Angiography has become a rarely used tool in the initial stage of diagnosis and treatment of traumatic brain injury (TBI) since the advent of CT scan, which has overwhelming ability in this setting. Because of this declination of angio­graphy from the first choice tool in the treatment of TBI, it sometimes became difficult to diagnose traumatic vascular disorders (TVD) in the head and the neck in the early stage of TBI. On the other hand, development of 3-dimensional CT angiography (3D-CTA) and MR angiography (MRA) have made it possible to screen TVD less invasively. Any of those image examinations is recommended to be done in case with a strong probability of TVD in the head and the neck as follows: i) neurological condition difficult to be explained only by TBI, ii) delayed and newly-developed neurological symptoms, iii) newly-developed hemorrhage or infarction on CT or MRI, iv) neck injuries (fracture in the cervical vertebra, hyperextension or hyper-rotation of the neck, etc.), v) cranial base fracture (bleeding from the nasal cavity or external auditory meatus, etc.), vi) thick, diffuse, severe subarachnoid hemorrhage or localized intense sub­arachnoid hemorrhage. Treatment is indicated when bleed­ing or non-bleeding TVD are detected and should be per­formed as soon as possible. Cerebral angiography is still being the gold standard technique because the entire vas­cular system from cervical to intracranial area can be examined in a single examination, and also it enables immediate endovascular treatment to be initiated. As for type of ves­sel injury, TVD comprise vascular rupture, arterial occlusion, sinus thrombosis, tramuatic aneurysm, arteriovenous fistula, and cerebral vasospasm after traumatic subarachnoid hemorrhage. In this manuscript, details of pathogenesis, symptoms and treatment are discussed with representative cases.

Acute subdural hematoma (ASDH) usually arise from the contusion of the cerebral cortex or sometimes arise from the laceration of bridging vein by high speed acceleration injuries. Bleedings from pinpoint source in cortical arteries are reported rarely, and the mechanism of the bleeding is unknown.

Between 1998 and 2010, 51 patients with ASDH underwent surgery with craniotomy in our hospital, and in 11 cases, the cause of the bleeding was rupture of single cortica­l artery. In microscopic observation, we found micro­aneurysm at the bleeding point in nearest 4 cases.

ASDH of arterial origin is thought to arise from the lacera­tion of the adhesion between a cortical artery and dura mater, or spontaneous rupture of an arterial twig from cortical artery, which is a point of potential weakness. On the other hand, rupture of the cerebral aneurysm can cause ASDH, and its onset is similar to that of “spontaneous” ASDH, which presents a stroke-like episode. We thought that micro­aneurysms of the cortical artery can be found more frequently in microscopic observation during the surgery of ASDH, and many cases of “spontaneous” ASDH can include rupture of the aneurysm, either traumatic or non-traumatic.

Purpose: Blunt traumatic cerebrocervical vascular injury (VI) provides a tremendous challenge to the neurosurgeons. The diagnosis and intravascular and/or surgical management of VI remains controversial, with direct surgical repair or endovascular surgery with parent artery preservation still presenting difficulties. The purpose of this study was to assess the long term results of surgical treatment of VI.

Materials: The delayed outcomes and graft patency rates of patients who underwent bypass procedures for VI were also studied from September 1997, 6 patients (4 male and 2 female patients; mean age, 35 yr) underwent 7 procedures for blunt traumatic VI.

Results: The type and number of injuries were; carotid cavernous fistula 3, intracranial carotid aneurysm 1, cervical extracranial carotid artery dissection 1, and distal anterior cerebral artery aneurysm 1. Diagnoses were made by using CT angiography, MRA, MRI, or digital subtraction angio­graphy. There were 4 radial artery graft bypasses (cervical external carotid artery to radial artery to middle cerebral artery anastomosis), 1 superficial temporal artery to middle cerebral artery bypasses, and 1 direct aneurysm clipping. The Glasgow outcome scale score was 5 in all patients at 1 year from the ictus without any additional neurological deficit. Follow up MRI and MRA (9 to 15 years) detected no new legion or graft occlusion.

