Angiomatous meningioma associated with rapidly aggravated peritumoral leptomeningitis: A case report.

Background: A special type of meningioma is known to have infiltrated inflammatory cells within the tumor, associated with peritumoral inflammation. However, there have been no reports of meningioma with inflammatory response only around the tumor, without inflammatory cells within the tumor itself. Case Description: A 70-year-old woman presented with transient right hemiparesis due to an extra-axial tumor on the left frontal convexity. The tumor appeared hypointense on T1-weighted magnetic resonance images and hyperintense on T2-weighted images without peritumoral edema, and was homogenously enhanced associated with the peritumoral leptomeningeal enhancement. Cerebrospinal fluid examination showed an increase in the number of inflammatory cells with a predominance of mononuclear cells. During the following 1 month, the tumor size was unchanged, but the peritumoral leptomeningeal enhancement was remarkably enlarged with uncontrolled focal seizures. The tumor was subtotally removed and semisolid substances in the subarachnoid space were biopsied. Pathological examination with immunostaining revealed angiomatous meningioma: the tumor had no inflammatory cell infiltration within it, but was associated with the infiltration of immunoglobulin G4-negative lymphocytes into the border zone between the tumor and the dura mater, as well as numerous neutrophils and fibrinous exudates in the peritumoral subarachnoid space. The tumor removal rapidly improved the leptomeningeal enhancement and inflammatory reactions. Conclusion: The authors reported the first case of angiomatous meningioma associated with massive peritumoral inflammation without inflammatory infiltrates within the tumor itself.

Advantages of Extradural Anterior Clinoidectomy and Extradural Approach with Dural Incision for Blood Blister Aneurysm or Pseudoaneurysm in the Internal Carotid Artery: Two Case Reports.

Blood blister aneurysms (BBAs) or pseudoaneurysms (PAs) in the internal carotid artery (ICA) have fragile necks; therefore, conventional neck clipping is difficult. The standard treatment for BBAs or PAs is trapping with high or low flow bypass. However, there is no consensus on whether or not anterior clinoidectomy should be performed together. Two patients with ruptured ICA PA (anterior protrusion) or BBA (posterior protrusion) were presented to our hospital. Complete trapping was safely performed for both types of aneurysms via extradural anterior clinoidectomy and the extradural approach with dural incision. The advantages of the procedure are 1) safe proximal clipping, 2) early identification of the ICA C3 portion, 3) minimized frontal lobe retraction, 4) optic canal opening to allow mobility of the optic nerve, and 5) dural ring incision to allow mobility of the ICA.

Endovascular therapy for cardiocerebral infarction associated with atrial fibrillation: A case report and literature review.

Background: Cardiocerebral infarction (CCI) is a rare entity that refers to the simultaneous occurrence of acute myocardial infarction and acute ischemic stroke. The management of CCI patients remains unclear. Case Description: An 86-year-old woman with a medical history of paroxysmal atrial fibrillation presented with a sudden onset of consciousness disturbance and right hemiplegia. Computed tomography of the head revealed no intracranial hemorrhage but the left hyperdense middle cerebral artery sign, associated with ST-segment elevation in II, III, and aVF noted on a routine 12-lead electrocardiogram at admission. The patient was immediately brought to the catheterization laboratory and percutaneous coronary intervention (PCI) was performed first, followed by mechanical thrombectomy, resulting in successful revascularization of the both diseases. Conclusion: Although the treatment strategy of CCI may depend on the condition of coronary and cerebral ischemia, it may be appropriate to prioritize coronary angiography and PCI if not acute ischemic stroke is critical.

A case of traumatic acute interhemispheric subdural hematoma due to injured dural branch of anterior cerebral artery.

Background: The precise causes of traumatic acute interhemispheric subdural hematoma (AISDH) are unclear in most cases, and there are few cases, where the sources of bleeding are directly confirmed intraoperatively. We report a rare case of traumatic AISDH, in which a damaged dural branch of anterior cerebral artery (ACA) to the cerebral falx was identified as the cause of bleeding during hematoma removal. Case Description: A 61-year-old man with a history of craniotomy for the left putaminal hemorrhage at the age of 50 fell from a bed, bruised his head, and lost consciousness. Computed tomography of the head showed AISDH of 2.5cm in thickness, which was removed through a parietal parasagittal craniotomy under the microscope. Intraoperatively, the bleeding source was revealed to be a damaged dural branch from ACA to the cerebral falx. There was no rebleeding during his stay in our hospital. Conclusion: In this case, intraoperative findings revealed that the cause of bleeding was a damage to the dural branch of ACA. A vascular study is mandatory to rule out a vascular malformation in similar cases.

Contrast extravasation from basilar artery without aneurysm formation on digital subtraction angiography in computed tomography angiogram-negative subarachnoid hemorrhage: A case report.

BACKGROUND: The causes of angiogram-negative subarachnoid hemorrhage (SAH) on initial angiography, which accounts for 10-30% of spontaneous SAH, are heterogeneous and still unclear. We report a case of nonaneurysmal SAH, in which initial computed tomographic angiography (CTA) showed no source of bleeding, but the subsequent digital subtraction angiography (DSA) revealed contrast extravasation from the basilar artery without aneurysms. CASE DESCRIPTION: A 67-year-old woman with a medical history of hypertension presented as SAH of World Federation of Neurological Surgeons Grade II. CTA on admission did not show any cause of bleeding and DSA was subsequently performed to show contrast extravasation from a perforator of the middle third of the basilar artery without aneurysms during the subsequent DSA, resulting in profound deterioration SAH and neurological status. The patient was conservatively treated. Follow-up DSAs on days 2 and 16 showed no source of bleeding as well. CONCLUSION: Although the precise cause of bleeding in this case is uncertain, SAH might be caused by local dissection of the basilar artery perforator, and the bleeding site might heal spontaneously without forming of a pseudoaneurysm.

