Studies of acute ischemic stroke with proton magnetic resonance spectroscopy: relation between time from onset, neurological deficit, metabolite abnormalities in the infarct, blood flow, and clinical outcome.
OBJECTIVE
Proton magnetic resonance spectroscopy (MRS) can be used to study metabolite abnormalities in the brains of stroke patients. We have used it to examine the relations between the metabolites in the infarct (N-acetylaspartate [NAA] and lactate) and the time lapse from stroke to MRS, the presenting neurological deficit, infarct size and swelling (on MRI), blood flow to the infarct (estimated by transcranial Doppler ultrasound), and clinical outcome.


METHODS
Patients with symptoms of a moderate to large cortical infarct underwent serial proton MRS (Siemens 1.5 Magnetom) within 4 days, from 5 to 10, and from 11 to 35 days after the stroke. A long echo time PRESS single voxel or chemical shift imaging acquisition was used. Transcranial Doppler ultrasound was performed daily in the first week and twice per week thereafter until the final MRS. Clinical features and baseline demographic data were collected independently by a stroke physician and 6-month outcome by postal questionnaire.


RESULTS
Fifty patients underwent at least 1 MRS examination. Reduced NAA in the infarct within the first 4 days was related to the clinical stroke syndrome, more extensive infarction, more severely reduced blood supply to the infarct, and the presence of lactate. The presence of lactate was related to large infarcts and reduced NAA. Swelling in the infarct was most closely associated with large infarcts and reduced blood supply but not reduced NAA or the presence of lactate. Clinical outcome was most closely related to the extent of the infarct (more than to the clinical syndrome)--the larger the infarct the worse the outcome--but not to the metabolite concentrations alone.


CONCLUSIONS
The reduction in NAA (but not the presence of lactate) in a visible infarct was related to the reduction in blood flow to the infarct, which in turn was related to infarct extent and clinical outcome.
Wardlaw
J M
JM
Department of Clinical Neurosciences, University of Edinburgh, Western General Hospital, Scotland. jmw@skull.dcn.ed.ac.uk
Marshall
I
I
Wild
J
J
Dennis
M S
MS
Cannon
J
J
Lewis
S C
SC
D000208:Acute Disease; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001224:Aspartic Acid / Q000031:analogs & derivatives / Q000032:analysis; D001921:Brain / Q000098:blood supply / Q000378:metabolism; D001923:Brain Chemistry / Q000502:physiology; D001929:Brain Edema / Q000000981:diagnostic imaging / Q000378:metabolism / Q000503:physiopathology; D002545:Brain Ischemia / Q000000981:diagnostic imaging* / Q000503:physiopathology / Q000628:therapy; D002536:Cerebral Arteries / Q000503:physiopathology; D002544:Cerebral Infarction / Q000000981:diagnostic imaging / Q000378:metabolism / Q000503:physiopathology; D002560:Cerebrovascular Circulation; D002561:Cerebrovascular Disorders / Q000000981:diagnostic imaging* / Q000503:physiopathology / Q000628:therapy; D002794:Choline / Q000032:analysis; D005500:Follow-Up Studies; D006801:Humans; D007773:Lactates / Q000378:metabolism; D008279:Magnetic Resonance Imaging; D008875:Middle Aged; D015999:Multivariate Analysis; D011237:Predictive Value of Tests; D011379:Prognosis; D011522:Protons; D013997:Time Factors; D016896:Treatment Outcome; D017585:Ultrasonography, Doppler, Transcranial
D007773:Lactates; D011522:Protons; D001224:Aspartic Acid; C000179:N-acetylaspartate; D002794:Choline