Hyperbaric hydrogen therapy improves secondary brain injury after head trauma.

Background: The pathophysiology of traumatic brain injury (TBI) is caused by the initial physical damage and by the subsequent biochemical damage (secondary brain injury). Oxidative stress is deeply involved in secondary brain injury, so molecular hydrogen therapy may be effective for TBI. Hydrogen gas shows the optimal effect at concentrations of 2% or higher, but can only be used up to 1.3% in the form of a gas cylinder mixed with oxygen gas, which may not be sufficiently effective. The partial pressure of hydrogen increases in proportion to the pressure, so hyperbaric hydrogen therapy (HBH2) is more effective than that at atmospheric pressure. Methods: A total of 120 mice were divided into three groups: TBI + non-treatment group (TBI group; n = 40), TBI + HBH2 group (n = 40), and non-TBI + non-treatment group (sham group; n = 40). The TBI and TBI + HBH2 groups were subjected to moderate cerebral contusion induced by controlled cortical impact. The TBI + HBH2 group received hyperbaric hydrogen therapy at 2 atmospheres for 90 minutes, at 30 minutes after TBI. Brain edema, neuronal cell loss in the injured hippocampus, neurological function, and cognitive function were evaluated. Results: The TBI + HBH2 group showed significantly less cerebral edema (p ≺ 0.05). Residual hippocampal neurons were significantly more numerous in the TBI + HBH2 group on day 28 (p ≺ 0.05). Neurological score and behavioral tests showed that the TBI + HBH2 group had significantly reduced hyperactivity on day 14 (p ≺ 0.01). Conclusion: Hyperbaric hydrogen therapy may be effective for posttraumatic secondary brain injury.

Eribulin prolongs survival in an orthotopic xenograft mouse model of malignant meningioma.

Meningioma is the most common intracranial tumor, with generally favorable patient prognosis. However, patients with malignant meningioma typically experience recurrence, undergo multiple surgical resections, and ultimately have a poor prognosis. Thus far, effective chemotherapy for malignant meningiomas has not been established. We recently reported the efficacy of eribulin (Halaven) for glioblastoma with a telomerase reverse transcriptase (TERT) promoter mutation. This study investigated the anti-tumor effect of eribulin against TERT promoter mutation-harboring human malignant meningioma cell lines in vitro and in vivo. Two meningioma cell lines, IOMM-Lee and HKBMM, were used in this study. The strong inhibition of cell proliferation by eribulin via cell cycle arrest was demonstrated through viability assay and flow cytometry. Apoptotic cell death in malignant meningioma cell lines was determined through vital dye assay and immunoblotting. Moreover, a wound healing assay revealed the suppression of tumor cell migration after eribulin exposure. Intraperitoneal administration of eribulin significantly prolonged the survival of orthotopic xenograft mouse models of both malignant meningioma cell lines implanted in the subdural space (P < .0001). Immunohistochemistry confirmed apoptosis in brain tumor tissue treated with eribulin. Overall, these results suggest that eribulin is a potential therapeutic agent for malignant meningiomas.

The ALK inhibitors, alectinib and ceritinib, induce ALK-independent and STAT3-dependent glioblastoma cell death.

Glioblastoma (GBM) is the most common, but extremely malignant, brain tumor; thus, the development of novel therapeutic strategies for GBMs is imperative. Many tyrosine kinase inhibitors (TKIs) have been approved for various cancers, yet none has demonstrated clinical benefit against GBM. Anaplastic lymphoma kinase (ALK) is a receptor tyrosine kinase (RTK) that is confirmed only during the embryonic development period in humans. In addition, various ALK gene alterations are known to act as powerful oncogenes and therapeutic targets in various tumors. The antitumor activity of various TKIs was tested against three human GBM cell lines (U87MG, LN229, and GSC23), which expressed substantially low ALK levels; second-generation ALK inhibitors, alectinib and ceritinib, effectively induced GBM cell death. In addition, treatment with either alectinib or ceritinib modulated the activation of various molecules downstream of RTK signaling and induced caspase-dependent/-independent cell death mainly by inhibiting signal transducer and activator of transcription 3 activation in human GBM cells. In addition, alectinib and ceritinib also showed antitumor activity against a U87MG cell line with acquired temozolomide resistance. Finally, oral administration of alectinib and ceritinib prolonged the survival of mice harboring intracerebral GBM xenografts compared with controls. These results suggested that treatment with the second-generation ALK inhibitors, alectinib and ceritinib, might serve as a potent therapeutic strategy against GBM.

