxylase (which converts glutamate to GABA) and reduced GABA receptor affinity in the inferior colliculus of rats (Bauer et al, 2000).…”

“…Choline and NAA both reflect neuronal density (Miller et al, 1996); therefore, we tested whether there were similar correlations with hearing loss and THI scores with NAA, as there were for choline, which might indicate a structural basis to observed changes. NAA did not correlate significantly with either mean hearing loss ( p ϭ 0.95 uncorrected) or THI score ( p ϭ 0.76 uncorrected).…”