Man-in-the-barrel syndrome after hemorrhagic shock.
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Adult↗
Biomedical subjects
Maurice Giroud
Publications and source records attributed to Maurice Giroud.
Reversible loss of N-acetyl-aspartate in rats subjected to long-term focal cerebral ischemia.
To evaluate the true meaning of N-acetyl-aspartate (NAA) measurements in ischemic stroke, the authors followed the temporal changes in brain NAA content in rats subjected to permanent focal ischemia. Ischemia was induced by photothrombotic cortical occlusion. At 1, 3, 8, and 30 d after onset of ischemia, NAA was measured in the infarct by high-performance liquid chromatography coupled to ultraviolet detection and histologic damage was examined. Cerebral content of NAA was markedly reduced in the lesioned tissue, reaching -90% after 3 d, a time at which viable neurons were no longer detected. N-Acetyl-aspartate concentrations after 8 and 30 d were higher than that observed after 3 d. This metabolic change coincided with an important microglial and astroglial activation. The results of this study raise questions regarding the use of NAA as a specific neuronal marker in chronic stage of stroke.
Animals↗
Spectroscopic data following stroke reveal tissue abnormality beyond the region of T2-weighted hyperintensity.
Cerebral tissue with T2 magnetic resonance imaging (MRI) abnormalities following stroke is generally considered infarcted, while surrounding regions with normal MRI appearance are believed to be healthy. To assess whether these surrounding regions consist of normal tissue, we explored the distribution of N-acetylaspartate (NAA) and lactate within and around the hyperintense area on T2-weighted MRI using proton MR spectroscopy. The study was carried out in 25 patients with middle cerebral artery occlusion imaged between 1 and 42 days after stroke onset. NAA/choline (Cho) ratios were significantly reduced in both areas of T2 hyperintensity and in surrounding tissue. The reduction was greater in the region of T2 hyperintensity than in the surrounding region (-50% vs. -28%, respectively) and was unrelated to the delay after the ictus. Lactate/Cho ratios increased massively within the abnormal T2 area, but did not differ from control values beyond the margin of hyperintensity. Overall data indicate that T2 visible lesions on MRI do not infer the entire injured tissue.
Aspartic Acid↗
5-Hydroxyindolacetic acid and homovanillic acid are not involved in the cerebrospinal fluid after a seizure in patients with Delirium Tremens.
Little is known about 5-hydroxyindolacetic acid (5-HIAA) and homovanillic acid (HVA) levels in cerebrospinal fluid of patients with Delirium Tremens revealed at onset by seizures. The aim of the study is to understand the biochemical abnormalities induced by seizures in the cerebrospinal fluid of patients involved by Delirium Tremens. Nine patients 42-62 years of age, who had experienced a Delirium Tremens after alcohol withdrawal, with one or two seizures at onset, were included in this study. The lumbar puncture (and a CT scan) were performed after the last seizure. Nine patients with neither Delirium Tremens nor seizure, needing a lumbar puncture for their medical problem, were matched by sex and by age. For the measures of 5-HIAA and HVA, we systematically took the first cm3. The mean value of 5-HIAA levels were 12.70 ng ml(-1) in the group of nine patients with Delirium Tremens versus 13.45 ng ml(-1) in the control group. The mean value of HVA levels were 19.81 ng ml(-1) in the group of nine patients with Delirium Tremens versus 25.25 ng ml(-1) in the control group. The differences were not statistically significant. During a Delirium Tremens with seizure at onset, there are no statistically significant changes in 5-HIAA and HVA levels in the cerebrospinal fluid. Our work raises the question of the role of Delirium Tremens in the normalization of the levels of neuro-mediators that usually decrease soon after seizures.
Adult↗
Subcortical gray matter N-acetylaspartate reduction in two cases of vascular dementia.
Many of the previous studies of vascular dementia using proton magnetic resonance (MR) spectroscopy had been carried out on white matter. However, no proton spectroscopic data of the subcortical gray matter are available in such disease. We report two cases suffering from vascular dementia, with an unilateral N-acetylaspartate (NAA) decrease on subcortical gray matter. This significant reduction in NAA ratios was associated with an increase of choline on the ipsilateral centrum semiovale. We discuss the pathophysiology of these cases.
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