Cerebral metabolism in man after acute stroke: New observations using localized proton NMR spectroscopy

Bruhn, H.; Frahm, Jens; Gyngell, Michael L.; Merboldt, Klaus‐Dietmar; Hänicke, W.; Sauter, R.

doi:10.1002/mrm.1910090115

Cited by 300 publications

(97 citation statements)

References 11 publications

(2 reference statements)

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“…This effect was more pronounced in ROIs, where normalized NAA levels were initially more dramatically reduced. NAA concentrations in the brain are high and it is mainly localized to neurons (35); therefore, it has been considered as a neuronal marker (36). Reduction of NAA was often ascribed to neuronal loss but today it is clear that alternative explanations should be considered, as recovery in NAA was reported.…”

Section: Discussionmentioning

confidence: 99%

Late stimulation of the sphenopalatine‐ganglion in ischemic rats: Improvement in N‐acetyl‐aspartate levels and diffusion weighted imaging characteristics as seen by MR

Bar‐Shir

Shemesh

Nossin-Manor

et al. 2010

Magnetic Resonance Imaging

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Purpose: To assess, by MR spectroscopy (MRS) and diffusion weighted imaging (DWI), the ability of electrical stimulation of the sphenopalatine ganglion (SPG) to augment stroke recovery in transient middle cerebral artery occluded (t-MCAO) rats, when treatment is started 18 6 2 h post-occlusion. Materials and Methods: 1 H-MRS imaging ( 1 H-MRSI) and DWI were used to evaluate ischemic brain tissue after SPG stimulation in rats subjected to 2 h of t-MCAO. Rats were examined by 1 H-MRSI, DWI, and behavioral tests at 16 6 2 h, 8 days, and 28 days post-MCAO.Results: N-Acetyl-aspartate (NAA) levels of the stimulated and control rats were the same 16 6 2 h post-MCAO (0.52 6 0.03, 0.54 6 0.03). At 28 days post-occlusion, NAA levels were significantly higher in the treated group (0.60 6 0.04) compared with those of the untreated animals (0.50 6 0.04; P < 0.05). This effect was more pronounced for regions with low NAA values (0.16 6 0.03) that changed to 0.32 6 0.03 (P ¼ 0.04) for the treated group and to 0.10 6 0.03 (P ¼ 0.20) for the controls. DWI data showed better ischemic tissue condition for the treated rats, but the measured parameters showed only a trend of improvement. The MR results were corroborated by behavioral examinations. Conclusion:Our findings suggest that SPG stimulation may ameliorate MR tissue characteristics following t-MCAO even if treatment is started 18 h post-occlusion.Key Words: Sphenopalatine ganglion (SPG); middle cerebral artery occlusion (MCAO); N-acetyl aspartate (NAA); MRI; MR spectroscopy (MRS)

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Section: Discussionmentioning

confidence: 99%

Late stimulation of the sphenopalatine‐ganglion in ischemic rats: Improvement in N‐acetyl‐aspartate levels and diffusion weighted imaging characteristics as seen by MR

Bar‐Shir

Shemesh

Nossin-Manor

et al. 2010

Magnetic Resonance Imaging

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“…The use of MRS in medical diagnosis of human neurological disease has also been described (Danielsen and Ross, 1999;Gillard et al, 2005;Lin et al, 2005). In human and animal studies, proton MRS and MRI have consistently demonstrated large increases in lactate levels, and significant decreases in NAA levels in ischemic brain tissue several hours after onset (Bruhn et al, 1989b;Di Costanzo et al, 2003;Fenstermacher and Narayana, 1990;Franke et al, 2000;Graham et al, 1994). However, there is a paucity of published information concerning the early response of neuronal NAA metabolism in human stroke patients.…”

