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Introduction It has been reported that brain tumor resection by craniotomy is a high risk for deep venous thrombosis (DVT), though few data is available in Japanese patients. The aim of this retrospective study was to evaluate the incidence and risk factors for DVT in Japanese adult patients with brain tumor surgery. Materials and methods Medical records of Japanese adult patients with craniotomy for brain tumor were reviewed. In addition to clinical variables including patients' age, sex, body mass index, previous history of DVT, leg paresis, medications, tumor histology, surgical factors, adjuvant therapy, infection, and duration of post-operative immobilization and hospitalization, plasma D-dimer levels were measured at pre-surgery (baseline), on post-operative day (POD) one to 30 and during adjuvant therapy, and were compared between patients with and without DVT. Results Thirteen of 61 patients (21.3%) had DVT after surgery with mechanical prophylaxis. All DVTs were asymptomatic. Multivariate analyses found post-operative infection (odds ratio, 12.15; 95% confidence interval, 1.09–134.98; P = 0.03) to be a sole independent risk factor for DVT. D-dimer levels were not significantly different between patients with and without DVT at baseline and POD 1–30, but were significantly elevated during adjuvant therapy in patients with DVT (P = 0.03). Conclusions Not a few Japanese patients developed DVT after brain tumor surgery with mechanical prophylaxis, and patients with infection should be carefully monitored for post-operative DVT.

BACKGROUND The drug manufacturer recommends postponing initiation of bevacizumab for malignant gliomas at least 4 weeks later postoperatively. Malignant glioma patients with significant neurological deficits due to postoperative residual tumors are preferably needed earlier bevacizumab therapy that expecting improvement of neurological state and brain edema. There is a literature review indicating that the timing for administration of postoperative bevacizumab was at least 2 weeks. The authors assessed the safety,tolerability,efficacy for bevacizumab therapy less than 4 weeks later postoperatively. METHODS Six patients of malignant gliomas with residual tumors and neurological deficits were treated by bevacizumab (10mg /kg every 2 weeks) therapy 2–3 weeks later postoperatively with chemoradiotherapy. Patients included 31-year-old female with thalamic-midbrain glioblastoma (initial),11-year-old female with anaplastic ependymoma (recurrent),71-year-old female with initial cervical cord anaplastic astrocytoma (initial),88-year-old female bilateral frontal glioblastoma (initial),27-year-old female with thalamic midbrain glioblastoma (initial) and 3-year-old female with brain stem glioblastoma (initial). RESULTS All the patients did not experienced hemorrhage and impair wound healing. Every patient neurological state and perifocal brain edema following bevacizumab therapy demonstrated early improvement. Earlier bevacizumab therapy did not delay and cease postoperative chemoradiotherapy. CONCLUSIONS Initiation of bevacizumab therapy 2–3 weeks later postoperatively seems to be safe and effective for malignant glioma patients with worse neurological state due to residual tumor and perifocal edema. The optimal interval which balances the risk of complications and the risk of tumor progression should be considered.

We present the first report of intraosseous meningioma accompanied by intradural cyst formation. A 76-year-old woman had previously undergone breast cancer treatment, so the preoperative diagnosis was metastatic breast cancer. This case reminds us that the possibility of meningioma should be kept in mind in patients with breast cancer, irrespective of neuroimaging findings.

Post-traumatic pituitary apoplexy is uncommon, most of which present with a sudden onset of severe headache and visual impairments associated with a dumbbell-shaped pituitary tumor. We experienced an unusual case of post-traumatic pituitary apoplexy with atypical clinical features. A 66-year-old man presented with mild cerebral contusion and an incidentally diagnosed intrasellar tumor after a fall accident with no loss of consciousness. The patients denied any symptoms before the accident. After 4 days, the left oculomotor nerve palsy developed and deteriorated associated with no severe headache. Repeated neuroimages suggested that pituitary apoplexy had occurred at admission and showed that the tumor compressed the left cavernous sinus. The patient underwent endonasal transsphenoidal surgery at 6 days after head injury, and the mass reduction improved the oculomotor nerve palsy completely within the following 14 days. The pathologic diagnosis was nonfunctioning pituitary adenoma with hemorrhage and necrosis.

