Donate Help Contact The AHA Sign In Home
American Heart Association
Stroke
Search: search_blue_button Advanced Search
Stroke. 2003;34:648-652
Published online before print February 13, 2003, doi: 10.1161/01.STR.0000058158.41581.41
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
34/3/648    most recent
01.STR.0000058158.41581.41v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Rutgers, D.R.
Right arrow Articles by van der Grond, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Rutgers, D.R.
Right arrow Articles by van der Grond, J.
Right arrowPubmed/NCBI databases
*Compound via MeSH
*Substance via MeSH
Hazardous Substances DB
*(L)-ASPARTIC ACID
*CHOLINE BITARTRATE
*CHOLINE CHLORIDE
Medline Plus Health Information
*Carotid Artery Disease
Related Collections
Right arrow Brain Circulation and Metabolism
Right arrow Computerized tomography and Magnetic Resonance Imaging
Right arrow Other imaging

(Stroke. 2003;34:648.)
© 2003 American Heart Association, Inc.


Original Contributions

Cerebral Hemodynamics and Metabolism in Patients With Symptomatic Occlusion of the Internal Carotid Artery

D.R. Rutgers, MD; M.J.P. van Osch, MSc; L.J. Kappelle, MD, PhD; W.P.T.M. Mali, MD, PhD J. van der Grond, PhD

From the Department of Radiology (D.R.R., W.P.T.M.M., J. vd G.), Image Sciences Institute (M.J.P. v O.), and Department of Neurology (L.J.K.), University Medical Center Utrecht, Utrecht, the Netherlands.

Correspondence to D.R. Rutgers, Department of Radiology, E01.132, University Medical Center Utrecht, Heidelberglaan 100, 3584 CX Utrecht, Netherlands. E-mail d.rutgers{at}azu.nl

Background and Purpose— The goals of this study were to investigate (1) whether the concentrations of choline, creatine, and N-acetyl aspartate (NAA) in cerebral white matter are changed in patients with symptomatic occlusion of the internal carotid artery (ICA) and (2) whether possible changes in metabolite concentration are related to regional cerebral perfusion or cerebral vasoreactivity.

Methods— In 19 patients (mean±SD age, 60±9 years), white matter metabolite concentrations were measured with proton MR spectroscopic imaging on average 4±2 months after symptoms occurred. In selected voxels, corresponding cerebral blood flow and volume, mean transit time, and time-to-bolus peak were determined with dynamic susceptibility contrast MRI. Cerebral CO2 reactivity was determined with transcranial Doppler sonography.

Results— No significant changes in choline and creatine concentrations were observed. NAA concentration was significantly reduced in the hemisphere on the side of the symptomatic ICA (9.1±1.7 mmol/L) compared with the contralateral hemisphere (10.5±1.7 mmol/L, P<0.005) and control subjects (10.5±0.9 mmol/L, P<0.01). Although no significant interhemispheric difference in NAA concentration was found in patients who presented with retinal ischemia, patients with cerebral ischemia had a significantly lower NAA concentration in the symptomatic hemisphere (9.0±1.7 mmol/L) compared with the asymptomatic hemisphere (10.4±1.6 mmol/L, P<0.05). In all patients, NAA concentration was not significantly correlated with quantitative cerebral perfusion parameters or CO2 reactivity.

Conclusions— Patients with symptomatic ICA occlusion may show chronic neuronal damage in cerebral white matter as evidenced by reduced NAA concentration. This seems to be related to previous symptomatology rather than to the cerebral hemodynamic status in a chronic stage.


Key Words: carotid artery diseases • choline • creatine • hemodynamics • N-acetyl aspartate • occlusion




This article has been cited by other articles:


Home page
HypertensionHome page
K. Kario, J. Ishikawa, S. Hoshide, Y. Matsui, M. Morinari, K. Eguchi, S. Ishikawa, and K. Shimada
Diabetic Brain Damage in Hypertension: Role of Renin-Angiotensin System
Hypertension, May 1, 2005; 45(5): 887 - 893.
[Abstract] [Full Text] [PDF]