Conclusion: Our results indicate that open direct surgery is an acceptable strategy and associated with excellent long-term outcomes and patency rates to treat complex VI.

Sport-related head injuries, especially in Judo, are still remained in common serious problems. Although it is urgent to reduce a high mortality rate, no detailed information regarding Judo-induced brain injury is yet available in Japan. In the present study, we investigated to clarify characteristics and preventive measures of Judo-induced TBI (Traumatic brain injury) school patients in Japan. Over the last 6-years period from 2006 to 2010, 24 students died and 60 students suffered severe injuries as a result of judo accidents in junior and senior high schools. The data was collected from the record of National Agency for the Advancement of Sports and Health (NAASH) and the all Japan Judo Federation, and characteristics were studied. Review of the record revealed that an annual number of student death was four cases. Among 24 dead students, 15 (62.5%) were in the first grade of junior and senior high schools. Among the 60 severe injury students, 28 (46.7%) were a freshman in junior and senior high schools, 21 (35.0%) were a freshman in senior high school. The incidence of fatality and severe injury were significantly high in beginners. Seventeen cases (70.8%) of 24 were died from brain injury. At least 9 cases resulted from acute subdural hematoma. Twenty seven cases (45.0%) of 60 were severe injury from brain and face injury, and 14 cases (23.3%) were cervical injury. The leading cause of throwing prior to TBI was Oosotogari (Major Outer Reaping) in 9 patients, to cervical injury was Seoinage (Shoulder Throw) and Haraigoshi (Sweeping hip throw) were with 10 patients’ cases respectively.

We explored that Oosotogari will cause a coup injury to beginners, and Seoinage and Haraigoshi will cause a neck injury to all players.

These results suggest the incidence of basic concept to have enough protective training such as Ukemi before fighting and to establish playing rules including safety guard devices for the prevention of fatal TBI in student Judo players.

Objective: Post-traumatic cerebral infarction (PTCI), an infarction in well-defined arterial distributions after traumatic brain injury (TBI), is a known complication in patients with severe head trauma. In this report, we analyzed the characteristics of cases associated with PTCI, and demonstrated an impact of cerebral infarction on TBI.

Methods: 2780 patients with TBI were admitted to our hospital from Jan. 1994 to Dec. 2010. In 2780 patients, fifty-two patients showed cerebral infarction during the hospitalization. We analyzed the characteristics of these patients. We classified the cause of PTCI into three groups, 1) cerebral infarction caused with direct traumatic factor, 2) cerebral infarction as cerebrovascular attack, and 3) miscellaneous group.

Results: Seventeen cases of the cerebral infarction were caused by brain herniation. Cases with brain herniation were excluded from this investigation. Finally thirty-five cases were enrolled in this study. Cerebral infarction caused with direct traumatic factors is dominating (19 patients; 54.3%). 7 patients (20%) had shown traumatic cerebral vaso­spasm as a cause of brain infarction. Only 10 patients presented cerebral infarction for cerebrovascular attack. In these 10 patients, five patients had shown cerebral embolism. TBI as­sociated with cerebral embolism demonstrated poor neurological prognosis. Three patients with cerebral embolism died during the hospitalization. Totally, 60% of patients with PTCI suffered from neurological deterioration on discharge.

Conclusion: PTCI aggravates symptoms and neurological outcome of TBI. Prevention against PTCI is important to improve the prognosis of TBI.

Introduction: To fully understand the pathology of head injury, we categorize severe head injury on the basis of injury type, and we compare clinical factors and biochemical markers between groups.

Subjects: A total of 55 patients with a mean age of 54.9 years (range, 15 – 84 years) were enrolled in the study after excluding those who died within 24 h of arrival, those with cardiopulmonary arrest on admission, and those with a Glasgow Coma Scale (GCS) score of ≤ 8.

Methods: Patients were divided into groups on the basis of diffuse injury (D), evacuated mass lesion (E), and non-evacuated mass lesion (NE) in accordance with National Traumatic Coma Data Bank (TCDB) computed tomography (CT) scan classification. Factors such as age, sex, GCS value, cause of injury, mortality rate, Glasgow Outcome Scale (GOS) value, coagulation factors, inflammatory condition, and escaped enzymes were compared, and the Student's t-test was used for statistical analysis.

