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ARTICLES:
J. van der Grond, A. F. van Raamt, Y. van der Graaf, W. P.T.M. Mali, and R. H.C. Bisschops
A fetal circle of Willis is associated with a decreased deep white matter lesion load
Neurology 2004; 63: 1452-1456
[Abstract][Full text][PDF]
A fetal circle of Willis is associated with a decreased deep white matter lesion load
Ken Ikeda, Hidetoshi Kashihara, Ken-ichi Hosozawa, Miou Shimoma, Yasumitsu Ichikawa, Osamu Igarashi, Jo Aoyagi, Masaki Tamura, and Yasuo Iwasaki
(1 March 2005)
Reply to Ikeda et al
J. van der Grond
(1 March 2005)
A fetal circle of Willis is associated with a decreased deep white matter lesion load
1 March 2005
Ken Ikeda, Department of Neurology, PL Tokyo Health Care Center 16-1, Kamiyamacho, Shibuyaku, Tokyo, 150-0047, Japan, Hidetoshi Kashihara, Ken-ichi Hosozawa, Miou Shimoma, Yasumitsu Ichikawa, Osamu Igarashi, Jo Aoyagi, Masaki Tamura, and Yasuo Iwasaki
We read the article by van der Grond
et al [1] with great interest. We also examined healthy adults to determined whether fetal
patterns are associated with risk factors of
cerebrovascular disease and white matter lesions (WMLs).
Our study included 3780 subjects (2600 men and 1180 women) who had
physicals including brain MRI and 3-dimensional
time-of-flight MR angiography (1.5 T; Hitachi Medical,
Japan) between September 2003 and October 2004 in PL Tokyo
Health Care Center. Mean age (SD) of the subjects was 51.8
(11.3) years. Frequency of fetal posterior configuration
of circle of Willis, deep and periventricular WMLs, and
cerebrovascular risk factors were determined. [2] Those data were analyzed and the
two groups were compared for absence or presence of fetal patterns. Fetal flows of
the unilateral or the bilateral posterior cerebral arteries
existed in 591 subjects (367 men and 224 women). A
sex difference of fetal patterns was seen in
men (14.1 %) and women (19.0 %). Age and prevalence of
hypertension, diabetes mellitus, hypercholesterolemia,
obesity and current smoking did not differ significantly
between the fetal and the non-fetal group. Presence of
deep and periventricular WMLs did not differ between the
fetal (11.2 and 5.8%) and the non-fetal group (13.5 and 7.8%). The number of those WMLs also had no differences
between both groups.
We would like to know the number of female subjects with a
fetal circle of Willis in the study of van der Grond et
al. [1] Atherosclerotic population of their study contains
210 men and 33 women in male-predominance. Logistic
regression analysis adjusted with age, sex and hypertension
shows significant reduction of small- and medium-sized WMLs
loads in the fetal posterior configuration group (n=70).
The selection bias of sex could contribute to WMLs load.
The number of female subjects may impact the
analyses of fetal patterns and WMLs. Accumulative rates
for deep WMLs are twice as high in Dutch elderly
women than men who had a history or risk of vascular
disease. [3] Our study showed female predominant occurrence
of fetal patterns and no association between fetal patterns
and asymptomatic WMLs in middle-aged healthy adults.
Further longitudinal studies in healthy and atherosclerotic
disease populations are needed to evaluate whether a fetal
circle of Willis can protect against appearance of WMLs.
References
1. Van der Grond J, van Raamt AF, van der Graaf Y, Mali
WPTM, Bisschops RHC. A fetal circle of Willis is associated
with a decreased deep white matter lesion load. Neurology
2004; 63: 1452-1456.
2. Ikeda K, Kashihara H, Hosozawa K, et al. Brain check-up-
based study of migraine in Japan. Headache Care. 2005, in
press.
3. Van der Heuvel DMJ, Admiraal-Behloul F, ten Dam VH, et
al. Different progression rates for deep white matter
hyperintensities in elderly men and women. Neurology 2004;
63: 1699-1701.
Reply to Ikeda et al
1 March 2005
J. van der Grond, Dept. of Radiology, Leiden University Medical Center Albinusdreef 2, 2300 RC Leiden, The Netherlands
I thank Dr. Ikeda et al for their comments and explanation of their
study in which large population configurations of the circle of Willis
were associated with the presence of white matter lesions. In contrast to
our study, no association between a fetal posterior variation of the
circle of Willis and the presence of white matter lesions was found.
Ikeda et al correctly suggest that this might be caused by a
high number of females in our fetal group. Of the 70 patients in the fetal
group, eight were female (173/22 in the non-fetal group, difference
p=0.95, chi-square). We do not believe that this could be the explanation
of differences in the results. The main difference between our study and
the study by Ikeda et al is that we included only patients with proven
atherosclerosis. These subjects had a relatively high white matter lesion
load, whereas Ikeda et al performed a population study, in which it is
expected that the white matter lesion load is lower.
Furthermore, differences in the way of white matter lesion
scoring could also be an underlying factor in the differences between
these two studies. In this respect I believe that segmentation of white
matter lesions and subsequent outcome of a white matter lesion load in
'ml', could be helpful.