Chronological analysis of caloric restriction-induced alteration of fatty acid biosynthesis in white adipose tissue of rats.

The beneficial actions of caloric restriction (CR) could be mediated in part by metabolic remodeling of white adipose tissue (WAT). Recently, we suggested that CR for 6 months increased the expressions of proteins involved in de novo fatty acid (FA) biosynthesis in WAT of 9-month-old rats. Herein, we compared the CR-induced chronological alterations of the expression of mRNAs and/or proteins involved in FA biosynthesis in the WAT and liver of rats subjected to CR starting from 3 months of age and their age-matched controls fed ad libitum. The findings suggested that CR was more effective on FA biosynthesis in WAT than in liver. In WAT, CR markedly increased the expressions of mRNAs and/or proteins involved in FA biosynthesis, including sterol regulatory element-binding protein 1c (SREBP1c), a master transcriptional regulator of FA biosynthesis, throughout the experimental period. Interestingly, the CR-enhanced upregulation was temporally attenuated at 5 months of age. CR markedly increased the nuclear phosphorylated form of Akt only at 3.5 months of age. In contrast, CR significantly reduced the expression of leptin at 9 months of age. The CR-induced upregulation was not observed in obese fa/fa Zucker rats homozygous for nonfunctional leptin receptor. Collectively, these data indicate that the V-shaped chronological alterations in WAT are regulated via SREBP1c, which is probably activated by CR duration-dependent modulation of both insulin and leptin signaling.

Bcl-2 homology domain 3-only proteins Puma and Bim mediate the vulnerability of CA1 hippocampal neurons to proteasome inhibition in vivo.

Bcl-2 homology domain 3 (BH3)-only proteins are pro-apoptotic Bcl-2 family members that play important roles in upstream cell death signalling during apoptosis. Proteasomal stress has been shown to contribute to the pathology of cerebral ischaemia and many neurodegenerative disorders. Here we explored the contribution of BH3-only proteins in mediating proteasome-inhibition-induced apoptosis in the murine brain in vivo. Stereotactic intrahippocampal microinjection of the selective proteasome inhibitor epoxomicin (2.5 nmol) induced a delayed apoptosis within only the CA1 hippocampal neurons and not neurons within the CA3 or dentate gyrus regions, a selective vulnerability similar to that seen during ischaemia. This injury developed over a time-course of 3 days and was characterized by positive terminal deoxynucleotidyl transferase dUTP nick end labelling staining and nuclear condensation. Previous work from our laboratory has identified the BH3-only protein p53-upregulated mediator of apoptosis (Puma) as mediating proteasome-inhibition-induced apoptosis in cultured neural cells. Genetic deletion of puma reduced the number of terminal deoxynucleotidyl transferase dUTP nick end labelling-positive cells within the CA1 following epoxomicin microinjection but it did not provide a complete protection. Subsequent studies identified the BH3-only protein Bim as also being upregulated during proteasome inhibition in organotypic hippocampal slice cultures and after epoxomicin treatment in vivo. Interestingly, the genetic deletion of bim also afforded significant neuroprotection, although this protection was less pronounced. In summary, we demonstrate that the BH3-only proteins Puma and Bim mediate the delayed apoptosis of CA1 hippocampal neurons induced by proteasome inhibition in vivo, and that either BH3-only protein can only partly compensate for the deficiency of the other.

Complete recovery from aneurysmal subarachnoid hemorrhage associated with out-of-hospital cardiopulmonary arrest.

Out-of-hospital cardiopulmonary arrest (OHCPA) because of aneurysmal subarachnoid hemorrhage (SAH) is almost always fatal, because devastating SAH causes OHCPA and the brain damage is aggravated by OHCPA. We report a rare case of a 63-year-old female patient who survived SAH-induced ventricular fibrillation OHCPA without neurologic sequelae. Early brain computed tomography scans were needed for the diagnosis, as most of SAH seemingly disappeared within 7 h after the onset and was associated with acute coronary syndrome-like findings. This case shows that even less severe SAH can cause ventricular fibrillation OHCPA and takotsubo cardiomyopathy, and that early diagnosis and appropriate treatment following immediate, successful resuscitation may lead to a surprisingly favorable outcome.

Tenascin-C is a useful marker for disease activity in myocarditis.

Tenascin-C (TNC) is an extracellular matrix protein which appears at active sites of tissue remodelling during embryogenesis or cancer invasion. In normal heart, TNC is only present during the early stages of development but reappears in pathological states. This study examined the diagnostic value of TNC for assessing disease activity of myocarditis. Expression of TNC was examined in myosin-induced autoimmune myocarditis mouse models. Sequential changes in amount, localization and the producing cells were analysed by reverse transcriptase-polymerase chain reaction, western blotting, immunohistochemistry and in situ hybridization and compared with the histological picture. The expression of TNC was upregulated at a very early stage of myocarditis. Immunostaining was detectable before cell infiltration and myocytolysis became histologically apparent, remained during the active stage while cell infiltration and necrosis continued, and disappeared in scar tissue with healing. TNC immunostaining was always observed at the periphery of necrotic or degenerating cardiomyocytes in foci of inflammation, the expression level correlating with histological evidence of inflammatory activity. Interstitial fibroblasts were the major source of TNC, expressing the large isoform containing alternative splicing sites. These data demonstrate that TNC is a useful marker for evaluation of disease activity in myocarditis.