Abnormal brain and muscle energy metabolism shown by
            <sup>31</sup>
            P magnetic resonance spectroscopy in patients affected by migraine with aura

Barbiroli, Bruno; Montagna, Pasquale; Cortelli, Pietro; Funicello, R.; Iotti, Stefano; Monari, L.; Pierangeli, Giulia; Zaniol, P; Lugaresi, E

doi:10.1212/wnl.42.6.1209

Cited by 201 publications

(138 citation statements)

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“…Our present findings confirm and extend previous results reported by Eleff et al (1990) and our group (Montagna et al, 1992) that impaired mitochondrial function of brain cortex may be associated with any of the clinical expressions of mitochondrial cytop athies, and that 31p MRS is able to uncover a deficit of brain energy metabolism not only in affected pa tients, but also in those patients without any brain symptoms and/or signs.…”

Section: Discussionsupporting

confidence: 92%

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Defective Brain Energy Metabolism Shown by in vivo³¹P MR Spectroscopy in 28 Patients with Mitochondrial Cytopathies

Barbiroli

Montagna

Martinelli

et al. 1993

J Cereb Blood Flow Metab

102

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Summary:We studied brain energy metabolism by phos phorus magnetic resonance spectroscopy e1p MRS) in 28 patients with mitochondrial cytopathies, and 20 normal control subjects. Fourteen patients had myopathy alone, six had only mild brain symptoms, and eight showed dif ferent degrees of brain involvement. Brain 31p MRS showed a low phosphocreatine content in all patients, accompanied by a high inorganic phosphate in 14 of 28 patients. The average value of the Pi concentration in the patient group was significantly (p = 0.009) different from the control group. The cytosolic pH was normal. From these data were derived a high concentration of ADP (calMitochondrial cytopathies are a heterogeneous group of diseases thought to be due to inherited disorders of mitochondrial function (Schneck et aI., 1973; Berenberg et aI., 1977; Di Mauro et aI., 1985), and characterized by a wide variety of clinical phe notypes (Schneck et aI., 1973; Berenberg et aI., 1977; Pavlakis et aI., 1984; Di Mauro et aI., 1985; Hurko and McKann, 1985; Bourd et aI., 1987; Frackowiak et aI., 1988;Wallace et at., 1988; Berk ovic et aI., 1989). Many patients show symptoms and signs involving multiple organs as in Kearns Sayre syndrome (KSS), in myoclonic epilepsy and Received July 30, 1992; final revision received December 9, 1992; accepted December 9, 1992.Address correspondence and reprint requests to Prof. B. Barbiroli at Istituto di Clinic a N eurologica, via U. Foscolo 7, 40123 Bologna, Italy.Abbreviations used: CPEO, chronic progressive external oph thalmoplegia; DRESS, depth-resolved surface-coil spectros copy; FID, free induction decay; KSS, Kearns-Sayre syndrome; LHON, Leber's hereditary optic neuropathy; MELAS, mito chondrial encephalomyopathy, lactic acidosis, and stroke-like episodes; MERRF, myoclonic epilepsy and ragged-red fibers; MRS, magnetic resonance spectroscopy; PCr, phosphocreatine; PP, phosphorylation potential. 469culated from the creatine kinase equilibrium), a high per cent value of V/V max for ATP biosynthesis, and a low phosphorylation potential, all features showing a de rangement of brain energy metabolism, in all patients with mitochondrial cytopathies. 31p MRS proved to be sensitive enough to disclose a deficit of mitochondrial functionality not only in the affected patients, but also in those without clinically evident brain symptoms. Key Words: Brain bioenergetics-Impaired brain energy me tabolism-Mitochondrial cytopathies-Brain MR spec troscopy.

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Section: Discussionsupporting

confidence: 92%

“…Phosphorus magnetic resonance spectroscopy 31p MR spectra were acquired by a GE 1.5 T Signa system with a spectroscopy accessory using a surface coil provided by General Electric (Milwaukee, WI, U.S.A.) as recently reported (Barbiroli et al, 1992). The pulse width and transmitter power were adjusted to obtain max imal signal intensity.…”

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confidence: 99%

Defective Brain Energy Metabolism Shown by in vivo³¹P MR Spectroscopy in 28 Patients with Mitochondrial Cytopathies

Barbiroli

Montagna

Martinelli

et al. 1993

J Cereb Blood Flow Metab

102

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“…One study, Boska et al, reported only a depletion of PCr in anterior brain regions of MwA and the occipital cortex of FHM patients (11). The calculated value of the phosphorylation potential was significantly decreased in migraine patients, as reported in a number of studies (8,9,(12)(13)(14)(15) hence has a lower energy reserve, was also frequently observed (8,9,(13)(14)(15)18). The percentage of v/v max was found to be significantly increased in migraine patients (8,9,14,15).…”

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confidence: 78%

“…pH i was measured in all abovementioned studies and no significant pH i -changes were observed in all but three studies (13,14,18). The pH i -changes found in these studies should be regarded carefully, though, because of the presence of large standard deviations (13), borderline significance (14) or migrainous stroke (18).…”

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confidence: 90%

Magnetic resonance spectroscopy in migraine: What have we learned so far?

