Abstract 191: Selective Frontal Lobe Metabolic Dysfunction After Sub-arachnoid Hemorrhage

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Abstract

Aneurysmal SAH results in high morbidity. Patients who make a good neurological recovery report significant neuropsychological impairment such as loss of motivation, interests, and concentration, all of which are commonly associated with frontal lobe dysfunction. We hypothesize that subclinical frontal lobe injury occurs in neurologically intact SAH patients and may be identified by measuring brain energy metabolism using regional N-acetyl aspartate (NAA) as an imaging marker of neuronal integrity and mitochondrial function, and CSF lactate, as a marker of anaerobic metabolism. We utilized MR Spectroscopy (MRS) to measure regional NAA in SAH patients who had suffered neither cerebral infarction nor neurological deficits. Only patients who underwent endovascular aneurysm coiling were included. Measurements were made in frontal, temporal, occipital lobes, lateral ventricles, and averaged in each hemisphere from 3 slices. Matching ROIs were placed on the most proximate CT perfusion maps to measure corresponding rCBF. MR spectra were compared to controls from our data library (7 subjects) and to rCBF. Average age was 58 years, Hunt Hess score was 2.43±1.09, modified Fisher score was 2.79±1.05. 3 patients had DCI and none had cerebral infarction. Median GCS at discharge was 15. MRS was done at 9.93±7.73 days from admission. 1 patient had no MRS data, 3 patients had no CT perfusion. SAH patients demonstrated significantly reduced NAA/RMS in frontal lobes (16.18±4.96 vs. 20.93±5.56, p=0.042) but not in temporal (16.49±4.37 vs. 19.37±4.38, p=0.09) or occipital lobes (20.62±4.50 vs. 21.05±4.23, p=0.41). CSF lactate was significantly higher in SAH patients (7.74±2.27 vs. 4.02±0.76, p=0.001). NAA/RMS did not correlate with CBF in pooled data (R2=0.02, p=0.40) or in frontal lobe rCBF (R2=0.001, p=0.92); nor with CSF lactate (R2=0.02, p=0.53). Total frontal lobe NAA is selectively reduced and CSF lactate is elevated in neurologically intact survivors after SAH. This preliminary data is suggestive of energy depletion and subclinical brain injury, which appears to be independent of cerebral blood flow. In addition to validating this pilot data, we will study the association with cognitive impairment in these patients.

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