Is There Any Leukoaraiosis in the Corpus Callosum? Analysis with Three Orthogonal Thin FLAIR Images.

A. Yamamoto1, Y. Miki1, H. Tomimoto2, M. Kanagaki1, T. Takahashi1, Y. Fushimi1, J. Konishi3, T. L. Haque1, J. Konishi1 1Department of Nuclear Medicine and Diagnostic Imaging, Graduate School of Medicine, Kyoto University, Kyoto, Kyoto, Japan, 2Department of Neurology, Graduate School of Medicine, Kyoto University, Kyoto, Kyoto, Japan, 3Department of Radiology, Graduate School of Medicine, Kobe University, Kobe, Hyogo, Japan Synopsis Leukoaraiosis refers to incidental diffuse T2-weighted hyperintensity in white matter mostly found in aged populations. Many patients with leukoaraiosis develop progressive cognitive impairment [1]. The most popular hypothesis of disease pathogenesis of leukoaraiosis is that acute disruption of blood supply in one perforating artery territory results in lacunar infarction, while a more chronic and widespread reduction in perfusion pressure causes leukoaraiosis [2,3]. The corpus callosum exhibits several unusual anatomic features compared with the central white matter [4]. Infarctions of the corpus callosum are not common and are attributed to a rich blood supply [5]. However, the question of whether leukoaraiosis is present in the corpus callosum remains unelucidated. We studied whether leukoaraiosis is present in the corpus callosum and correlates with the severity of leukoaraiosis in periventricular and deep white matter. Methods Twenty-one patients who underwent MRI for screening brain pathology (6 men, 15 women, age 51-83 years, mean 72 years) were included in this prospective study. We excluded subjects with cortical infarcts or subcortical infarcts more than 15 mm in maximum diameter and subjects known to have demyelinating disease, brain tumors, hydrocephalus, past trauma, and other known callosal abnormalities. MR studies were performed on a 1.5T whole body system with a head coil. In addition to routine MRI sequences, FLAIR (TR=10000, TE=147, TI=2200 or 2500, NEX=1) in three orthogonal plane (axial, sagittal and coronal) contiguous 3 mm slices were obtained to provide whole corpus callosum coverage. According to Fazekas’ rating scale, leukoaraiosis in the periventricular white matter and that in the deep white matter were graded as follows, respectively; periventricular hyperintensity (PVH) was graded as 0 = absence, 1=”caps” or pencil-thin lining, 2=smooth “halo”, 3=irregular PVH extending into the deep white matter; deep white matter hyperintense signals (DWMH) were rated as 0=absence, 1=punctate foci, 2=beginning confluence of foci, 3=large confluent areas [6,7]. Leukoaraiosis in the corpus callosum was considered present when hyperintensity was identified in the corpus callosum on all axial, coronal, and sagittal images with FLAIR sequence. Statistical analysis was performed to see if there is any correlation between the presence of leukoaraiosis in the corpus callosum and grade of leukoaraiosis in the white matter, using Pearson chi-square test. Results PVH consisted of Grade 1 was seen in 15 patients, Grade 3 in five patients, and PVH was absent in one patient. Grade 1 DWMH was seen in nine patients, Grade 2 in five patients and Grade 3 in six patients, and DWMH was absent in one patient. Leukoaraiosis in the corpus callosum were considered present in 7 out of the 21 patients. In these 7 patients who showed hyperintensities in the corpus callosum, three patients had Grade 1 PVH and four had Grade 3 PVH; three patients showed Grade 2 DWMH and four showed Grade 3 DWMH. Statistical analysis yielded significant correlation between leukoaraiosis in the corpus callosum and the severity of PVH (p = 0.04) and DWMH (p = 0.02). Discussion In the present investigation, we have elucidated the presence of hyperintensities with FLAIR images in the corpus callosum, which correlated with severity of periventricular and deep white matter