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Objective: With the increase in the aged population, geriatric traumatic brain injury (gTBI) is also rapidly increasing in Japan. There is thus a need to review the effect of intensive treatments for gTBIs. The aim of this study was 1) to assess how intensive treatments influenced patient outcome and 2) to identify the refractory factor against these intensive treatments in gTBI, from the Japan Neurotrauma Data Bank (JNTDB)., Methods: Of all 3194 patients in the JNTDB, 1165 (≥ 65 years old) with severe gTBIs were enrolled in this study. The clinical features and their outcomes based on the Glasgow Outcome Scale on discharge and 6 months after injury were compared., Results: Intensive treatments were administered to 71.4% of all patients with severe gTBI showing a significant increase over 15 years. Accordingly, mortality decreased significantly (from 62.7% to 51.1%, P = 0.001). On the other hand, severely disabled dependent survivors, who need daily help from others for living, increased accordingly (from 63.2% to 68.4%). The existence of intraventricular hemorrhage (IVH) rather than the patient's age was identified as the strongest refractory factor (odds ratio, 5.762; 95% confidence interval, 1.317-25.216) against intensive treatment., Conclusions: This study clarified that 1) intensive treatments are associated with higher survival rates (however, they also increase the incidence of severely disabled survivors) and 2) the strongest refractory factor for intensive treatment in cases of severe gTBI was not age but the existence of IVH. These results warrant further establishment of a seamless strategy for both the acute and the chronic phase of gTBI., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Traumatic cerebrovascular injury (TCVI) is a serious complication of severe head injury, with a high mortality rate. To establish a proper treatment strategy for TCVI, we investigated patients with a high risk of TCVI according to the Guidelines for the Management of Severe Head Injury (hereafter "the Guidelines") to elucidate the validity of the criteria for TCVI in the Guidelines and the appropriate screening timing and methods. Of those transported to our facility between December 2008 and June 2012, 67 individuals with a high risk of TCVI were evaluated to reveal the proper timing and methods of vascular evaluation. Of the 67 patients, 21 had a diagnosis of TCVI based on cerebral angiography, three-dimensional computed tomography angiography (3DCTA), or magnetic resonance imaging (MRI), accounting for 6.4% of all patients with severe head injury and as high as 31.3% of patients with a high risk of TCVI according to the Guidelines. In addition, according to the Glasgow Outcome Scale (GOS), outcomes were three deaths due to primary brain injury, six cases of persistent vegetative state, five cases of severe disability, three cases of moderate disability, and four cases of good recovery. Although 3DCTA is a simple and convenient diagnostic method, cerebral angiography is necessary to evaluate dissecting lesions. If patients have any signs or symptoms of TCVI, as described in the Guidelines, cerebral angiography or 3DCTA should be performed as an initial screening method within 72 hours of admission, followed by cerebral angiography on postadmission Day 14 ± 2 to prevent failed diagnosis.

Background: The aim of this study was to evaluate the time course of recovery from cerebral vulnerability, using microdialysis (MD) technique and cerebral vascular autoregulation measurement, to clarify the appropriate timing of subsequent major surgical procedures, and to minimize the possibility of secondary brain injury in patients with severe traumatic brain injury (STBI)., Methods: In 3,470 MD samples of 25 patients with STBI, cerebral extracellular biomarkers (glucose, lactate, pyruvate, glycerol, and glutamate) were measured. In addition, to estimate cerebral vascular autoregulaton, the pressure reactivity index (PRx) was calculated with intracranial pressure (ICP) and mean arterial pressure. The data with ICP, cerebral perfusion pressure (CPP), and PRx were collected hourly for 7 days after injury and they were compared with MD biomarkers daily., Results: During the study period, the average ICP and CPP remained stable and were within the threshold of STBI treatment guidelines. After injury, the extracellular glucose concentration decreased, and the levels of glycerol, glutamate, and lactate/pyruvate ratio (LPR), which indicate cerebral ischemia and neural cell damage, increased. On the fourth day after injury, the extracellular glucose concentration improved, and the value of LPR decreased. The average PRx decreased daily and became negative on the fifth day after injury., Conclusion: Our results indicated that cerebral vascular autoregulation would recover on the fourth day after STBI, and cerebral perfusion might be increased by recovery of autoregulation. Thus, subsequent nonemergent surgery should be performed at least 4 days after STBI to prevent secondary brain injury. In addition, we should keep in mind that the cerebral vulnerability might persist for 4 days after suffering STBI.

