Brain metastasis from invasive thymoma mimicking intracerebral hemorrhage: case report.

A 55-year-old man with an 8-year history of invasive thymoma presented with sudden onset of left hemiparesis. Computed tomography (CT) and magnetic resonance (MR) imaging showed a right frontal lobe intracerebral hemorrhage and the possibility of brain metastasis could not be rejected. The patient underwent removal of the hematoma. Histological examination showed brain metastasis from invasive thymoma. To the best of our knowledge, this is the first reported case of hemorrhagic brain metastasis from invasive thymoma (non-cancerous) mimicking intracerebral hemorrhage.

Expression of the TGF-ß-ALK-1 pathway in dura and the outer membrane of chronic subdural hematomas.

Neovascularization of the outer membrane plays a critical role in the development and enlargement of chronic subdural hematomas (CSHs) and vascular endothelial growth factor (VEGF) may promote their progression. However, the precise mechanisms remain to be determined. We focused on the signaling pathway upstream of VEGF, transforming growth factor ß (TGF-ß), and activin receptor-like kinase 1 (ALK-1) to identify the mechanisms underlying the neovascularization of the outer membrane of CSH. Retrospective comparative study was conducted on 15 consecutive patients diagnosed as CSH with burr-hole drainage. Dura and the outer membrane were collected. We immunohistochemically examined the expression of VEGF, integrin-α, TGF-ß, and ALK-1 on the outer membrane and dura of CSH and compared our findings with control samples and the signal intensity of hematomas on computed tomography (CT) scans. VEGF and integrin-α expression was markedly up-regulated in both the dura and outer membrane of CSH, the expression of TGF-ß and ALK-1 in the dura was slightly increased in the dura and markedly up-regulated in the outer membrane. There was no significant correlation between their expression and CT density. Here we first report the expression of TGF-ß and ALK-1 in the outer membrane and dura mater of CSH. We suggest that the TGF-ß-ALK-1 pathway and VEGF affect neovascularization and the progression of CSH.

Subarachnoid hemorrhage after an ischemic attack due to a bacterial middle cerebral artery dissecting aneurysm: case report and literature review.

A 78-year-old woman suffered sudden-onset left hemiparesis. There were no remarkable infectious findings. Computed tomography (CT) demonstrated a low-intensity area supplied by the right middle cerebral artery (MCA). The diagnosis was cerebral ischemia and she was conservatively treated with hyperosmotic fluids. Two days after the ischemic stroke she suddenly became comatose. CT showed diffuse subarachnoid hemorrhage (SAH) in the basal cistern associated with a right intra-Sylvian and a right frontal subcortical hematoma. Three-dimensional (3D)-CT angiography demonstrated occlusion of the M2 portion of the right MCA. Four days after the ischemic onset she died of brain herniation. Autopsy revealed arterial dissection in the intermediate membrane of the right MCA bifurcation and occlusion of the M2 portion of the thrombosed right MCA. Gram staining showed remarkable bacterial infection in the thrombus. SAH after an ischemic attack due to MCA dissection is extremely rare. We suspect that bacterial infection was involved in the formation of her fragile dissecting aneurysm.

[An operated case of a meningioma causing acute subdural hematoma].

We report a rare case of a meningioma causing acute hematoma. A 67-year-old woman presented with sudden headache. No evidence of trauma was seen. CT demonstrated a subdural hematoma in the convexity of the fronto-temporal lobe. Magnetic resonance imaging showed marked signal heterogeneity in the convexity of the frontal lobe. One week later, the patient underwent hematoma evacuation and tumor resection including the attached dura mater. The histological diagnosis was meningothelial meningioma. The clot was connected directly to the tumor and the origin of the subdural hematoma was identified as the meningioma. Postoperative course was uneventful, and the headache improved. Meningiomas have a relatively benign course but rarely present with hemorrhage. Surgical exploration is the effective and recommended treatment.

Lung squamous cell carcinoma arising in a patient with adult-onset recurrent respiratory papillomatosis.

