[Selective coil embolization of a distal anterior choroidal artery aneurysm associated with moyamoya disease: a case report].

Intracranial hemorrhage in patients with moyamoya disease is often caused by rupture of the associated aneurysms. Of these aneurysms, distal anterior choroidal artery (AChoA) aneurysms are rare. In patients with moyamoya disease, the AChoA constitutes collateral vessels and the aneurysm requires careful treatment strategy. However, reported cases of distal AChoA aneurysms include various procedures including conservative therapy, direct surgery, and endovascular therapy. Herein, we report a case of coil embolization of a distal AChoA aneurysm associated with moyamoya disease and discuss the treatment strategy. A 39-year-old female presented with severe headache and subsequent deep coma. Computed tomography (CT) revealed thick intraventricular hemorrhage, and three-dimensional CT angiography revealed a right distal AChoA aneurysm. Bilateral ventricular drainage was performed and subsequent ventriculoperitoneal (VP)shunt was performed. The persisting distal AChoA aneurysm was coil embolized without any complication. Rebleeding did not occur during the 1-year follow-up period. Endovascular treatment is effective for distal AChoA aneurysms associated with moyamoya disease to preserve collateral circulation.

Evaluation of recurrence factors and Gorei-san administration for chronic subdural hematoma after percutaneous subdural tapping.

Recent reports have shown that administration of Gorei-san (Tsumura, Tokyo, Japan) can prevent recurrence of chronic subdural hematoma (CSDH). However, no report has shown its potential, including its correlation with other recurrent clinical factors. We retrospectively evaluated the recurrent factors and the effects of Gorei-san on CSDH using percutaneous subdural tapping. Between April 2009 and February 2012, we performed percutaneous subdural tapping on 160 patients with intact CSDH. Of this population, 125 patients with unilateral hematoma and measurable initial hematoma pressure were included in this study. From April 2010, Gorei-san was routinely administered to patients. Patient characteristics such as age, sex, neurological grading, alcohol, diabetes mellitus, antiplatelet agent, anticoagulant agent, trauma, midline shift on CT images, hematoma volume on CT images, initial hematoma pressure, volume of the removed hematoma, and administration of Gorei-san were analyzed. Recurrence was recognized in 35/125 (28.0%) patients. Multivariate analysis revealed that a greater midline shift on CT images (p = 0.033) and initial hematoma pressure (p = 0.031) predicted recurrence. Gorei-san was administered to 94/125 (75.2%) patients, but they showed no changes in recurrence (27.7% vs. 29.0%; p = 1.0). Among 13 patients for whom Gorei-san administration was started before surgery, CSDH recurrence was reported in only 1 (7.7%). However, the group showed a significantly lower number of recurrent factors. Patients with a greater midline shift in their CT images or higher initial hematoma pressure need close postsurgical observation. The potential of Gorei-san for preventing recurrence of CSDH needs further examination.

[Case with intracranial pial arteriovenous fistulas].

A 25-year-old man presented with right hemiparesis and was admitted to the local hospital. CT scan revealed an intracerebral hematoma in the left motor cortex. He was treated conservatively, the hematoma passed without increase and his right hemiparesis improved gradually. The cause of hemorrhage was examined at the local hospital without resolution. He came to our hospital for further examination. Angiography revealed pial arteriovenous fistulas near the hematoma. The fistulas were fed by small branches of the left anterior cerebral artery and drained into an abnormal cortical vein. Left parietal craniotomy was performed. A red dilated cortical vein existed under the thickened, cloudy arachnoid membrane. Retrograde observation of the red vein showed some small branches connected directly to the red vein at the central sulcus. There was no nidus. The color of the red vein changed to blue after disconnection of the fistulas by electrocoagulation. The dilated cortical vein was resected. Postoperative angiography revealed the disappearance of the fistulas. He was discharged without any new neurological deficits. Intracranial pial arteriovenous fistulas are rare cerebrovascular lesions. As symptomatic patients managed conservatively have a poor prognosis, radical treatment should be undertaken as soon as possible.

The transcriptional programme of antibody class switching involves the repressor Bach2.

