OBJECTIVEThis study examined the biochemical metabolism by proton magnetic resonance spectroscopy ('H-MRS) in order to explore the value of 'H-MRS in idiopathic epilepsy in children.

METHODSThirty-three children with idiopathic epilepsy (14 cases with history of febrile seizures and 19 cases without) and six normal controls experienced MRI of the skull and brain and single-voxel 'H-MRS examinations of the hippocampi-temporal lobe. The signal intensities of N-acetylaspartate (NAA), eatine+phosphocreatine (Cr), choline-containing compounds (Cho) and lactate (Lac) and the ratios of NAA/ (Cho+Cr) and Lac/Cr were compared between the patients and normal controls.

RESULTSMRI examination showed that only one child with epilepsy had myelin dysplasia. 'H-MRS examination showed that the ratio of NAA/ (Cho+Cr) in the epilepsy group was lower than that in the control group (0.64+/-0.07 vs 0.73+/-0.05; P<0.01). The epileptic children with history of febrile seizures had a more decreased ratio of NAA/ (Cho+Cr) compared with those without the history (0.61+/-0.07 vs 0.66+/-0.06; P<0.05). There were no significant differences in the ratio of Lac/Cr between the epilepsy and the control groups.

CONCLUSIONS'H-MRS may provide early information on brain injury sensitively and non-invasively in children with epilepsy. It may be used for diagnosis and prognosis evaluation of epilepsy.

Aspartic Acid ; analogs & derivatives ; analysis ; Child ; Child, Preschool ; Choline ; analysis ; Epilepsy ; diagnosis ; metabolism ; Female ; Humans ; Magnetic Resonance Imaging ; Magnetic Resonance Spectroscopy ; methods ; Male ; Phosphocreatine ; analysis ; Protons

This study was conducted to investigate the metabolic changes in the motor and motor association cortices following axonal injury in the internal capsule that was caused by deep intracerebral hematoma. Using proton magnetic resonance spectroscopy (1H MRS), the authors studied the primary motor cortices (M-1) and sup-plementary motor areas (SMA) of 9 hemiparetic patients with documentable hemi-paresis of varying severity, and we studied 10 normal volunteers as controls. To measure the M-1 and SMA biochemical changes, 4 separate single volumes of inter-est(VOIs) were located bilaterally in the affected and unaffected hemisphere (AH and UH).1H MRS provided a neuronal and axonal viability index by measuring levels of N-acetylaspartate (NAA) and creatine/phosphocreatine (Cr). The M-1/SMA NAA/Cr ratios of the AH and UH in patients, and the AH and normal volunteers were com-pared. The NAA/Cr ratios of the M-1 and SMA in AH, and the SMA in UH were sig-nificantly lower than those of normal volunteers. These 1H MRS findings indicate that axonal injury in the descending motor pathway at the level of internal capsule could induce metabolic changes in the higher centers of the motor pathway.
Adult ; Aged ; Aged, 80 and over ; Aspartic Acid/*analogs & derivatives/metabolism ; Basal Ganglia Hemorrhage/metabolism/*pathology ; Creatine/metabolism ; Female ; Humans ; *Magnetic Resonance Spectroscopy ; Male ; Middle Aged ; Motor Cortex/metabolism/*pathology ; Paresis/metabolism/*pathology ; Phosphocreatine/metabolism ; Protons ; Pyramidal Tracts/metabolism/*pathology

OBJECTIVETo study the changes of the hippocampus metabolites with MRS to provide some clues for exploring the possible underlying unrecognised factors and pathophysiological mechanisms of psychogenic erectile dysfunction (ED).

METHODSFifteen cases of psychogenic erectile dysfunction and 15 normal volunteers (the control) were studied by a clinical 1. 5T MRI/MRS system. Proton multi-voxel spectroscopy imaging (1H-MRSI) was obtained from both sides of the hippocampus region. N-acetylaspartate (NAA), creatine and phosphocreatine (Cr) and choline-containing compounds (Cho) were determined and the ratios of NAA/Cr and Cho/Cr were calculated respectively.

RESULTSThe NAA/Cr ratio was significantly lower in the ED patients than in the control (P < 0.05). There was no significant difference in the Cho/Cr ratio between the two groups (P > 0.05).

CONCLUSIONPsychogenic erectile dysfunction may not be simply a functional disease. The hippocampus may be involved in the pathophysiology of psychogenic ED. The disease may have some previously unrecognised underlying aetiological factors and pathophysiological mechanisms.

Adult ; Aspartic Acid ; analogs & derivatives ; analysis ; Case-Control Studies ; Creatine ; analysis ; Erectile Dysfunction ; metabolism ; physiopathology ; Hippocampus ; chemistry ; physiopathology ; Humans ; Magnetic Resonance Spectroscopy ; Male ; Phosphocreatine ; analysis ; Sexual Dysfunctions, Psychological ; metabolism ; physiopathology

We sought to know whether a free radical spin trap agent, alpha-phenyl-N-tert-butyl nitrone (PBN) influences brain cell membrane function and energy metabolism during and after transient global hypoxia-ischemia (HI) in the newborn piglets. Cerebral HI was induced by temporary complete occlusion of bilateral common carotid arteries and simultaneous breathing with 8% oxygen for 30 min, followed by release of carotid occlusion and normoxic ventilation for 1 hr (reoxygenationreperfusion, RR). PBN (100 mg/kg) or vehicle was administered intravenously just before the induction of HI or RR. Brain cortex was harvested for the biochemical analyses at the end of HI or RR. The level of conjugated dienes significantly increased and the activity of Na+, K+-ATPase significantly decreased during HI, and they did not recover during RR. The levels of ATP and phosphocreatine (PCr) significantly decreased during HI, and recovered during RR. PBN significantly decreased the level of conjugated dienes both during HI and RR, but did not influence the activity of Na+, K+-ATPase and the levels of ATP and PCr. We demonstrated that PBN effectively reduced brain cell membrane lipid peroxidation, but did not reverse ongoing brain cell membrane dysfunction nor did restore brain cellular energy depletion, in our piglet model of global hypoxic-ischemic brain injury.
Adenosine Triphosphate/metabolism ; Animals ; Animals, Newborn ; *Anoxia ; Brain/*drug effects/metabolism/pathology ; Cell Membrane/*metabolism ; Cerebral Cortex ; *Ischemia ; Lipid Peroxidation ; Na(+)-K(+)-Exchanging ATPase/metabolism ; Neuroprotective Agents/*pharmacology ; Nitrogen Oxides/*pharmacology ; Phosphocreatine/*analogs & derivatives/metabolism ; Reperfusion Injury/*drug therapy ; Support, Non-U.S. Gov't ; Swine ; Time Factors