(Stroke. 1997;28:984-987.)
© 1997 American Heart Association, Inc.
Articles |
From the Department of Neurosurgery, Nasu Neurosurgical Center, Kuroiso, Tochigi, Japan.
| Abstract |
|---|
|
|
|---|
Methods One hundred thirty-five neurologically normal subjects were divided into four grades of WML on the basis of their MR images. rCBF values in the centrum semiovale were measured by xenon contrast CT methods.
Results Advanced age and associated hypertension were significant risk factors for higher grade WMLs. Centrum semiovale rCBF values on the left side were 24.27±2.60 mL·100 g-1·min-1 in grade 0, 23.52±2.78 in grade I, 19.35±2.81 in grade II, 15.82±2.05 in grade III, and 11.31±2.56 in grade IV. Differences were significant between grades (P<.005 between grade 0 and grades II, III, and IV; between grade II and grades III and IV; and between grades III and IV). Patients with hypertension had lower rCBF values than those without in grades 0, I, II, and III, with significant difference in grade I (P<.005). Age-matched studies between patients 61 to 70 years old confirmed a significant difference between WML grades.
Conclusions WMLs in centrum semiovale are associated with greater age, hypertension, and reduced rCBF values.
Key Words: cerebral blood flow leukoaraiosis magnetic resonance imaging tomography, x-ray computed white matter
| Introduction |
|---|
|
|
|---|
The present study compared rCBF in the centrum semiovale among patients with various grades of WML using xenon contrast CT.
| Subjects and Methods |
|---|
|
|
|---|
MR imaging involved a spin-echo protocol for T1-weighted imaging (TR, 600 ms; TE, 15 ms) and T2-weighted imaging (TR, 3000 ms; TE, 80 ms) made in the orbitomeatal plane with 7.5-mm slice thickness (1.5-T superconductive MR system, Toshiba). The display matrix was 256x256. WMLs were defined as high-intensity foci on T2-weighted images that were isointense with normal brain parenchyma on T1-weighted images and were 1 mm or more in diameter on hard copy film (true dimensions, 2 to 3 mm or more). Frank lacuner infarcts and PVLs were excluded. WMLs were counted and the patients graded as grade 0, no lesions; grade I, fewer than 10 scattered focal lesions; grade II, more than 10 scattered but not confluent focal lesions; grade III, partially confluent lesions; and grade IV, bilateral and diffuse confluent lesions.15
Xenon CT was performed with an Xpeed CT scanner (Toshiba). Patients
inhaled a mixture of 30% xenon in oxygen for 3 minutes, during which a
series of 8-second CT scans was made parallel to the orbitomeatal line.
To match the slices of CT and MR imaging, the CT table was adjusted to
the same slice width as that of the MR imaging. Regions of interest
were circular with diameters greater than 22.26 mm. An AZ-7000
image processing system (Anzai Corp) was used to calculate CBF data
with the end-tidal chamber scan method. The confidential image was used
to detect motion artifacts, and a 6x6 filter was also used. Xenon CT
was performed within 1 to 40 days (mean interval, 21 days) of MR
imaging. Statistical analysis was performed with Student's
t test or
2 test.
| Results |
|---|
|
|
|---|
|
Main clinical complaints of patients with WMLs were headache and
dizziness, accounting for approximately 82%, but there were no
significant differences between grades (Table 1
).
Table 2
shows CBF values in the centrum
semiovale according to grade. Representative
rCBF maps are shown in the Figure
. There were no
significant differences in CBF values between grades 0 and I, but there
were significant differences between grade 0 and grades II, III, and
IV, between grade II and grades III and IV, and between grades III and
IV (P<.005). CBF values in age-matched patients (61 to 70
years) also showed significant differences between grades (Table 3
). CBF values in patients with hypertension tended to
be lower than in those without hypertension, but significant
differences were present only in grade I (P<.005)
(Table 4
).
|
|
|
|
| Discussion |
|---|
|
|
|---|
Previous cerebral perfusion and metabolic studies have used the 133Xe injection method, positron emission tomography, single-photon emission CT, and xenon contrast CT, but these studies were based on smaller series of patients, usually with neurological deficits or with both WML and PVL in the same patients.7 8 10 28 29 31 32 33 34 35 Our study included only patients without neurological deficits and excluded those with both PVL and WML or frank lacunar infarcts and WML.