A 75-year-old male was admitted to our hospital in December 2011 with a mass in the right upper pulmonary lobe. He was incidentally diagnosed as having tracheal papillomas 10 years ago. Bronchoscopy revealed multiple polypoid papillomas in the dorsal lesion of the trachea. Polymerase chain reaction amplification detected human papillomavirus type 11 DNA in the papilloma tissues. A computed tomography scan demonstrated the occlusion of the right superior segment bronchus with distal consolidation. Furthermore, F-18 fluoro-2-deoxy-D-glucose positron emission tomography and computed tomography showed intense tracer uptake in the right superior segment of the lung. He underwent a right upper lobectomy. The tumor was seen as a rounded nodule, ≈ 2 cm in diameter. Histological examination of the tumor revealed squamous papilloma with papillary and solid architecture surrounded by accumulation of acute inflammatory cells. Furthermore, in a part of the tumor, squamous cell carcinoma was also present. The lymph nodes were free of tumor. After the surgery, he continued to undergo endoscopic microwave resection. Recurrent respiratory papillomatosis is a rare disease that can cause life-threatening airway compromise and malignant transformation. The present case indicates that F-18 fluoro-2-deoxy-D-glucose positron emission tomography and computed tomography is indispensable for early detection of lung cancer arising in a patient with recurrent respiratory papillomatosis.

Fatal subarachnoid hemorrhage caused by Aspergillus arteritis without angiographic abnormalities.

No source of bleeding is detected by angiogram in 15-20% of patients with nonaneurysmal subarachnoid hemorrhage (SAH). This negative angiographic finding might suggest a benign prognosis. We describe a case of fatal SAH caused by Aspergillus arteritis without formation of fusiform dilatation or aneurysms. A 76-year-old man with a 2-month history of progressive visual loss due to pachymeningitis around the optic nerves suffered from SAH in the bilateral sylvian fissures. Repetitive serum galactomannan assay and angiography showed no abnormality. Post mortem examination revealed marked proliferation of Aspergillus in the granulomas of the frontal base dura mater. In addition, major trunks and several branches of the bilateral middle cerebral arteries were invaded by Aspergillus hyphae, which destroyed the walls in the absence of dilatation and aneurysms. Invasive aspergillosis of the CNS often forms a mycotic aneurysm. However, four autopsy cases of nonaneurysmal SAH due to invasive aspergillosis have been reported. The present case is the second autopsy case of Aspergillus arteritis without angiographic abnormality, resulting in fatal SAH. Aggressive and continuous antifungal therapy is absolutely necessary in suspected cases of invasive aspergillosis of the CNS, even if angiography is negative and therapeutic markers of aspergillosis are normal.

Myocardial fat at cardiac imaging: how can we differentiate pathologic from physiologic fatty infiltration?

Myocardial fat is often seen at cardiac computed tomography (CT) and magnetic resonance (MR) imaging of healthy adults and patients with myocardial diseases. Physiologic myocardial fat develops with aging and is commonly seen at CT in the anterolateral right ventricular (RV) free wall and RV outflow tract with normal or thickened RV myocardium and a normal-sized RV in elderly patients. Pathologic conditions with myocardial fat include healed myocardial infarction (MI); arrhythmogenic RV cardiomyopathy or dysplasia (ARVC); and others, such as cardiac lipoma, lipomatous hypertrophy of the interatrial septum, tuberous sclerosis complex, dilated cardiomyopathy, and cardiomyopathy with muscular dystrophy. In patients with healed MI, CT and MR imaging show fat in left ventricular myocardium that is of normal thickness or thin and follows the distribution of the coronary artery; CT often depicts fat in mostly subendocardial regions. In patients with ARVC, characteristic CT and MR imaging findings include a thin RV outflow tract and free wall caused by subepicardial fatty infiltration; fat in the RV moderator band, trabeculae, and ventricular septum; and RV enlargement and wall motion abnormality. Recognition of patient age, characteristic locations of myocardial fat, myocardial thickness, and ventricular size helps in differentiating physiologic and pathologic myocardial fat at cardiac imaging; findings of wall motion abnormality and late gadolinium enhancement at MR imaging help narrow the diagnosis.

Primary signet-ring cell carcinoma of the lung: a report of 2 cases.

