In 2007, the second edition of the Japan Society of Neurotraumatology (JSNT) Guidelines for the Management of Severe Head Injury were published and disseminated. Also, the third edition of the Brain Trauma Foundation (BTF) guidelines were established in the US in 2007. In these guidelines, the use of intracranial pressure monitoring is recommended in severe traumatic brain injury (TBI) patients, and several additional neuromonitorings were also added as optional recommendations. In the US guideline, brain tissue oxygenation monitoring was added as a new topic. In Japan, clinical microdialysis use was approved in 2007, and it has been applied for the estimation of cerebral circulation and metabolism in severe TBI patients. In this article, we review up-to-date neuromonitorings from the viewpoint of the latest Japanese and US guidelines, and we discuss the topics and problems with them.

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No treatment method for severe traumatic brain injury (TBI) has proven effective to replace hypothermia therapy, emphasizing the major role of this therapy for patients with TBI. To improve the effectiveness of hypothermia therapy, earlier hypothermia induction is necessary, and management of brain temperature should be based on individual pathophysiology through neuromonitoring during the maintenance and rewarming periods of this therapy. Recently, the protective effects of hypothermia therapy have been confirmed for patients with severe TBI after craniotomy. The outcome of TBI patients with hypothermia therapy is expected to improve with the use of the brain temperature management method and selection of appropriate pathophysiology.

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Introduction: Higher brain dysfunction is the major problem of patients who recover from neurotrauma the prevents them from returning to their previous social life. Many such patients do not have focal brain damage detected with morphological imaging. We focused on studying the focal brain dysfunction that can be detected only with functional imaging with positron emission tomography (PET) in relation to the score of various cognition batteries. Methods: Patients who complain of higher brain dysfunction without apparent morphological cortical damage were recruited for this study. Thirteen patients with diffuse axonal injury (DAI) or cerebral concussion was included. They underwent a PET study to image: 1) glucose metabolism by ^<18>F-FDG, and 2) central benodiazepine receptor (cBZD-R) (marker of neuronal body) by ^<11>C-flumazenil, together with cognition measurement by WAIS-R, WMS-R, and WCST etc. PET data were compared with age matched normal controls using SPM2. Results: 1) DAI patients had a significant decrease in glucose matabolism and cBZD-R distribution in the cingulated cortex than normal controls. 2) Patients diagnosed with concussion because of shorter consciousness disturbance also had abnormal FDG uptake and cBZD-R distribution. 3) Cognition test scores were variable among patients. Degree of decreased glucose metabolism and cBZD-R distribution in the dominant hemishphere corresponded well to the severity of cognitive disturbance. Conclusions: PET molecular imaging was useful to depict focal cortical dysfunction of neurotrauma patients even when morphological change was not apparent. This method may be promising to clarify the pathophysiology of higher brain dysfunction of patients with diffuse axonal injury or chronic traumatic encephalopathy.

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Intracranial hypotension is a syndrome in which the predominating symptom is orthostatic headache due to cerebrospinal fluid leakage. It has been known for over 70 years, so this syndrome is not a newly established clinical entity. However, this syndrome is attracting much attention today, because there are currently many discussions about the relationship between this syndrome and "Whiplash" after traffic accidents. The terms "Cerebrospinal fluid hypovolemia" and "Intracranial hypotension" are often used synonymously. The former is used more often recently because there are patients whose intracranial pressures are normal. In order to clarify the clinical characteristics of intracranial hypotension following head injury, the Japan Society for Neurotraumatology reviewed over 300 articles about this syndrome. According to their report, the clinical entity of intracranial hypotension following head injury treated in Japan seems to differ from that treated in foreign countries. As mentioned above, there is still controversy about the mechanism and diagnosis of cerebrospinal fluid hypovolemia including intracranial hypotension following head injury. From 2007, the "Cerebrospinal fluid hypovolemia research group" granted by the Ministry of Health, Labour and Welfare has worked to solve issues about this syndrome. In this paper, we want to present a concept for and several issues of intracranial hypotension following head injury, based on the interim report of that research group.