Results: The number of patients in groups D, E, and NE was 28, 26, and 1, respectively. The mean age was 52.3 years and 58.8 years in groups D and E, respectively. With regard to cause of injury, group D had an overwhelmingly high rate of traffic-related injury. The mortality rate was 7% in group D and 23% in group E. A comparison of biochemical markers revealed that while LDH was significantly high in group D, group E had significantly high stress index (Glu/K) levels. In addition, group E tended to have more severe coagulation abnormalities.

Discussion: Group D patients were characterized by relatively young age and high-energy trauma. Despite minor coagulation abnormalities and a low mortality rate, the patients had poor functional outcome. On the other hand, group E patients presented with multifactorial injuries, such as different forms of hematomas, and it was therefore difficult to identify specific characteristics.

Background: Although penetrating brain injury is relatively rare, this should be treated with the appropriate strategy. Showing our recent two cases, we would like to show our therapeutic strategy for this injury.

Case Report: Case No.1; Working in a factory, a 65-year-old man felled down and a steel column penetrated his neck. This steel column was removed and he was transferred to our emergency room. At the arrival, his consciousness was slightly impaired. After the procedure of neck wound, he was getting drowsy. Because brain CT revealed skull base fracture and intracranial hemorrhage in the left frontal lobe, an emergency operation was performed. Case No.2; After drinking alcohol, a 54-year-old man fell down in the garden and a gardening strut penetrated his left orbita. Without removing the gardening strut, he was transferred to our emergency room. At the arrival, he was alert, but, his eye of movement (EOM) was limited to the all directions. Brain CT revealed the edge of the gardening strut was in the intracranial, and a broken tip of skull bone was invaginated into the frontal lobe. Intracranial air and hemorrhage are also found in the frontal lobe and in the ventricles. 3DCTA and 3DCTV revealed no damage of the major vessels. Under the general anesthesia, bicoronal craniotomy was performed and the damaged dura was removed. Then the gardening strut was removed from the outside of clean operation area, and the invaginated tip of skull bone was also removed. The damaged dura was repaired by pericranial flap and the defect of the orbital roof was repaired by a titanium plate. Disorder of EOM disappeared one month after the operation and EOM has not been got worse even one year after the operation.

Discussion & Conclusion: To treat penetrating brain injury, proper operation strategy, proper major vessels evaluation before operation and proper infection control as well as prevention of cerebrospinal rhinorrhea after operation are required. In the operation for penetrating brain injury, using foreign bodies such as a titanium plate to repair the bone defect of the orbita may be controversial, however, this method would be useful for the long term preservation of EOM.

In development of support system for higher brain dys­function mainly related to traumatic brain injury, Ibaraki prefecture seemed to have two main problems as follows:　1) network formation among related organizations did not effectively progress 2) development of support system in acute and recovery phase was insufficient. Therefore we started 2 trials to solve these two problems. First, we established “Association of support and cooperation for higher brain dysfunction in Ibaraki prefecture”, including almost all related organizations as voluntary sponsors in June 2011, for the main purpose of acceleration of network for­mation among them. This association already held 3 lec­ture meetings in a year and actually gave the opportunities to get friendship among participants. Second, we established a screening system for evaluation of higher brain dysfunction –i HBF battery– in recovery phase in October 2010. Both trials are still going on and in the future we would like to start further trials such as establishment of regional alliance path for higher brain dysfunction, cultivation of life supporter, and so on.

