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Background: Guillain-Barré syndrome (GBS) is a polyradiculoneuropathy mediated by the immune system and is the primary reason for acute flaccid paralysis. Intravenous immunoglobulin (IVIg) is a recognized immunotherapeutic drug that can accelerate recovery from GBS. Limited literature exists concerning cerebral infarction complications with IVIg following its use in the treatment of GBS. Case presentation: A patient was diagnosed with the acute inflammatory demyelinating polyradiculoneuropathy subtype of GBS, while another patient was diagnosed with the acute bulbar palsy variant of GBS 2 years prior and experienced a relapse of GBS. Both patients received immunoglobulin therapy, during which multiple acute cerebral infarctions were detected using magnetic resonance imaging. Both patients had a history of coronary artery atherosclerotic heart disease and vertebral artery stenosis, and D-dimer and fibrinogen degradation products were significantly elevated after immunoglobulin therapy. Conclusions: The risk of cerebral infarction associated with IVIg is generally low in patients with different GBS variants. Nevertheless, the occurrence of cerebral infarction associated with IVIg might not be insignificant in older patients with vascular risk factors and should be carefully monitored.

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BACKGROUND: Idiopathic nephrotic syndrome (NS) presents as a hypercoagulable state, of which thromboembolism (TE) is a well-known life-threatening complication. Although TE is more likely to occur in venous vessels than arterial vessels, arterial TE is important because it may cause after-effects, including tissue necrosis and cerebral infarction (CI); therefore, prompt diagnosis and appropriate treatment are required. We report a pediatric NS case with multiple CIs. CASE PRESENTATION: A 14-year-7-month-old Japanese girl was diagnosed with frequent relapsing NS, accompanied by headache and disturbance of consciousness during the second relapse. Brain magnetic resonance imaging (MRI) and four-dimensional computed tomography revealed multiple CIs, vasogenic edema, and cerebral venous sinus thrombosis (CVST). The patient had no underlying thrombophilia other than hypercoagulability due to NS and prednisolone (PSL), and no cardiac arrhythmia; however, a right-to-left shunt through the patent foramen ovale (PFO) was observed with the Valsalva maneuver by echocardiography. Therefore, we assumed that a potential cause of multiple CIs might be an embolic stroke, caused by thrombosis formed from a hypercoagulable state due to NS and PSL treatment and reached through PFO. Antiplatelet and anticoagulant therapies were administered for TE. She was treated with PSL and mycophenolate mofetil (MMF) for NS. Rituximab (RTX) was administered to prevent NS relapse after complete remission (CR). She underwent transcatheter PFO closure at age 14 years and 9 months because we considered that the right-to-left shunt through the PFO would be one of the risks for recurrent cerebral embolism when NS relapses. One year after the onset of CIs, an MRI indicated that the CVST had resolved, leaving no neurological sequelae due to CI; therefore, anticoagulant therapy was discontinued. And then she has been in CR for NS with only MMF therapy. CONCLUSIONS: CI is a serious complication in patients with NS. The pathogenesis of multiple CIs is various, including right-to-left shunt through PFO, in addition to the hypercoagulability due to NS. It is important to investigate and manage underlying risks such as PFO, besides preventing the relapses of NS by aggressive treatments using MMF and RTX, in patients with NS.