Section: Magnetic Resonance Spectroscopy and Imaging Of Naamentioning

confidence: 96%

N-Acetylaspartate in the CNS: From neurodiagnostics to neurobiology

Moffett

Ross

Arun

et al. 2007

Progress in Neurobiology

1,213

1,126

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The brain is unique among organs in many respects, including its mechanisms of lipid synthesis and energy production. The nervous system-specific metabolite N-acetylaspartate (NAA), which is synthesized from aspartate and acetyl-coenzyme A in neurons, appears to be a key link in these distinct biochemical features of CNS metabolism. During early postnatal CNS development, the expression of lipogenic enzymes in oligodendrocytes, including the NAA-degrading enzyme aspartoacylase (ASPA), is increased along with increased NAA production in neurons. NAA is transported from neurons to the cytoplasm of oligodendrocytes, where ASPA cleaves the acetate moiety for use in fatty acid and steroid synthesis. The fatty acids and steroids produced then go on to be used as building blocks for myelin lipid synthesis. Mutations in the gene for ASPA result in the fatal leukodystrophy Canavan disease, for which there is currently no effective treatment. Once postnatal myelination is completed, NAA may continue to be involved in myelin lipid turnover in adults, but it also appears to adopt other roles, including a bioenergetic role in neuronal mitochondria. NAA and ATP metabolism appear to be linked indirectly, whereby acetylation of aspartate may facilitate its removal from neuronal mitochondria, thus favoring conversion of glutamate to alpha ketoglutarate which can enter the tricarboxylic acid cycle for energy production. In its role as a mechanism for enhancing mitochondrial energy production from glutamate, NAA is in a key position to act as a magnetic resonance spectroscopy marker for neuronal health, viability and number. Evidence suggests that NAA is a direct precursor for the enzymatic synthesis of the neuron specific dipeptide N-acetylaspartylglutamate, the most concentrated neuropeptide in the human brain. Other proposed roles for NAA include neuronal osmoregulation and axon-glial signaling. We propose that NAA may also be involved in brain nitrogen balance. Further research will be required to more fully understand the biochemical functions served by NAA in CNS development and activity, and additional functions are likely to be discovered.

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“…15 - 19 The decrease appears to occur mainly between 6 (in one patient) and 24 hours after the clinical incident. The loss of NAA seems to be greater in the central than in the outer part of the VOI, suggesting a heterogeneous distribution of NAA within the infarcted area as visualized by MRI.…”

Section: Discussionmentioning

confidence: 99%

Early time course of N-acetylaspartate, creatine and phosphocreatine, and compounds containing choline in the brain after acute stroke. A proton magnetic resonance spectroscopy study.

Gideon

Henriksen

Sperling

et al. 1992

Stroke

165

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Background and Purpose:The early time course after acute stroke of cerebral JV-acetylaspartate, creatine and phosphocreatine, and compounds containing choline was studied in vivo by means of localized water-suppressed proton magnetic resonance spectroscopy.Methods: Eight patients with acute stroke were studied serially in the acute phase, 1 week after, and 2-4 weeks after the onset of clinical symptoms. Ten healthy volunteers served as controls. A stimulated echo (STEAM) sequence was used for measurement of the brain metabolites in a volume of interest located within the infarcted area as visualized by magnetic resonance imaging. For quantification, the unsaturated water signal was used as the internal standard. Regional cerebral blood flow in the infarcted area was measured relative to a symmetrically located unaffected area by means of single-photon emission computed tomographic scanning, using

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Cerebral metabolism in man after acute stroke: New observations using localized proton NMR spectroscopy

Cited by 300 publications

References 11 publications

Late stimulation of the sphenopalatine‐ganglion in ischemic rats: Improvement in N‐acetyl‐aspartate levels and diffusion weighted imaging characteristics as seen by MR

Late stimulation of the sphenopalatine‐ganglion in ischemic rats: Improvement in N‐acetyl‐aspartate levels and diffusion weighted imaging characteristics as seen by MR

N-Acetylaspartate in the CNS: From neurodiagnostics to neurobiology

Early time course of N-acetylaspartate, creatine and phosphocreatine, and compounds containing choline in the brain after acute stroke. A proton magnetic resonance spectroscopy study.

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