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LARGE VIRCHOW-ROBIN SPACES IN TWO CHILDREN
Seiji KIMURA
Department of Pediatrics, Yokohama City University School of Medicine (Received June 22, 1993)
Large symmetrical Virchow--Robin spaces in the bilateral cerebral white matter,
dominant in the occipital area, were observed in two children on magnetic resonance imaging. Large Virchow-Robin spaces have been reported as non-specific white matter
lesions, which are sometimes misdiagnosed as lacunar infarcts, and have been seen mainly in the aging brain. To our knowledge, there has been no report of large
Virchow-Robin spaces in young children. We present herein the cases of two children with large Virchow-Robin spaces who developed generalized seizures. Each patient had had an episode of perinatal asphyxia.
Introduction
The Virchow-Robin space is a subadventitial
space that encircles capillaries in the central nervous system (CNS). Recently, dilated
Virchow--Robin spaces have been visualized ･by magnetic
resonance <MR) imagingi)N3). Large Virchow-Robin spaces are seen in the brain in association with aging and miscellaneous conditions3}N7). We herein
present our experience of prominent Virchow-Robin spaces in two children with generalized
seizure disorder.
Case Reports
Case 1. A 5-year-old boy; born to
non-consan-guineous healthy parents with a body weight of
3,206 g at 41 gestational weeks, turbid amniotic
fluid and initial tachypnea and cyanosis which
disappeared by day 3 after birth without supple-mental oxygen therapy. Developsupple-mental milestones were normal. At age 5, he developed a generalized motor seizure disorder. He had no intracranial
'
pyramidal or extrapyramidal signs. The verbal IQ was 87 while the performance IQ was 100. Routine laboratory examinations including serum chemis-tries and cerebrospinal fluid analysis showed no abnormalities. Screening for amino acids, lyso-somal enzymes, and long chain fatty acids in the
serum and for urinary organic acids was negative. Case 2. A 3-year-old boy; born at 25 gestational
weeks with a body weight of 688 g. The patient
was mechanically ventilated at birth. The serum IgM at birth was 54 mg/dl (normal <20). A chest
radiograph at 7 days was consistent with the Wilson-Mikity syndrome. Mechanical ventilation and oxygen therapy were terminated at days 93 and 240, respectively. The patient developed a
generalized seizure at age 1 1/2 and also speech
disability, though his motor development was
normal. His speech disability improved until the age of 5, and his IQ at the age of 6 was 98.
MR Studies
Case 1. An MR scan of the brain was obtained at age 5. The general configuration of the brain was well preserved, though parallel linear or tubular lesions were demonstrated. These lesions showed low and high intensity attenuation on Ti (TR/TE
==440/15) and T2 (TR/TE=2500/100) weighted
images, respectively (Fig. 1-1-4). The lesions were isointense relative to the cerebrospinal fluid.
Ab-normalities were found in the white matter
bilaterally, mainly in the occipital area (Fig. 1-lt-3). Lesions were oriented vertically between the periventricular white matter and the subcortices (Fig. 1-4). Branches emanating from these lesions
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Flg. 1 MRIofPatient1Multiple low intensity tubular lesions are seen in the bilateral occipital white matter (arrowheads), almost
symmetrically, on a Ti (TRITE =440115) image (1). On a T2 (TRITE =25001100) image, tubular lesions
showing isointensity with cerebrospinal fluid are remarkably more visible (arrowheads) than these on a Ti
image. Thin linear high intensity lesions show a parallel arrangement, and some linear lesions are
connected with cerebral cortices as indicated by arrows (2). Low intensity spotty lesions are dominant in
the occipital area (arrowhead) (TRITE=45/13) (3). On a sagittal section (T2 image), the parallel
arrangement of tubular lesions is more remarkable than that seen on other sections (arrowheads). They run vertically between periventricular white matter and cortices (arrowheads) (4).
were connected to the subarachnoid space of the cortical surface (Fig. 1-2). On MR angiography there was no arteriovenous malformation. Case 2. MR findings were similar to those of
Case 1 (Fig. 2--5, 6), though the lesions were less
prominent than in Case 1. Tubular or linear
lesions were located only in the occipital white matter.
Follow up MR studies performed one year after the first examinations of both patients showed no interval change.
MR
scansDiscussion
of two children revealed a parallel
arrangement of linear or tubular lesions in the cerebral white matter. Abnorrnalities were 1ocated
throughout the cerebrum, but were most
promi-nent in the occipital area. Lesions showed low and high intensities by Ti- and T2-weighted imaging, respectively, and were isointense relative to the cerebrospinal fluid. In some of the MR scan slices, continuity of these lesions with the subarachnoid spaces of the cerebral cortices was visible. These lesions were consistent with large Virchow-Robin spacesi}N3). Large Virchow-Robin spaces have been reported in the aging brain and in miscellaneous conditionsi}N7), but most are non-specific white matter lesions. A recent study by Heier et a13)
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Fig. 2 MRIofPatient2
On a T2 image, tubular lesions showing isointensity with cerebrospinal fluid are present (arrows). These lesions are almost same as those seen in Fig. I--2 of Patient 1 (5). A sagittal section (T2 image) shows the parallel arrangement of tubular lesions. They run vertically between the periventricular white matter and
cortices (6).
concluded that large Virchow-Robin spaces are
another phenomenon of the aging brain. A large Virchow-Robin space is sometimes mistaken for a lacunar infarctioni}2). In the present cases, the lesions were symmetrical in the two hemispheres and were isointense relative to the cerebrospinal fluid. Abnormalities were vertically oriented be-tween the periventricular white matter and the cerebral cortices. These findings are consistent
with Virchow-Robin spaces rather than lacunar
infarctioni)ny3). Both of our patients had experi-enced perinatal asphyxia of mild degree, though Patient 2 had required mechanical ventilation for about 3 months. Perinatal asphyxia causes mis-cellaneous white matter lesions, which are easily recognized by MR scan if the lesions are marked. However, brain lesions caused by mild perinatal asphyxia are not well understood, because normal children without a history of perinatal asphyxia
are rarely examined by MR scans. Mild diffuse
brain atrophy, a sequela of mild perinatal
as-phyxia, may cause large Virchow-Robin spaces, which may mimic the atrophy seen in the aging
brain.
References
1) Jungreis CA, Kanal E, Hirsch W et al; Normal
perivascular spaces mimicking lacunar infarction: MR imaging. Radiolczgy 169: 101-104, 1988
2) Braffman BH, Zimmerman RA, Trojanowski JQ
et al: Pathologic correlation with gross and pathology. 1. Lacunar infarction and Virchow-Robin spaces. AJNR 151: 551-558, 1988
3) Heier LA, Bauer CJ, Schwartz L et al: Large Virchow-Robin spaces: MR-clinical correlation. AJNR
10: 929-936, 1989
4) Mirfakhraee M, Crofford MJ, Guinto FC et al: A path of spread in neurosarcoidosis. Radiology 158: 715-720, 1986
5) Wehn SM, Heinz ER, Burger PC et al: Dilated
Virchow-Robin spaces in cryptococcal meningitis
ciated with AIDS: CT and MR findings. J Comput Assist Tomogr 13: 756-762, 1989
6) Sheerman JL, Stern BJ: Sarcoidosis of the CNS: Comparison of unenhanced and enhanced MR images. AJNR 11: 915-923, 1990
7) Tien RD, Chu PK, Hesselink JR et al: Intracranial cryptococcosis in immunocompromised patients: CT
and MR findings in 29 cases. ANJR 12: 283-289, 1991
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