Cerebral Blood Flow and Oxygen Metabolism in Leuko-Araiosis

161

127

Background-White matter lesions in cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) are underlaid by severe ultrastructural changes of the arteriolar wall. Although chronic ischemia is presumed to cause the tissue lesions, the pattern of perfusion abnormalities and hemodynamic reserve in CADASIL, particularly within the white matter, remains unknown. Methods-We used the MRI bolus tracking method in 15 symptomatic patients with CADASIL (5 with dementia) and 10 age-matched control subjects before and 20 minutes after the intravenous injection of acetazolamide (ACZ, 17 mg/kg). Cerebral blood flow (CBF), blood volume (CBV), and mean transit time (MTT) were calculated both in the cortex and in the white matter according to the singular value decomposition technique. Perfusion parameters were obtained in regions of hyperintensities and within the normal-appearing white matter as observed on T2-weighted images. Analysis was performed with both absolute and relative (region/whole brain) values. Results-A significant reduction in absolute and relative CBF and CBV was found within areas of T2 hyperintensities in white matter in the absence of significant variations of MTT. This reduction was more severe in demented than in nondemented patients. No significant change in absolute CBF and CBV values was observed in the cortex of patients with CADASIL. A decrease in relative CBF and CBV values was detected in the occipital cortex. After ACZ administration, CBF and CBV increased significantly in both the cortex and white matter of affected subjects, but the increase in absolute CBF was lower within areas of increased signal on T2-weighted images in patients than in the white matter of control subjects. Conclusions-In CADASIL, both basal perfusion and hemodynamic reserve are decreased in areas of T2 hyperintensities in the white matter. This hypoperfusion appears to be related to the clinical severity. The significant effect of ACZ on CBF and CBV suggests that cerebral perfusion might be increased using pharmacological vasodilation in CADASIL.

Section: Discussionmentioning

confidence: 96%

Cerebral Hemodynamics in CADASIL Before and After Acetazolamide Challenge Assessed With MRI Bolus Tracking

Chabriat

Pappatà

Østergaard

et al. 2000

161

127

“…Using PET with 18 F-fluoromethane as a CBF tracer, Herholz et al 24 found focal reductions in the cortical CBF overlying the large white matter lesions in patients with atherosclerotic carotid artery disease, suggesting a transneural depression of CBF. De Reuck et al 25 found decreased blood flow and metabolism in demented patients with leukoaraiosis. Those results support the view that the cerebral hemodynamics in patients with leukoaraiosis involves several contributing factors.…”

Section: Discussionmentioning

confidence: 98%

Decreased cerebrovascular dilatory capacity in subjects with asymptomatic periventricular hyperintensities.

Isaka

Okamoto

Ashida

et al. 1994

Background and PurposeThe clinical significance of the periventricular hyperintensity incidentally found on magnetic resonance images of the brain is questionable. We evaluated resting cerebral blood flow and cerebrovascular dilatory capacity of subjects with asymptomatic periventricular hyperintensities to study their cerebral hemodynamics.Methods Magnetic resonance imaging of the brain was performed in 28 asymptomatic subjects with cerebrovascular risk factors to determine the severity of periventricular hyperintensity. Mean gray matter flow was computed by a "'Xeclearance technique in subjects at rest and after the administration of 1 g acetazolamide. Flow values were correlated with the scores for periventricular hyperintensity.

“…6,8,9,21 Impaired cerebral autoregulation and altered pulsatility characteristics measured by TCD were found in patients with vascular dementia and lacunes [22][23][24][25] ; however, most of these studies did not distinguish between cerebral microangiopathy and lacunar and territorial brain infarction.…”

Section: Discussionmentioning

confidence: 99%

“…[1][2][3][4][5][6] Cerebral microangiopathy is characterized anatomically by lipohyalinosis of cerebral arteries and arterioles and hemodynamically by decreased cerebral blood flow and loss of autoregulation. [7][8][9][10] Impaired VMR is thought to cause further ischemic infarctions and progression of Binswanger's disease. 5,11 NIRS measures changes in concentration of the chromophores HbO 2 and Hb, and enables the assessment of cerebral hemodynamics noninvasively (see References 12 through 14).…”

mentioning

confidence: 99%

Reduced Vasomotor Reactivity in Cerebral Microangiopathy

Terborg

Gora

Weiller

et al. 2000

129

Background and Purpose-Reduction of cerebral blood flow and vasomotor reactivity (VMR) are thought to play an important role in the pathogenesis of cerebral microangiopathy. The aim of our study was to determine whether near-infrared spectroscopy (NIRS) can detect a reduced VMR in patients with microangiopathy, whether NIRS reactivities correlate with VMR assessed by transcranial Doppler sonography (TCD), and whether the differing extents of patients' microangiopathy demonstrated on MRI or CT can be distinguished by both noninvasive techniques. Methods-We compared the VMR of 46 patients with cerebral microangiopathy with 13 age-matched control subjects.Patients were classified with the Erkinjuntti scale. We monitored cerebral blood flow velocity (CBFV) in both middle cerebral arteries by TCD, changes in concentration of oxyhemoglobin (HbO 2 ), deoxyhemoglobin (Hb) and blood volume (HbT) by NIRS, mean arterial blood pressure, and end-tidal CO 2 (EtCO 2 ) during normocapnia and hypercapnia. VMRs were calculated as percent change of CBFV (NCR) and as absolute change in concentration of HbO 2 , Hb, and HbT per 1% increase in EtCO 2 (CR-HbO 2 , CR-Hb, CR-HbT). Results-NCR and NIRS reactivities were significantly reduced in patients with cerebral microangiopathy. CR-HbO 2 and CR-Hb showed a close correlation with NCR, and NCR and NIRS reactivities were related to the severity of cerebral microangiopathy according to the Erkinjuntti scale. Validity of NCR and NIRS reactivities were similar. Conclusions-VMR