ABSTRACT
A seventy-year-old man developed color change in his left toes and was treated for frostbite. Eight months later, he developed cognitive impairment and was admitted to our hospital. A remarkable increase of eosinophils was observed in peripheral blood. Brain MRI revealed abnormal lesions in the fornix, corpus callosum, basal ganglia and frontal lobe. Steroid therapy ameliorated his symptom temporarily, but he suddenly developed cardiopulmonary arrest. His autopsy revealed severe pulmonary hemorrhage with alveolar vasculitis and cholesterol crystals in the brain, kidneys, liver, and the other organs. It was possible that cholesterol embolization to multiple organs including the brain induced systemic vasculitis that caused pulmonary hemorrhage and his critical prognosis. Cholesterol embolization should be considered when we see a patient with brain lesions accompanied with eosinophilia.
Subject(s)
Cognition Disorders/etiology , Embolism, Cholesterol/complications , Hemorrhage/etiology , Lung Diseases/etiology , Aged , Humans , Male , SyndromeABSTRACT
The patient was a 58-year-old man with 1-year history of cognitive decline, which was diagnosed as Alzheimer's disease in another hospital. He was admitted to our hospital for extreme fatigue, weight loss, and dysphagia, subsequent to the left peripheral facial paresis. Brain magnetic resonance (MR) imaging showed bilateral diffuse white matter lesions and hippocampal atrophy. After admission, he presented with sudden high fever, recurrent exacerbations of consciousness, and increased C-reactive protein level with marked neutrophilia, with the result that he underwent mechanical ventilation. Routine cerebrospinal fluid findings at the exacerbation were normal i.e. 4.7 cells/mm(3), 40 mg/dl of protein, but IL-6 concentration was mildly elevated to 22.2 pg/ml. After confirming the positivity of HLA (human leukocyte antigen) B54 and Cw1, we administered steroid to him and his physical activity and state of consciousness significantly improved. During the course of treatment, dermal lesion characterisitic of Sweet disease was absent. We diagnosed this case was possible neuroSweet disease proposed by Hisanaga in 2005.
Subject(s)
Central Nervous System Diseases/diagnosis , Consciousness Disorders/complications , Sweet Syndrome/diagnosis , HLA Antigens/analysis , Humans , Interleukin-6/cerebrospinal fluid , Male , Middle AgedABSTRACT
The patient is a 66-year-old man with hereditary telangiectasia. He was diagnosed with pulmonary arteriovenous malformation (PAVM), which was revealed by contrast-enhanced chest computed tomography at the age of 65. He developed headache, right homonymous hemianopsia, and right hemiparesis and was admitted to our hospital. Contrast-enhanced magnetic resonance imaging revealed multiple lesions in the left hemisphere, which indicates brain abscesses. Thus, the diagnosis of brain abscess mediated through PAVM was established. Following management with drainage and coil embolization, all neurological symptoms resolved. Therefore, coil embolization should be considered for PAVM at an early stage to prevent brain abscess, even if it is asymptomatic.
Subject(s)
Arteriovenous Malformations/complications , Arteriovenous Malformations/therapy , Brain Abscess/etiology , Fusobacterium Infections/etiology , Pulmonary Artery/abnormalities , Pulmonary Veins/abnormalities , Telangiectasia, Hereditary Hemorrhagic/complications , Aged , Anti-Bacterial Agents/administration & dosage , Arteriovenous Fistula , Arteriovenous Malformations/diagnosis , Brain Abscess/diagnosis , Brain Abscess/microbiology , Brain Abscess/therapy , Drainage/methods , Drug Therapy, Combination , Embolization, Therapeutic/methods , Fusobacterium Infections/diagnosis , Fusobacterium Infections/microbiology , Fusobacterium Infections/therapy , Fusobacterium nucleatum/isolation & purification , Humans , Magnetic Resonance Imaging , Male , Treatment OutcomeABSTRACT
We previously demonstrated that the deficiency of class A macrophage scavenger receptor type I/II was involved in the delayed phagocytosis of degraded myelin by macrophages in class A macrophage scavenger receptor type I/II knockout mice after crush injury of the sciatic nerve [Naba et al. (2000) Exp. Neurol., 166, 83-89]. In order to elucidate the role of CD36, one of the scavenger receptors, here we inflicted crush injury to the sciatic nerves of CD36 knockout mice and investigated the remyelination after crush injury in comparison with that of class A macrophage scavenger receptor type I/II knockout mice. Although we previously reported a lot of onion-bulbs in class A macrophage scavenger receptor type I/II knockout mice at 3 weeks, the number of onion-bulbs was limited both in CD36 knockout mice and wild-type mice. In the morphometry, the remyelination was seriously delayed, and the infiltrating macrophages into the nerve fascicles were quite frequent in CD36 knockout mice compared with wild-type mice at 3 and 6 weeks postinjury. The immunohistochemistry with the monoclonal antibody reacted with oxidized phosphatidylcholine and oil red O staining were positive in wild-type mice, but were negative in CD36 knockout mice, suggesting that the oxidation of phosphatidylcholine and the generation of neutral lipids in macrophages were disturbed in CD36 knockout mice. We hypothesize that the delayed phagocytosis by macrophages and the defect in reuse of lipids from degraded myelin are related to seriously delayed remyelination and a small number of onion-bulbs in CD36 knockout mice.