Background Blood blister-like aneurysms (BBAs) are a subgroup of aneurysms located on nonbranching sites of the internal carotid artery (ICA) and characterized by small size, a fragile wall, and a poorly defined broad-based neck. Both direct surgery and endovascular treatment for BBAs are often challenging. Some of the BBAs have been reported to look like true saccular aneurysms, and the misdiagnosis of BBA might result in catastrophic outcomes. The purpose of this study is to clarify the clinical and intraoperative findings of saccular BBAs. Methods We analyzed clinical and intraoperative findings in consecutive 11 patients with subarachnoid hemorrhage caused by ruptured BBA. BBAs were divided into typical BBAs, which were defined as typical tiny, broad-based, blister-like aneurysms, and saccular BBAs, which seemingly looked like true saccular aneurysms but were demonstrated to be BBAs by the intraoperative findings of the laceration of the ICA. The characteristics of saccular BBAs were analyzed. Results There were 4 patients with saccular BBAs in which the admission day was diverse from the onset day to several days after the onset. The origin of saccular BBAs was the medial (n = 2) or anterior (n = 2) walls of the ICA. Three of the 4 saccular BBAs pointed toward the optic nerve, whereas none of the typical BBAs pointed toward the optic nerve. Conclusions Saccular BBAs may not merely develop secondarily from typical BBAs, but also form by the surrounding structures-dependent mechanisms when an aneurysm points toward the optic nerve. The findings in this study suggest that saccular-shaped aneurysms at nonbranching sites of the ICA toward the optic nerve should be considered as saccular BBAs.

Temporal lobe epilepsy is a common, chronic neurological disorder characterized by recurrent spontaneous seizures. MicroRNAs (miRNAs) are small, noncoding RNAs that regulate post-transcriptional expression of protein-coding mRNAs, which may have key roles in the pathogenesis of neurological disorders. In experimental models of prolonged, injurious seizures (status epilepticus) and in human epilepsy, we found upregulation of miR-134, a brain-specific, activity-regulated miRNA that has been implicated in the control of dendritic spine morphology. Silencing of miR-134 expression in vivo using antagomirs reduced hippocampal CA3 pyramidal neuron dendrite spine density by 21% and rendered mice refractory to seizures and hippocampal injury caused by status epilepticus. Depletion of miR-134 after status epilepticus in mice reduced the later occurrence of spontaneous seizures by over 90% and mitigated the attendant pathological features of temporal lobe epilepsy. Thus, silencing miR-134 exerts prolonged seizure-suppressant and neuroprotective actions; determining whether these are anticonvulsant effects or are truly antiepileptogenic effects requires additional experimentation. © 2012 Nature America, Inc. All rights reserved.

Brief, non-harmful seizures can activate endogenous protective programmes which render the brain resistant to damage caused by prolonged seizure episodes. Whether protection in epileptic tolerance is long-lasting or influences the subsequent development of epilepsy is uncertain. Presently, we investigated the relationship between hippocampal pathology, neuropeptide Y rearrangement and spontaneous seizures in sham- and seizure-preconditioned mice after status epilepticus induced by intra-amygdala kainate. Seizure-induced neuronal death at 24 h was significantly reduced in the ipsilateral hippocampal CA3 and hilus of tolerance mice compared to sham-preconditioned animals subject to status epilepticus. Damage to the CA3-hilus remained reduced in tolerance mice 21 days post-status. In sham-preconditioned mice subject to status epilepticus correlative statistics showed there was a strong inverse relationship between CA3, but not hilar, neuron counts and the number of spontaneous seizures. A strong positive association was also found between neuropeptide Y score and spontaneous seizure count in these mice. In contrast, there was no significant association between spontaneous seizure count and CA3 neuron loss or neuropeptide Y rearrangement in the tolerance mice. These data show that tolerance-conferred neuroprotection is long-lasting and that tolerance disrupts the normal association between CA3 damage, synaptic rearrangement and occurrence of spontaneous seizures in this model.

Mesial temporal lobe epilepsy is the most common, intractable seizure disorder in adults. It is associated with an asymmetric pattern of hippocampal neuron loss within the endfolium (hilus and CA3) and CA1, with limited pathology in extra-hippocampal regions. We previously developed a model of focally-evoked seizure-induced neuronal death using intra-amygdala kainic acid (KA) microinjection and characterized the acute hippocampal pathology. Here, we sought to characterize the full extent of hippocampal and potential extra-hippocampal damage in this model, and the temporal onset of epileptic seizures. Seizure damage assessed at four stereotaxic levels by FluoroJade B staining was most prominent in ipsilateral hippocampal CA3 where it extended from septal to temporal pole. Minor but significant neuronal injury was present in ipsilateral CA1. Extra-hippocampal neuronal damage was generally limited in extent and restricted to the lateral septal nucleus, injected amygdala and select regions of neocortex ipsilateral to the seizure elicitation side. Continuous surface EEG recorded with implanted telemetry units in freely-moving mice detected spontaneous, epileptic seizures by five days post-KA in all mice. Epileptic seizure number averaged 1–4 per day. Hippocampi from epileptic mice 15 days post-KA displayed unilateral CA3 lesions, astrogliosis and increased neuropeptide Y immunoreactivity suggestive of mossy fiber rearrangement. These studies characterize a mouse model of unilateral hippocampal-dominant neuronal damage and short latency epileptogenesis that may be suitable for studying the cell and molecular pathogenesis of human mesial temporal lobe epilepsy.