Xenon contrast CT has the advantage of providing high resolution, especially in deep white matter regions. Normal CBF values in white matter using the xenon inhalation method are reported to be 26.0±4.9 mL·100 g-1·min-1 on the basis of data from 20 normal subjects ranging from 20 to 100 years old.35 Although significant age-related declines in CBF values were observed for all cortical and subcortical gray and white matter regions, the slope of the regression line for mean white matter rCBF values was significantly less than for cortical and subcortical gray matter.35 However, the absence of a significant difference in white matter regions with aging has been reported.36 Therefore, rCBF values for the centrum semiovale may still be controversial. The present study showed that rCBF values in the centrum semiovale of patients with grade 0 WML was 24.27 mL·100 g-1·min-1, and this value declined with grade severity to 11.31 mL·100 g-1·min-1 with grade IV WML. Age-matched comparisons also showed that rCBF values in centrum semiovale decreased with advancing grades. Patients with hypertension had significantly lower rCBF values than those without hypertension in grade I, and similar trends were seen in the other grades.
CBF values measured in patients with both lacunar infarction and leukoaraiosis using single-photon emission CT and xenon contrast CT showed that leukoaraiosis was closely related to the CBF in the putamen and thalamus, suggesting that blood flow reduction in deep perforating areas might be the cause of leukoaraiosis29 33 ; however, marked WMLs without lacunar infarctions have an incomplete or milder pathology than WML with lacunar infarction.29 Our patients had WMLs in only the centrum semiovale and did not have lacunar infarctions or PVL. However, histological studies have shown that WMLs also have features of milder vascular disease.37 38 39 Our study shows that WMLs in the centrum semiovale increase with age and hypertension and are associated with reduced CBF in the centrum semiovale. Patients with grade III and IV WML have low rCBF in the centrum semiovale and are at risk for stroke because WMLs have the milder pathological features of vascular disease. Therefore, the management of such patients requires preventive care, especially among those with hypertension.
| Selected Abbreviations and Acronyms |
|---|
|
| Footnotes |
|---|
Received January 3, 1997; revision received February 20, 1997; accepted February 21, 1997.
| References |
|---|
|
|
|---|
2. McDonald WM, Ranga R, Krishnan R, Doraiswarmy PM, Figiel CG, Husain MM, Boyko OB, Heyman A. Magnetic resonance findings in patients with early-onset Alzheimer's disease. Biol Psychiatry.. 1991;29:799-810.[Medline] [Order article via Infotrieve]
3. Brun A. Pathology and pathophysiology of cerebrovascular dementia: pure subgroups of obstructive and hypoperfusive etiology. Dementia.. 1994;5:145-147.
4. Ogata J. Silent cerebral infarction: postmortem pathological study [in Japanese]. Gendai Iryo.. 1994;26:3253-3255.
5.
Awad IA, Spetzler RF, Hodak JA, Awad CA, Carey
R. Incidental subcortical lesions identified on magnetic
resonance imaging in the elderly, I: correlation with age and
cerebrovascular risk factors. Stroke.. 1986;17:1084-1089.
6.
Lechner H, Schmidt R, Bertha G, Justich E, Offenbacher
H, Schneider G. Nuclear magnetic resonance image of white matter
lesions and risk factors for stroke in normal individuals.
Stroke.. 1988;19:263-265.
7.
Fazekas F, Niederkorn K, Schmidt R, Offenbacher H,
Horner S, Bertha G, Lechner H. White matter signal abnormalities
in normal individuals: correlation with carotid ultrasonography,
cerebral blood flow measurements, and cerebrovascular risk
factors. Stroke.. 1988;19:1285-1288.
8. Fazekas F. Magnetic resonance signal abnormalities in asymptomatic individuals: their incidence and functional correlates. Eur Neurol.. 1989;29:164-168.[Medline] [Order article via Infotrieve]
9. Hendrie HC, Farlow MR, Austrom MG, Edwards MK, Williams MA. Foci of increased T2 signal intensity on brain MR scans of healthy elderly subjects. AJNR Am J Neuroradiol.. 1989;10:703-707.[Abstract]
10. Meguro K, Hatazawa J, Yamaguchi T, Itoh M, Matsuzawa T, Ono S, Miyazawa H, Hishimura T, Yanai K, Sekita Y, Yamada K. Cerebral circulation and oxygen metabolism associated with subclinical periventricular hyperintensity as shown by magnetic resonance imaging. Ann Neurol.. 1990;28:378-383.[Medline] [Order article via Infotrieve]
11.
Wahlund LO, Agartz I, Almqvist O, Basun H, Forssell L,
Saaf J, Wetterberg L. The brain in healthy aged individuals: MR
imaging. Radiology.. 1990;175:675-679.
