Changes in NAA and lactate following ischemic stroke: a serial MR spectroscopic imaging study.
OBJECTIVE
Although much tissue damage may occur within the first few hours of ischemic stroke, the duration of tissue injury is not well defined. We assessed the temporal pattern of neuronal loss and ischemia after ischemic stroke using magnetic resonance spectroscopic imaging (MRSI) and diffusion-weighted imaging (DWI).


METHODS
We measured N-acetylaspartate (NAA) and lactate in 51 patients with acute ischemic stroke at five time points, from admission to 3 months, in voxels classified as normal, possibly or definitely abnormal (ischemic) according to the appearance of the stroke lesion on the admission DWI. We compared changes in NAA and lactate in different voxel classes using linear mixed models.


RESULTS
NAA was significantly reduced from admission in definitely and possibly abnormal (p < 0.01) compared to contralateral normal voxels, reaching a nadir by 2 weeks and remaining reduced at 3 months. Lactate was significantly increased in definitely and possibly abnormal voxels (p < 0.01) during the first 5 days, falling to normal at 2 weeks, rising again later in these voxels.


CONCLUSIONS
The progressive fall in N-acetylaspartate suggests that some additional neuronal death may continue beyond the first few hours for up to 2 weeks or longer. The mechanism is unclear but, if correct, then it is possible that interventions to limit this ongoing subacute tissue damage might add to the benefit of hyperacute treatment, making further improvements in outcome possible.
Muñoz Maniega
S
S
University of Edinburgh, Division of Clinical Neurosciences, Western General Hospital, Crewe Road, Edinburgh, EH4 2XU, UK. s.m.maniega@ed.ac.uk
Cvoro
V
V
Chappell
F M
FM
Armitage
P A
PA
Marshall
I
I
Bastin
M E
ME
Wardlaw
J M
JM
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001224:Aspartic Acid / Q000031:analogs & derivatives* / Q000032:analysis / Q000378:metabolism; D015415:Biomarkers / Q000032:analysis / Q000378:metabolism; D001921:Brain / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D002545:Brain Ischemia / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D001931:Brain Mapping; D016923:Cell Death / Q000502:physiology; D038524:Diffusion Magnetic Resonance Imaging; D018450:Disease Progression; D015536:Down-Regulation / Q000502:physiology; D004734:Energy Metabolism / Q000502:physiology; D005260:Female; D006801:Humans; D019344:Lactic Acid / Q000032:analysis / Q000378:metabolism*; D016014:Linear Models; D009682:Magnetic Resonance Spectroscopy / Q000379:methods*; D008297:Male; D008875:Middle Aged; D009410:Nerve Degeneration / Q000175:diagnosis / Q000378:metabolism / Q000503:physiopathology; D020521:Stroke / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D013997:Time Factors
D015415:Biomarkers; D001224:Aspartic Acid; D019344:Lactic Acid; C000179:N-acetylaspartate