Age may be an independent predictor of outcomes in traumatic brain injury (TBI), but the causes of the poor outcomes in elderly patients remain unclear. To clarify the differences between elderly and young patients with TBI, brain metabolism parameters were monitored with the microdialysis method in 30 patients with severe TBI (Glasgow Coma Scale scores 3-8). The microdialysis probe was inserted in the penumbra area of the brain and extracellular levels of glucose, glutamate, glycerol, lactate, and pyruvate were measured hourly for the initial 168 hours (7 days) after operation. The lactate/pyruvate ratio, which is considered to be a good indicator of neuronal ischemia, was also calculated. The patients were divided into the elderly group aged 65 years or older and the young group aged less than 65 years, and the biochemical markers were compared daily between these two groups. The value of extracellular glucose concentration was significantly lower in the elderly group than in the young group, and continued until the 7th day after injury. Moreover, the lactate/pyruvate ratio peaked on the 5th day after injury in the elderly group, later than in the young group. We concluded that neural vulnerability persisted longer in elderly patients than in young patients with TBI, and this should be considered to prevent the occurrence of additional secondary brain injury.

We demonstrate that in head injuries the degree of cerebral endothelial activation or injury depends on the type of brain injury and the patients age, and that in severe head injuries measuring the serum levels of thrombomodulin (TM) and von Willebrand factor (vWF) is useful in evaluating cerebral endothelial injury and activation. The values of vWF in the cases of focal brain injury were significantly higher than in the cases of diffuse axonal injury. The serum levels of TM in focal brain injuries were higher than in diffuse axonal injuries, but the differences were not statistically significant. In patients with delayed traumatic intracerebral hematoma (DTICH), vWF levels were much higher than in patients without DTICH. The values of TM and vWF in elderly patients were significantly higher than in younger patients. These findings indicate that: 1) the degree of endothelial activation in focal brain injury is significantly higher than in diffuse brain injury; 2) the degree of cerebral endothelial injury in patients with DTICH is much higher than in those without DTICH; and 3) the degree of cerebral endothelial activation and injury in elderly head injury patients is significantly higher than in younger patients.

Elevated serum levels of thrombomodulin (TM) and von Willebrand factor (vWf) are good indicators of injury and activation of cerebral endothelium in patients with severe simple head injury. The present study evaluated cerebral endothelial injury or activation as the serum levels of TM and vWf in elderly and younger patients with similar brain trauma, to evaluate the primary parenchymal injury of the brain. Patients with head injury were classified into the young group (16-30 years), the middle-aged group (31-65 years), and the elderly group (over 66 years). There was no difference in Glasgow Coma Scale on admission between the three groups. The serum levels of TM and vWf at 2 hours after injury were significantly higher in the elderly group than in the other groups. However, the serum levels of TM and vWf were not significantly different at 3 and 7 days after injury. Cerebral endothelial activation and injury were significantly higher in elderly patients just after head injury than in younger patients, which suggests that greater sensitivity to endothelial injury and activation may be important in the worse outcome after head injury in elderly patients compared with younger patients.

Ciliary neurotrophic factor (CNTF) is known as a neuro-survival factor in the developing and developed CNS, as well as in the CNS following injury. However, little is known about the expression of CNTF or that of its receptor (CNTFR-alpha) in cases of intracerebral hemorrhage (ICH). We investigated the temporal and spatial profiles of CNTF and CNTFR-alpha expression using a collagenase-induced ICH rat model. CNTF expression was up-regulated from the day following ICH induction and reached a peak level at 5 to 14 days, with increased expression observed in brain tissue surrounding the hematoma lesion and white matter structures in association with astroglial proliferation. Further, CNTFR-alpha was transiently expressed in the cerebral cortex surrounding the hematoma, with a peak at 5 days. Administration of exogenous CNTF into the lesion following initiation of ICH resulted in a prolonged expression of CNTFR-alpha on cortical neurons neighboring the hematoma. Our findings suggest differential regulation of CNTF and CNTFR-alpha, and the possibility of a therapeutic strategy using CNTF administration for ICH.

