Functional 1H-MRS findings in migraine patients with and without aura assessed interictally. Neuroimage

Neuroscience Department, University of Perugia, Policlinico Monteluce, Via E Dal Pozzo, 06126 Perugia, Italy.
NeuroImage (Impact Factor: 6.36). 03/2005; 24(4):1025-31. DOI: 10.1016/j.neuroimage.2004.11.005
Source: PubMed


The present study was aimed at investigating changes in brain metabolites due to visual cortex activation in migraineurs and normal subjects by (1)H-magnetic resonance spectroscopy (MRS). Twenty-two migraine patients with aura, 22 migraine patients without aura, and 10 control subjects were assessed. The volume of interest (about 8 cm(3)) was placed on the visual cortex area and the visual stimulus was applied using MR-compatible goggles with a flashing red light at a frequency of 8 Hz and an intensity of 14 lx. Data were acquired over 36'40". The experimental time course was: baseline phase, from 0 to 3'40" (1 spectrum); on phase (flashing light condition), from 3'40" to 29'20" (1540") (7 spectra), and off phase, from 29'20" to the end of the experiment at 36'40" (2 spectra). The main result of photic stimulation in patients with migraine with aura is the more consistent decrease (-14.61%) of the N-acetylaspartate (NAA) signal, which is significantly greater than that found in migraine patients without aura and control subjects. A parallel slight increase in the lactate peak was also detected. The above findings support little differences in brain metabolites between the two patient groups assessed in interictal periods, which suggests a less efficient mitochondrial functioning in migraine with aura patients.

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Available from: Giuseppe Stipa, Apr 26, 2014
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    • "The development of proton magnetic resonance spectroscopy (1H-MRS) has been used to assess noninvasively the metabolic status of human brain [43]. Several studies have employed 1H-MRS achieving numerous results for metabolites including N-acetylaspartate (NAA), as a marker of neuronal functioning [44], choline (Cho), as a marker for membrane turnover [45], total creatine (tCr) and lactate, for energy metabolism [46], and myo-inositol (a glial marker) [47]. With the exception of NAA, the results obtained for these molecules are heterogeneous and sometimes contradictory. "
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    ABSTRACT: The term omics consist of three main areas of molecular biology, such as genomics, proteomics and metabolomics. The omics synergism recognise migraine as an ideal study model, due to its multifactorial nature. In this review, the plainly research data featuring in this complex network are reported and analyzed, as single or multiple factor in pathophysiology of migraine. The future of migraine biomolecular research shall be focused on networking among these different and hierarchical disciplines. We have to look for its Ariadne's tread, in order to see the whole painting of migraine molecular biology.
    The Journal of Headache and Pain 07/2013; 14(1):55. DOI:10.1186/1129-2377-14-55 · 2.80 Impact Factor
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    • "Both studies used visual stimuli and paradigms similar to ours. Sarchielli et al. (10) found a decrease in NAA levels during visual stimulation for three groups of subjects: 22 patients with migraine with aura, 22 patients with migraine without aura, and 10 healthy subjects. The decrease was more marked for the first group (14.6% for the patients with migraine with aura). "
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    ABSTRACT: N-acetyl-aspartyl-glutamate (NAAG) and its hydrolysis product N-acetyl-L-aspartate (NAA) are among the most important brain metabolites. NAA is a marker of neuron integrity and viability, while NAAG modulates glutamate release and may have a role in neuroprotection and synaptic plasticity. Investigating on a quantitative basis the role of these metabolites in brain metabolism in vivo by magnetic resonance spectroscopy (MRS) is a major challenge since the main signals of NAA and NAAG largely overlap. This is a preliminary study in which we evaluated NAA and NAAG changes during a visual stimulation experiment using functional MRS. The paradigm used consisted of a rest period (5 min and 20 s), followed by a stimulation period (10 min and 40 s) and another rest period (10 min and 40 s). MRS from 17 healthy subjects were acquired at 3T with TR/TE = 2000/288 ms. Spectra were averaged over subjects and quantified with LCModel. The main outcomes were that NAA concentration decreased by about 20% with the stimulus, while the concentration of NAAG concomitantly increased by about 200%. Such variations fall into models for the energy metabolism underlying neuronal activation that point to NAAG as being responsible for the hyperemic vascular response that causes the BOLD signal. They also agree with the fact that NAAG and NAA are present in the brain at a ratio of about 1:10, and with the fact that the only known metabolic pathway for NAAG synthesis is from NAA and glutamate.
    Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas / Sociedade Brasileira de Biofisica ... [et al.] 08/2012; 45(11):1031-6. DOI:10.1590/S0100-879X2012007500128 · 1.01 Impact Factor
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    • "In addition, the NAA reduction detected by 1H-MRS was specially observed in migraine with aura patients under the cortical activation induced by photic stimulation, while the NAA reduction observed in migraine without aura was only slightly more evident than in controls [2]. In our migraine series, the NAA levels were reduced in both types of migraine, including the chronic form evolved from migraine without aura, though patients experiencing aura symptoms were characterized by the lowest serum NAA. "
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    ABSTRACT: Serum levels of N-acetyl-aspartate (NAA) may be considered a useful marker of neuronal functioning. We aimed to measure serum NAA in cohorts of migraine and tension-type headache patients versus controls, performing correlations with main clinical features. A total of 147 migraine patients (including migraine without aura, with aura and chronic migraine), 65 tension-type headache (including chronic and frequent episodic tension-type headache) and 34 sex- and age-matched controls were selected. Serum was stored at -80 °C. Quantification of NAA was achieved by the standard addition approach and analysis was performed with liquid-chromatography-mass-spectrometry (LC/MS) technique. The NAA levels were significantly decreased in migraine group (0.065 ± 0.019 mol/L), compared with both tension-type headache patients (0.078 ± 0.016 mol/L) and controls (0.085 ± 0.013 mol/L). Control subjects were significantly different from migraine with and without aura and chronic migraine, who differed significantly from episodic and chronic tension-type headache. Migraine with aura patients showed lower NAA levels when compared to all the other headache subtypes, including migraine without aura and chronic migraine. In the migraine group, no significant correlation was found between NAA serum levels, and headache frequency, allodynia and interval from the last and the next attack. The low NAA in the serum may be a sign of neuronal dysfunction predisposing to migraine, probably based on reduced mitochondria function.
    The Journal of Headache and Pain 04/2012; 13(5):389-94. DOI:10.1007/s10194-012-0448-3 · 2.80 Impact Factor
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