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Neuroradiology |
1 From the Departments of Radiology (R.v.d.B., M.A.v.B.), Clinical Genetics (S.A.J.L.O.), and Neurology (M.D.F., J.H.), Leiden University Medical Center, C2S, Albinusdreef 2, 2333 ZA Leiden, the Netherlands; and Department of Neurology, Rijnland Hospital, Leiderdorp, the Netherlands (J.H.). From the 2002 RSNA scientific assembly. Received October 22, 2002; revision requested January 7, 2003; final revision received April 16; accepted May 20. Address correspondence to R.v.d.B. (e-mail: r.van_den_boom@lumc.nl).
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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MATERIALS AND METHODS: Forty patients with CADASIL in different age groups (20–30 years, n = 5; 31–40 years, n = 4; 41–50 years, n = 16; 51–60 years, n = 15) underwent transverse MR imaging with T1-weighted dual fast spin-echo, fluid-attenuated inversion-recovery, and T2*-weighted gradient-echo sequences. Images were analyzed by one neuroradiologist for the presence of areas of hyperintensity, lacunar infarcts, microbleeds, and subcortical lacunar lesions (SLLs) in different anatomic locations. Descriptive statistics were obtained for the presence of MR imaging abnormalities in various brain areas and for distribution according to age.
RESULTS: The mean age of the 40 mutation carriers (21 women, 19 men) was 45 years ± 10 (SD). In patients with CADASIL who were 20–30 years old, characteristic hyperintense lesions in the anterior temporal lobe (100% [five of five]) and SLLs (20% [one of five]) were the only abnormalities seen on MR images. In patients who were 30–40 years old, lacunar infarcts were found in 75% (three of four) of cases. More areas of hyperintensity were noted, and they frequently involved the external capsule, basal ganglia, and brainstem. In patients 41–50 years old, microbleeds were observed in 19% (three of 16). In patients older than 50 years, areas of hyperintensity (100% [15 of 15]), SLLs (73% [11 of 15]), lacunar infarcts (93% [14 of 15]), and microbleeds (47% [seven of 15]) were frequently observed.
CONCLUSION: The four types of brain lesions that are observed in patients with CADASIL were seen in patients of different age groups.
© RSNA, 2003
Index terms: Brain, diseases, 13.78, 13.87 • Brain, infarction • Brain, MR, 13.121411, 13.121412, 13.121413 • Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), 10.7229
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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The definite diagnosis of CADASIL is established with detection of NOTCH3 mutations, and detection of these mutations is a laborious process that is performed at a limited number of specialized centers. Presently, NOTCH3 mutation analysis is considered only in patients who have unexplained neurologic symptoms, such as ischemic episodes, cognitive deficits, and a positive family history of these symptoms, and who have suggestive MR imaging abnormalities. The radiologic findings of patients with advanced stages of the disease are well documented. On the basis of these descriptions, radiologists can adequately help in the identification of patients with an indication for further molecular or pathologic testing for CADASIL (4–6,10–12). However, the radiologic appearances during earlier stages of the disease have not been described in detail, and this lack of information may lead to inadequate guidance of patients through the diagnostic work-up.
To our knowledge, findings of the only published study about the development of cerebral changes over time in patients with CADASIL were reported by Chabriat et al (5). In that study, the development of areas of hyperintensity and of lacunar infarcts was studied in the periventricular and subcortical white matter, the basal ganglia, and the infratentorial areas. However, after publication of that study, other radiologic hallmarks of CADASIL, such as SLLs, microbleeds, and areas of hyperintensity in the anterior temporal lobe and in the external capsule, were detected (7–9,11). The temporal evolution of these more recently described radiologic phenomena of CADASIL remains to be elucidated. Thus, the purpose of our study was to depict various brain lesions that have been described in patients who have CADASIL with prospective performance of standardized MR imaging in patients of different age groups.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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The families included in this study were all of the families seen between August 1999 and July 2000. To ensure informed consent, only cognitively capable subjects were included in this study. The institutional medical ethics committee approved the study protocol. Since one individual of the 63 participants did not consent to undergo MR imaging, the final number of subjects was 62; 40 of these subjects had a mutation in the NOTCH3 gene and 22 did not.
