|
|
J Neurol Neurosurg Psychiatry. 1998 September; 65(3): 317–321. | PMCID: PMC2170260 |
Cerebral blood flow and metabolism in patients with silent brain
infarction: occult misery perfusion in the cerebral cortex H. Nakane, S. Ibayashi, K. Fujii, S. Sadoshima, K. Irie, T. Kitazono, and M. Fujishima Second Department of Internal Medicine, Faculty of Medicine, Kyushu University, Fukuoka, Japan. OBJECTIVES—Silent
brain infarction (SBI) is of growing interest as a possible risk factor
for symptomatic stroke. Although morphological characteristics of SBI
have been well defined, their characteristic patterns of cerebral blood
flow (CBF) and metabolism are in dispute. The purpose of this study was
to elucidate CBF and metabolism in patients with SBI in relation to
symptomatic stroke.
METHODS—The patients
underwent PET and were separated into three groups; control group (C
group), with no lesions on CT (n=9, mean age 57), SBI group, with no
neurological signs or history of stroke, but with ischaemic lesions on
CT (n=9, mean age 63), and brain infarction group (BI group), with
neurological deficits and compatible CT lesions in the area supplied by
perforating arteries (n=19, mean age 56). Regional CBF, oxygen
extraction fraction (OEF), cerebral metabolic rate for oxygen
(CMRO2), and cerebral blood volume (CBV) were measured by PET.
RESULTS—Mean values
for CBF to the cerebral cortex and deep grey matter were lower in the
SBI group (31.6 (SD 5.8) and 34.3 (SD 6.9) ml/100 g/min, respectively)
and in the BI group (30.8 (SD 5.2), 33.9 (SD 5.9), respectively) than
in the C group (36.0 (SD 6.6) and 43.5 (SD 9.5), respectively).
Although mean CMRO2 of deep grey matter (2.36 (SD 0.52)
ml/100 g/min) was significantly decreased in the SBI group compared
with the C group (2.76 (SD 0.480), p<0.01), CMRO2 of the
cortical area was as well preserved in the SBI patients (2.36 (SD
0.39)) as in the controls (2.48 (SD 0.32)) with a compensatory increase
of mean OEF (0.45 (SD 0.06) and 0.41 (SD 0.05), respectively).
CONCLUSIONS—Patients
with SBI showed decreased CBF and CMRO2 in deep grey
matter. On the other hand, decreased CBF with milder increased OEF,
resulting in preserved CMRO2 in the cerebral cortex
indicates the presence of occult misery perfusion, suggesting that
patients with SBI have reduced cerebral perfusional reserves.
The Full Text of this article is available as a PDF (126K). These references are in PubMed. This may not be the complete list of references from this article. - Kase CS, Wolf PA, Chodosh EH, Zacker HB, Kelly-Hayes M, Kannel WB, D'Agostino RB, Scampini L. Prevalence of silent stroke in patients presenting with initial stroke: the Framingham Study. Stroke. 1989 Jul;20(7):850–852. [PubMed]
- Shinkawa A, Ueda K, Kiyohara Y, Kato I, Sueishi K, Tsuneyoshi M, Fujishima M. Silent cerebral infarction in a community-based autopsy series in Japan. The Hisayama Study. Stroke. 1995 Mar;26(3):380–385. [PubMed]
- Davis PH, Clarke WR, Bendixen BH, Adams HP, Jr, Woolson RF, Culebras A. Silent cerebral infarction in patients enrolled in the TOAST Study. Neurology. 1996 Apr;46(4):942–948. [PubMed]
- Herderscheê D, Hijdra A, Algra A, Koudstaal PJ, Kappelle LJ, van Gijn J. Silent stroke in patients with transient ischemic attack or minor ischemic stroke. The Dutch TIA Trial Study Group. Stroke. 1992 Sep;23(9):1220–1224. [PubMed]
- Jørgensen HS, Nakayama H, Raaschou HO, Gam J, Olsen TS. Silent infarction in acute stroke patients. Prevalence, localization, risk factors, and clinical significance: the Copenhagen Stroke Study. Stroke. 1994 Jan;25(1):97–104. [PubMed]
- Laloux P, Ossemann M, Jamart J. Stroke subtypes and risk factors associated with silent infarctions in patients with first-ever ischemic stroke or transient ischemic attack. Acta Neurol Belg. 1994;94(1):17–23. [PubMed]
- Petersen P, Madsen EB, Brun B, Pedersen F, Gyldensted C, Boysen G. Silent cerebral infarction in chronic atrial fibrillation. Stroke. 1987 Nov–Dec;18(6):1098–1100. [PubMed]
