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Roberto C. Heros

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Toru Horikoshi, Arata Watanabe, Mikito Uchida and Hiroyuki Kinouchi


Magnetic resonance imaging may show a fluid collection in the spinal epidural space of patients with spontaneous intracranial hypotension syndrome (SIHS), but the chronological changes remain unclear.


Brain and spine MR imaging findings were analyzed in 16 patients (9 women and 7 men, mean age 48.6 years) with SIHS before and after treatment.


Diffuse dural enhancement was seen in 15 patients, and the epidural fluid collection in the spinal canal was clear in 15 and equivocal in 1. Symptoms disappeared after bed rest in 1 patient, and an epidural blood patch was performed in 15 patients, resulting in complete resolution of symptoms in 13. After the follow-up period (range 1–20 months, mean 5.0 months), 1 patient had persistent mild headache that gradually worsened in the afternoon, and another patient complained of heaviness of the eyes. Follow-up MR imaging demonstrated disappearance of the dural enhancement in all patients, but a fluid collection in the spinal canal remained in 4. Two of the 4 patients had persistent symptoms, but the other patients exhibited complete resolution of the symptoms.


An epidural blood patch is effective for sealing of CSF leaks, but the resolution of SIHS-related symptoms does not always imply complete eradication of the leakage.

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Hiroyuki Kinouchi, Kazuo Mizoi, Akira Takahashi, Yoshihide Nagamine, Keiji Koshu and Takashi Yoshimoto

Object. A retrospective analysis was conducted of 10 patients (three women and seven men) who were treated for spinal dural arteriovenous shunts (AVSs) located at the craniocervical junction. This analysis was performed to evaluate the characteristics of this unusual location in contrast with those of the more common thoracic and lumbar AVSs.

Methods. Seven patients presented with subarachnoid hemorrhage (SAH) and one with slowly progressive quadriparesis and dyspnea due to myelopathy. The other two cases were detected incidentally and included a transverse—sigmoid dural AVS and a cerebellar arteriovenous malformation. Angiographic studies revealed that the spinal dural AVSs at the C-1 and/or C-2 levels were fed by the dural branches of the radicular arteries that coursed from the vertebral artery and drained into the medullary veins. Venous drainage was caudally directed in the patient with myelopathy. In contrast, the shunt flow drained mainly into the intracranial venous system in patients with SAH. Furthermore, in four of these patients a varix was found on the draining vein. In all patients, the draining vein was interrupted surgically at the point at which this vessel entered the intradural space, using intraoperative digital subtraction angiography to monitor flow. The postoperative course was uneventful in all patients and no recurrence was confirmed on follow-up angiographic studies obtained in seven patients at 6 months after discharge.

Conclusions. If computerized tomography scanning shows SAH predominantly in the posterior fossa and no abnormalities are found on intracranial four-vessel angiographic study, proximal vertebral angiography should be performed to detect dural AVS at the craniocervical junction. The results of surgical intervention for this disease are quite satisfactory.

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Clément Dubost, François-Xavier Arnaud and Thomas Geeraerts

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Toshio Sasajima, Hiroyuki Kinouchi, Noriaki Tomura, Jiro Watarai and Kazuo Mizoi

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Katsuhiro Kuroda, Hiroyuki Kinouchi, Kazuya Kanemaru, Takuma Wakai, Nobuo Senbokuya and Toru Horikoshi

This 44-year-old woman presented with a ruptured anterior communicating artery aneurysm. Intraoperative indocyanine green (ICG) videoangiography demonstrated the aneurysm neck and dome, which were buried in subarachnoid clots. Dissection and aspiration of the clots around the neck were safely performed without touching the ruptured points. The aneurysm was successfully clipped. The patient's postoperative course was excellent. This case illustrates the use of intraoperative ICG videoangiography to provide information about the anatomical location of the aneurysm neck and dome despite their being completely obscured by subarachnoid clots. Intraoperative ICG videoangiography allowed safer dissection of the ruptured aneurysm from the blood clots.

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Hiroyuki Kinouchi, Haiyen Huang, Shouichi Arai, Kazuo Mizoi and Takashi Yoshimoto

Object. Recently, two different cyclooxygenase (COX) genes, COX-1 and -2, were identified. In this study, topographic and chronological profiles of COX-2 messenger (m)RNA and c-fos mRNA expression were investigated using in situ hybridization after focal cerebral ischemia.

Methods. Rats undergoing permanent ischemia were decapitated at 30 and 90 minutes and at 2, 4, 8, and 24 hours after middle cerebral artery (MCA) occlusion, and rats undergoing transient ischemia were decapitated at 4, 8, and 24 hours after MCA occlusion that lasted for either 30 or 90 minutes. After brief transient MCA occlusion, c-fos mRNA was induced in the whole MCA territory, adjacent cortex (cingulate cortex), and distant brain regions such as the hippocampus and substantia nigra. In contrast, COX-2 mRNA was not induced in the ischemic core (lateral striatum) but only in the penumbral area (MCA cortex). Long transient and permanent MCA occlusion did not induce c-fos and COX-2 mRNAs in the ischemic core but strongly induced both mRNAs in the penumbral area (medial striatum and periphery of MCA cortex) and adjacent cortex (cingulate cortex). In brain regions distant from the ischemic territory, although c-fos mRNA was induced in the thalamus, substantia nigra, and hippocampus after extended transient and permanent occlusion, COX-2 mRNA was only induced in the bilateral hippocampi. The induction of COX-2 mRNA persisted in all locations even at 24 hours after MCA occlusion.

