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• Vol.50 No.9
• CLINICA NEUROL, 50: 651−655, 2010
• Vol.50 No.9 contents

Case Report

An autopsy case of senile dementia suspected to be influenced by cerebral amyloid angiopathy with multiple cortical microinfarcts

Yasushi Iwasaki, M.D.¹⁾, Keiko Mori, M.D.¹⁾, Masumi Ito, M.D.¹⁾, Akira Deguchi, M.D.²⁾, Taizo Shiraishi, M.D.³⁾, Maya Mimuro, M.D.⁴⁾, Mari Yoshida, M.D.⁴⁾ and Yoshio Hashizume, M.D.⁴⁾

¹⁾Department of Neurology, Oyamada Memorial Spa Hospital
²⁾Department of Internal Medicine, Oyamada Memorial Spa Hospital
³⁾Department of Pathologic Oncology, Mie University Graduate School of Medicine
⁴⁾Department of Neuropathology, Institute for Medical Science of Aging, Aichi Medical University

A Japanese male showed gradually progressing dementia with psychiatric symptoms including abnormal behavior, night and day reversal, nocturnal delirium, loud shouting, agitation, resistance to care, and loud soliloquy. The patient had a history of right cerebral embolism due to atrial fibrillation 1 month before the onset of dementia. Head CT revealed widespread cerebral infarction in the right cerebral hemisphere with bilateral lateral ventricular dilatation. The patient died at the age of 83, 10 months after the onset of cerebral embolism. The clinical diagnosis was mixed-type dementia.
On autopsy the brain weighed 1,160 g. Widespread cerebral amyloid angiopathy (CAA) was observed, with distribution most severe in the cerebral cortical vessels and slightly milder in the leptomeningial and subarachnoid vessels. The artery, arteriole, and capillary walls were thickened by the deposition of amorphous, eosinophilic and β-protein immunopositive amyloid. Aβ-deposition was more severe in capillaries and CAA tended to be more severe in the occipital regions. Multiple cortical microinfarcts were found, particularly in the crests of the cerebral gyri of watershed zones. Cerebral white matter, basal ganglia, thalamus, brainstem and spinal cord were relatively preserved from CAA. Infarction was not apparent, except for an embolic lesion in the right cerebral hemisphere and the cortical microinfarcts. We did not observe fibrinoid necrosis, granulomatous angiitis or giant cell reaction associated with CAA-vasculopathies. Rare instances were observed of neurofibrillary tangles and senile plaques corresponding to Braak stages II and A, respectively.
We thought the multiple cortical microinfarcts occurred due to chronic hypoperfusion associated with CAA-associated vasculopathies of capillaries in the cerebral cortex. We suspected that the dementia was influenced by the CAA with multiple cortical microinfarcts. Pathologic findings of the patient suggest that CAA without AD-related Aβ-deposition might exist and that capillary Aβ-deposition might be an important factor of hemodynamic perturbation.
Full Text of this Article in Japanese PDF (754K)

(CLINICA NEUROL, 50: 651−655, 2010)
key words: cerebral amyloid angiopathy, cortical microinfarct, dementia, psychiatric symptom, watershed zone

(Received: 4-Mar-10)