In cases with traumatic brain injury (TBI), main purposes of surgery is to control intracranial pressure (ICP), increased by both intracranial hematomas and edema. In this paper, basic techniques, variations and pitfalls of surgical treatments for TBI are presented.
  In acute epidural hematoma, the whole area of the hematoma should be involved in the craniotomy in order to remove the hematoma and to access the bleeding point. Craniotomy, consisting of a couple of bone windows across the dural sinus, is useful for dural tenting to obtain effective hemostasis in cases with dural sinus injuries. In acute subdural hematoma, large craniotomy is generally selected concerning subsequent decompressive craniectomy. In such craniotomy/craniectomy, injuries of dural sinuses and/or bridging veins should be carefully avoided, and the middle fossa should be effectively decompressed. In cases with urgent tentorial herniation, one burr-hole craniectomy or trephination is useful to achieve quick ICP reduction by partial hematoma evacuation. Since ICP reduction is only temporary only by such procedures, subsequent craniotomy is required. Contusion necrotomy is applied in cases with uncontrollable intracranial hypertension and/or clinical deterioration mainly due to contusional hematomas. In cases with severe TBI without significant intracranial hematomas, uni-or bilateral decompressive craniectomy may be required as the need arises from ICP monitoring, such as acute brain swelling.
  Surgical treatments for TBI are simple, and advanced technical skills may not be required. Since combined procedures are often required in various clinical settings, mastering basic surgical techniques is important as well as avoiding pitfalls.

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  The guidelines for the management of severe traumatic brain injury, 3rd revised edition, were published in 2013 by the Guideline Committee on the Management of Severe Head Injury, the Japan Society of Neurotraumatology. These guidelines were prepared to serve an academic purpose for use by primary care physicians dealing with head injuries such as neurosurgeons and emergency care physicians. In the 3rd edition, the chapters on the emergency care system and neurosurgery, initial treatment to protect the brain, ICU management, surgical indications and procedures, management of craniofacial injuries, management of pediatric and geriatric patients, and management of mild or moderate head injuries were subject to revisions and corrections following in the 2nd edition's footsteps. A chapter on radiological examinations was newly prepared, and items on sports head injury, neuropsychological disorders following head injury and intracranial hypotension accompanied by trauma were also prepared as a supplement. In the present manuscript, the chapter-updated 3rd edition is explained, and an examination is made of how the guidelines influence the treatment of severe traumatic brain injury based on data from the Japan Neurotrauma Data Bank.

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  Disordered haemostasis is a known complication following traumatic brain injury. In the event of brain parenchymal injury, coagulapathy is significantly prolonged to support activation of the extrinsic pathway of the coagulation cascade by tissue thromboplastin. We experienced such a difficult to treat brain parenchymal hemorrhage in decompression craniotomy that resulted in a poor outcome.
  In this study, we focus on hemorrhage due to the fibrinogenolysis effect of second brain injury and patient outcome. We also show the importance of monitoring haemostatic markers when treating traumatic brain injury and provide practical guidelines.
  The objective of this study was to determine the clinical significance of coagulation and fibrinogenolysis in 247 patients with traumatic brain injury and compare the shift of haemostatic markers.
  Univariate analyses for survival and non-survival was performed by determining the association between clinical factor (age, GCS, ISS), hemocoagulative factor and mortality. When simultaneously adjusting for all these factors in multivariate analysis, patient age, initial GCS and plasma D-dimer values were found to be independent predicting factors of mortality. Mortality was most strongly related to an age greater than 57 years, an initial GCS of 7 points and a less than 50 μg/ml of plasma D-dimer value level. As for haemostatic marker shifting dynamic change in the short-term after traumatic brain injury, we found that coagulation and fibrinogenolysis initially increase within the first 3 hours, the secondary inhibitor of fibrinogenolysis increases within 6 hours, and that fibrinogen increases over 6 hours after brain injury. The most important factor in haemostatic shift was the peak of plasma D-dimer values within 3 hours after brain injury.
  Fibrinogenolysis with an increased plasma D-dimer value was associated with a prediction of mortality and the degree that the brain parenchymal damage influenced systemic haemostasis in the early phase within 1 hour after brain injury and increases within 3 hours after brain injury. There is also an initial hypercoagulable stage that follows 6 hours after brain injury. Therefore, it is important for us to recognize haemostatic disorders when treating brain injury in the acute phase and practical use should be made of haemostatic shift values after brain injury.

