Cerebral metabolism after transient ischemic attack. A 1H MR spectroscopy study

Metabolic changes induced by cerebral infarction or by stenosis and occlusion of the internal carotid artery have been previously described in 1H Magnetic Resonance Spectroscopy (1H MRS). These changes are essentially characterized by decreased N-acetyl-aspartate (NAA) and increased lactate concentration. Little is known about the metabolic changes observed in the three days following a transient ischemic attack (TIA), in the absence of stenosis or occlusion of the internal carotid artery, and without visible infarction on Magnetic Resonance Imaging (MRI). We studied five patients with a TIA lasting between 30 min and 3 h, affecting the sensory and motor functions of the brachio-facial territory with or without aphasia. A Computerized Tomography Scan (CT-scan), an electro-encephalogram, cervical Doppler ultrasound and MRI with proton magnetic resonance spectroscopy were performed on the affected cerebral area and on the normal contralateral homologous cerebral area within three days of the onset of TIA. None of the five patients had stenosis or occlusion of the internal carotid artery on Doppler ultrasound, or cerebral infarction on MRI. From 1H MRS ratio measurements, we did not observe any significant changes in the NAA/Creatine ratio. However, a rise in Lactate/Creatine ratio was observed in the symptomatic non-infarcted area compared with the normal cerebral tissue. During the first three days following a transient ischemic attack, there is an increase in lactate production. This change may reflect transient local hypoperfusion which could be long enough to stimulate lactate production, but short enough not to induce infarction. This region could be at risk from infarction in the long term.