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BACKGROUND: Cerebrovascular diseases in cancer patients significantly aggravate their condition and prognosis; therefore, prompt and accurate diagnosis and treatment are important. The purpose of this study was to investigate patient demographics, laboratory data, brain magnetic resonance imaging (MRI) findings, and prognosis among patients with stroke and cancer, especially cancer-associated ischemic stroke (CAIS). METHODS: We performed a retrospective, single-center study. We enrolled consecutive patients who had acute stroke and were admitted to our hospital between January 2011 and December 2021. We collected general demographic characteristics, cancer histopathological type, laboratory data, brain MRI findings, and prognosis data. RESULTS: Among 2040 patients with acute stroke, a total of 160 patients (7.8%) had active cancer. The types of strokes were cerebral infarction, cerebral hemorrhage, subarachnoid hemorrhage, and transient ischemic attack in 124, 25, 5, and 6 patients, respectively. Among the patients with ischemic stroke, there were 69 cases of CAIS. Pancreas and adenocarcinoma were the most frequent types of primary tumor and histopathology. Patients with adenocarcinoma and those with cerebral infarctions in both bilateral anterior and posterior cerebral circulation areas showed higher D-dimer levels. Pancreatic cancer and high plasma D-dimer levels were associated with poor survival rate. CONCLUSION: CAIS was seen more frequently in patients with pancreatic cancer and adenocarcinoma. Pancreatic cancer and high plasma D-dimer levels were potential factors of poor prognosis in patients with CAIS.

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BACKGROUND AND OBJECTIVE: Traditional disease diagnosis is usually performed by experienced physicians, but misdiagnosis or missed diagnosis still exists. Exploring the relationship between changes in the corpus callosum and multiple brain infarcts requires extracting corpus callosum features from brain image data, which requires addressing three key issues. (1) automation, (2) completeness, and (3) accuracy. Residual learning can facilitate network training, Bi-Directional Convolutional LSTM (BDC-LSTM) can exploit interlayer spatial dependencies, and HDC can expand the receptive domain without losing resolution. METHODS: In this paper, we propose a segmentation method by combining BDC-LSTM and U-Net to segment the corpus callosum from multiple angles of brain images based on computed tomography (CT) and magnetic resonance imaging (MRI) in which two types of sequence, namely T2-weighted imaging as well as the Fluid Attenuated Inversion Recovery (Flair), were utilized. The two-dimensional slice sequences are segmented in the cross-sectional plane, and the segmentation results are combined to obtain the final results. Encoding, BDC- LSTM, and decoding include convolutional neural networks. The coding part uses asymmetric convolutional layers of different sizes and dilated convolutions to get multi-slice information and extend the convolutional layers' perceptual field. RESULTS: This paper uses BDC-LSTM between the encoding and decoding parts of the algorithm. On the image segmentation of the brain in multiple cerebral infarcts dataset, accuracy rates of 0.876, 0.881, 0.887, and 0.912 were attained for the intersection of union (IOU), dice similarity coefficient (DS), sensitivity (SE), and predictive positivity value (PPV). The experimental findings demonstrate that the algorithm outperforms its rivals in accuracy. CONCLUSION: This paper obtained segmentation results for three images using three models, ConvLSTM, Pyramid-LSTM, and BDC-LSTM, and compared them to verify that BDC-LSTM is the best method to perform the segmentation task for faster and more accurate detection of 3D medical images. We improve the convolutional neural network segmentation method to obtain medical images with high segmentation accuracy by solving the over-segmentation problem.

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The patient is a 73-year-old woman. She presented with dysarthria, and a head MRI revealed multiple acute cerebral infarctions in the bilateral cerebral hemisphere and cerebellar hemisphere. Transesophageal echocardiography after admission revealed a 16 mm large mobile calcification of the mitral annulus (caseous calcification of the mitral annulus; CCMA) on the posterior apex of the mitral valve annulus. Since the CCMA had a high risk of relapse, and a new infarction was detected on the 8th day, resection of the mass and mitral valve replacement surgery were performed. CCMA is a subtype of mitral annular calcification (MAC). When calcification progresses from the MAC state to form a mass, it is called a calcified amorphous tumor; CAT. Reports of embolic cerebral infarction caused by CAT are rare, but this is a rare report of an embolic cerebral infarction from CCMA presenting as CAT.