hyperintensities. Changes in the cerebral hemispheric white matter, detectable with increasing frequency by modern neuroimaging methods, are associated with aging and may contribute to the development of specific cognitive deficits [1]. The pathogenesis of these cerebral white matter abnormalities (leukoaraiosis) is incompletely understood [2]. The neurological and histological abnormalities associated with leukoaraiosis are nonspecific [8,9]. The most popular hypothesis of disease pathogenesis of leukoaraiosis is ischemic injury [2]. Histologic changes of leukoaraiosis were showed to be inhomogeneous associated with different types of white matter hyperintensities [7,10]. Hyperintense caps and a small halo are caused by altered periventricular fluid dynamics [7]. Punctate, early confluent, and confluent DWMH reflect increasing severity of ischemic tissue damage [7]. Irregular PVH extending into the deep white matter also indicates arteriosclerotic disease of a similar degree as present with confluent DWMH [7]. Recently, pathologic study revealed that the white matter is more susceptible to chronic cerebral hypoperfusion than the gray matter, with an involvement of both axonal and myelin components in the rat and immunohistochemistry for some peptides may become a useful tool to investigate white matter lesions caused by various pathoetiologies [11]. Three orthogonal plane thin slice FLAIR images are useful for assessment of lesions in the corpus callosum. Evaluation of hyperintensities in the corpus callosum by only one anatomical plane (e.g. axial) or by only two planes (e.g. axial and sagittal) may mislead hyperintensities located outside the corpus callosum as located inside the corpus callosum. In this study, hyperintensities in cavity of septum pellucidum with axial and sagittal FLAIR images were confirmed with coronal FLAIR image as hyperintensities located outside the corpus callosum. Lesion in the corpus callosum have been described in patients with diseases such as tumors, demyelinating diseases, vascular processes, trauma [12,13]. Infarctions of the corpus callosum are uncommon and may present atypically with slowly evolving and non-localizing signs and symptoms that are more suggestive of tumor [14]. The corpus callosum exhibits a several interesting anatomic features [4] and in some degree, these features may contribute imaging features of the corpus callosum in some pathologic status. This study revealed that leukoaraiosis may present in the corpus callosum, which correlated leukoaraiosis in the white matter. Hyperintensity in the corpus callosum may reflect increasing severity of ischemic tissue damage. Acknowledgements We thank Ari Kobayashi, Yoko Yoshida, and Akira Hiraga for their technical assistance. References [1] Yamauchi H et al, Stroke 2000; 31: 1515-1520. [2] Pantoni L et al, Stroke 1997; 28: 652-659. [3] O'Sullivan M et al, Neurology 2002; 59: 321-326. [4] Moody DM et al, AJNR Am J Neuroradiol 1988; 9: 1051-1059. [5] Ture U et al, Neurosurgery 1996; 39: 1075-1084; discussion 1084-1075. [6] Fazekas F et al, AJR Am J Roentgenol 1987; 149: 351-356. [7] Fazekas F et al, Neurology 1993; 43: 1683-1689. [8] Pantoni L et al, Stroke 1995; 26: 1293-1301. [9] Chimowitz MI et al, Arch Neurol 1992; 49: 747-752. [10] Fazekas F et al, J Neural Transm Suppl 1998; 53: 31-39. [11] Wakita H et al, Brain Res 2002; 924: 63-70. [12] Bourekas EC et al, AJR Am J Roentgenol 2002; 179: 251-257. [13] Georgy BA et al, AJR Am J Roentgenol 1993; 160: 949-955. [14] Kasow DL et al, AJNR Am J Neuroradiol 2000; 21: 1876-1880.

Figure: Coronal, sagittal and axial thin FLAIR images of the corpus callosum. Hyperintensities are noted at the lateral inferior portion of the corpus callosum bilaterally on all coronal, sagittal, and axial images (arrowheads). Simultaneously, Grade 3 periventricular and Grade 3 deep white matter hyperintensities are shown.

Proc. Intl. Soc. Mag. Reson. Med. 11 (2003) 2067