Thrombomodulin (TM), which is located in the surface of the endothelium in the arteries, veins, and capillaries of major organs such as the brain, lungs, liver, kidneys, skeletal muscles, and gastrointestinal tract, is one of several indicators of endothelial injury. Von Willebrand factor (vWf), which is synthesized by endothelial cells, is also an endothelial specific glycoprotein. The serum level of vWf increases in response to various stimuli without endothelial injury. An elevated serum level of vWf may suggest endothelial activation in severe head injury. We hypothesize that the degree of cerebral endothelial activation or injury depends on the type of head injury and that measuring the TM and vWf is useful for predicting delayed traumatic intracerebral hematoma (DTICH), produced by weakness of the vessel wall, occuring either as a direct or indirect effect of head injury. The values of vWf in focal brain injury (ranging from 332.5 +/- 52.8% to 361.7 +/- 86.2%) were significantly higher than those in diffuse axonal injury from 2 h to 7 days after the injury occurred (ranging from 201.6 +/- 59.5% to 242.5 +/- 51.7%). The serum level of TM in focal brain injury (ranging from 3.84 +/- 1.54 to 4.12 +/- 1.46 U/mL) was higher than that in diffuse axonal injury (ranging from 2.96 +/- 0.63 to 3.67 +/- 1.70 U/mL), but these differences were not statistically significant. In patients with DTICH, TM was significantly higher than in patients without DTICH (p < 0.01). The results of our study demonstrate that the degree of endothelial activation in focal brain injury was significantly higher than in diffuse brain injury. In addition, the serum level of TM in patients with DTICH was significantly higher than in patients without DTICH. These findings suggest that cerebral tissue injury is often accompanied by cerebral endothelial activation, and that these two phenomena should be distinguished from each other. The levels of serum TM and vWf appear to be good indicators of the cerebral endothelial injury and of endothelial activation in severe head injury.

Nine patients with CNS damage who had been transferred to our critical care unit were treated with a commercially available kit for percutaneous dilational tracheostomy (PDT). The mean procedure time was about 11 minutes, and the perioperative complication rate was 22% (2/9). Only one complication, wound infection, occurred, and the patient was cured with conventional therapy. On the other hand, premature extubation of the translaryngeal tube occurred in one case. Long-term complications like tracheal stenosis and tracheal malacia were not experienced in two patients. They were discharged from the hospital after decannulation. In conclusion, the advantages of PDT include a short procedure time, the ability to perform the procedure at the bedside, and reduced stimulation of the trachea. Because of the safety and simplicity of the procedure, we recommend PDT for patients with CNS damage.

The course of intracranial pressure (ICP) and the finding of auditory brain stem response (ABR) was discussed in the cases diagnosed as diffuse axonal injury (DAI) established by Gennarelli. ICP was measured in twenty-six cases which were divided into three groups according to the course of ICP: Group (1), in which ICP remained below 20 mmHg (group I, 9 cases). Group (2), in which ICP rose above 20 mmHg but was controlled by therapy (group II, 8 cases). Group (3), in which ICP rose above 20 mmHg and could not be controlled by any therapies (group III, 9 cases). Glasgow outcome scale 3 months after the injury in the cases of group I and II was severe disability (SD) and/or persistent vegetative state (PVS), but all of the cases in group III died. The findings of serial ABR were divided into 3 groups. These were group A (2 cases) which showed normal record, group B (5 cases) which showed elongation of latencies between the first and fifth waves, and group C (5 cases) in which there was no response in ABR. GOS in group A or B was SD and/or PVS, but all of the cases in group C were shown to be dead in GOS. Our studies suggest that the level of ICP in DAI is rather higher than that published in previous reports, and the continuous measurements of ICP and serial records of ABR are useful for evaluating the outcome of DAI.