Activated B cells differentiate to plasma cells to secrete IgM or, after undergoing class switch recombination (CSR), to secrete other classes of immunoglobulins. Diversification of antibody function by CSR is important for humoral immunity. However, it remains unclear how the decision for the bifurcation is made. Bach2 is a B-cell-specific transcription repressor interacting with the small Maf proteins whose expression is high only before the plasma cell stage. Here we show that Bach2 is critical for CSR and somatic hypermutation (SHM) of immunoglobulin genes. Genetic ablation of Bach2 in mice revealed that Bach2 was required for both T-cell-independent and T-cell-dependent IgG responses and SHM. When stimulated in vitro, Bach2-deficient B cells produced IgM, as did wild-type cells, and abundantly expressed Blimp-1 (refs 9, 10) and XBP-1 (ref. 11), critical regulators of the plasmacytic differentiation, indicating that Bach2 was not required for the plasmacytic differentiation itself. However, they failed to undergo efficient CSR. These findings define Bach2 as a key regulator of antibody response and provide an insight into the orchestration of CSR and SHM during plasma cell differentiation.

Regulation of heme oxygenase-1 by transcription factor Bach1 in the mouse brain.

Oxidative stress has been implicated in tissue damage from traumatic brain injury. Heme oxygenase-1 (HO-1) is an inducible enzyme that degrades prooxidant heme to radical-scavenging biliverdin/bilirubin in order to protect cells from oxidative stress. Although HO-1 is induced after induction of brain damage, the regulatory mechanism of HO-1 in the brain is still unclear. Bach1 is a transcriptional repressor of the HO-1 gene, and plays a critical role in tissue protection from oxidative stress by reperfusion injury of the myocardium. In this study, we examined the role of Bach1 in HO-1 regulation of the various brain sites by investigating the expression of Bach1 and HO-1 in brain tissues of mice bearing Bach1-deficient (Bach1(-/-)) or wild-type (Bach1(+/+)) genes. While the expression levels of Bach1 mRNA in the olfactory bulb were significantly higher than other brain areas, those at the cortex showed the lowest activity. Bach1(-/-) mice showed significantly higher HO-1 mRNA expression levels than Bach1(+/+) mice in all brain sites studied. Moreover, higher induction of HO-1 was observed around damaged tissues after cold injury in Bach1(-/-) than Bach1(+/+) mice. Thus, Bach1 plays an important role in regulating the constitutive and inducible expression levels of HO-1 in the brain. Although a significantly higher level of HO-1 was observed in Bach1(-/-) than Bach1(+/+) mice, genetic ablation of the Bach1 gene failed to show any tissue protective effect after cold injury was inflicted on the cortex.

[A case of Rathke's cleft cyst in association with a ruptured aneurysm of the anterior cerebral artery mimicking pituitary apoplexy].

We present a rare case of a Rathke's cleft cyst in association with a ruptured aneurysm of the anterior cerebral artery (ACA). A 44-year-old man suffered from sudden onset of headache. Initial computed tomographic (CT) scan revealed a high-density mass lesion in the suprasellar region and a diffuse high-density area in the basal cistern. Using emergent magnetic resonance imaging (MRI), we found a cyst showed homogeneously high and iso-intensity on T1 and T2-weighted image, respectively. The cyst showed no enhancement of the cyst wall, but on Gd-DTPA, it was shown to compress the normal pituitary gland. Angiography showed an aneurysm at the A1 portion of the left ACA. Based on/these findings, we were able to diagnose Rathke's cleft cyst and a ruptured aneurysm. An operation was performed through the interhemispheric approach. The suprasellar cystic mass compressed the optic nerves and chiasm upward. Neck clipping of the aneurysm and opening of the cyst were performed. We confirmed the cause of the subarachnoid hemorrhage as being a ruptured aneurysm at the A1 portion of the left ACA. Histological diagnosis was Rathke's cleft cyst. Postoperative course was uneventful. There has been only one reported case of Rathke's cleft cyst in association with a ruptured aneurysm. When we encounter a case presenting subarachnoid hemorrhage with suprasellar mass and intracerebral aneurysm, we must discriminate between ruptured aneurysm and pituitary apoplexy in the acute stage as the cause of the subarachnoid hemorrhage. If the mass is Rathke's cleft cyst, we speculate that the cause of the subarachnoid hemorrhage is a ruptured aneurysm, because there are no reports of Rathke's cleft cyst with subarachnoid hemorrhage.