MR Imaging and Interpretation
All MR imaging examinations were performed with a 1.5-T MR system (Philips Medical systems, Best, the Netherlands). Participants underwent MR imaging with a standardized protocol that included the following: conventional T1-weighted spin-echo (repetition time msec/echo time msec, 600/20; section thickness, 6.0 mm; intersection gap, 0.6 mm; matrix, 256 x 205; field of view, 220 x 165 mm), dual T2-weighted fast spin-echo (3,000/27, 120; section thickness, 3.0 mm; intersection gap, 0 mm; matrix, 256 x 205; field of view, 220 x 220 mm), and fast fluid-attenuated inversion-recovery (FLAIR) (repetition time msec/echo time msec/inversion time msec, 8,000/100/2,000; section thickness, 3.0 mm; intersection gap, 0 mm; matrix, 256 x 192; field of view, 220 x 176 mm) sequences. In addition, a T2*-weighted gradient echo planar (2,598/48; section thickness, 6.0 mm; intersection gap, 0.6 mm; matrix, 256 x 192; field of view, 220 x 198 mm; echo-planar imaging factor, 25) sequence was performed to detect hemosiderin deposits. All images were obtained in the transverse plane parallel to the inferior border of the genu and splenium of the corpus callosum.
Areas of hyperintensity were defined as areas of brain parenchyma with increased signal intensity on intermediate, T2-weighted, and FLAIR MR images, and they were rated from hard copies of transverse dual T2-weighted fast spin-echo MR images with the semiquantitative visual scoring system described by Scheltens et al (14). In this scale, the brain is anatomically divided into deep white matter, basal ganglia, and infratentorial regions. For each region, a score of 0–6 is assigned according to the following scale: score 0, absent; score 1, up to five areas of white matter hyperintensity of less than 3 mm in diameter; score 2, six or more areas of white matter hyperintensity of less than 3 mm in diameter; score 3, as many as five areas of white matter hyperintensity of 4–10 mm in diameter; score 4, six or more areas of white matter hyperintensity of 4–10 mm in diameter; score 5, one or more areas of white matter hyperintensity of more than 10 mm in diameter; and score 6, confluent areas of white matter hyperintensity. In addition, scores were assigned to the frontal and occipital periventricular "caps" and periventricular "bands" as follows: score 0, absent; score 1, as much as 5 mm in diameter; and score 2, more than 5 mm in diameter. Because the Scheltens scoring system does not fully reflect the characteristic lesion distribution in patients who have CADASIL, three anatomic locations were added to the Scheltens score: external and internal capsule and the temporal region. The external and internal capsules were assigned separate scores for the presence of areas of subcortical hyperintensity, and the temporal region was assigned a separate score for the presence of areas of periventricular hyperintensity. In our experience, areas of hyperintensity in young patients who have CADASIL often are located in the anterior temporal lobe; for this reason, we assigned separate scores for the presence of areas of hyperintensity in the anterior temporal lobe and the posterior temporal lobe. We defined the border between the anterior temporal lobe and the posterior temporal lobe as the posterior margin of the amygdala (11). To obtain an overall supratentorial lesion load score, the periventricular score was added to the Scheltens subcortical score. To calculate the prevalence of areas of hyperintensity, a Scheltens score of 1 or higher was considered to be positive for areas of hyperintensity, and a score of 0 implied absence of areas of hyperintensity.
Lacunar infarcts were defined as parenchymal defects that did not extend to the cortical gray matter, with a signal intensity similar to that of cerebrospinal fluid with all pulse sequences, irrespective of size. There are three locations where lacunar infarcts can be difficult to distinguish from normal Virchow-Robin spaces: the basal ganglia, the subinsular region, and the semiovale center. To differentiate a lacunar infarct from a Virchow-Robin space, we excluded lesions in the following areas because they were most likely to represent a Virchow-Robin space: (a) basal ganglia—lesions that were isointense to cerebrospinal fluid with all pulse sequences and were located in the lower one-third of the corpus striatum (15,16); (b) subinsular region—areas with a featherlike configuration that were isointense to cerebrospinal fluid on T1- and T2-weighted MR images but did not have high signal intensity on FLAIR images (17); (c) semiovale center—all lesions with a transverse diameter of 2 mm or smaller or with a tubular appearance following the course of perforating arteries (18).
Microbleeds were defined as focal areas of signal intensity loss on T2-weighted fast spin-echo MR images that increased in size on the T2*-weighted gradient-echo images ("blooming effect") (7). In this way, microbleeds were differentiated from areas of signal loss that were based on vascular flow voids. Areas of symmetric hypointensity of the globus pallidus that were likely to represent calcification or nonhemorrhagic iron deposits were excluded.