12.
Matsubayashi K, Shimada K, Kawamoto A, Ozawa T.
Incidental brain lesions on magnetic resonance imaging and
neurobehavioral functions in the apparently healthy elderly.
Stroke.. 1992;23:175-180.
13.
Schmidt R, Fazekas F, Kleinert G, Offenbacher H, Gindl
K, Payer F, Freidl W, Niederkorn K, Lechner H. Magnetic
resonance imaging signal hyperintensities in the deep and subcortical
white matter. Arch Neurol.. 1992;49:825-827.
14. Fukuyama H, Ogawa M. Hyperintensity foci on T2-weighted MR imaging in neurological-free subjects [in Japanese]. Ther Res.. 1993;14:1259-1261.
15. Horikoshi T, Yagi S, Fukamachi A. Incidental high-intensity foci in white matter on T2-weighted magnetic resonance imaging: frequency and clinical significance in symptom-free adults. Neuroradiology.. 1993;35:151-155.[Medline] [Order article via Infotrieve]
16.
Ylikoski R, Ylikoski A, Erkinjuntti T, Sulkava R,
Raininko R, Tilvis R. White matter changes in healthy elderly
persons correlate with attention and speed of mental
processing. Arch Neurol.. 1993;50:818-824.
17.
Breteler MMB, van Swieten JC, Bots ML, Grobbee DE,
Claus JJ, van den Hout JHW, van Harskamp F, Tanghe HLJ, de Jong PTVM,
van Gijn J, Hofman A. Cerebral white matter lesions, vascular
risk factors, and cognitive function in a population-based study: the
Rotterdam study. Neurology.. 1994;44:1246-1252.
18. Lindgren A, Roijer A, Rudling O, Norrving B, Larsson E-M, Eskilsson J, Wallin L, Olsson B, Johansson BB. Cerebral lesions on magnetic resonance imaging, heart disease, and vascular risk factors in subjects without stroke. Stroke.. 1994;25:929-934.[Abstract]
19.
Ylikoski A, Erkinjuntti T, Raininko R, Sarna S, Sulkava
R, Tilvis R. White matter hyperintensities on MRI in the
neurologically nondiseased elderly: analysis of cohorts of
consecutive subjects aged 55 to 85 years living at home.
Stroke.. 1995;26:1171-1177.
20.
Hachinski VC, Potter P, Merskey H.
Leukoaraiosis. Arch Neurol.. 1987;44:21-23.
21. Udaka F, Shitsuya M, Kameyama M. Silent cerebral infarction on MRI [in Japanese]. Gendai Iryo.. 1994;26:3263-3268.
22.
Sullivan P, Pary R, Telang F, Rifai AH, Zubenko
GS. Risk factors for white matter changes detected by magnetic
resonance imaging in the elderly. Stroke.. 1990;21:1424-1428.
23.
Erkinjuntti T, Ketonen L, Sulkava R, Sipponen J,
Vuorialho M, Iivanainen M. Do white matter changes on MRI and CT
differentiate vascular dementia from Alzheimer's
disease? J Neurol Neurosurg Psychiatry.. 1987;50:37-42.
24. Raininko R, Elovaara I, Virta A, Valanne L, Haltia M, Valle S-L. Radiological study of the brain at various stages of human immunodeficiency virus infection. Neuroradiology.. 1992;34:190-196.[Medline] [Order article via Infotrieve]
25. van Swieten JC, Geyskes GG, Derix MMA, Peeck BM, Ramos LMP, van Latum JC, van Gijn J. Hypertension in the elderly is associated with white matter lesions and cognitive decline. Ann Neurol.. 1991;30:825-830.[Medline] [Order article via Infotrieve]
26. Hirai T. Silent cerebral infarction in outcome patients [in Japanese]. Gendai Iryo.. 1994;26:3260-3262.
27. Okamoto K, Itoh J, Tokiguchi S. White matter changes in vascular diseases [in Japanese]. Medicina.. 1994;31:1690-1696.
28. Sakayori O, Komiyama T, Kitamura S, Terashi A. Hyperintensity (PVH) lesions and dementia in multiple cerebral infarction: the aspects of cerebral blood flow and metabolism using positron emission tomography [in Japanese]. Jpn J Stroke.. 1993;15:176-188.
29. Yamamoto Y, Oiwa K, Satoi H. The comparison of severity and regional cerebral blood flow in patients with lacunar infarction and leukoaraiosis of basal ganglia. In: Proceedings of the Perfusamine Conference; July 17, 1993; Tokyo, Japan; 9:61-64.