Lomustine and nimustine exert efficient antitumor effects against glioblastoma models with acquired temozolomide resistance.

Glioblastomas (GBM) often acquire resistance against temozolomide (TMZ) after continuous treatment and recur as TMZ-resistant GBM (TMZ-R-GBM). Lomustine (CCNU) and nimustine (ACNU), which were previously used as standard therapeutic agents against GBM before TMZ, have occasionally been used for the salvage therapy of TMZ-R-GBM; however, their efficacy has not yet been thoroughly examined. Therefore, we investigated the antitumor effects of CCNU and ACNU against TMZ-R-GBM. As a model of TMZ-R-GBM, TMZ resistant clones of human GBM cell lines (U87, U251MG, and U343MG) were established (TMZ-R-cells) by the culture of each GBM cells under continuous TMZ treatment, and the antitumor effects of TMZ, CCNU, or ACNU against these cells were analyzed in vitro and in vivo. As a result, although growth arrest and apoptosis were triggered in all TMZ-R-cells after the administration of each drug, the antitumor effects of TMZ against TMZ-R-cells were significantly reduced compared to those of parental cells, whereas CCNU and ACNU demonstrated efficient antitumor effects on TMZ-R-cells as well as parental cells. It was also demonstrated that TMZ resistance of TMZ-R-cells was regulated at the initiation of DNA damage response. Furthermore, survival in mice was significantly prolonged by systemic treatment with CCNU or ACNU but not TMZ after implantation of TMZ-R-cells. These findings suggest that CCNU or ACNU may serve as a therapeutic agent in salvage treatment against TMZ-R-GBM.

Signal transduction pathways and resistance to targeted therapies in glioma.

Although surgical techniques and adjuvant therapies have undergone progressive development for decades, the therapeutic outcomes for treating glioblastoma (GBM) remain poor. The main reasons for the poor prognosis of gliomas are that limited tumor tissue that can be resected (to preserve brain functions) and that residual tumors are often resistant to irradiation and chemotherapy. Therefore, overcoming the resistance of residual tumors against adjuvant therapy is urgently needed for glioma treatment. Recent large cohort studies of genetic alterations in GBM demonstrated that both genetic information and intracellular molecular signaling are networked in gliomas and that such information may help clarify which molecules or signals serve essential roles in resistance against radiation or chemotherapy, highlighting them as potential novel therapeutic targets against refractory gliomas. In this review, we summarize the current understanding of molecular networks that govern glioma biology, mainly based on cohort studies or recent evidence, with a focus on how intracellular signaling molecules in gliomas associate with each other and regulate refractoriness against current therapy.

Extracellular α-synuclein enters dopaminergic cells by modulating flotillin-1-assisted dopamine transporter endocytosis.