SLLs were defined as linearly arranged groups of rounded circumscribed lesions that were just below the cortex at the gray matter–white matter junction and had a signal intensity that was identical to that of cerebrospinal fluid with all pulse sequences (9).
One experienced neuroradiologist (M.A.v.B.) who was blinded to the diagnosis of CADASIL assessed the presence of areas of hyperintensity, lacunar infarcts, microbleeds, and SLLs in all 62 participants. For lacunar infarcts and microbleeds, size and number were assessed in the following brain areas: supratentorial region (frontal, temporal, occipital, and parietal lobes and internal and external capsules), infratentorial region (cerebellum, pons, medulla oblongata, and mesencephalon), thalamus, and basal ganglia (globus pallidus, caudate nucleus, and putamen). The presence of SLLs was assessed in each patient who had CADASIL.
Statistical Analyses
Descriptive statistics were obtained in regard to the presence of MR imaging abnormalities in various areas of the brain according to age (percentage of patients affected per anatomic structure per decade). Differences in areas of hyperintensity, lacunar infarcts, and microbleeds between male and female patients who had CADASIL were investigated with the Student t test for unpaired data. Differences in SLLs were tested by using the 
2 test. A difference with P < .05 was considered significant. A statistical software package (SPSS-10; SPSS, Chicago, Ill) was used for data analysis.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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As early as the 3rd decade, cerebral abnormalities can be found in patients who have CADASIL. In this study, supratentorial areas of hyperintensity were observed in all patients, and SLLs were observed in one patient. A notable site of predilection of the areas of hyperintensity is the anterior temporal lobe. These areas of hyperintensity are found in all patients of this age group, invariably as a highly characteristic pattern of bilateral hyperintense areas located directly below the cortical ribbon. Although this type of abnormality has been described by others (12) as a characteristic finding in patients who have CADASIL, the early involvement of the anterior temporal lobe has not been reported before, to our knowledge. A pattern of multiple, although often few, small patches with high signal intensity was observed in other locations. Periventricular white matter areas of hyperintensity are frequently seen as smooth caps around the frontal horns and seldom are seen around the posterior and temporal horn of the lateral ventricles. In young patients, SLLs were another characteristic observation, and SLLs always were observed in conjunction with the observation of areas of hyperintensity in the anterior temporal lobe. SLLs are a recently described abnormality that is considered to be specific for CADASIL (9). The radiologic phenomenon of SLLs is based on the presence of dilated perivascular spaces of perforating arteries at the level of the gray matter–white matter junction and spongiosis in the surrounding parenchyma. Detection of areas of hyperintensity with or without SLLs in the anterior temporal lobes in young patients is highly characteristic of findings in young patients with CADASIL, and detection of these areas of hyperintensity suggests the diagnosis.
In the 4th decade, in addition to areas of hyperintensity and SLLs, lacunar infarcts were seen in patients who have CADASIL. These lacunar infarcts are found in 75% of patients of this age group, and they occur in the supratentorial white matter and in the basal ganglia. In the supratentorial white matter, areas of hyperintensity in the external capsule are a new finding in this age group, and this finding can be observed in 25% of patients. The prevalence of subcortical areas of hyperintensity increases in all lobes, and larger periventricular areas of hyperintensity are present. Subcortical and periventricular areas of hyperintensity may become confluent. The areas of hyperintensity in the anterior temporal lobe increase in size and expand posteriorly in the temporal lobe. Apart from the supratentorial white matter, areas of hyperintensity are now also observed in the basal ganglia, the thalamus, and the brainstem. Although the number of patients in whom SLLs are observed does not increase, the number of SLLs per patient is higher than it is in the preceding age group, and the distribution of SLLs follows the expanding white matter areas of hyperintensity of the anterior temporal lobes.
In patients in the 5th decade, microbleeds may be observed in addition to areas of hyperintensity, SLLs, and lacunar infarcts. Microbleeds are found in 19% of patients in this age group, and they can be observed in the thalamus, the brainstem, and the supratentorial white matter. The number of patients in whom areas of hyperintensity are observed further increases, although there are still patients in whom areas of hyperintensity are not observed in the infratentorial white matter, in the basal ganglia, or in the thalamus. The number and size of areas of hyperintensity further increase, giving rise to large confluent areas of high signal in subcortical and periventricular white matter. Areas of hyperintensity can also involve the internal capsule. The prevalence of lacunar infarcts (94%) and SLLs (56%) increases. Now lacunar infarcts also are present in the brainstem and the thalamus.