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OBJECTIVES: To investigate the patient demographics, survival after diagnosis, and prognostic factors among patients with multiple-territory cerebral infarctions due to cancer-associated ischemic stroke (multiple CAIS). MATERIALS AND METHODS: We performed a retrospective review of the medical records from a 10-year period of consecutive patients with multiple CAIS, defined as (1) newly developed multiple cerebral infarctions involving two or more cerebrovascular territories, (2) association with active cancer diagnosed or treated <6 months before or after stroke, and (3) exclusion of obvious etiologies other than cancer-associated coagulopathy in routine screening. We extracted demographic features, stroke severity and characteristics, cancer characteristics, comorbidities, and laboratory data. Univariable Cox proportional hazards regression was used to idenify the prognostic factors. RESULTS: The median age was 74 years (interquartile range, 68.3-80.5), and the median survival after diagnosis was 44.5 (27.3-76.8) days in 26 patients with complete follow-up. The median National Institutes of Health Stroke Scale was 5.5 (2.0-9.0). Twenty (76.9%) patients had received a cancer diagnosis prior to the diagnosis of multiple CAIS, and most patients (25 patients, 96.2%) had stage IV cancer. Univariate analysis showed that high serum albumin (hazard ratio, 0.31; 95% confidence interval, 0.11-0.88) was significantly associated with prolonged survival, whereas stroke severity and comorbidities were not associated with survival. CONCLUSION: Multiple CAIS predominantly occurred in elderly patients with advanced cancer, and their survival was short. Serum albumin levels were significantly associated with prognosis, indicating the poor general condition associated with cancers may affect prognosis.

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BACKGROUND: Calcified amorphous tumor (CAT) of the heart is a rare non-neoplastic intracardiac mass, a calcium deposition surrounded by amorphous fibrous tissue, and possibly causes cerebral embolism. Even rarer is CAT associated with infection, and no CAT with antecedent infection has been reported to our knowledge. In addition, although some CAT in patients on hemodialysis has been reported to grow rapidly, no case has been reported on CAT that grew and diminished rapidly in a short period of time. Here, we report the case of an 82-year-old Japanese woman with normal renal function who developed multiple cerebral infarctions due to CAT that grew rapidly, associated with inflammation from an antecedent infection, and diminished rapidly by detachment of fibrin on the mass surface and antithrombotic drugs. CASE PRESENTATION: The patient developed fever after dental treatment and found musical hallucination on the left ear worsened in degree and frequency. In a nearby clinic, she was treated with antibiotics, and her body temperature turned to normal in approximately 1 month. She presented to our hospital for workup on the worsened musical hallucination. Magnetic resonance imaging (MRI) showed multiple cerebral infarctions, and transthoracic echocardiography (TTE) revealed an immobile hyperechoic mass with an acoustic shadow arising from a posterior cusp of the mitral valve. CAT was suspected and treated with apixaban and aspirin. Follow-up MRI and TTE showed newly developed multiple cerebral infarctions and rapidly diminished CAT. Cardiac surgery was performed to resect the CAT. The pathological findings showed calcifications surrounded by amorphous fibrous tissue including fibrin, indicating CAT. The patient's symptoms improved and no cerebral infarctions recurred in 4 months follow-up. CONCLUSION: Inflammation from an antecedent infection can cause CAT to grow rapidly. Fibrous tissue including fibrin may attach to the surface of CAT, resulting in multiple cerebral infarctions. Fibrous tissue may detach and disappear by antithrombotic drugs, leading to a rapid diminishment of CAT in size.

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BACKGROUND: Heat-related illnesses include symptoms such as heat syncope/cramps, heat exhaustion, and life-threatening heat stroke. Usually, a heat stroke causes cerebellar ataxia, cognitive impairment, dysphagia, and aphasia. We report a very rare case of a patient who developed severe heat stroke complicated by multiple cerebral infarctions. CASE PRESENTATION: An 80-year-old Asian woman was found lying unconscious at her house, with no air conditioner and closed windows; the highest outside temperature was 36.1 °C. She was brought to our hospital unconscious with a high bladder temperature (42.5 °C) and disseminated intravascular coagulation (DIC score 4). She was diagnosed with severe heat stroke and managed with rapid cooling, intravenous fluids therapy, antibiotic therapy, and anti-coagulation therapy for DIC. Anti-coagulation therapy consisted of treatment with recombinant thrombomodulin for 4 days (days 1-4) and recombinant antithrombin for 1 day (day 1). A head computed tomography (CT) and magnetic resonance imaging (MRI) examination were performed on day 3, because she was still unconscious. Diffuse-weighted imaging showed high-signal intensities, indicating multiple lesions. An intracranial magnetic resonance angiography showed normal results. Imaging indicated new multiple cerebellar infarctions complicated with DIC. A tracheotomy was performed on day 9 because her conscious condition had not improved. She was transferred to another hospital for subacute care on day 23. CONCLUSIONS: Early management of heat stroke using anti-DIC, anti-bacterial, and fluid resuscitation therapy can help prevent complications such as intracranial hemorrhaging.

