• 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.

• 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.

• 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.

• 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 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.

• Toxicological Research
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• v.17
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• pp.71-77
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• 2001

The brain of the aged dog possesses senile plaques and amyloid angiopathy, which characterize Alzheimer's disease brains. We have defined the dementia condition of aged dogs and examined which mechanism(s) is responsible for the condition. A series of studies revealed that the dementia condition in aged dogs is significantly related to the number of apoptotic brain cells including both neurons and glial cells, but not to the number of senile plaques. On the other hand, 5-azacytidine (5AzC) is a cytidine analogue, and is thought to induce kinds of cell differentiation possibly through hypomethylation of genomic DNA. We have revealed neuronal apoptosis induced in 5AzC-treated fetal mice and PC12 cells. The ribosomal protein L4 (rpL4) gene is expressed prior to the apoptosis in the PC12 cell system. Therefore, the involvement of the rpL4 gene expression in age-related brain cell apoptosis in dogs may contribute to the investigation of Alzheimer's dementia.

• 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.