- Watanabe N, Imai Y, Nagai K, Tsuji I, Satoh H, Sakuma M, Sakuma H, Kato J, Onodera-Kikuchi N, Yamada M, Abe F, Hisamichi S, Abe K. Nocturnal blood pressure and silent cerebrovascular lesions in elderly Japanese. Stroke. 1996 Aug;27(8):1319–1327. [PubMed]
- Nakamura K, Oita J, Yamaguchi T. Nocturnal blood pressure dip in stroke survivors. A pilot study. Stroke. 1995 Aug;26(8):1373–1378. [PubMed]
- Bornstein NM, Gur AY, Treves TA, Reider-Groswasser I, Aronovich BD, Klimovitzky SS, Varssano D, Korczyn AD. Do silent brain infarctions predict the development of dementia after first ischemic stroke? Stroke. 1996 May;27(5):904–905. [PubMed]
- Chodosh EH, Foulkes MA, Kase CS, Wolf PA, Mohr JP, Hier DB, Price TR, Furtado JG., Jr Silent stroke in the NINCDS Stroke Data Bank. Neurology. 1988 Nov;38(11):1674–1679. [PubMed]
- Ricci S, Celani MG, La Rosa F, Righetti E, Duca E, Caputo N. Silent brain infarctions in patients with first-ever stroke. A community-based study in Umbria, Italy. Stroke. 1993 May;24(5):647–651. [PubMed]
- Boon A, Lodder J, Heuts-van Raak L, Kessels F. Silent brain infarcts in 755 consecutive patients with a first-ever supratentorial ischemic stroke. Relationship with index-stroke subtype, vascular risk factors, and mortality. Stroke. 1994 Dec;25(12):2384–2390. [PubMed]
- Heathfield KW, Croft PB, Swash M. The syndrome of transient global amnesia. Brain. 1973 Dec;96(4):729–736. [PubMed]
- Fisher CM. Transient global amnesia. Precipitating activities and other observations. Arch Neurol. 1982 Oct;39(10):605–608. [PubMed]
- Caplan L, Chedru F, Lhermitte F, Mayman C. Transient global amnesia and migraine. Neurology. 1981 Sep;31(9):1167–1170. [PubMed]
- Fujii K, Sadoshima S, Ishitsuka T, Kusuda K, Kuwabara Y, Ichiya Y, Fujishima M. Regional cerebral blood flow and metabolism in patients with transient global amnesia: a positron emission tomography study. J Neurol Neurosurg Psychiatry. 1989 May;52(5):622–630. [PubMed]
- Zorzon M, Antonutti L, Masè G, Biasutti E, Vitrani B, Cazzato G. Transient global amnesia and transient ischemic attack. Natural history, vascular risk factors, and associated conditions. Stroke. 1995 Sep;26(9):1536–1542. [PubMed]
- Frackowiak RS, Lenzi GL, Jones T, Heather JD. Quantitative measurement of regional cerebral blood flow and oxygen metabolism in man using 15O and positron emission tomography: theory, procedure, and normal values. J Comput Assist Tomogr. 1980 Dec;4(6):727–736. [PubMed]
- Lammertsma AA, Jones T. Correction for the presence of intravascular oxygen-15 in the steady-state technique for measuring regional oxygen extraction ratio in the brain: 1. Description of the method. J Cereb Blood Flow Metab. 1983 Dec;3(4):416–424. [PubMed]
- Fujii K, Sadoshima S, Okada Y, Yao H, Kuwabara Y, Ichiya Y, Fujishima M. Cerebral blood flow and metabolism in normotensive and hypertensive patients with transient neurologic deficits. Stroke. 1990 Feb;21(2):283–290. [PubMed]
- Kobayashi S, Okada K, Yamashita K. Incidence of silent lacunar lesion in normal adults and its relation to cerebral blood flow and risk factors. Stroke. 1991 Nov;22(11):1379–1383. [PubMed]
- Chamorro A, Saiz A, Vila N, Ascaso C, Blanc R, Alday M, Pujol J. Contribution of arterial blood pressure to the clinical expression of lacunar infarction. Stroke. 1996 Mar;27(3):388–392. [PubMed]
- Gibbs JM, Wise RJ, Leenders KL, Jones T. Evaluation of cerebral perfusion reserve in patients with carotid-artery occlusion. Lancet. 1984 Feb 11;1(8372):310–314. [PubMed]
- Meguro K, Hatazawa J, Yamaguchi T, Itoh M, Matsuzawa T, Ono S, Miyazawa H, Hishinuma T, Yanai K, Sekita Y, et al. Cerebral circulation and oxygen metabolism associated with subclinical periventricular hyperintensity as shown by magnetic resonance imaging. Ann Neurol. 1990 Sep;28(3):378–383. [PubMed]
- Powers WJ, Raichle ME, Grubb RL., Jr Positron emission tomography to assess cerebral perfusion. Lancet. 1985 Jan 12;1(8420):102–103. [PubMed]
|