30. Masawa N. Pathological findings of silent cerebral infarction [in Japanese]. Gendai Iryo.. 1994;26:3277-3281.
31. Ohsawa N, Takahashi S, Yonezawa H. Cerebral blood flow patterns in patients with leukoaraiosis and lacuna infarction [in Japanese]. Rinsho Shinkeigaku.. 1994;34:443-448.[Medline] [Order article via Infotrieve]
32. Kobari M, Meyer JS, Ichijo M, Oravez WT. Leukoaraiosis: correlation of MR and CT findings with blood flow, atrophy, and cognition. AJNR Am J Neuroradiol.. 1990;11:273-281.[Abstract]
33.
Kawamura J, Meyer JS, Terayama Y, Weathers S.
Leukoaraiosis correlates with cerebral hypoperfusion in vascular
dementia. Stroke.. 1991;22:609-614.
34.
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;22:1379-1383.
35.
Tachibana H, Meyer JS, Okayasu H, Kandula P.
Changing topographic patterns of human cerebral blood flow with age
measured by xenon CT. AJR Am J Radiol.. 1984;142:1027-1034.
36.
Davis SM, Ackerman RH, Correia JA, Alpert NM, Chang J,
Buonanno F, Kelley RE, Rosner B, Taveras JM. Cerebral blood flow
and cerebrovascular CO2 reactivity in stroke-age normal
controls. Neurology.. 1983;33:391-399.
37.
Fazekas F, Kleinert R, Offenbacher H, Schmidt R,
Kleinert G, Payer F, Radner H, Lechner H. Pathologic correlates
of incidental MRI white matter signal hyperintensities.
Neurology.. 1993;43:1683-1689.
38.
Awad IA, Johnson PC, Spetzler RF, Hodak JA.
Incidental subcortical lesions identified on magnetic resonance imaging
in the elderly, II: postmortem pathological correlations.
Stroke.. 1986;17:1090-1097.
39.
Munoz DG, Hastak SM, Harper B, Lee D, Hachinski
VC. Pathologic correlates of increased signals of the centrum
ovale on magnetic resonance imaging. Arch Neurol.. 1993;50:492-497.
This article has been cited by other articles:
![]() |
T.J. Huynh, B. Murphy, J.A. Pettersen, H. Tu, D.J. Sahlas, L. Zhang, S.P. Symons, S. Black, T.-Y. Lee, and R.I. Aviv CT Perfusion Quantification of Small-Vessel Ischemic Severity AJNR Am. J. Neuroradiol., November 1, 2008; 29(10): 1831 - 1836. [Abstract] [Full Text] [PDF] |
||||
![]() |
P. Sachdev, W. Wen, R. Shnier, and H. Brodaty Cerebral Blood Volume in T2-Weighted White Matter Hyperintensities Using Exogenous Contrast Based Perfusion MRI J Neuropsychiatry Clin Neurosci, February 1, 2004; 16(1): 83 - 92. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. O'Sullivan, D. J. Lythgoe, A. C. Pereira, P. E. Summers, J. M. Jarosz, S. C.R. Williams, and H. S. Markus Patterns of cerebral blood flow reduction in patients with ischemic leukoaraiosis Neurology, August 13, 2002; 59(3): 321 - 326. [Abstract] [Full Text] [PDF] |
||||
![]() |
N. Miyazawa, K. Hashizume, M. Uchida, and H. Nukui Long-term Follow-up of Asymptomatic Patients with Major Artery Occlusion: Rate of Symptomatic Change and Evaluation of Cerebral Hemodynamics AJNR Am. J. Neuroradiol., February 1, 2001; 22(2): 243 - 247. [Abstract] [Full Text] [PDF] |
||||
![]() |
H S Markus, D J Lythgoe, L Ostegaard, M O'Sullivan, and S C R Williams Reduced cerebral blood flow in white matter in ischaemic leukoaraiosis demonstrated using quantitative exogenous contrast based perfusion MRI J. Neurol. Neurosurg. Psychiatry, July 1, 2000; 69(1): 48 - 53. [Abstract] [Full Text] [PDF] |
||||
![]() |
N. Miyazawa, M. Uchida, A. Fukamachi, I. Fukasawa, H. Sasaki, and H. Nukui Xenon Contrast-Enhanced CT Imaging of Supratentorial Hypoperfusion in Patients with Brain Stem Infarction AJNR Am. J. Neuroradiol., November 1, 1999; 20(10): 1858 - 1862. [Abstract] [Full Text] |
||||
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
Stroke Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 1997 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |