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Cerebral Blood Flow and Metabolism in Patients with Silent Brain Infarction J Neurol Neurosurg Psychiatry 1998;65:317–321 317 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.65.3.317 on 1 September 1998. Downloaded from Cerebral blood flow and metabolism in patients with silent brain infarction: occult misery perfusion in the cerebral cortex Hiroshi Nakane, Setsuro Ibayashi, Kenichiro Fujii, Seizo Sadoshima, Katsumi Irie, Takanari Kitazono, Masatoshi Fujishima Abstract Recent advances in neuroimaging techniques Objectives—Silent brain infarction (SBI) have disclosed frequent silent brain infarctions is of growing interest as a possible risk (SBIs). Many reports have focused on the factor for symptomatic stroke. Although morphological characteristics of SBIs. Silent morphological characteristics of SBI have brain infarctions are usually located in the basal been well defined, their characteristic ganglia,1–4 and the size and number of SBIs are patterns of cerebral blood flow (CBF) and less than those of symptomatic brain 25 metabolism are in dispute. The purpose of infarctions. Aging, hypertension, and atrial 2–467 this study was to elucidate CBF and fibrillation are closely related to SBIs. metabolism in patients with SBI in rela- Moreover, nocturnal hypotension may play an 89 tion to symptomatic stroke. important part in the development of SBIs. Whether SBIs a ect cognitive function,510 Methods—The patients underwent PET V recurrence of vascular disease,11 12 residual and were separated into three groups; 51314 511 control group (C group), with no lesions handicap, and mortality is still contro- on CT (n=9, mean age 57), SBI group, with versial. Thus it is important to evaluate changes in cerebral blood flow (CBF) and no neurological signs or history of stroke, metabolism among patients with SBIs in com- but with ischaemic lesions on CT (n=9, parison with those with symptomatic brain inf- mean age 63), and brain infarction group arction or control patients. Only a few reports (BI group), with neurological deficits and are available about CBF and metabolism in copyright. compatible CT lesions in the area supplied patients with SBIs and results are controversial. by perforating arteries (n=19, mean age The purpose of this study was to investigate 56). Regional CBF, oxygen extraction CBF and oxygen metabolism among patients fraction (OEF), cerebral metabolic rate with or without SBI, using PET. for oxygen (CMRO2), and cerebral blood volume (CBV) were measured by PET. Results—Mean values for CBF to the cer- Materials and methods ebral cortex and deep grey matter were Two hundred and twenty nine patients were lower in the SBI group (31.6 (SD 5.8) and admitted to our clinic in Kyushu University 34.3 (SD 6.9) ml/100 g/min, respectively) hospital from 1986 to1993 for PET to evaluate and in the BI group (30.8 (SD 5.2), 33.9 brain function. This study was approved by an (SD 5.9), respectively) than in the C group institutional review committee and patients http://jnnp.bmj.com/ (36.0 (SD 6.6) and 43.5 (SD 9.5), respec- gave informed consent. We focused on patients tively). Although mean CMRO2 of deep who had symptomatic or asymptomatic lesions grey matter (2.36 (SD 0.52) ml/100 g/min) in the territory of perforating arteries because Second Department of was significantly decreased in the SBI SBIs usually occur in this area. Patients who Internal Medicine, group compared with the C group (2.76 had cardiogenic embolism, atherothrombotic Faculty of Medicine, (SD 0.480), p<0.01), CMRO of the cortical brain infarction, brain haemorrhage, dementia, Kyushu University, 2 Fukuoka, Japan area was as well preserved in the SBI metabolic encephalopathy, or other cerebral H Nakane patients (2.36 (SD 0.39)) as in the controls diseases were excluded. Patients with either on September 26, 2021 by guest. Protected S Ibayashi (2.48 (SD 0.32)) with a compensatory occlusion or severe stenosis (more than 70%) Ko Fujii increase of mean OEF (0.45 (SD 0.06) and of the internal carotid or middle cerebral arter- S Sadoshima 0.41 (SD 0.05), respectively). ies were also excluded. We included patients KIrie who had transient global amnesia in this study. T Kitazono Conclusions—Patients with SBI showed The cause of transient global amnesia remains M Fujishima decreased CBF and CMRO2 in deep grey matter. On the other hand, decreased unclear and several underlying conditions, 15 16 Correspondence to: CBF with milder increased OEF, resulting such as transient ischaemic attacks, epilepsy, Dr Hiroshi Nakane, Second and migraine,17 are reported to be possible Department of Internal in preserved CMRO2 in the cerebral Medicine, Faculty of cortex indicates the presence of occult candidates. We previously reported that CBF Medicine, Kyushu misery perfusion, suggesting that patients and cerebral oxygen metabolism in patients University, Maidashi 3–1–1, with recent transient global amnesia were bet- Fukuoka 812, Japan. with SBI have reduced cerebral per- Telephone 0081 92 642 ter preserved compared with those with fusional reserves. 18 5271; fax 0081 92 632 2551. transient ischaemic attacks. The patients with transient global amnesia seem to have less vas- (J Neurol Neurosurg Psychiatry 1998;65:317–321) Received 10 September 1997 cular disease and vascular risk factors than and in revised form 5 19 January 1998 Keywords: cerebral infarction; positron emission tom- those with transient ischaemic attacks. Con- Accepted 14 January 1998 ography; cerebral blood flow sidering these findings together, we think that 318 Nakane, Ibayashi, Fujii, et al J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.65.3.317 on 1 September 1998. Downloaded from Table 1 Classification of patients (total of 229) examined by PET Brain PET studies in chronic stages were performed within two months of admission. No symptoms and no lesions on CT 9 → Control group Brain infarction (BI) 122 Regional (r) CBF and oxygen extraction → 15 Asymptomatic 9 SBI group fraction (OEF) were measured by the H2 O Symptomatic 94 continuous infusion method, according to the Cardiogenic embolism 5 Thrombosis 80 oxygen-15 steady state technique described by ICA or MCA occlusion or severe stenosis: Frackowiak et al.20 Regional cerebral metabolic +56 − rates for oxygen (CMRO2) were calculated as 24 × × Cortical lesion: rCMRO2 = rCBF rOEF arterial oxygen con- +5tent. Both rOEF and rCMRO were corrected −19 → BI group 2 Unclassified 9 using regional cerebral blood volume (rCBV) 15 Transient ischaemic attack 20 measured using a single inhalation of C O2 Brain haemorrhage 7 gas.21 We excluded patients who had extremely Dementia 33 Brain tumour 5 low or high arterial pCO2 because of hyperven- Neurological degenerative disease 18 tilation or respiratory disease. The Metabolic encephalopathy 10 Others 24 HEADTOME-III device (Shimadzu Inc, Kyoto, Japan and Akita Noken, Akita, Japan) ICA=internal carotid artery; MCA=middle cerebral artery. with a spatial resolution of 8.2 mm full width at half maximum was used as previously cerebral ischaemia is not a major mechanism of 22 transient global amnesia. Therefore, 37 pa- described. In each brain, the values in four tients were included in the present study. They slices parallel to the orbitomeatal (OM) line were divided into three groups; control sub- (35, 50, 65, and 80 mm above the OM line) jects, who had no neurological deficits, no epi- were analysed. As shown in figure 1, 18×14 mm sodes of stroke, and no lesions on CT (C regions of interest (ROIs) were selected group), patients with SBI, who had no bilaterally in the frontal, temporal, parietal, and neurological symptoms or history of stroke, but occipital cortices, striatum, and thalamus by had silent CT infarcts (SBI group), and the use of CT images corresponding to each patients with symptomatic brain infarctions, PET slice. We used ROIs which did not include who had neurological deficits and infarcts in infarcted tissue. Values of all pixels in each ROI the territory of the perforating arteries (BI were averaged, and rCBF, rOEF, rCMRO2, and group). There were nine patients in the C rCBV were determined. Mean values for the group (mean age 57 (9) years, MABP 114 (24 cerebral cortex were calculated by combining mm Hg), nine in the SBI group (mean age 64 measurements in all cortical regions and for copyright. (3 years, MABP 120 (20) mm Hg), and 19 in deep grey matter they were calculated by com- the BI group (mean age 56 (11) years, MABP bining values in the striatum and thalamus. We 107 (17) mm Hg) in this study (table 1). also evaluated brain lesions on CT and http://jnnp.bmj.com/ on September 26, 2021 by guest. Protected Figure 1 Schematic drawings showing locations of regions of interest (ROIs) placed symmetrically for each hemisphere. The numerals below each slice indicate distance from the orbitomeatal (OM) line in mm. Cerebral blood flow and metabolism in patients with silent brain infarction 319 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.65.3.317 on 1 September 1998. Downloaded from Table 2 Profiles of patients in control group and silent 20 brain infarction (SBI) group Cases Age/sex Diagnosis Control group: 1 53/M HT 2 53/M TGA 3 73/F HT 4 65/F HT 5 49/F HT 10 6 47/F HT 7 53/F HT 8 58/F HT 9 65/F HT SBI group: Ischaemic lesions (n) 1 66/M DM 2 65/M Otogenic vertigo 3 62/F TGA 4 58/M HT 0 5 65/M TGA SBI group BI group 6 67/F TGA 7 64/F HT Figure 2 Number of ischaemic lesions in the brain, either 8 62/M DM symptomatic or asymptomatic in each patient in SBI and 9 62/M Transient visual loss BI groups.
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