The authors present two cases of syncope presenting as falls. A 62-year-old man hit on the forehead after an un­explained fall, whose dissecting aortic aneurysm turned out the cause of the collapse and a 72-year-old man presented with chronic subdural hematoma after frequent falls, whose arrhythmia (sick sinus syndrome) was proved responsible for the repeated faintness. With a careful history and physical examination, the victims of syncope should be detected among a great number of patients with head injury brought to the emergency departments, because they require different management from simple head injury. To get a clue to distinguish them more effectively, the authors compared the clinical features between 1027 patients with head injury after an accidental fall (group A) and 48 patients with head injury after syncope (group B). As a result, 221 frontofacial injuries (22%), 43 facial fractures (4.2%), and 801 upper limb injuries (78%) were found in group A and 18 (38%), 8 (17%), and 16 (33%) respectively in group B. During a fall, hands and arms are more often injured, because the upper extremities are usually extended to protect head and trunk due to postural reflexes. After syncope, global cerebral hypoperfusion might restrain those reflexes from working normally and consequently head and face may get more directly hurt without upper limbs protection. These results show that patients with head and face injury after an unexplained fall, especially when neither hands nor arms are injured, are most likely to be related with syncope and need further investigation.

Objective: The objective of this study is to evaluate risk factor of embolism and bleeding, and prognosis in patients with chronic subdural hematoma (CSH) under anticoagulant therapy (ACT).

Materials & Method: The subjects consisted of 92 patients with CSH who had been hospitalized from January to December 2010. INR values at the time of hospitalization, CHADS₂ score (the risk score of embolism), and HAS-BLED score (the risk score of bleeding), in 13 patients with ACT were compared to those of 79 CSH patients without ACT (control group). Dementia and history of stroke, age, head injury were also examined. In view of change of mRS score from admission to discharge, we divided into two groups, an exacerbate group and a no-change group.

Results: The ratio of dementia and history of stroke in ACT group was significantly higher than in control group. In ACT group, INR values at the time of hospitalization were 1.1 – 3.1 (mean 1.99). In one patient, the INR value was higher than therapeutic range. Six patients with low CHADS₂ score (low embolism risks), and 11 patients with high HAS-BLED score (high bleeding risk) were detected. The ratio of the exacerbate group in ACT group was higher than that of control group and the average age of the exacer­bate group was significantly higher than that of the no-change group.

Conclusion: The prognosis of CSH patients with ACT was poor. We should pay more attention in ACT to patients with low CHADS₂ score and high HAS-BLED score.

Objective. To investigate the cause of poor prognosis of traumatic acute subdural hematoma (TaSDH) in patients on pre-injury antiplatelets and/or anticoagulants (antithrombotic agents), we retrospectively reviewed our own cases.

Materials and Methods. From 2001 to 2011, we managed 7 surgically treated patients with TaSDH on pre-injury anti­thrombotic agents (antithrombotic group) and 63 without antithrombotic agents (non antithrombotic group). Age and gender of the patients, the mechanisms of injury, cause of antithrombotic agents on antithrombotic group, post­operative clinical course and outcomes were analyzed.

Results. On antithrombotic group, 6 were male, 1 female. The average age of injury was 77.6 years. Warfarin was prescribed in 3 cases for atrial fibrillation and in 1 for deep venous thrombosis, combination of warfarin and aspirin prescribed in 2 for myocardial infarction, ticlopidine in 1 for MI. The mechanisms of injury included involvement of traffic accident in 3 cases, fall downstairs in 3 and fall on the road in 1. Decompressive craniectomy, evacuation of hematoma, placement of external ventricular drainage and intracranial pressure monitoring and normothermia were carried out on acute stage. Outcomes at discharge were severely disabled in 3 cases, persistent vegetative status in 1 and dead in 2. Compared with the cases on non anti­thrombotic group, patient's age was significantly higher than that on nonantithrombotic group (77 years old vs. 63 years old; p<0.05).

Conclusions. Patients with TaSDH on pre-injury anti­thrombotic agents have older age and poorer outcomes than those without antithrombotic agents. Physicians should beware of prescribing antithrombotic agents for elderly patients to avoid excessive primary hemorrhagic cause.

A 4-month-old girl was suddenly suffered from generalized convulsion probably caused by meningitis, which was diagnosed at a previous hospital, and transferred to our hospital in emergency. On admission to our PICU, she grew worse with intractable convulsion without consciousness, and was diagnosed as an acute encephalopathy introduced by meningitis with the findings of routine MRI at hospitalization. One week later, however, the results of head 3D-CT and MRI re-checked by neurosurgeons raised a suspicion of head injury caused by child abuse. The closer hearing of clinical course with her parents proved the abuse by her grandmother. This case suggests that it should be necessary to consider a possibility of child abuse for even a case once diagnosed as an acute encephalopathy, and to apply various kinds of image studies and examination with a fundoscopy.

