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Small-Vessel Disease in the Basal Ganglia: Lacune or Microbleed?
Case Report
Small-Vessel Disease in the Basal Ganglia: Lacune or Microbleed? Tomohisa Nezu, MD, Shoji Arihiro, MD, Kazunori Toyoda, MD, and Kazuo Minematsu, MD
Brain microbleeds (BMBs) can be detected on the gradient-echo T2*-weighted magnetic resonance imaging and are considered a risk factor for cognitive impairment and intracerebral hemorrhage. Detailed radiologic findings on the etiology of BMBs and their changes remain scarce. We present a case of subacute change in a BMB in the basal ganglia that mimicked a subacute lacunar infarct. Our findings underscore the need for physicians to be careful to not erroneously diagnose BMBs as lacunar infarctions and prescribe unnecessary antiplatelet medication. Key Words: Cerebrovascular disease—intracerebral hemorrhage— gradient-echo T2*-weighted magnetic resonance imaging. Ó 2012 by National Stroke Association
Case Report A 79-year-old man with hypertension visited our clinic with a complaint of memory impairment. On magnetic resonance imaging (MRI), an old intracerebral hemorrhage (ICH) was identified in the right putamen (Fig 1, A), which did not seem to affect memory function. One year later, walking had become gradually more difficult for the patient, prompting another visit to our clinic. He presented with a mildly shuffling gait and postural instability. A computed tomography (CT) scan detected no highdensity areas (Fig 1, B). Although T1-weighted MRI performed on the day of the visit did not reveal any abnor-
From the Department of Cerebrovascular Medicine, National Cerebral and Cardiovascular Center, Suita, Japan. Received March 8, 2011; revision received May 8, 2011; accepted May 13, 2011. Supported in part by Grants-in-Aid H23-Junkanki-Ippan-010 and H21-Junkanki-Ippan-017 from the Ministry of Health, Labor and Welfare of Japan. Address correspondence to Tomohisa Nezu, MD, Department of Cerebrovascular Medicine, National Cerebral and Cardiovascular Center, Fujishirodai 5-7-1, Suita, Osaka 565-8565, Japan. E-mail: [email protected]. 1052-3057/$ - see front matter Ó 2012 by National Stroke Association doi:10.1016/j.jstrokecerebrovasdis.2011.05.020
malities (Fig 1, C), T2-weighted MRI and fluid-attenuated inversion recovery MRI (FLAIR) examination showed a new high-intensity area with a low-intensity core in the left putamen (Fig 1, D and E). Although diffusionweighted MRI (DWI) seemed to show a slightly higher intensity at this lesion (Fig 1, F), apparent diffusion coefficient (ADC) imaging did not demonstrate low intensity (Fig 1, G). These MRI series were performed according to our routine stroke MRI sequences, and thus gradientecho T2*-weighted MRI (GRE) was not performed at this point. We considered this new lesion an atypical subacute lacunar infarction. Thirteen days later, the high-intensity area appeared slightly smaller on FLAIR (Fig 1, H), and was identified as a round low-intensity core surrounded by a high-intensity rim on GRE (Fig 1, I). The slight high intensity of that lesion disappeared on DWI (Fig 1, J). On day 60, the lesion changed to a low-intensity dot without the surrounding high-intensity area on FLAIR (Fig 1, K), and finally appeared as an ovoid low-intensity spot without the rim on GRE (Fig 1, L). During this period, CT and T1-weighted MRI found no abnormalities in the left basal ganglia. The patient’s blood pressure on admission was 168/74 mm Hg, and his systolic blood pressure ranged between 160 mm Hg and 170 mm Hg during the first 2 weeks. He was given antihypertensive therapy without antithrombotic
Journal of Stroke and Cerebrovascular Diseases, Vol. 21, No. 8 (November), 2012: pp 905.e5-905.e6
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Figure 1. Changes in the BMB (white arrows) detected on MRI studies. (A) The initial FLAIR MRI. (B) CT scan on the day of the visit (1 year after the FLAIR image in A). (C) T1-weighted MRI on the day of the visit. (D) T2-weighted MRI on the day of the visit. (E) FLAIR on the day of the visit. (F) DWI MRI on the day of the visit. (G) ADC image on the day of the visit. (H) FLAIR on day 13 after the visit. (I) GRE on day 13. (J) DWI on day 13. (K) FLAIR on day 60. (L) GRE on day 60.
drugs or other medications. The left putaminal lesion was finally diagnosed as a brain microbleed (BMB).