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A 60-year-old woman was urgently admitted to our hospital because of vertigo and left hemiplegia. Laboratory examination showed thrombocytopenia, high levels of D-dimer and carcinoembryonic antigen. Brain magnetic resonance imaging (MRI) revealed multiple bilateral cerebral infarctions. Chest computed tomography (CT) showed an irregularly shaped tumor in the upper lobe of the left lung and mediastinal node swelling. The histopathological findings revealed adenocarcinoma negative for anaplastic lymphoma kinase fusion gene, sensitive epidermal growth factor receptor mutations. A diagnosis of lung adenocarcinoma initially presenting as arterial thromboembolism was made, and she was treated with direct oral anticoagulant (DOAC). Subsequently, pembrolizumab therapy was initiated because tumor cells were positive for programmed cell death protein 1 (PD-L1;60%), and resulted in reduction of the tumor with normalization of the platelet count and d-dimer. The treatment has been continued for over one year without any recurrence of the disease or thromboembolism.

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A 56-year-old man presented to our hospital as he presented progressive hemiplegia of the right upper limb with no other symptoms, including chest pain. Inter-arm blood pressure difference was not observed. Laboratory investigations revealed an elevated D-dimer value (2.4 µg/ml). Chest X-ray study showed normal findings without widened mediastinum. Brain MRI showed acute multiple brain infarcts in the left posterior limb of the internal capsule and right pons on diffusion-weighted imaging. Bilateral internal carotid arteries were non-occlusive in MRA. Carotid duplex ultrasonography revealed normal internal carotid artery flow velocities bilaterally. Because ischemic lesions were found in multiple vascular territories, and D-dimer value was elevated, the patient underwent thoracic contrast-enhanced-CT to exclude malignant tumors. Stanford type A aortic dissection limited to the ascending aorta was detected. As the plaque had accumulated in the false lumen, we suspected that plaque in the false lumen could be an embolic source. After ascending aortic replacement surgery, brain infarction did not recur during hospitalization. In cases of ischemic stroke wherein multiple vascular territories are detected, and D-dimer value is elevated, even in patients without chest pain, the possibility of painless Stanford type A aortic dissection should be ruled out as an embolic source.

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A 76-year-old man, who had undergone surgery for esophageal cancer in 2010, presented to our hospital in April 2017 complaining of prolonged slight fever, loss of appetite, and dysphagia. Initial evaluation revealed a paralyzed left vocal cord, slight muscle weakness of the extremities, left facial paralysis, hoarseness, left sternocleidomastoid and trapezius muscle weakness, tongue deviation to the left, and left hypacusia-suggesting a diagnosis of Garcin's syndrome. Laboratory tests revealed increased white blood cells and C-reactive protein. Cerebrospinal fluid (CSF) analysis showed mild pleocytosis (predominantly polymorphonuclear cells), elevated protein, and low CSF/plasma glucose ratio. CT showed mild clival erosion, with no evidence of carcinoma recurrence. Brain contrast-enhanced MRI showed abnormal clival marrow, enhanced soft tissue and dura matter from the clivus to the atlantoaxial joint, enhanced soft tissue around the left ear canal, multiple cerebral infarctions in the left watershed zones, and left internal carotid stenosis. There was excessive ear wax and inflammation of the left external acoustic meatus but no otorrhea or otalgia. On the basis of his overall presentation, he was diagnosed with atypical skull base osteomyelitis due to external otitis. He was treated with antibiotic treatment that included ceftazidime for the Pseudomonas aeruginosa detected on bacterial cultures. He did not respond to treatment and died approximately 4 months later. Skull base osteomyelitis is thus an important differential diagnosis candidate after finding unilateral, multiple cranial neuropathy, underscoring the importance of prompt treatment when suspected.

