Single-voxel 1H-MRS investigation of brain metabolic changes during lactate-induced panic

Dager, Stephen R.; Richards, Todd L.; Strauss, Wayne; Artru, Alan A.

doi:10.1016/s0925-4927(97)00066-8

Cited by 49 publications

(43 citation statements)

References 31 publications

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“…Three studies have assessed lactate metabolism in small samples of remitted PD patients. Two found that elevated brain lactate responses to a lactate infusion were still present after PD patients were treated and in clinical remission, 28,30 and the third found a significantly elevated brain lactate response to hyperventilation in remitted PD patients. 16 This suggests that abnormal lactate metabolism is not merely a consequence of recent panic attacks.…”

Section: Discussionmentioning

confidence: 99%

“…This confirms and extends the findings of prior studies showing elevated brain lactate responses during metabolic challenges in patients with PD. 16,[28][29][30] Increased local oxygen availability, rather than hypoxia, in response to stimulus-induced neural activation is one of the most well-established observations in neuroscience. 44,45 Since the hypoxia model attributes the consistently elevated brain lactate responses observed in PD to ischemic hypoxia, 16,20,21 it predicts that the characteristic elevation of brain lactate would not be observed in the visual cortex in PD patients during visual stimulation.…”

Section: Discussionmentioning

confidence: 99%

“…Three studies of sodium lactate infusions and one study of hyperventilation have all observed significantly greater increases in brain lactate in PD patients. 16,[28][29][30] Some investigators proposed that the abnormal lactate response resulted from a disturbance in the dynamics of lactate metabolism in PD, 14 while others attributed it to cerebral hypoxia due to an exaggerated cerebral vasoconstriction response to alkalosis in PD. 16,20,21 It is well known that lactate accumulates under hypoxic conditions.…”

Section: Introductionmentioning

confidence: 99%

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Elevated brain lactate responses to neural activation in panic disorder: a dynamic 1H-MRS study

et al. 2008

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Converging evidence suggests that patients with panic disorder have a metabolic disturbance that may influence the regulation of arousal systems and confer vulnerability to 'spontaneous' panic attacks. The consistent finding of elevated brain lactate responses to various metabolic challenges in panic disorder appears to support this model, although the mechanism of this effect is not understood. Several mechanisms have been proposed to account for elevated brain lactate responses in panic disorder, including (1) brain hypoxia due to excessive cerebral vasoconstriction, and (2) a metabolic disturbance affecting lactate metabolism. Recent studies have shown that neural activation (for example, sensory stimulation) causes local lactate accumulation in the presence of increased oxygen availability. The current study used proton magnetic resonance spectroscopic measures of visual cortex lactate changes during visual stimulation in 15 untreated patients with panic disorder and 15 matched volunteers to critically test these two proposed mechanisms of elevated brain lactate responses in panic disorder. Visual cortex lactate/N-acetylaspartate increased during visual stimulation in both groups. The increase was significantly greater in the panic patients than in the comparison group. There were no group differences in end-tidal pCO 2 . The finding that visual stimulation leads to significantly greater visual cortex lactate responses in panic patients is not predicted by the hypoxia model. These results suggest that a metabolic disturbance affecting the production or clearance of lactate is the cause of the elevated brain lactate responses consistently observed in panic disorder and provide further support for metabolic models of vulnerability to this illness.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Elevated brain lactate responses to neural activation in panic disorder: a dynamic 1H-MRS study

et al. 2008

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“…21 and references therein). After NMR parameters were adjusted, [2][3][4][5][6][7][8][9][10][11][12][13] C]glucose (20% wt/vol) was infused i.v. at 8 ml/hr over the first 5 min, followed by continuous infusion at a lower rate, which was adjusted over a small range to maintain plasma glucose concentration at hyperglycemic levels (23.3 Ϯ 2.6 mM).…”

Section: Animal Preparationmentioning

confidence: 99%

In vivo ¹³C saturation transfer effect of the lactate dehydrogenase reaction

Yang

Shen

2007

Magnetic Resonance in Med

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Lactate dehydrogenase (LDH, EC 1.1.1.27) catalyzes an exchange reaction between pyruvate and lactate. It is demonstrated here that this reaction is sufficiently fast to cause a significant magnetization (saturation) transfer effect when the 13 C resonance of pyruvate is saturated by a continuous-wave (CW) RF pulse. Infusion of [2-13 C]glucose was used to allow labeling of pyruvate C2 at 207.9 ppm to determine the pseudo first-order rate constant of the unidirectional lactate 3 pyruvate flux in vivo. During systemic administration of GABA A receptor antagonist bicuculline, this pseudo first-order rate constant was determined to be 0.08 ؎ 0.01 s ؊1 (mean ؎ SD, N ‫؍‬ 4) in halothane-anesthetized adult rat brains. In 9L and C6 rat glioma models, the 13 C saturation transfer effect of the LDH reaction was also detected in vivo. Our results demonstrate that the 13 C magnetization transfer effect of the LDH reaction may be useful as a novel marker for utilizing noninvasive in vivo MRS to study many physiological and pathological conditions, such as cancer. Magn Reson Med 57:258 -264, 2007.

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“…[10][11][12][13][14] Little is known about the neurobiology of 'physiological' anxiety in normal subjects, ie the anxiety of normal everyday behavior, and there is no consensus about the primary brain regions involved in physiologic anxiety. 15,16 A few in vivo magnetic resonance spectroscopy ( 1 H-MRS) studies have examined brain chemistry changes in panic disorder, [17][18][19] and showed increases in brain lactate concentration during lactate-induced panic. The aim of this study was to examine relationships between regional brain chemistry (as identified by localized in vivo single-voxel 1 H-MRS) and anxiety (as measured by the State-Trait Anxiety Inventory (STAI)).…”

Section: Introductionmentioning

confidence: 99%

Anxiety in healthy humans is associated with orbital frontal chemistry

Grachev

Apkarian

2000

Mol Psychiatry

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Single-voxel 1H-MRS investigation of brain metabolic changes during lactate-induced panic

Cited by 49 publications

References 31 publications

Elevated brain lactate responses to neural activation in panic disorder: a dynamic 1H-MRS study

Elevated brain lactate responses to neural activation in panic disorder: a dynamic 1H-MRS study

In vivo ¹³C saturation transfer effect of the lactate dehydrogenase reaction

Anxiety in healthy humans is associated with orbital frontal chemistry

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Single-voxel 1H-MRS investigation of brain metabolic changes during lactate-induced panic

Cited by 49 publications

References 31 publications

Elevated brain lactate responses to neural activation in panic disorder: a dynamic 1H-MRS study

Elevated brain lactate responses to neural activation in panic disorder: a dynamic 1H-MRS study

In vivo 13C saturation transfer effect of the lactate dehydrogenase reaction

Anxiety in healthy humans is associated with orbital frontal chemistry

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In vivo ¹³C saturation transfer effect of the lactate dehydrogenase reaction