Discussion BMBs can be detected on GRE and are considered a risk factor for cognitive impairment and ICH.1 Detailed radiologic findings showing how BMBs occur and how they change remain scarce. Unique characteristics of this patient’s BMB were a tiny, round core with a relatively large surrounding area of edema. The intensity of this lesion was slightly high on DWI but was not low on ADC imaging, indicating that the changes seen on DWI were due to the T2 shine-through phenomenon. The surrounding high-intensity area visible on FLAIR diminished within a period of several months, indicating vasogenic edema. There were size imbalances between the core hematoma and surrounding area of edema com-
pared with previous reports.2,3 As shown in Figure 1, E, this BMB mimicked a lacunar infarct. The present case suggests that physicians must be careful to not erroneously diagnose BMBs as lacunar infarctions and thus avoid prescribing unnecessary antiplatelet medications. The GRE was useful for discriminating this CT- and DWI-undetectable lesion from a silent lacune.
References 1. Greenberg SM, Vernooij MW, Cordonnier C, et al. Cerebral microbleeds: A guide to detection and interpretation. Lancet Neurol 2009;8:165-174. 2. Arima H, Wang JG, Huang Y, et al. Significance of perihematomal edema in acute intracerebral hemorrhage: The INTERACT trial. Neurology 2009;73:1963-1968. 3. Lee SH, Kim BJ, Roh JK. Silent microbleeds are associated with volume of primary intracerebral hemorrhage. Neurology 2006;66:430-432.
Small-Vessel Disease in the Basal Ganglia: Lacune or Microbleed? Tomohisa Nezu, MD, Shoji Arihiro, MD, Kazunori Toyoda, MD, and Kazuo Minematsu, MD
Brain microbleeds (BMBs) can be detected on the gradient-echo T2*-weighted magnetic resonance imaging and are considered a risk factor for cognitive impairment and intracerebral hemorrhage. Detailed radiologic findings on the etiology of BMBs and their changes remain scarce. We present a case of subacute change in a BMB in the basal ganglia that mimicked a subacute lacunar infarct. Our findings underscore the need for physicians to be careful to not erroneously diagnose BMBs as lacunar infarctions and prescribe unnecessary antiplatelet medication. Key Words: Cerebrovascular disease—intracerebral hemorrhage— gradient-echo T2*-weighted magnetic resonance imaging. Ó 2012 by National Stroke Association
Case Report A 79-year-old man with hypertension visited our clinic with a complaint of memory impairment. On magnetic resonance imaging (MRI), an old intracerebral hemorrhage (ICH) was identified in the right putamen (Fig 1, A), which did not seem to affect memory function. One year later, walking had become gradually more difficult for the patient, prompting another visit to our clinic. He presented with a mildly shuffling gait and postural instability. A computed tomography (CT) scan detected no highdensity areas (Fig 1, B). Although T1-weighted MRI performed on the day of the visit did not reveal any abnor-
From the Department of Cerebrovascular Medicine, National Cerebral and Cardiovascular Center, Suita, Japan. Received March 8, 2011; revision received May 8, 2011; accepted May 13, 2011. Supported in part by Grants-in-Aid H23-Junkanki-Ippan-010 and H21-Junkanki-Ippan-017 from the Ministry of Health, Labor and Welfare of Japan. Address correspondence to Tomohisa Nezu, MD, Department of Cerebrovascular Medicine, National Cerebral and Cardiovascular Center, Fujishirodai 5-7-1, Suita, Osaka 565-8565, Japan. E-mail: [email protected]. 1052-3057/$ - see front matter Ó 2012 by National Stroke Association doi:10.1016/j.jstrokecerebrovasdis.2011.05.020