Giant cell reparative granuloma (GCRG) is an uncommon and nonneoplastic reactive tumor that involves the maxilla and mandible in the region of the head and neck. It is rare in the nasal cavity, and it might be misdiagnosed. We reported a very aggressive GCRG with intracranial invasion, which was treated surgically via a combined approach of a lateral rhinotomy with a craniotomy by bilateral coronal incision. The pathology was consistent with GCRG. A short literature review about diagnosis, clinical behavior, and treatment of this tumor entity is given.

When an otherwise harmful insult to the brain is preceded by a brief, noninjurious stimulus, the brain becomes tolerant, and the resulting damage is reduced. Epileptic tolerance develops when brief seizures precede an episode of prolonged seizures (status epilepticus). MicroRNAs (miRNAs) are small, noncoding RNAs that function as post-transcriptional regulators of gene expression. We investigated how prior seizure preconditioning affects the miRNA response to status epilepticus evoked by intra-amygdalar kainic acid in mice. The miRNA was extracted from the ipsilateral CA3 subfield 24 hours after focal-onset status epilepticus in animals that had previously received either seizure preconditioning (tolerance) or no preconditioning (injury), and mature miRNA levels were measured using TaqMan low-density arrays. Expression of 21 miRNAs was increased, relative to control, after status epilepticus alone, and expression of 12 miRNAs was decreased. Increased miR-132 levels were matched with increased binding to Argonaute-2, a constituent of the RNA-induced silencing complex. In tolerant animals, expression responses of >40% of the injury-group-detected miRNAs differed, being either unchanged relative to control or down-regulated, and this included miR-132. In vivo microinjection of locked nucleic acid-modified oligonucleotides (antagomirs) against miR-132 depleted hippocampal miR-132 levels and reduced seizure-induced neuronal death. Thus, our data strongly suggest that miRNAs are important regulators of seizure-induced neuronal death.

Preconditioning brain with a sub-lethal stressor can temporarily generate a damage-refractory state. Microarray analyses have defined the changes in hippocampal gene expression that follow brief preconditioning seizures, but not the transcriptome after a prolonged and otherwise injurious seizure in previously preconditioned brain. Presently, microarray analysis was performed 24 h after status epilepticus in mice that had received previously either seizure preconditioning (tolerance) or sham-preconditioning (injury). Transcriptional changes in the hippocampal CA3 subfield of >or=2 fold were detected for 1357 genes in the tolerance group compared to a non-seizure control group, with 54% up-regulated. Of these regulated genes, 792 were also regulated in the injury group. Among the remaining 565 genes regulated only in tolerance, 73% were down-regulated. Analysis of the genes differentially suppressed in tolerance identified calcium signaling, ion channels and excitatory neurotransmitter receptors, and the synapse as over-represented among pathways, functions and compartments. Finally, 12 days continuous EEG recordings determined mice with induced tolerance had fewer spontaneous electrographic seizures compared to the injury group. Our data suggest the transcriptional phenotype of neuroprotection in tolerance may be dictated by the biology of the preconditioning stressor, functions by transcriptional reduction of vulnerability to excitotoxicity, and has anti-epileptogenic effects.

A 64-year-old man who had undergone single burr hole drainage twice prior to this admission was hospitalized with a recurrent right chronic subdural hematoma. A head CT showed a mixed density subdural hematoma on the right frontotemporoparietal region. Based on the intraoperative findings of the previous surgeries, the hematoma was known to be organized. Therefore, we decided to do a small craniotomy under general anesthesia, and remove the organized subdural hematoma and thick outer membrane while leaving the thickened dura matter intact. The inner membrane was left untouched. One week later, despite adequate decompression, the hematoma recurred with midline shift on head CT. It is likely that the uniquely thick and vascular enriched outer membrane and dura contributed to such an early recurrence. Finally, we performed an extensive craniotomy, removing all the organized hematoma, outer membrane and dura. Again, the inner membrane was left intact. On one year follow-up the patient has been asymptomatic with complete resolution of the subdural hematoma on CT scan. The successful treatment of organized chronic subdural hematoma can be challenging. We strongly recommend an extensive removal of the organized hematoma, outer membrane and excision of the dura mater in order to achieve a successful outcome after failed burr hole evacuation.