The white matter in centrum semiovale is particularly susceptible area to hypoperfusion because it is the most distal white matter part which perfused by the cortical branches of carotid arteries. This area is most likely one of the first to have ischemic injury affection when blood flow decrease.
From a technical point of view, the centrum semiovale is suited for performing accurate spectroscopy of white matter without contamination by gray matter or subcutaneous fat.
Findings of 1H-MRSI in patients with symptomatic internal carotid artery stenosis or occlusion revealed a decrease in the NAA and an increase in the choline in cerebral white matter on the stenosed or occluded side.
The creatine peak is a multicomposed peak comprising of creatine and phosphocreatine. This peak may be used as a control value because it remains fairly stable even in circumstances of disease. But creatine peak cannot be used as an internal reference in some occasions such as cerebral infarction, because its concentration differs with the anaerobic tissue conditions as in our study.
Many authors have found a decrease in the concentration of creatine in infarcted areas.
For this reason we used the peak area of NAA, choline, and creatine (rNAA, rCho, and rCr) as a parameters contrary to NAA/creatine and choline/creatine, when we studied metabolic changes and compared them between the affected side and contralateral side of the patients who had no infarction.
As there was no detectable infarction on MRI in patients with internal carotid artery stenosis or occlusion, we believe that the creatine peak may be presumed to be fairly stable and it is acceptable to use it as a control value in these patients.
A decrease in NAA is generally viewed as a neuronal loss, as NAA is mostly considered a neuronal marker. Since neurons do not regenerate, this is considered as an irreversible damage.
However, previous studies have reported that NAA decrease in the hemisphere ipsilateral to the symptomatic ICA stenosis or occlusion revealed a trend toward recovery due to gradually improved collateral circulation.
We assume that the NAA reduction in these patients is not caused merely by a loss of neurons. The observed reduction may have been caused by changes in the axonal volume in the white matter or by a reversible mitochondria dysfunction, since NAA is synthesized in mitochondria.
We observed an increase in choline in the hemisphere ipsilateral to ICA occlusion or stenosis. The main parts of choline peak involves choline, phosphocholine, and glycerolphosphocholine, which are involved in membrane synthesis. The main source of free choline is breakdown in cells.
In our study, lactate peaks were observed in 8 of 30 patients with ICA stenosis or occlusion.
Lactate appears in ischemic brain and indicates a switch from oxidative metabolism to anaerobic glycolysis. Lactate production is a sensitive marker of brief local hypoperfusion.
The increased lactate observed in the hemisphere ipsilateral to ICA stenosis or occlusion could be explained by an increase in the anerobic glycolysis caused by hypoperfusion. This hypoperfusion would appear to be long enough to bring about significant changes in the anerobic metabolism, but not enough to produce infarction. The regions with lactate may be at particular risk for cerebral infarction if perfusion further decreases.
The patients with a lactate signal are probably at high risk for infarction. The absence of lactate peaks in some patients may be attributed to a few factors. The hypoperfusion may not be severe enough to induce anerobic glycolysis and the lactate concentration may be very low due to transient anaerobic glycolysis.
1H-MRSI can reveal abnormal metabolic changes which occur in cerebral tissues with no infarction, however with internal carotid artery may show stenosis or occlusion at an initial stage, which in turn may help guide management decisions and preoperative assessment.
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