BACKGROUND AND PURPOSE: 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.
BACKGROUND AND PURPOSE: 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, TIApatients did not have altered flow volume in any of the arteries and had normal flow distribution through the circle of Willis. In TIApatients, 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 TIApatients without a prior TIA. CONCLUSIONS:TIApatients 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.