BACKGROUND: Signet-ring cell carcinoma is a distinct subtype of mucin-producing adenocarcinoma that originates in various organs, particularly the stomach. However, primary signet-ring cell carcinoma of the lung is an extremely rare condition. The preoperative identification of signet-ring cells by cytologic examination is vital because signet-ring cell carcinoma of the lung has been reported to have a worse prognosis than ordinary adenocarcinoma. In this study, we present 2 cases of primary signet-ring cell carcinoma of the lung in conjunction with their cytomorphologic features. CASES: Bronchial brush and wash samples were obtained from the lungs of a 63-year-old woman and a 65-year-old man for the evaluation of lung tumors. Examination of the bronchial samples revealed many large clusters of atypical cells containing abundant intracytoplasmic mucin. Although the clusters were equivocal in the first case, the presence of more atypical cell clusters led to the diagnosis of adenocarcinoma. CONCLUSION: Signet-ring cell carcinoma should be considered when many atypical round cells with abundant intracytoplasmic mucin--namely, signet-ring cells--are observed along with adenocarcinomatous cells.

Detection of lymphatic invasion in resected cases of primary pancreatic cancer based on immunohistochemistry of D2-40.

We investigated the presence of lymphatic invasion detected by D2-40 immunostaining compared to conventional hematoxylin-eosin (HE) staining in primary pancreatic cancer. We also compared the alkaline phosphatase-fast red detection method with the 3,3'-diaminobenzidine (DAB) detection method. We reviewed 25 cases of pancreatic cancer with lymph node (LN) metastases and 15 cases without LN metastases and evaluated the detection rate of lymphatic invasion by HE stain slide alone and D2-40 immunostains. Regarding the cases with positive LN metastasis, 4 (16%) of the 25 cases showed lymphatic invasion by HE slide alone, whereas 7 cases (28%) demonstrated positive lymphatic invasion by D2-40 immunostain. On the other hand, even in cases with negative LN metastasis, 3 of the 15 cases revealed lymphatic invasion by D2-40 immunostaining. Lymphatic invasion was easily detected by alkaline phosphatase-fast red technique, especially at the lower magnification. Regarding the location of lymphatic invasion, it was recognized not only at the peripheral portion but also in the central part of the tumors by D2-40 immunostains; this was difficult to identify by HE stain slide alone. Our study indicates that lymphatic invasion may be overlooked when only HE stain slides are used. In addition, the alkaline phosphatase-fast red detection method (vivid red color) is a distinctive advantage compared with the DAB detection method (brown color), especially in detecting lymphatic invasion at the lower magnification.

Extranodular background liver parenchyma of focal nodular hyperplasia: histopathological characteristics.

Focal nodular hyperplasia (FNH) of the liver is considered to develop as a hyperplastic response to a preexisting vascular abnormality. From the pathogenic point of view, we studied histological alterations in the extranodular background liver tissue of FNH (FNH-bg-liver). We compared ten FNH-bg-livers with ten non-FNH cases (non-FNH-liver) and found small uniform nodule formations with ring-like siderosis in the FNH-bg-livers (4/7, 57%) but not in the non-FNH-livers. Abnormal small arteries not accompanied by portal tracts were observed in six of six FNH-bg-livers for which immunohistochemical study was available, while this was observed in only three of the ten non-FNH-livers. CD34-positive sinusoids around the portal tracts were observed in only the FNH-bg-livers (3/6, 50%). Further, two of ten FNH-bg-livers had ectopic pancreatic tissue. Ring-like siderosis, abnormal small arteries, CD34-positive sinusoids, and ectopic pancreatic tissue were characteristic in the extranodular background liver tissue in cases of FNH.

Lymphoglandular bodies in malignant tumors: with special reference to histologic specimens.