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BACKGROUND: Benign gynecologic tumor, such as uterine adenomyosis, has been suggested to develop hypercoagulability. Although some cases of cerebral infarction associated with adenomyosis have been reported, the mechanism of hypercoagulation initiated by adenomyosis is still not clear, and the therapeutic strategy is uncertain. CASE PRESENTATION: A 44-year-old woman was presented to our department with headache, left hand weakness, and gait disturbance during her menstrual phase. She had a history of adenomyosis and infertility treatment for 18 years and heavy menstrual bleeding. Magnetic resonance imaging on admission showed multiple hyperintense lesions in cortical and subcortical areas in the cerebrum and cerebellum on diffusion-weighted imaging. Transesophageal echocardiography showed neither embolic sources nor existence of foramen ovale. Her laboratory data revealed anemia, a high D-dimer level, and elevated levels of a mucinous tumor marker. She had adenomyosis and no malignancy was detected. Anticoagulation therapy with intravenous heparin followed by rivaroxaban did not prevent recurrence of cerebral infarction. We discontinued rivaroxaban, and started warfarin therapy with pseudomenopause treatment, which prevented recurrence for 6 months. Five months after her last pseudomenopause treatment, multiple cerebral infarctions occurred. Total hysterectomy was performed, which prevented recurrence of the multiple cerebral infarctions for 2 years without anticoagulation therapy. CONCLUSIONS: Our findings reveal for the first time that anticoagulation therapy, including novel oral anticoagulants, had no preventive effect against cerebral infarctions associated with adenomyosis in a middle-aged woman. Although pseudomenopause treatment temporarily prevented recurrence, resection of the adenomyosis might be the most effective therapy in these cases.

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The association between thrombosis and cancer has been recognized since Trousseau's report in 1865. We present a case of bladder squamous cell carcinoma associated with multiple cerebral infarctions. This patient was diagnosed as having Trousseau's syndrome and received radiotherapy for bladder cancer treatment, along with anticoagulation therapy.

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A 69-year-old woman had syncope and aphasia. Magnetic resonance imaging showed multiple cerebral infarctions in both hemispheres. Cardiogenic embolisms were suspected, but no arrhythmic causes were shown. Transesophageal echocardiography revealed a highly calcified mitral annulus (MAC) with a rough intraluminal surface and mild mitral regurgitation, but no thrombus or tumor in the left heart system. However, recurrent multiple cerebral embolisms occurred in spite of strict anticoagulation therapy. We speculated that spontaneous rupture of the MAC was the cause of the scattered cerebral embolisms, and we therefore planned to remove the MAC as safely as possible and to endothelialize the deficit of MAC with autologous pericardium. Operative findings revealed that the MAC in P2-P3 had ruptured longitudinally and the ostium of the left atrium was connected to the ostium of the left ventricle as an inter-atrioventricular tunnel beneath the posterior mitral annulus with a fragile calcified wall. The finding suggested that calcified particles that had peeled away from the MAC by normal heart beating resulted in the cerebral infarctions. Therefore, she underwent resection of the MAC and mitral valve replacement with reinforcement of the decalcified posterior mitral annulus between the posterior left ventricular wall and the left atrial wall using autologous pericardium, which enabled both appropriate insertion of a mechanical prosthetic valve and endothelial continuity covering the surface of the residual MAC. No systemic embolism has occurred for two and a half years after surgery. This is the first case report of cerebral embolism caused by a spontaneously ruptured MAC.