Hemodynamic and metabolic changes in transient ischemic attack patients: a magnetic resonance angiography and (1)H-magnetic resonance spectroscopy study performed within 3 days of onset of a transient ischemic attack.
OBJECTIVE
We investigated whether patients with transient ischemic attack (TIA) have systemic low flow to the brain or an abnormal intracranial flow distribution caused by an abnormal anatomy of the circle of Willis. Furthermore, we investigated whether metabolic changes were present in the brain.


METHODS
Forty-four patients with clinically diagnosed TIA were prospectively included in our study. Clinical and neurological data were compiled. MR imaging; quantitative flow measurements of the internal carotid, middle cerebral, and basilar arteries; MR angiography of the circle of Willis; and (1)H-MR spectroscopy were performed in all patients within 3 days of onset of symptoms.


RESULTS
Compared with control subjects, TIA patients did not have altered flow volume in any of the arteries and had normal flow distribution through the circle of Willis. In TIA patients, the N-acetylaspartate (NAA)/choline ratio in noninfarcted regions was significantly decreased in the symptomatic hemisphere (1.73+/-0.16) compared with the asymptomatic hemisphere (1.84+/-0.19, P<0.05) and control subjects (1.90+/-0.17, P<0.001). In the symptomatic hemisphere, the lactate/NAA ratio was significantly increased (0.04+/-0.08) compared with control subjects (0.00+/-0.01, P<0.05). Patients with a history of prior TIA had a significantly decreased NAA/choline ratio in both the symptomatic (P<0.05) and asymptomatic (P<0.05) hemispheres compared with TIA patients without a prior TIA.


CONCLUSIONS
TIA patients have neurological deficits that are transient; however, metabolic damage to the brain is present up to 3 days after the onset of the symptoms. These metabolic changes are not restricted to the symptomatic hemisphere or to areas close to ischemic lesions.
Bisschops
Robertus H C
RH
Department of Radiology, University Medical Center Utrecht, Utrecht, the Netherlands. r.h.c.bisschops@azu.nl
Kappelle
L J
LJ
Mali
Willem P T M
WP
van der Grond
Jeroen
J
D000328:Adult; D000368:Aged; D001224:Aspartic Acid / Q000031:analogs & derivatives* / Q000378:metabolism; D001921:Brain / Q000098:blood supply / Q000378:metabolism / Q000503:physiopathology; D002536:Cerebral Arteries / Q000503:physiopathology; D002560:Cerebrovascular Circulation; D002794:Choline / Q000378:metabolism; D002941:Circle of Willis / Q000002:abnormalities / Q000503:physiopathology; D017352:Echo-Planar Imaging / Q000379:methods; D005260:Female; D006439:Hemodynamics; D006801:Humans; D006859:Hydrogen; D002546:Ischemic Attack, Transient / Q000175:diagnosis / Q000378:metabolism* / Q000503:physiopathology*; D019344:Lactic Acid / Q000378:metabolism; D018810:Magnetic Resonance Angiography / Q000379:methods*; D009682:Magnetic Resonance Spectroscopy / Q000379:methods*; D008297:Male; D008875:Middle Aged; D012039:Regional Blood Flow; D013997:Time Factors
D001224:Aspartic Acid; D019344:Lactic Acid; D006859:Hydrogen; C000179:N-acetylaspartate; D002794:Choline