The neuropathological hallmarks of Parkinson's disease (PD) include the appearance of α-synuclein (α-SYN)-positive Lewy bodies (LBs) and the loss of catecholaminergic neurons. Thus, a potential mechanism promoting the uptake of extracellular α-SYN may exist in susceptible neurons. Of the various differentially expressed proteins, we are interested in flotillin (FLOT)-1 because this protein is highly expressed in the brainstem catecholaminergic neurons and is strikingly up-regulated in PD brains. In this study, we found that extracellular monomeric and fibrillar α-SYN can potentiate FLOT1-dopamine transporter (DAT) binding and pre-endocytic clustering of DAT on the cell surface, thereby facilitating DAT endocytosis and down-regulating its transporter activity. Moreover, we demonstrated that α-SYN itself exploited the DAT endocytic process to enter dopaminergic neuron-like cells, and both FLOT1 and DAT were found to be the components of LBs. Altogether, these findings revealed a novel role of extracellular α-SYN on cellular trafficking of DAT and may provide a rationale for the cell type-specific, functional, and pathologic alterations in PD.-Kobayashi, J., Hasegawa, T., Sugeno, N., Yoshida, S., Akiyama, T., Fujimori, K., Hatakeyama, H., Miki, Y., Tomiyama, A., Kawata, Y., Fukuda, M., Kawahata, I., Yamakuni, T., Ezura, M., Kikuchi, A., Baba, T., Takeda, A., Kanzaki, M., Wakabayashi, K., Okano, H., Aoki, M. Extracellular α-synuclein enters dopaminergic cells by modulating flotillin-1-assisted dopamine transporter endocytosis.

[A Case of Primary Intracranial Malignant Melanoma Mimicking a Traumatic Brain Contusion].

Primary intracranial malignant melanoma(PIMM)is a rare neoplasm of the central nervous system, accounting for 1% of cases of malignant melanomas and 0.1% of cases of brain tumors. Here, we report a case of PIMM that was initially considered to be a traumatic brain contusion. A 44-year-old man was transferred to a local hospital because of general tonic convulsion after falling while riding a bike. CT showed an irregular high-density area in the left temporal pole, which was diagnosed as a traumatic contusion. MRI performed 3 months after the initial episode revealed an enlarged temporal lesion with surrounding edema, suggestive of a neoplasm. The MRI showed the lesion as mixed signal intensity, suggesting both solid and cystic components. Subtotal resection was performed, except for the tumor adhering to the peripheral middle cerebral arteries(MCAs). The definitive diagnosis was made based on pathological findings and no evidence of extracranial lesions. Gamma knife surgery was performed for the remnant tumor adjacent to MCAs. The radiologically positive tumor chronologically regressed, and the patient remained progression-free for 18 months. Radiological findings of PIMM vary but typically include high density on CT and hyperintensity on T1-weighted MRI. Close observation enabled early diagnosis based on the suspicion of a neoplasm according to atypical radiological findings. PIMM has a poor prognosis with an overall survival of 12.0 months without confirmative treatment. Gamma knife surgery might achieve suppression of this highly progressive tumor.

Concomitant administration of radiation with eribulin improves the survival of mice harboring intracerebral glioblastoma.

Glioblastoma is the most common and devastating type of malignant brain tumor. We recently found that eribulin suppresses glioma growth in vitro and in vivo and that eribulin is efficiently transferred into mouse brain tumors at a high concentration. Eribulin is a non-taxane microtubule inhibitor approved for breast cancer and liposarcoma. Cells arrested in M-phase by chemotherapeutic agents such as microtubule inhibitors are highly sensitive to radiation-induced DNA damage. Several recent case reports have demonstrated the clinical benefits of eribulin combined with radiation therapy for metastatic brain tumors. In this study, we investigated the efficacy of a combined eribulin and radiation treatment on human glioblastoma cells. The glioblastoma cell lines U87MG, U251MG and U118MG, and SJ28 cells, a patient-derived sphere culture cell line, were used to determine the radiosensitizing effect of eribulin using western blotting, flow cytometry and clonogenic assay. Subcutaneous and intracerebral glioma xenografts were generated in mice to assess the efficacy of the combined treatment. The combination of eribulin and radiation enhanced DNA damage in vitro. The clonogenic assay of U87MG demonstrated the radiosensitizing effect of eribulin. The concomitant eribulin and radiation treatment significantly prolonged the survival of mice harboring intracerebral glioma xenografts compared with eribulin or radiation alone (P < .0001). In addition, maintenance administration of eribulin after the concomitant treatment further controlled brain tumor growth. Aberrant microvasculature was decreased in these tumors. Concomitant treatment with eribulin and radiation followed by maintenance administration of eribulin may serve as a novel therapeutic strategy for glioblastomas.

Intracellular cholesterol level regulates sensitivity of glioblastoma cells against temozolomide-induced cell death by modulation of caspase-8 activation via death receptor 5-accumulation and activation in the plasma membrane lipid raft.

Development of resistance against temozolomide (TMZ) in glioblastoma (GBM) after continuous treatment with TMZ is one of the critical problems in clinical GBM therapy. Intracellular cholesterol regulates cancer cell biology, but whether intracellular cholesterol is involved in TMZ resistance of GBM cells remains unclear. The involvement of intracellular cholesterol in acquired resistance against TMZ in GBM cells was investigated. Intracellular cholesterol levels were measured in human U251 MG cells with acquired TMZ resistance (U251-R cells) and TMZ-sensitive control U251 MG cells (U251-Con cells), and found that the intracellular cholesterol level was significantly lower in U251-R cells than in U251-Con cells. In addition, treatment by intracellular cholesterol remover, methyl-beta cyclodextrin (MßCD), or intracellular cholesterol inducer, soluble cholesterol (Chol), regulated TMZ-induced U251-Con cell death in line with changes in intracellular cholesterol level. Involvement of death receptor 5 (DR5), a death receptor localized in the plasma membrane, was evaluated. TMZ without or with MßCD and/or Chol caused accumulation of DR5 into the plasma membrane lipid raft and formed a complex with caspase-8, an extrinsic caspase cascade inducer, reflected in the induction of cell death. In addition, treatment with caspase-8 inhibitor or knockdown of DR5 dramatically suppressed U251-Con cell death induced by combination treatment with TMZ, MßCD, and Chol. Combined treatment of Chol with TMZ reversed the TMZ resistance of U251-R cells and another GBM cell model with acquired TMZ resistance, whereas clinical antihypercholesterolemia agents at physiological concentrations suppressed TMZ-induced cell death of U251-Con cells. These findings suggest that intracellular cholesterol level affects TMZ treatment of GBM mediated via a DR5-caspase-8 mechanism.

Modified Extradural Temporopolar Approach for Paraclinoid Aneurysms: Operative Nuance and Surgical Result.

BACKGROUND: Extradural temporopolar approach can provide extensive exposure of the anterior clinoid process, which can prevent intraoperative neurovascular injury in anterior clinoidectomy for paraclinoid aneurysms. The present study investigates the usefulness of this modified technique, and operative nuances are discussed here. METHODS: We retrospectively reviewed the medical charts of 30 consecutive patients with paraclinoid aneurysms who underwent treatment with this modified extradural temporopolar approach between September 2009 and March 2016. RESULTS: Worsening of visual acuity was documented postoperatively in three patients (10.0%), and visual field function worsened in three patients (10.0%). Postoperative outcome was good recovery in all patients. No operation-related mortality occurred in the series. CONCLUSION: Extradural anterior clinoidectomy via the modified extradural temporopolar approach is safe and may be recommended for surgical treatment of paraclinoid aneurysms to reduce the risk of intraoperative optic neurovascular injury.

Multistaged, multidirectional strategy for safe removal of large meningiomas in the pineal region.

OBJECTIVE Pineal region meningiomas are rare and tend to be discovered only after they grow. Several simultaneous multidirectional approaches performed as a single operation have been proposed, but the best strategy to remove these deeply situated large meningiomas involving the deep vital venous system remains to be established. The authors advocate a multistaged, multidirectional approach to safely remove these challenging tumors. METHODS Four consecutive cases of meningioma in the pineal region were treated between April 2013 and June 2016. The 3 large (> 40 mm diameter) tumors were removed via multistaged, multidirectional approaches (2 surgeries in 2 patients and 3 surgeries in 1 patient) with gravity retraction of the occipital or parietal lobe. The large occipital skin incision extending bilaterally was used for the next operation from the contralateral side. Combinations of the occipital transtentorial approach with or without the transfalcine approach, occipital bitranstentorial/falcine approach, combined supra-/infratentorial transsinus approach, and contralateral parietal interhemispheric transcallosal approach were used. RESULTS Transient visual field deficits occurred after 2 of the 8 operations, but all tumors were removed grossly or subtotally without permanent surgery-related morbidity. The galenic venous system and straight sinus remained intact in all patients. During the follow-up period (mean 29.5 months [range 13-52 months]), there were no recurrences after the final operation. CONCLUSIONS A multistaged, multidirectional strategy with an intentional large occipital scalp incision and gravity retraction of the occipital lobe is a good choice for the safe removal of large meningiomas in the pineal region.