Forty cases diagnosed as diffuse brain injury (DBI) were studied by magnetic resonance imaging (MRI) performed within 3 days after injury. These cases were divided into two groups, which were the concussion group and diffuse axonal injury (DAI) group established by Gennarelli. There were no findings on computerized tomography (CT) in the concussion group except for two cases which had a brain edema or subarachnoid hemorrhage. But on MRI, high intensity areas on T2 weighted imaging were demonstrated in the cerebral white matter in this group. Many lesions in this group were thought to be edemas of the cerebral white matter, because of the fact that, on serial MRI, they were isointense. In mild types of DAI, the lesions on MRI were located only in the cerebral white matter, whereas, in the severe types of DAI, lesions were located in the basal ganglia, the corpus callosum, the dorsal part of the brain stem as well as in the cerebral white matter. As for CT findings, parenchymal lesions were not visualized especially in mild DAI. Our results suggested that the lesions in cerebral concussion were edemas in cerebral white matter. In mild DAI they were non-hemorrhagic contusion; and in severe DAI they were hemorrhagic contusions in the cerebral white matter, the basal ganglia, the corpus callosum or the dorsal part of the brain stem.

One hundred seventy-seven patients who had incurred head trauma were studied with magnetic resonance imaging (MRI). Patients varied from those with mild injury without any focal neurological deficit to those with severe injury with post-traumatic coma. Altogether, 177 lesions were demonstrated by MRI in 123 of 177 patients within 3 days of injury using T2-weighted (SE2000/40,2000/111) and T1-weighted (IR1500/500/40) multislice sequences. In contrast, computerized tomography (CT) demonstrated 103 lesions in 90 patients. MRI was superior to CT in the diagnosis of nonhemorrhagic contusions demonstrated as a high-intensity area on T2-weighted imaging. MRI provided some information to evaluate the severity of diffuse axonal injury or to predict delayed traumatic intracerebral hematoma (DTICH).

Barbiturate therapy was performed on 84 head trauma patients which were measured on GCS score of 8 or less, through October 1979 to December 1982. More than 3 g/day of thiamylal or more than 1.5 g/day of pentobarbital were administered for barbiturate therapy. Barbiturate therapy was discontinued in patients whose ICP remained less than 20 mmHg for more than 36 hours. In patients whose ICP sustained higher level, barbiturate was administered continuously until brain death was confirmed or non-filling was recognized. The patients were divided into two groups; Group I in which barbiturate therapy was carried out for 72 hours or less, and Group II in which it was administered for more than 72 hours. The patients in each group were further divided into responder and survivor (a), responder but late death (b), and no-responder or acute brain death (c), As far as age of patients concern, 19 out of 26 patients whose age was less than 20, 22 out of 35 patients whose age was 20-50 and 13 out of 23 patients whose age was more than 50 years responded well to the barbiturate therapy. But one patient died among young age, 4 patients died among middle age and 9 patients died among aged group at later stage. As for Group I (51 patients), Group I a consisted of 22 patients (mean age; 26.2 years, mean GCS score; 6.04, mean initial and maximal ICP; 11.9 and 27.8 mmHg), I b of 8 (52.5 years, 4.75, 17.0 and 27.8 mmHg), and I c of 21 (41.4 years, 4.57, 38.1 and 98.0 mmHg respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