2012

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Objective: To summarize and evaluate proton (1H) and phosphorus (31P) magnetic resonance spectroscopy (MRS) findings in migraine. Methods: A thorough review of 1H and/or 31P-MRS studies in any form of migraine published up to September 2011. Results: Some findings were consistent in all studies, such as a lack of ictal/interictal brain pH change and a disturbed energy metabolism, the latter of which is reflected in a drop in phosphocreatine content, both in the resting brain and in muscle following exercise. In a recent interictal study ATP was found to be significantly decreased in the occipital lobe of migraine with aura patients, reinforcing the concept of a mitochondrial component to the migraine threshold, at least in a subgroup of patients. In several studies a correlation between the extent of the energy disturbance and the clinical phenotype severity was apparent. Less consistent but still congruent with a disturbed energy metabolism is an observed lactate increase in the occipital cortex of several migraine subtypes (MwA, migraine with prolonged aura). No increases in brain glutamate levels were found. Conclusion: The combined abnormalities found in MRS studies imply a mitochondrial component in migraine neurobiology. This could be due to a primary mitochondrial dysfunction or be secondary to, for example, alterations in brain excitability. The extent of variation in the data can be attributed to both the variable clinical inclusion criteria used and the variation in applied methodology. Therefore it is necessary to continue to optimize MRS methodology to gain further insights, especially concerning lactate and glutamate.

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“…74,75 Reduced PCr concentrations have also been reported in migraine, which has been postulated to be associated with abnormal mitochondrial function. 76,77 Several 31 P MRS studies have suggested a connection between decreased levels of PCr and bipolar disorder (Table 5). A study by Kato et al 78 of bipolar patients across the full range of mood states (depressed, manic, and euthymic) observed significantly 22 Consequently, it is possible that the decreased PCr levels observed in these studies were due to the pharmacological effects of these treatments.…”

Section: Elevated Lactate In Bipolar Disordermentioning

confidence: 99%

Mitochondrial dysfunction in bipolar disorder: evidence from magnetic resonance spectroscopy research

2005

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Magnetic resonance spectroscopy (MRS) affords a noninvasive window on in vivo brain chemistry and, as such, provides a unique opportunity to gain insight into the biochemical pathology of bipolar disorder. Studies utilizing proton ( 1 H) MRS have identified changes in cerebral concentrations of N-acetyl aspartate, glutamate/glutamine, choline-containing compounds, myo-inositol, and lactate in bipolar subjects compared to normal controls, while studies using phosphorus ( 31 P) MRS have examined additional alterations in levels of phosphocreatine, phosphomonoesters, and intracellular pH. We hypothesize that the majority of MRS findings in bipolar subjects can be fit into a more cohesive bioenergetic and neurochemical model of bipolar illness that is both novel and yet in concordance with findings from complementary methodological approaches. In this review, we propose a hypothesis of mitochondrial dysfunction in bipolar disorder that involves impaired oxidative phosphorylation, a resultant shift toward glycolytic energy production, a decrease in total energy production and/or substrate availability, and altered phospholipid metabolism. Molecular Psychiatry (2005) 10, 900-919.

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Abnormal brain and muscle energy metabolism shown by ³¹ P magnetic resonance spectroscopy in patients affected by migraine with aura

Cited by 201 publications

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Defective Brain Energy Metabolism Shown by in vivo³¹P MR Spectroscopy in 28 Patients with Mitochondrial Cytopathies

Defective Brain Energy Metabolism Shown by in vivo³¹P MR Spectroscopy in 28 Patients with Mitochondrial Cytopathies

Magnetic resonance spectroscopy in migraine: What have we learned so far?

Mitochondrial dysfunction in bipolar disorder: evidence from magnetic resonance spectroscopy research

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Abnormal brain and muscle energy metabolism shown by 31 P magnetic resonance spectroscopy in patients affected by migraine with aura

Cited by 201 publications

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Defective Brain Energy Metabolism Shown by in vivo31P MR Spectroscopy in 28 Patients with Mitochondrial Cytopathies

Defective Brain Energy Metabolism Shown by in vivo31P MR Spectroscopy in 28 Patients with Mitochondrial Cytopathies

Magnetic resonance spectroscopy in migraine: What have we learned so far?

Mitochondrial dysfunction in bipolar disorder: evidence from magnetic resonance spectroscopy research

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Product

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Abnormal brain and muscle energy metabolism shown by ³¹ P magnetic resonance spectroscopy in patients affected by migraine with aura

Defective Brain Energy Metabolism Shown by in vivo³¹P MR Spectroscopy in 28 Patients with Mitochondrial Cytopathies

Defective Brain Energy Metabolism Shown by in vivo³¹P MR Spectroscopy in 28 Patients with Mitochondrial Cytopathies