Superficial Temporal Artery to Anterior Cerebral Artery Hemi-bonnet Bypass Using Radial Artery Graft for Prevention of Complications after Surgical Treatment of Partially Thrombosed Large/Giant Anterior Cerebral Artery Aneurysm.

BACKGROUND: Partially thrombosed large/giant aneurysm of the anterior cerebral artery is still challenging because this complex aneurysm requires arterial revascularization in the deep operation field. Therefore, direct neck clipping is often impossible. We describe our experiences with extracranial-intracranial bypass as an insurance bypass prior to clipping of partially thrombosed anterior cerebral artery aneurysms, and discuss the microsurgical technique and strategy. CLINICAL PRESENTATION: Consecutive, single-surgeon experience with the surgical treatment of partially thrombosed anterior cerebral artery aneurysms was retrospectively reviewed. Three cases of partially thrombosed anterior cerebral artery aneurysms, 2 anterior communicating artery aneurysms, and 1 postcommunicating artery (A2 segment of the anterior cerebral artery) aneurysm, presented as mass effect symptoms from giant aneurysms in 2 patients and incidentally discovered aneurysm in one patient. Superficial temporal artery-radial artery graft-anterior cerebral artery hemi-bonnet bypass was performed as an insurance bypass prior to clipping of the partially thrombosed anterior cerebral artery aneurysms. Complete aneurysm obliteration and bypass patency were demonstrated in all 3 patients. No neurological sequelae occurred. CONCLUSIONS: Superficial temporal artery-radial artery graft-anterior cerebral artery hemi-bonnet bypass prior to aneurysm dissection can avoid ischemic complication during temporary occlusion and secures permanent revascularization after complete obliteration of partially thrombosed large/giant anterior cerebral artery aneurysm.

[A Case of Retro-Odontoid Pseudotumor in a Very Elderly Individual].

Retro-odontoid pseudotumors are mainly caused by aging or rheumatoid arthritis. We treated a very elderly patient with retro-odontoid pseudotumor. A 92-year-old man was admitted with the chief complaints of difficulty walking and progressive numbness in the right upper and lower extremities. Neurological examination revealed muscle weakness and exaggerated tendon reflexes of the right upper and lower extremities, and disturbance in skilled motor activities of the fingers, bilaterally. He had no bladder or rectal disturbances. The Japanese Orthopaedic Association(JOA)score for cervical myelopathy was 10/17. Rheumatoid arthritis was interpreted as negative. Radiography of the neck showed no atlanto-axial instability. Cervical magnetic resonance(MR)imaging revealed a mass located posterior to the C2 odontoid process, severely compressing the cervical cord. The patient underwent a C1 laminectomy and C2 half laminectomy without fixation to achieve cord decompression. Postoperatively, muscle weakness in the right upper and lower extremities was remarkably improved, and gait disturbance was also improved. However, skilled motor activities of the fingers on the right hand during tasks such as writing letters, holding a cup, and using chopsticks, were not improved. JOA score was improved to 14/17. Postoperative radiography revealed no atlanto-axial instability and MR imaging revealed adequate decompression of the spinal canal. Laminectomy without fixation is recommended as an effective and less invasive treatment for retro-odontoid pseudotumor, especially in very elderly patients without atlanto-axial instability.

[A Case of Foramen Magnum Meningioma Manifesting as Hypoglossal Nerve Palsy].