In patients in the 6th decade, no new types of lesions are seen, and areas of hyperintensity, SLLs, lacunar infarcts, and microbleeds are observed in most patients. Areas of hyperintensity are always found in all lobes, in the brainstem, in the basal ganglia, and in the thalamus. In almost all cases, areas of hyperintensity are also found in the internal and external capsule. During this stage, most of the supratentorial white matter may show a symmetric pattern of large homogeneous areas of increased signal intensity involving the subcortical and periventricular white matter. Lacunar infarcts are found in more than 90% of cases. SLLs are found in 73% of cases; microbleeds, in 47%. SLLs may now be observed in the temporal lobe, in the subinsular white matter, and in the operculum of the frontal lobe.
In patients older than 30 years, CADASIL shares several radiologic characteristics with other diseases accompanied by small vessel disease, which implies that differentiating CADASIL from these disorders based on findings of radiologic examinations may be difficult. Nonspecific areas of hyperintensity in the periventricular, the frontal, the parietal, and the occipital regions are seen in a number of other small vessel diseases (19). Brainstem abnormalities located predominantly at the rostrocaudal center of the pons are frequently observed in patients who have CADASIL, but they can also be found in patients who have atherosclerosis (20). The occurrence of lacunar infarcts and microbleeds is also considered to be characteristic of cerebral small vessel disease in general and is not characteristic of only CADASIL (21,22). Still, the distribution of the areas of hyperintensity and the presence of SLLs seem to specifically suggest the diagnosis of CADASIL. By using image postprocessing software that is based on statistical parametric mapping, Auer et al (12) compared patterns of areas of hyperintensity in a group of patients who had CADASIL and a group of patients who had Binswanger disease. In that study, it was suggested that the presence of white matter areas of hyperintensity in the anterior temporal lobe was characteristic of patients who had CADASIL (12). The image processing technique used in that study only permitted detection of differences between groups and did not help in determination of the diagnosis in patients. In our study, the characteristic areas of hyperintensity in the anterior temporal lobe were present in 39 of 40 patients who had CADASIL, and this result demonstrates that the prevalence of this finding in patients who have CADASIL is high, which makes it a useful radiologic hallmark of the disease. The presence of areas of hyperintensity in the external capsule also has been described to be characteristic of CADASIL (11). Because of its high prevalence (94%) among patients with CADASIL after the age of 40, this is another sign that is helpful in the suggestion of the diagnosis later during the course of the disease. Finally, the prevalence of SLLs increases considerably in patients older than 40 years, and therefore, this lesion is helpful for detection of the disease in patients with increasing age.
In our study, men were more frequently affected by lacunar infarcts and SLLs than were women. For this observation, there is no simple explanation. A difference in age at death between men and women who have CADASIL has been found (1). Death occurs at a significantly younger age in men, and although this difference may reflect the generally observed difference in life expectancy, it may also be caused by differences in the disease dynamics in men and women.
In summary, in patients who have CADASIL, imaging abnormalities are found in the brain earlier than expected clinically. In young patients who have CADASIL, cerebral abnormalities are highly characteristic, although limited. The areas of hyperintensity in the anterior temporal lobe and the SLLs that are observed in these young patients continue to help in the recognition of the underlying condition later in life.
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FOOTNOTES |
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Author contributions: Guarantors of integrity of entire study, R.v.d.B., M.A.v.B.; study concepts, R.v.d.B., M.A.v.B., J.H.; study design, R.v.d.B., M.A.v.B.; literature research, R.v.d.B., M.A.v.B.; clinical studies, R.v.d.B., S.A.J.L.O.; data acquisition, R.v.d.B., S.A.J.L.O.; data analysis/interpretation, R.v.d.B., M.A.v.B.; statistical analysis, R.v.d.B., M.A.v.B.; manuscript preparation and definition of intellectual content, R.v.d.B, M.A.v.B.; manuscript editing, R.v.d.B.; manuscript revision/review, M.A.v.B, M.D.F., J.H.; manuscript final version approval, all authors
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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