ABSTRACT
We report the results of brain metabolic studies (using magnetic resonance spectroscopy) in three groups of individuals: (1) demented patients with multiple subcortical ischemic lesions (n = 18); (2) nondemented, age-matched controls (n = 21); and (3) demented patients with neurodegenerative disease, probably of the Alzheimer type (n = 19). Patients with dementia with subcortical vascular lesions, as demonstrated by appropriate imaging studies, had an increase of phosphate energy charge in areas of the cerebral cortex (especially prominent in the frontal regions) superficial to and excluded from the subcortical lesions. We hypothesize that this increased energy charge might be caused by reduced metabolic activity of disconnected brain tissue or by astrocytic hypertrophy and hyperplasia that accompanies subtle ischemic, cortical alterations.
Subject(s)
Alzheimer Disease/metabolism , Brain/metabolism , Energy Metabolism , Ischemic Attack, Transient/metabolism , Adenosine Triphosphate/metabolism , Aged , Alzheimer Disease/complications , Brain Chemistry , Female , Humans , Ischemic Attack, Transient/complications , Magnetic Resonance Spectroscopy , Male , Middle Aged , Phosphates/metabolism , Phosphocreatine/metabolism , Phosphorus/metabolismABSTRACT
We investigated the effect of moderate post-ischemic hypothermia on neuropathological outcome and cerebral high energy phosphate metabolism, intracellular pH and Mg2+ concentration in the rat. Three groups of animals were investigated: (1) Wistar rats subjected to 12 min of forebrain ischemia under normothermic conditions (n = 17), (2) rats subjected to the identical procedure of ischemia, except that 30 degrees C hypothermia was induced post-ischemia and maintained for 2 h of reperfusion (n = 6), and (3) control hypothermic rats not subjected to ischemia (n = 4). In vivo 31P NMR spectroscopy was performed prior to ischemia, and at intervals up to 168 h after ischemia. Histological analysis of brain tissues was performed 7 days after ischemia. No significant differences in cortical and hippocampal neuronal damage was detected between the two experimental groups. Significantly lower pH values were detected in the hypothermic ischemic animals at 24 h (P = 0.0001) and 48 h (P = 0.018) post-ischemia compared to the normothermic ischemic animals. Normothermic ischemic animals exhibited significantly lower [Mg2+] at 72 h (P less than 0.006) compared to the pre-ischemia level. Our data indicate that post-ischemic hypothermia modifies the profiles of post-ischemic brain tissue pH and Mg2+ concentration, and this modification is not associated with histopathological outcome 7 days after ischemia.
Subject(s)
Brain/metabolism , Energy Metabolism , Hypothermia, Induced , Ischemic Attack, Transient/metabolism , Ischemic Attack, Transient/pathology , Neurons/pathology , Prosencephalon/physiopathology , Adenosine Triphosphate/metabolism , Animals , Blood Glucose/metabolism , Brain/pathology , Carbon Dioxide/blood , Glial Fibrillary Acidic Protein/analysis , Magnetic Resonance Spectroscopy/methods , Male , Neurons/metabolism , Oxygen/blood , Partial Pressure , Phosphates/metabolism , Phosphocreatine/metabolism , Phosphorus , Rats , Rats, Inbred StrainsABSTRACT
An uncommon type of stroke in children is presented. An intracranial arteriovenous malformation in a 13-year-old boy spontaneously occluded about 22 months after surgical intervention. Precipitating factors, such as bacterial infections, could not be demonstrated in this patient, who had been attending school since the time of the craniotomy. The histological features of venous encephalomalacia in the galenic territory are contrasted with hemorrhagic encephalomalacia as seen after arterial occlusions: in the former, hemorrhages are more widespread and edema is more pronounced.