We report a case of foramen magnum meningioma manifesting as hypoglossal nerve palsy. A 72-year-old woman presented with progressive hypoglossal nerve palsy and lingual atrophy on the left side. Gadolinium-enhanced T1-weighted magnetic resonance imaging revealed a heterogeneously enhanced mass lesion with dural tail sign partially extending into the hypoglossal canal. The transcondylar approach was performed to expose the hypoglossal canal and resect the tumor completely. Histological examination revealed a transitional meningioma. The postoperative course was uneventful. Hypoglossal nerve palsy improved gradually after the operation.

[Surgical Treatment of a Giant Olfactory Groove Schwannoma:A Case Report].

Schwannomas originating from the olfactory nerve are extremely rare because the olfactory nerve does not normally contain Schwann cells. We describe a case of a giant schwannoma of the olfactory groove. A 73-year-old woman presented with anosmia persisting for 10 months. Head computed tomography(CT)for head trauma at another hospital demonstrated a tumor lesion located in the left frontal lobe and paranasal sinus. She had never suffered epilepsy, and past medical history and family history identified no indicators. Neurological examination revealed anosmia and dementia. Head CT demonstrated a tumor lesion with bone erosion, causing a defect of about 5cm in the frontal base. Head magnetic resonance(MR)imaging with contrast medium indicated a lesion that was 6cm in diameter, with heterogeneous enhancement and severe perifocal edema in the left frontal base, extending into the paranasal cavity. The tumor was resected through a left extradural subfrontal approach with bicoronal frontal craniotomy. The endoscopic approach was also performed simultaneously to remove the tumor in the paranasal sinus. The cystic tumor was soft and easy to bleed. Intraoperatively the right olfactory nerve was confirmed, but the left olfactory nerve could not be identified because of replacement by the tumor, suggesting that the tumor had originated from the left olfactory nerve. The defect of the dura was repaired with femoral fascia, the pedunculated periosteal flap was laid over the frontal base, and the bone defect was repaired with the inner plate of the frontal calvaria. Postoperative head MR imaging with contrast medium revealed no residual lesion. The patient was discharged 25 days after surgery, without new neurological deficits. Histological examination identified mixed Antoni type A and Antoni type B schwannoma on hematoxylin and eosin staining and S-100 protein on immunostaining.

[A Case of Coexistent Glossopharyngeal Neuralgia and Hemifacial Spasm Successfully Treated with Transposition of the Vertebral Artery].

A case of coexistent glossopharyngeal neuralgia and hemifacial spasm was treated by transposition of the vertebral artery. A 60-year-old man was referred to our hospital due to pain in the left posterior part of the tongue that was difficult to control with oral medication at a local hospital. The diagnosis was left glossopharyngeal neuralgia based on the symptoms, imaging findings, and lidocaine test results. Moreover, the patient had left hemifacial spasm. Microvascular decompression was performed, which confirmed that the vertebral artery was compressing the lower cranial nerve and the posterior inferior cerebellar artery was compressing the root exit zone of the facial nerve. The vertebral artery and posterior inferior cerebellar artery were transposed using TachoSil®. After the surgery, both glossopharyngeal neuralgia and hemifacial spasm disappeared, and the patient was discharged.

[Primary Intracranial Malignant Lymphoma Associated with Acquired Immunodeficiency Syndrome(AIDS):A Case Report].

The spread of human immunodeficiency virus(HIV)infection may result in an increased likelihood of surgery in patients with HIV infection. We treated a patient with intracranial malignant lymphoma associated with acquired immunodeficiency syndrome(AIDS)caused by HIV infection. The recommendations of the countermeasure manual for AIDS were followed. Only surgical staff without finger injury or inflammation were permitted to be involved in the operation. All staff were dressed in a waterproof, full-body surgical gown, and wore double gloves, double foot covers, and an N95 mask. The surgery could be performed safely with such infection control measures. Histological examination revealed a diffuse large B-cell lymphoma. The patient was referred to the Division of Infectious Diseases and Respiratory Medicine for chemotherapy.

Recurrent neomorphic mutations of MTOR in central nervous system and testicular germ cell tumors may be targeted for therapy.