Lymphoglandular bodies (LGBs) have been described as cytoplasmic fragments of lymphocytes and a specific feature of organized lymphoid tissue. The recognition of LGBs is useful in distinguishing malignant lymphomas from carcinomas and sarcomas in cytology specimens, especially in Giemsa-stained tissues. So far, there has been no description of LGBs in hematoxylin and eosin (HE)-stained histologic specimens in the literature. Therefore, we evaluated LGBs in HE sections, especially regarding malignant tumors. We reviewed 110 biopsy and surgical materials including malignant lymphoma, carcinoma, and other malignant tumors and evaluated the frequency, number, size, and significance of LGBs. We also performed the terminal deoxyribosyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) method on LGBs. Lymphoglandular bodies were found in about 40% of cases with malignant lymphoma, whereas only 3 (3.8%) nonlymphoma cases showed LGBs. These were undifferentiated carcinoma, seminoma, and multiple myeloma. The size of LGBs was usually less than half the size of a red blood cell. No apoptotic cells were detected in any of the cases by TUNEL method regarding LGBs. Our study suggests that LGBs can be found in HE sections. As observed in cytologic specimens in the literature, the presence of LGBs around cytologically malignant cells favors a diagnosis of malignant lymphoma rather than nonlymphoma malignancies, even in HE histologic sections.

[A case of subacute necrotizing lymphadenitis with recurrent aseptic meningitis 11 years after the first episode].

We report a 29-year-old man with subacute necrotizing lymphadenitis (SNL) associated with recurrent aseptic meningitis following an 11-year remission period. In both episodes, headache and fever were followed by lymphadenopathy, with increased serum IgE level. Although pleocytosis in cerebrospinal fluid was confirmed at admission in the first episode, it appeared at one week after admission in the second episode. Administration of glucocorticoid was effective for treating meningitis. The present case suggests a pathomechanism for SNL that involves both an immunological background and an acute viral infection as triggers of exacerbation of aseptic meningitis.

Multinucleated astrocytes in old demyelinated plaques in a patient with multiple sclerosis.

A 51-year-old woman with MS of 26 years duration is reported. The patient's MS history began at the age of 25 years with an initial relapsing-remitting course, followed by slow progression without distinct relapses. She became bed-ridden at the age of 40 years. A post-mortem examination revealed numerous demyelinated plaques that exhibited fibrillary gliosis with Rosenthal fibers, but without lymphocytic cuffing or foamy macrophages. Activated microglia were found mainly in the marginal portion of the plaques. These plaques were consistent with so-called 'slowly expanding plaques'. Interestingly, multinucleated astrocytes were observed within the plaques, being more numerous in the area where microglial infiltration had occurred. These findings suggest that mild persistent inflammatory processes are present even in old plaques and that certain inflammatory stimuli cause multinucleation of astrocytes. This might explain the gradual deterioration without definite relapses observed in the late stage of MS.

Hydranencephaly with extensive periventricular necrosis and numerous ectopic glioneuronal nests.

The case reported here relates to a male infant with hydranencephaly who was born at 37 weeks of gestation and died immediately after birth. Post-mortem examination revealed that the cerebral hemispheres had been replaced by fluid-filled cavities within a normal-sized cranium. The membranous hemispheric wall was composed of gliosed tissue with multiple foci of necrosis and hemosiderin-laden macrophages. The ependyma was absent. Many necrotic foci containing hemosiderin were also found around the aqueduct and fourth ventricle. These findings suggest that hemorrhagic necrosis had occurred throughout the periventricular region, and more severely in the cerebral hemispheres. Moreover, numerous glioneuronal nests were found throughout the subarachnoid space and ventricles. Glioneuronal nests, if present, are usually minimal in hydranencephaly, whereas it is one of the pathological features of multicystic encephalopathy. The transition of multicystic encephalopathy to hydranencephaly has been demonstrated repeatedly. The former is a condition resulting from a severe circulatory disturbance, most often at the end of gestation or in the perinatal period. These lesions date later than hydranencephaly. Considering that numerous glioneuronal nests were found in the present case, it is likely that the encephaloclastic process developed toward the end of gestation.

Change in the postmortem formation of hypostasis in skin preparations 100 micrometers thick.

Twenty-three paired skin samples from 19 autopsies without putrefaction were taken from areas of livor mortis that (1). did not blanch with finger pressure and (2). blanched with strong pressure by tweezers. Three-dimensional microscopic viewing of 100-microm benzidine-stained skin sections demonstrated small blood vessels filled with red blood cells. The diameters of the clumps of red blood cells were greater in the sections from non-blanched areas than in the blanched areas, suggesting that fixation of hypostasis soon after death depends on sedimentation of intravascular red blood cells and passive dilatation of small vessels rather than on postmortem hemolysis.