• Journal of Korean Neurosurgical Society
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• v.39 no.6
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• pp.447-450
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• 2006

Cerebral amyloid angiopathy[CAA] is characterized by the deposition of amyloid ${\beta}-protein$ in the walls of small to medium-sized arteries of the leptomeninges and cerebral cortex. While often asymptomatic, CAA can develop into intracerebral hemorrhage facilitated by arterial hypertension. We report the case of a 52-year-old man with CAA and arterial hypertension who developed recurrent cerebral hemorrhages on three different occasions and in multiple non-overlapping loci over a period of nine years. Based on our findings, we recommend brain biopsies for all patients undergoing evacuation of multiple recurrence or atypical pattern intracerebral hemorrhages.

• Dementia and Neurocognitive Disorders
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• v.22 no.3
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• pp.87-99
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• 2023

Background and Purpose: According to the amyloid cascade hypothesis, fibrillary amyloid-beta load in the brain causes Alzheimer's disease (AD) with toxic effects. Recently, perivascular spaces (PVSs), fluid-filled cavities around small penetrating arterioles and venules in the brain, and the glymphatic system relationship with type 2 diabetes mellitus (DM2) and AD has been an important research topic from a physiopathological point of view. There are two types of PVSs that are associated with sporadic atherosclerosis and cerebral amyloid angiopathy. In this study, we evaluated the relationship between the number and localization of enlarged PVSs in AD. Methods: A total of 254 patients with AD and 125 healthy controls were included in this study All the patients were evaluated with neurological and cognitive examinations and magnetic resonance imaging (MRI). PVSs on MRI were graded by recording their number and location. The study was a retrospective study. Results: In our study, the number of white matter convexity-central semiovale localized PVSs was higher in patients than in the control group. In addition, the number of PVSs in this localization score was higher in patients with DM2. Cerebral PVS counts were higher in patients with AD than in the control group. Conclusions: These results suggest the important role of cerebral amyloid angiopathy, one of the vascular risk factors, and the glymphatic system in the pathogenesis of AD. In addition, the results of our study suggest that the evaluation of PVSs levels, especially at the (centrum semiovale), using imaging studies in AD is a potential diagnostic option.

• Journal of Korean Neurosurgical Society
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• v.58 no.1
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• pp.30-35
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• 2015

Objective : The clinical and pathological characteristics of 10 cases of cerebral amyloid angiopathy (CAA)-related cerebral lobar hemorrhage (CLH) that was diagnosed at autopsy were investigated to facilitate the diagnosis of this condition. Methods : The clinical characteristics of 10 cases of CAA-related CLH were retrospectively reviewed, and a neuropathological examination was performed on autopsy samples. Results : The 10 cases included two with a single lobar hemorrhage and eight with multifocal lobar hemorrhages. In all of the cases, the hemorrhage bled into the subarachnoid space. Pathological examinations of the 10 cases revealed microaneurysms in two, double barrel-like changes in four, multifocal arteriolar clusters in five, obliterative onion skin-like intimal changes in four, fibrinoid necrosis of the vessels in seven, neurofibrillary tangles in eight, and senile plaques in five cases. Conclusion : CAA-related CLHs were located primarily in the parietal, temporal, and occipital lobes. These hemorrhages normally consisted of multiple repeated CLHs that frequently bled into the subarachnoid space. CAA-associated microvascular lesions may be the pathological factor underlying CLH.

• Annals of Clinical Neurophysiology
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• v.23 no.1
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• pp.65-67
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• 2021

• Journal of the Korean Society of Radiology
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• v.84 no.5
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• pp.1140-1145
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• 2023

Cerebral amyloid angiopathy-related inflammation (CAA-RI) is an encephalopathy caused by inflammation of β-amyloid peptide deposition in cerebrovascular vessels. It is a rare disease that mainly occurs in the elderly and is characterized by rapidly progressive dementia, headache, seizures, and focal neurologic deficits. CAA-RI can demonstrate characteristic brain MRI findings and can be reversed by steroids or other immunosuppressive therapies. Here, we report a case of CAA-RI, which was initially misdiagnosed as a subacute infarction but was diagnosed while reviewing follow-up brain MRI images, and spontaneous remission was achieved.

• Journal of the Korean neurological association
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• v.36 no.4
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• pp.314-317
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• 2018

Focal subarachnoid hemorrhage occasionally presents as transient focal neurologic episodes mimicking transient ischemic attack (TIA). Unless properly diagnosed, it may aggravate cerebral hemorrhage by administering antithrombotic agents. Therefore, clinicians need to be aware that such focal subarachnoid hemorrhage sometimes cannot be detected on noncontrast computed tomography and blood-sensitive magnetic resonance imaging can detect even a small amount of hemorrhage. We describe an 85-year-old woman with focal subarachnoid hemorrhage and possible cerebral amyloid angiopathy who presented transient left arm weakness recurrently, which mimicked TIA.

• Dementia and Neurocognitive Disorders
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• v.17 no.3
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• pp.73-82
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• 2018

Cerebral microbleeds (CMBs) are increasingly recognized neuroimaging findings, occurring with cerebrovascular disease, dementia, and aging. CMBs are associated with subsequent hemorrhagic and ischemic stroke, and also with an increased risk of cognitive deterioration and dementia. They occur in the setting of impaired small vessel integrity due to hypertension or cerebral amyloid angiopathy. This review summarizes the concepts, cause or risk factors, histopathological mechanisms, and clinical consequences of CMBs.

• Journal of Korean Medical Science
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• v.33 no.46
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• pp.289.1-289.10
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• 2018

Background: Cerebral microbleeds (CMBs) are associated with cerebrovascular risk factors and cognitive dysfunction among patients with Parkinson's disease (PD). However, whether CMBs themselves are associated with PD is to be elucidated. Methods: We analyzed the presence of CMBs using 3-Tesla brain magnetic resonance imaging in non-demented patients with PD and in age-, sex-, and hypertension-matched control subjects. PD patients were classified according to their motor subtypes: tremor-dominant, intermediate, and postural instability-gait disturbance (PIGD). Other cerebrovascular risk factors and small vessel disease (SVD) burdens were also evaluated. Results: Two-hundred and five patients with PD and 205 control subjects were included. The prevalence of CMBs was higher in PD patients than in controls (16.1% vs. 8.8%; odds ratio [OR], 2.126; P = 0.019); CMBs in the lobar area showed a significant difference between PD patients and controls (11.7% vs. 5.9%; OR, 2.234; P = 0.032). According to the motor subtype, CMBs in those with PIGD type showed significant difference from controls with respect to the overall brain area (21.1% vs. 8.9%; OR, 2.759; P = 0.010) and lobar area (14.6% vs. 4.9%; OR, 3.336; P = 0.016). Among PD patients, those with CMBs had higher age and more evidence of SVDs than those without CMBs. Conclusion: We found that CMBs are more frequent in PD patients than in controls, especially in those with the PIGD subtype and CMBs on the lobar area. Further study investigating the pathogenetic significance of CMBs is required.