Germ cell tumors constitute a heterogeneous group that displays a broad spectrum of morphology. They often arise in testes; however, extragonadal occurrence, in particular brain, is not uncommon, and whether they share a common pathogenesis is unknown. We performed whole exome sequencing in 41 pairs of central nervous system germ cell tumors (CNS GCTs) of various histology and their matched normal tissues. We then performed targeted sequencing of 41 selected genes in a total of 124 CNS GCTs, 65 testicular germ cell tumors (tGCTs) and 8 metastatic GCTs to the CNS. The results showed that mutually exclusive mutations of genes involved in the MAPK pathway were most common (48.4 %), typically in KIT (27.4 %), followed by those in the PI3K pathway (12.9 %), particularly in MTOR (6.5 %), among the 124 CNS GCTs. Pure germinomas and non-germinomatous germ cell tumors (NGGCTs), as well as CNS and testicular GCTs, showed similar mutational profiles, suggesting that GCTs share a common molecular pathogenesis. Mutated MTOR identified in CNS GCTs upregulated phosphorylation of the AKT pathway proteins including AKT and 4EBP1 in nutrient-deprived conditions and enhanced soft-agar colony formation; both events were suppressed in a dose-dependent manner by addition of the MTOR inhibitor pp242. Our findings indicate that the dominant genetic drivers of GCTs regardless of the site of origin are activation of the MAPK and/or PI3K pathways by somatic point mutations. Mutated MTOR represents a potential target for novel targeted therapies for refractory GCTs.

Retrograde Suction Decompression Through Direct Puncture of the Common Carotid Artery for Paraclinoid Aneurysm.

BACKGROUND: Surgical clipping of paraclinoid aneurysm can be very difficult because strong adhesions may hinder the dissection of the perforators and surrounding anatomical structures from the aneurysm dome. We describe our experience with using retrograde suction decompression during the clipping of paraclinoid aneurysms and discuss the relative advantages and pitfalls. MATERIALS AND METHODS: This study included 23 patients with large and giant paraclinoid aneurysms who underwent surgical treatment consisting of direct clipping with suction decompression between March 2004 and August 2014. Direct puncture of the common carotid artery (CCA) was performed with a 20-gauge needle. The aneurysm was temporarily trapped by clamping of the CCA and external carotid artery (ECA), followed by temporary clipping of the intracranial internal carotid artery (ICA) distal to the aneurysm neck. Blood was then gently aspirated through a catheter introduced into the cervical ICA, resulting in collapse of the aneurysm. Therefore, safe aneurysm dissection was feasible during interruption of the blood flow, which could be maintained for up to 5 min. This procedure was repeated until dissection and clipping of the aneurysm were completed. RESULTS: Seven patients were admitted with SAH, 11 with asymptomatic unruptured aneurysm, and 5 with symptomatic unruptured aneurysm. The aneurysms were located on the paraclinoidal segment of the ICA in 15 cases, on the ICA-posterior communicating artery (PComA) in 6, at the ICA bifurcation in 1, and on the anterior wall of the ICA in 1. None of them suffered complications related to the CCA puncture. Surgical outcome was good recovery in 13 patients, moderate disability in 4, severe disability in 4, and vegetative state in 1. CONCLUSION: Retrograde suction decompression through direct puncture of the common carotid artery is a useful adjunct technique for the clipping of paraclinoid ICA aneurysms.

[A Surgical Case of Tuberculoma with Visual Disturbance].

We herein report a surgical case of multiple cerebral calculi located within the chiasmatic cistern resulting in visual disturbance. A 61-year-old man experienced homonymous lower right quadrantanopsia a few years prior. Non-enhanced head CT revealed multiple calcified lesions of about 7-mm within the basal cistern. MRI showed the lesion compressing the left optic tract. We could not remove the entire lesion because of severe adhesion to the optic tract. A pathological test showed calcified lesions with lymphocyte infiltration. We diagnosed tuberculoma caused by tuberculous meningitis with degeneration of the calcified lesion because of a history of tuberculosis at a fetal age. After the surgery, the patient was discharged without improvement of the visual disturbance.