Conclusions. The distribution of COX-2 mRNA induction was apparently different from that of c-fos mRNA after MCA occlusion. These results pertaining to COX-2 mRNA agree well with the previous observations of changes in prostaglandin metabolism induced by focal cerebral ischemia. However, whether this induction of the COX-2 gene contributes to the histopathological outcome of cerebral ischemia remains to be elucidated.

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Nobuo Senbokuya, Hideyuki Yoshioka, Takashi Yagi, Yuji Owada and Hiroyuki Kinouchi


Elucidating the mechanisms of neuronal injury is crucial for the development of spinal cord injury (SCI) treatments. Brain-type fatty acid–binding protein 7 (FABP7) is expressed in the adult rodent brain, especially in astrocytes, and has been reported to play a role in astrocyte function in various types of brain damage; however, its role after SCI has not been well studied. In this study, the authors evaluated the expression change of FABP7 after SCI using a mouse spinal cord compression model and observed the effect of FABP7 gene knockout on neuronal damage and functional recovery after SCI.


Female FABP7 knockout (KO) mice with a C57BL/6 background and their respective wild-type littermates were subjected to SCI with a vascular clip. The expression of FABP7, neuronal injury, and functional recovery after SCI were analyzed in both groups of mice.


Western blot analysis revealed upregulation of FABP7 in the wild-type mice, which reached its peak 14 days after SCI, with a significant difference in comparison to the control mice. Immunohistochemistry also showed upregulation of FABP7 at the same time points, mainly in proliferative astrocytes. The number of surviving ventral neurons in the FABP7-KO mice at 28 days after SCI was significantly lower than that observed in the wild-type mice. In addition, motor functional recovery in the FABP7-KO mice was significantly worse than that of the wild-type mice.


The findings of this study indicate that FABP7 could have a neuroprotective role that might be associated with modulation of astrocytes after SCI. FABP7 could potentially be a therapeutic target in the treatment of SCI.

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Mitsuto Hanihara, Tomoyuki Kawataki, Kyoko Oh-Oka, Kentaro Mitsuka, Atsuhito Nakao and Hiroyuki Kinouchi


Indoleamine 2,3-dioxygenase (IDO), a key enzyme of tryptophan (Trp) metabolism, is involved in tumor-derived immune suppression through depletion of Trp and accumulation of the metabolite kynurenine, resulting in inactivation of natural killer cells and generation of regulatory T cells (Tregs). It has been reported that high expression of IDO in cancer cells is associated with suppression of the antitumor immune response and is consistent with a poor prognosis. Thus, IDO may be a therapeutic target for malignant cancer. The authors have recently shown that IDO expression is markedly increased in human glioblastoma and secondary glioblastoma with malignant change, suggesting that IDO targeting may also have therapeutic potential for patients with glioma. The aim of this study was to investigate the antitumor effect of IDO inhibition and to examine the synergistic function of IDO inhibitor and temozolomide (TMZ) in a murine glioma model.


Murine glioma GL261 cells and human glioma U87 cells were included in this study. The authors used 3 mouse models to study glioma cell growth: 1) a subcutaneous ectopic model, 2) a syngeneic intracranial orthotopic model, and 3) an allogenic intracranial orthotopic model. IDO inhibition was achieved via knockdown of IDO in GL261 cells using short hairpin RNA (shRNA) and through oral administration of the IDO inhibitor, 1-methyl-l-tryptophan (1-MT). Tumor volume in the subcutaneous model and survival time in the intracranial model were evaluated.


In the subcutaneous model, oral administration of 1-MT significantly suppressed tumor growth, and synergistic antitumor effects of 1-MT and TMZ were observed (p < 0.01). Mice containing intracranially inoculated IDO knockdown cells had a significantly longer survival period as compared with control mice (p < 0.01).


These results suggest that IDO expression is implicated in immunosuppression and tumor progression in glioma cells. Therefore, combining IDO inhibition with standard TMZ treatment could be an encouraging therapeutic strategy for patients with malignant glioma.

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Takashi Sato, Takeshi Sugiyama, Tomoyuki Kawataki, Eiji Sato, Toru Horikoshi, Kanji Sugita and Hiroyuki Kinouchi

This 11-year-old boy presented with a rare case of Castleman syndrome caused by a clear cell meningioma manifesting as persistent fever of unknown origin, 2 years after glomerulonephritis. Laboratory investigation of the patient showed an increased inflammatory reaction, as well as elevated polyclonal gamma globulin titer and serum level of C-reactive protein. Magnetic resonance imaging revealed a tumor at the cerebellopontine angle. Neurosurgical intervention was performed under the presumptive diagnosis of Castleman syndrome caused by intracranial tumor. Histological examination of the tumor verified that it was clear cell meningioma with infiltration of lymphoplasma cells, and surgical removal resulted in complete resolution of the patient's symptoms and biochemical abnormalities. The present case of clear cell meningioma manifesting as Castleman syndrome shows that the possibility of a brain tumor should be considered in patients presenting with fever of unknown origin, anemia, hypergammaglobulinemia, or other systemic illness.