malities (Fig 1, C), T2-weighted MRI and fluid-attenuated inversion recovery MRI (FLAIR) examination showed a new high-intensity area with a low-intensity core in the left putamen (Fig 1, D and E). Although diffusionweighted MRI (DWI) seemed to show a slightly higher intensity at this lesion (Fig 1, F), apparent diffusion coefficient (ADC) imaging did not demonstrate low intensity (Fig 1, G). These MRI series were performed according to our routine stroke MRI sequences, and thus gradientecho T2*-weighted MRI (GRE) was not performed at this point. We considered this new lesion an atypical subacute lacunar infarction. Thirteen days later, the high-intensity area appeared slightly smaller on FLAIR (Fig 1, H), and was identified as a round low-intensity core surrounded by a high-intensity rim on GRE (Fig 1, I). The slight high intensity of that lesion disappeared on DWI (Fig 1, J). On day 60, the lesion changed to a low-intensity dot without the surrounding high-intensity area on FLAIR (Fig 1, K), and finally appeared as an ovoid low-intensity spot without the rim on GRE (Fig 1, L). During this period, CT and T1-weighted MRI found no abnormalities in the left basal ganglia. The patient’s blood pressure on admission was 168/74 mm Hg, and his systolic blood pressure ranged between 160 mm Hg and 170 mm Hg during the first 2 weeks. He was given antihypertensive therapy without antithrombotic
Journal of Stroke and Cerebrovascular Diseases, Vol. 21, No. 8 (November), 2012: pp 905.e5-905.e6
905.e5
T. NEZU ET AL.
905.e6
Figure 1. Changes in the BMB (white arrows) detected on MRI studies. (A) The initial FLAIR MRI. (B) CT scan on the day of the visit (1 year after the FLAIR image in A). (C) T1-weighted MRI on the day of the visit. (D) T2-weighted MRI on the day of the visit. (E) FLAIR on the day of the visit. (F) DWI MRI on the day of the visit. (G) ADC image on the day of the visit. (H) FLAIR on day 13 after the visit. (I) GRE on day 13. (J) DWI on day 13. (K) FLAIR on day 60. (L) GRE on day 60.
drugs or other medications. The left putaminal lesion was finally diagnosed as a brain microbleed (BMB).
Discussion BMBs can be detected on GRE and are considered a risk factor for cognitive impairment and ICH.1 Detailed radiologic findings showing how BMBs occur and how they change remain scarce. Unique characteristics of this patient’s BMB were a tiny, round core with a relatively large surrounding area of edema. The intensity of this lesion was slightly high on DWI but was not low on ADC imaging, indicating that the changes seen on DWI were due to the T2 shine-through phenomenon. The surrounding high-intensity area visible on FLAIR diminished within a period of several months, indicating vasogenic edema. There were size imbalances between the core hematoma and surrounding area of edema com-
pared with previous reports.2,3 As shown in Figure 1, E, this BMB mimicked a lacunar infarct. The present case suggests that physicians must be careful to not erroneously diagnose BMBs as lacunar infarctions and thus avoid prescribing unnecessary antiplatelet medications. The GRE was useful for discriminating this CT- and DWI-undetectable lesion from a silent lacune.
References 1. Greenberg SM, Vernooij MW, Cordonnier C, et al. Cerebral microbleeds: A guide to detection and interpretation. Lancet Neurol 2009;8:165-174. 2. Arima H, Wang JG, Huang Y, et al. Significance of perihematomal edema in acute intracerebral hemorrhage: The INTERACT trial. Neurology 2009;73:1963-1968. 3. Lee SH, Kim BJ, Roh JK. Silent microbleeds are associated with volume of primary intracerebral hemorrhage. Neurology 2006;66:430-432.