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  After suffering traumatic brain injury (TBI), there may be a substantial number of disabled people whose impairment is not recognized socially because their disabilities are limited to cognitive, emotional and behavioral domains, with no obvious physical deficits. The Japanese Government has provided medico-social services for such patients diagnosed with impairments of executive brain function (IEBF), since 2006. One of the administrative criteria for diagnosis of IEBF to receive medico-social services is the confirmation of organic injured lesions in the brain by neuroimaging modalities. Consequently, some people with chronic stage TBI have been excluded from receiving services because no lesions were apparent on conventional CT or MRI. Recent development of SPECT, PET and new MRI neuroimaging modalities make it possible to detect regions of metabolic dysfunction where organic injured lesions may be absent or have not been detected on conventional CT or MRI.
  One of the most crucial diagnostic findings of diffuse TBI in the chronic stage on conventional CT or MRI is diffuse brain atrophy. T2^* weighted imaging (WI) and susceptibility WI (SWI) are extremely sensitive methods to detect hemosiderin-lading lesions even in the chronic stage. Another method, diffusion tensor imaging (DTI), permits the evaluation of white matter structural integrity in the brain. One index used in DTI is the fractional anisotropy (FA) value. A region of interest (ROI) study of FA values in patients with diffuse TBI revealed significant decreases in the corpus callosum, coronal radiation, centrum semiovale, cingulated gyrus. Tractogram derived by fiber tracking on FA map is an innovative neuroimaging technique, which reveals axonal deficits visually. Another innovative neuroimaging tool derived from DTI is the FA-SPM image. This permits the detection of lesions with significantly decreased FA values objectively and over the whole brain. Alternatively, FDG-PET and ECD-SPECT are functional neuroimaging modalities which can uncover the regions with metabolic dysfunction in the brain. In patients with diffuse TBI, metabolic dysfunction is characteristically shown in the medial part of the prefrontal region and the base of the bilateral frontal lobes, the bilateral cingulated gyri, and the bilateral thalami, in the chronic stage.
  The findings suggesting the existence of minute lesions due to TBI on these new neuroimaging modalities may be useful evidence for diagnosing IEBF administratively, and also serve as a tool for elucidating the mechanisms of IEBF after TBI.

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  We performed microvascular decompression for spontaneous trigeminal neuralgia, with the aim of separating all compressing or contacting vessels from the trigeminal nerve, and investigated the effects of the type and number of compressing or contacting vessels, and the pattern of the compression or connection observed intraoperatively on the incidences of complication and recurrence, and rate of cure. The outcomes of the present and previous procedures were compared to validate the effectiveness. A total of 116 consecutive patients were followed up for 1 to 9 years (mean 3.6 years). Postoperative complications were temporary in 17% and persistent in 1%, and the incidence of complications was high in patients with 3 or more compressing or contacting vessels, or in whom the superior cerebellar artery was not the compressing vessel. Residual symptoms or recurrence was found in 13 patients, but was not related to intraoperative findings. The incidence of persistent complications was 1%, recurrence rate was 9%, and cure rate was 97% immediately after the operation and 91-88% at 1-3 years postoperatively.
  These findings indicate that our present procedure emphasizing the identification and separation of all compressing or contacting vessels and prevention of recurrence caused by postoperative change in location of such vessels resulted in increased incidence of temporary complications in patients with complex angiographic structure, but decreased incidence of persistent complications or recurrence and increased cure rate. Therefore, we recommend our treatment strategy.

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  Papillary glioneuronal tumors (PGNT) are a rare tumor type, which were only recently recognized and histologically characterized by their pseudopapillary architecture associated with compact areas composed of neuronal elements in different maturation states.
  The authors present 17-year-old woman with papillary glioneuronal tumor. She was admitted to our institute because of a temporal mass discovered accidentally. Imaging showed a demarcated, mainly solid and partly cystic subcortical tumor in the right temporal lobe. The patient underwent surgery for total resection of the lesion. Histologically, it was a biphasic tumor characterized by small cuboidal GFAP-positive astrocytes around hyalinised blood vessels and synaptophysin-positive interpapillary collections of neurocytes. After surgery, she remains asymptomatic with no tumor recurrence at her one-year follow-up.

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  A 21-year-old man presented with a 1-month history of right orbital pain and a 2-week history of progressive ptosis and diplopia. Neurological examination revealed right third nerve palsy. Magnetic resonance imaging (MRI) demonstrated a mass lesion which was of mixed intensity on T1-and T2-weighted images in the cavernous sinus. During surgery, the tumor was found to be entirely within the dural layers of the lateral wall of the cavernous sinus. Histological analysis confirmed a diagnosis of mature teratoma. Teratoma of the lateral wall of the cavernous sinus is extremely rare and only five cases have been reported. The clinical course along with the computed tomography (CT) and MRI findings of the present case are discussed, and the literature on this rare location of teratoma is reviewed.

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