ABSTRACT
Prosthetic valve endocarditis (PVE) can cause large cerebral vessel occlusion. Many reports suggested that mechanical thrombectomy (MT) is effective and useful for early diagnosis from the histopathological findings of thrombus. We present the case of a 62-year-old man, with a history of prosthetic aortic valve replacement and pulmonary vein isolation for his atrial fibrillation, who developed a high fever and an acute neurological deficit, with left hemiplegia and speech disorder. He was diagnosed as having an acute right middle cerebral artery embolism and underwent an MT. The embolic source was found to be a PVE vegetation. However, histopathological analysis of the thrombus could not detect the actual diagnosis. Although he was treated for bacterial endocarditis, his blood culture revealed a rare fungal infection with Exophiala dermatitidis not until >3 weeks after admission. Subsequently, a ß-D-glucan assay also indicated elevated levels. Although he underwent an aortic valve replacement on day 36, MRI showed multiple minor embolic strokes till that day. Early diagnosis of fungal endocarditis and detection of the causative pathogen are still challenging, and the disease has a high risk of occurrence of early and repeated embolic stroke. In addition to clinical findings and pathological studies, ß-D-glucan assay might be a good tool for the diagnosis and evaluation of fungal endocarditis.
ABSTRACT
INTRODUCTION: We report a case of embolic stroke with an atypical course after endovascular therapy performed during the subacute stage of progressive stroke, where symptom relapse could not be controlled despite medical treatment. CASE PRESENTATION: An 81-year-old woman developed slight weakness in her left leg and was hospitalized three days after the onset of symptoms. On admission, her consciousness was almost clear and she exhibited left hemiparesis. The computed tomography(CT)and magnetic resonance imaging(MRI)revealed a cerebral infarction in the right caudate head and corona radiata, and CT perfusion showed no difference in the cerebral blood flow. However, three-dimensional computed tomography angiography showed right M1 occlusion. Considering the clinical course of the leg weakness without atrial fibrillation, antiplatelet therapy for atherosclerotic cerebral infarction was administered. Five days after the symptom onset, the left hemiparesis deteriorated. CT and diffusion-weighted MRI showed increasing edema associated with the cerebral infarction, and CTP showed decreased cerebral blood flow in the right middle cerebral artery region. Because angiography revealed an obstruction involving a long lesion with loss of contrast, we suspected an embolic stroke. Endovascular surgery was performed successfully using the Penumbra system. Postoperatively, the hemiparesis resolved and the patient was transferred to the rehabilitation hospital. CONCLUSION: In rare cases, patients with an embolic stroke develop gradual progression of symptoms. To differentiate between cardioembolic stroke and atherosclerotic cerebral infarction in such patients, a follow-up examination of the brain blood flow must be performed, especially when there is a change in symptoms. This may provide useful information for intravascular treatment even in the subacute period.
Subject(s)
Atrial Fibrillation , Cerebral Infarction , Intracranial Embolism , Aged, 80 and over , Diffusion Magnetic Resonance Imaging , Female , Humans , ThrombectomyABSTRACT
A 65-year-old man had suffered contusion of the left frontal lobe of the brain with a skull base fracture, pneumocephalus, and cerebrospinal fluid (CSF) leakage. He was treated with ceftriaxone 4 g/day for 14 days, but after 1 month he developed multiple cranial nerve palsies (bilateral III-X). CSF contained increased levels of protein (96 mg/dl) and mononuclear cells (72 cells/mm³), and low glucose levels (40 mg/dl, blood sugar 120 mg/dl), but no malignant cells were detected. Magnetic resonance imaging (MRI) disclosed swelling in multiple cranial nerves with Gd enhancement. Anti-biotic and antifungal therapy remitted the facial, glossopharyngeal, and vagus nerve palsies and reduced the Gd-enhancement lesion, as detected by MRI. However, the eyes were bilaterally dilated and medially fixed, and hearing impairments persisted. After 3 months, follow-up MRIs revealed the presence of Gd-enhanced small masses at the ventral pontine base, medulla, and cervicomedullary junctions despite a lack of change in neurological symptoms. Those lesions subsided favorably upon treatment with intravenous and oral corticosteroids. After 1 year and 9 months, Gd-enhanced small cystic masses appeared on the medulla and cerebellum. An open biopsy of the cerebellar tonsillar lesions revealed diffuse large B cell lymphoma. Although the development of primary central nervous system lymphoma after open head injury and infection has not been reported to date, central nervous system lymphomas may mimic diverse neurological diseases. Brain biopsy remains the only definitive diagnosis, and thus should be pursued if blood and CSF markers appear normal.