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A blast wave (BW) is generated by an explosion and is comprised of a lead shock wave followed by a subsequent supersonic flow. Pressure induced damage accounts for the occurrence of blast-induced TBI (bTBI) (primary bTBI) in addition to mechanisms observed in civilian traumatic brain injury. Fracture, hemorrhage, massive and rapid edema progression, and cerebral vasospasm characterize the clinical findings of bTBI in the acute phase, whereas cognitive dysfunction and posttraumatic disorder do in the chronic period. Since BW is invisible, and impacts the brain in an extremely short period of time in contrast to penetrating (secondary bTBI) and direct impact mechanism (tertiary bTBI) injury, it is often difficult to screen out the patients who are at high risk. In addition, there have been few animal models experiments that can be conducted in the laboratory and validated in terms of SW physics, which precluded us from understanding the mechanism and pathophysiology of bTBI. On the other hand, we have successfully formed organized infrastructures and accumulated knowledge of SW and BW at the Institute of Fluid Science since 1980s both for engineering issues and medical application. Our translational research platform now covers a broad range of issues related to SW (BW) and brain injury, including the development of a clinically relevant bTBI model as a bedside to bench approach, and the development of a surgical instrument applying shock bubble interaction (one of the mechanisms of SW-induced tissue injury) as a bench to bedside approach. The medical instrument is now clinically applied in neurosurgery as a laser-induced liquid jet, and has shown advantages over conventional surgical instruments. Efforts to utilize the system in minimally invasive surgery and to expand the application in endoscopic surgery became our current goal. In the present article, we describe the mechanism of bTBI and current research problems from the perspectives of SW physics. We also describe our translational research platform aiming to facilitate understanding of TBI and improve clinical treatment for TBI.

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The Great East Japan Earthquake on March, 2011 and the subsequent extremely destructive tsunami struck a wide area of eastern Japan and took a heavy toll of lives. The epicenter was 130 kilometers east of the Oshika Peninsula, which is a part of the City of Ishinomaki. The northeastern area of Miyagi prefecture, the region closest to the epicenter, was a one of the areas most severely damaged by this catastrophe. Ishinomaki Red Cross Hospital, which is located on the Pacific coast in the northeastern area of Miyagi prefecture, was the only reference hospital in the area at the time of the earthquake, and was practically the only medical facility remaining in operation in the aftermath of the disaster. Accordingly, our hospital was swarming with patients and had considerable difficulty in providing appropriate neurosurgical service. To understand the impact of the disaster on neurosurgical service at our hospital, the number of new outpatients presenting with neurological disorders in the following 5 weeks was evaluated and compared with the average number during the same time of year in the past 3 years. The object diseases were cerebrovascular disease, head trauma, epilepsy, syncope, nonorganic headache and vertigo, and chronic subdural hematoma. Cerebrovascular disease and head trauma increased in number as well as in average ages immediately following the disaster. Accordingly, the number of chronic subdural hematoma cases increased 1-3 month after the disaster. Cases of epilepsy and syncope notably increased in the first week after the earthquake. The increase in the numbers of patients with these conditions may have resulted both from the increased number of patients seeking treatment at our hospital as well as from genuine increases in the prevalence of these conditions.

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Removal of the anterior clinoid process (ACP) is an essential technique in skull base surgery. The trans-superior orbital fissure (SOF) extradural anterior clinoidectomy (trans-SOF method) is a recently developed method involving resection of the meningo-orbital band, peeling the dura propria from the SOF, exposing the entire ACP, and drilling away the ACP. If cutting the medial tentorial edge is added after the trans-SOF method, we can transpose to the extradural temporopolar trans-cavernous approach. We illustrate this method using the three-dimensional skull base model with artificial cavernous sinus and intraoperative photographs. We performed the trans-SOF method in the 21 patient. The incidences of postoperative visual acuity (5%) and field disturbance (10%) were relatively low. The trans-SOF method is safe to remove the ACP under direct operative view and can be transposed to the trans-cavernous approach if necessary.

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Intracranial osteoma without connection to the dura mater/inner table of the skull has rarely been reported in the literature and there were thought to be only six such cases. In the present study, we reported a case with sudden-onset headache followed by intermittent headache caused by an intracranial osteoma located in the subarachnoid space without any involvement at the dura mater/inner table of the skull in the right parietal region. The tumor was thought to be an osteoma or ossified meningoma. It was surgically removed. It was totally located in the subarachnoid space and there were no connection between the tumor and the dura mater except for a few fine vessels connected between them. Pathological study showed benign osteoma.

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