There is increasing evidence from human and experimental studies that the most important factor governing the outcome in head injury is the severity of diffuse axonal injuries. The authors have experienced 18 cases of severe diffuse axonal injury which showed post-traumatic coma for more than 24 hours and CT findings resembling those of shearing injuries of the cerebral white matter such as have been presented by Zimmerman et al. (1978). The consciousness levels on admission were 6 or less on the Glasgow Coma Scale and all cases were shown clinically to have primary brain stem injury. The main type of head trauma resulted from road traffic accidents (83%). Skull fractures were found in only 5 cases (28%). These findings suggested that acceleration/deceleration injury produce in the patients severe diffuse axonal injury. Initial ICP was below 20 mmHg in 11 cases out of 13 (85%). Parenchymal small hemorrhagic lesions of initial CT were basal ganglia (7 cases), corpus callosum (4 cases), pons (4 cases), midbrain (3 cases) and thalamus (2 cases). Extraparenchymal hemorrhagic lesions included intraventricular hemorrhage (6 cases) and subarachnoid hemorrhage (6 cases). Two autopsied cases of severe diffuse axonal injury (acute case and chronic case) showed remarkable congestion and edema in the deep part of the frontal white matter. Microscopic examination revealed marked axonal degeneration including axonal retraction ball in the corpus callosum, in the internal capsule and in the white matter of the brain stem. Glasgow Outcome Scale of the 18 patients at 3 months after the trauma made us concerned that no patients indicated good recovery or even only moderate disability.(ABSTRACT TRUNCATED AT 250 WORDS)

Three heavy drinkers, the patients fell down stairs while inebriated and were hit on their heads. Utilizing CT, we found that the hematomas in all three cases were accompanied by ventricular hemorrhage which, in two of the cases, were similar to hypertensive intracerebral hematoma in the basal ganglia. None of the three had a history of hypertension. We are of the opinion that the vulnerability of cerebral arteries, especially in the basal ganglia, of such heavy drinkers added to the traumatic force and led to the pathogenic bleeding. We were unable to find a correlation between the intracerebral hematoma and the site of the hit. It is assumed that immediate removal of the hematoma in cases of intracerebral hematoma with ventricular bleeding can result in the survival of the patient.

During four year period from April, 1977 to March, 1981, 53 cases with acute traumatic epidural hematoma had been encountered out of 430 acute head injured patients examined by computerized tomography (CT) within 24 hours after incurring the trauma at the Department of Neurosurgery and Critical Care Medicine of Nippon Medical School, Sendagi, Tokyo, Japan. Besides the initial CT, the authors performed contrast enhanced CT (41 cases) and serial CT scanning (31 cases). There were 49 cases of epidural hematoma existing in the supratentorial region, Two cases infratentorial region and 2 cases in the both regions. Two cases of vertex epidural hematoma had been encountered, one of them required vertical scan technique. In 22 (41%) of the 53 patients, the initial CT showed evidence of other cerebral lesions. The most frequent lesion was pneumocephalus (11 cases), 3 cases of them existed in the epidural hematoma. There were also intracerebral hematoma (6 cases), subdural hematoma (4 cases), cerebral contusion (2 cases), intraventricular hemorrhage (2 cases) and 2 cases of them demonstrated "diffuse traumatic cerebral injury" (Zimmerman, 1979). During contrast enhanced CT, 11 cases out of 41 cases indicated several enhancement pattern. There were total enhancement of epidural hematoma (2 cases), partial enhancement of hematoma (2 cases) and enhancement of internal margin of hematoma (2 cases). Serial CT scans was performed in 36 out of the 53 patients. Common findings on the serial CT scans were decreased density collection in the subdural space such as subdural effusions or chronic subdural hematomas (8 cases) and enlargement of small epidural hematomas (3 cases).(ABSTRACT TRUNCATED AT 250 WORDS)