The typical clinical manifestation of Type I Chiari malformation is slowly progressive mainly in the adults. Therefore, it is rare to see the patient in acute progression of the disease, especially in the childhood. We had a 7-year-old boy with mild head trauma associated with formerly unknown Type I Chiari malformation. He had no neurological deficit other than nystagmus and headache right after the blow in the left retroauricular area. Computed tomography revealed hemorrhagic contusion in the left cerebellar tonsil. Magnetic resonan­ce (MR) image revealed tonsillar herniation to the foramen magnum and a hypoplasia of the corpus callosum, which were the strong evidence of the Type I Chiari malformation. The headache gradually improved without any invasive treatment. In the literature, some authors pointed out that the cerebellar contusion occasionally results in acute neurological deterioration. When it happens to the Chiari Type I malformation patient whose cerebellar tonsils are already herniated, the symptom could be worse. We have to be aware of such traumatic pediatric patients harboring Chiari Type I malformation.

We report a case of reversible findings of ¹²³I-IMZ-SPECT in a patient with traumatic epilepsy. A 78-years-woman suffered from traumatic acute subdural hematoma without cerebral contusion. She underwent emergent surgical hematoma evacuation on the same day. Though her post operative course was uneventful, epileptic seizure occurred on day 11. Her symptoms was prolonged, then improved gradually. On the first study (day16) ¹²³I-IMZ-SPECT showed cortical accumulation loss in the right hemisphere, and these accumulation loss recovered on second study (day 44). Generally, accumulation loss in ¹²³I-IMZ-SPECT indicates irreversible neuronal damage. In the present case with traumatic epilepsy, improvement of accumulation loss was observed. It is thought that ¹²³I-IMZ-SPECT can detect both irreversible and reversible brain damages.

Based on the Japan Society of Neurotraumatology guidelines for management of severe head injury, delayed-onset traumatic cerebrospinal fluid (CSF) leakage should be treated by the surgical repair, because it is hard to cure the leakage completely by conservative therapy. However, it is not always easy to determine the location of the leak to be repaired when the leak is intermittent.

This time, we treated a 62-year-old male with delayed-onset traumatic CSF rhinorrhea. He had a closed head injury and lost his left eye sight in the motor cycle accident 37 years ago. We performed a left frontal craniotomy to repair the CSF fistula. During the operation, we confirmed a fistula of the left fronto-basal bone. But intraoperative CT revealed that the location of the fistula was different from where we had predicted before operation. Very thin bone was observed there. We covered both the leak point and the very thin bone using pericranial flap. He had no recurrence of rhinorrhea in 11 months of follow-up.

We have reported three patients with acute subdural hematoma (ASDH) due to second head injury in concussion state during snowboarding. The outcome of two cases was good and that of the other one was fatal.

Patient 1; 19-year-old man suffered from an occipital hit and causing nausea with transient loss of consciousness (LOC). CT scan on that day was normal. Next day, he had another neck injury and got CT scan again, which showed thin ASDH not requiring evacuation. Patient 2; 22-year-old woman experienced transient LOC after occipital hit, suf­fered from head injury again on the next day. She became comatose rapidly after the second injury. Immediate re­moval of ASDH restored her consciousness although she had permanent diplopia. Patient 3; 32-year-old man suf­fered from an occipital hit and presented transient LOC followed by amnesia. He continued snowboarding ignoring the physician's restraint. He fell down four hours after the first hit and was transferred to our institute in coma. Severe brain swelling was confirmed in emergent craniotomy and the patient died sixteen days later.

Concussion is most common head injury in sports and the subsequent second impact in post concussive state might result in poor outcome, as known as second impact syndrome (SIS). Patient 3 might correspond to SIS caused even in non-contact recreational snowboarding. An importance of appropriate conceptual education must contribute to the safety management of this sport to avoid severe head injury. Enlightenment and knowledge of SIS should be recognized for the sports physicians as well as the snowboarders.