Metabolic changes induced by cerebral infarction or by stenosis and occlusi
on of the internal carotid artery have been previously described in 1H Magn
etic Resonance Spectroscopy (1H MRS). These changes are essentially charact
erized by decreased N-acetyl-aspartate (NAA) and increased lactate concentr
ation. Little is known about the metabolic changes observed in the three da
ys following a transient ischemic attack (TIA) in the absence of stenosis o
r occlusion of the internal carotid artery, and without visible infarction
on Magnetic Resonance imaging (MRI). We studied five patients with a TIA la
sting between 30 min and 3 h, affecting the sensory and motor functions of
the brachio-facial territory with or without aphasia. A Computerized Tomogr
aphy Scan (CT-scan) an electro-encephalogram, cervical Doppler ultrasound a
nd MRI with proton magnetic resonance spectroscopy were performed on the af
fected cerebral area and on the normal contralateral homologous cerebral ar
ea within three days of the onset of TIA. None of the five patients had ste
nosis or occlusion of the internal carotid artery on Doppler ultrasound, or
cerebral infarction on MRI. From 1H MRS ratio measurements, we did not obs
erve any significant changes in the NAA/Creatine ratio. However, a rise in
Lactate/Creatine ratio was observed in the symptomatic non-infarcted area c
ompared with the normal cerebral tissue. During the first three days follow
ing 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 inf
arction. This region could be at risk from infarction in the long term.