In severe head injuries, delayed intracerebral hematoma appearing lately is noted due to the spread use of serial CT scan. The authors experienced the autopsy of 5 cases who presented diffuse axonal injury (DAI) among these new lesions in repeated CT scan findings and report the pathohistological findings. Subjects were as follows: The age range of the patients was 15 to 25 years. The consciousness levels of the 5 cases on admission were 6 or less by the Glasgow coma scale. CT findings of DAI were revealed hemorrhage of the corpus callosum, basal ganglia, tegmentum of pons, intraventricular, and acute brain swelling. Total clinical courses were 2 to 29 days, but most of them were 9 or less days. In the macroscopic findings, marked congestion and edema revealed mainly in deep part of the white matter of the frontal lobe in all 5 cases. Callosal disruption and hematoma adjacent the corpus callosum revealed in 4 out of 5 cases. Cerebral contusion with hemorrhage revealed in 3 out of 5 cases. Intraventricular hemorrhage and traumatic subarachnoid hemorrhage revealed in 2 out of 5 cases. Hemorrhage of basal ganglia and base of pons revealed in 2 cases. Microscopic examination of all 5 cases revealed pallor of myelin in the corpus callosum and white matter surrounding hemorrhagic lesion, and abnormal tortuous, swelling and fragmentation of axons in stained preparation. Axonal retraction ball was recognized in 3 out of 5 cases. In conclusion, five autopsied cases who presented acute brain swelling and hemorrhage of corpus callosum and tegmentum of pons in serial CT scan were examined.(ABSTRACT TRUNCATED AT 250 WORDS)

Measurement of the serum level of anterior pituitary hormones (GH, TSH, LH and FSH) and the response of these hormones to their releasing hormones were made in 45 uncomplicated head injury patients within 24 hours after injury. We classified these 45 patients into three groups according to the Glasgow Outcome Scale of six months after head injury, such as good outcome group (GR or MD), poor outcome group (SD or PVS) and dead group. The serum level of the anterior pituitary hormones in dead group were higher than those in the good or poor outcome group, especially the level of GH. The serum level of GH was 14.7 +/- 3.0 ng/ml in the dead group, whereas 5.8 +/- 0.9 ng/ml in the good outcome group and 4.0 +/- 2.1 ng/ml in the poor outcome group. The response of TSH, LH or FSH to the administration of TRH or LH-RH were depressed in the dead group. On the other hand, there were normal response of TSH, LH or FSH following administration of TRH or LH-RH in the other two survival groups. These findings suggested that the measurement of the anterior pituitary hormones and the response of these hormones to their releasing hormones were useful to evaluate the severity of head injury.

Advantages of magnetic resonance imaging (MRI) to computed tomography (CT) on a diagnosis of diffuse axonal injury (DAI) were discussed. Sixteen patients diagnosed as DAI defined by the criteria of Gennarelli were studied with CT and MRI. Lesions were demonstrated as high intensity areas on MRI of T2 weighted imaging (SE 2000/111) in all of the patients. These lesions were located only in a cerebral white matter in the cases of mild DAI, whereas in the cases of severe DAI located in a basal ganglia, corpus callosum, dorsal part of the brain stem as well as in the cerebral white matter. As for the findings of CT, these parenchymal lesions were not visualized in nine cases including six cases without any pathological findings. Our series suggest that MRI is superior to CT on the diagnosis of DAI and provides some information to evaluate the severity of DAI.

Traumatic intracranial aneurysm is rare lesion which is complicated severe head injury. In spite of this rarity, this aneurysm is well known by the fact of high probability of rupture, and high mortality rate. Ninety-four cases of traumatic aneurysms, including 5 cases of our own are discussed. In 94 cases, 83 cases (88.3%) are located at the middle cerebral arteries and/or the anterior cerebral arteries. There are only 2 cases (2.1%) located at the posterior fossa. All of these 94 aneurysms are situated at the peripheral arteries and/or cortical branches, in the distance of Willis' arterial ring. There are 8 cases which lead to be cured spontaneously without any surgical treatment. It was reported by some authors that the traumatic intracranial aneurysms expecting spontaneous healing had some characteristics by the cerebral angiography, such as irregular shapes, and unclear connections from parent arteries. However, these characteristics are sometimes common in the traumatic intracranial aneurysms. Therefore, it is actually difficult to differentiate spontaneous healing aneurysms from deteriorating ones. As for the prognosis of these 79 cases which are able to be examined, the mortality rate of non-surgical group is 4 times higher compared with that of the surgical group, that is the former 40%, and the latter 11%, respectively. According to these facts, authors concluded that the principle therapy of traumatic intracranial aneurysm is surgical treatment.