ライフサイエンスコーパス: head injury

1 ctly (eg, raised intracranial pressure after head injury).

2 tested interaction between Rep1 genotype and head injury.

3 a fallen patient who has sustained a closed head injury.

4 isrupted among DMN key structures after mild head injury.

5 150 g is the most commonly used criteria for head injury.

6 abilities that are particularly sensitive to head injury.

7 uld modulate bacterial invasion in rats with head injury.

8 st, and then also for smoking and history of head injury.

9 o-severe injury, and many patients with mild head injury.

10 ative capability in patients after traumatic head injury.

11 uch as Alzheimer disease, Down syndrome, and head injury.

12 aracteristic of both Alzheimer's disease and head injury.

13 n, demonstrated in a paradigm of mild closed head injury.

14 ions evolve following relatively mild closed head injury.

15 ortant role in managing patients with severe head injury.

16 ative effect in the treatment of significant head injury.

17 ed prehospital care for patients with severe head injury.

18 portant strategy in the management of severe head injury.

19 lele is associated with a poor outcome after head injury.

20 neurosurgical care on mortality after severe head injury.

21 elivered greater benefit to patients without head injury.

22 rtaken in the thalamus of humans after blunt head injury.

23 eers and 20 patients within 6 days of closed head injury.

24 attainable for treatment of human accidental head injury.

25 n determining treatment strategies for acute head injury.

26 fective treatment of cognitive deficits post head injury.

27 oss populations of patients with significant head injury.

28 e distinction between accidental and abusive head injury.

29 serious sequelae may increase with repeated head injury.

30 tinguish accidental head injury from abusive head injury.

31 influence patient outcome following a severe head injury.

32 of depression increased with severity of the head injury.

33 long-term risk of depression associated with head injury.

34 tetanic stimulation in the hippocampus after head injury.

35 formed on anesthetized mice following closed head injury.

36 ions and mesiofrontal areas) is common after head injury.

37 bution of abnormalities in focal and diffuse head injury.

38 to be highest in those who have had a severe head injury.

39 of depressive illness 50 years after closed head injury.

40 manner in infants and children after severe head injury.

41 and can be debilitating in the months after head injury.

42 odegenerative conditions, such as stroke and head injury.

43 in the cerebrospinal fluid (CSF) 24 h after head injury.

44 ential of CN-105 in a murine model of closed head injury.

45 tical and hippocampal cell populations after head injury.

46 , nonmilitary trauma, alcohol use, and prior head injury.

47 4.0 (PedsQL-4.0) at 4, 8, and 12 weeks after head injury.

48 accounting for the effects of PTSD and prior head injury.

49 itive nature of sports- and military-related head injury.

50 orrhages in potential cases of nonaccidental head injury.

51 clinical symptoms with a medical history of head injury.

52 isk for AD-associated pathology changes with head injury.

53 outcome observed in patients after a single head injury.

54 ld model of TBI with parallels to concussive head injury.

55 ric disorders following hospital contact for head injury.

56 e in risk for all psychiatric outcomes after head injury.

57 -up study of veterans with focal penetrating head injuries.

58 isorders, including brain edema, stroke, and head injuries.

59 ine the need for CT imaging in children with head injuries.

60 137 children and adolescents attending with head injuries.

61 stablish the presence and severity of closed head injuries.

62 e importance of protecting young people from head injuries.

63 mon comorbidity of stroke and other bleeding head injuries.

64 isorders in 113,906 persons who had suffered head injuries.

65 ultiple sclerosis, 1.7 (95% CI, 1.6-1.7) for head injury, 1.3 (95% CI, 1.2-1.3) for stroke, and 1.7 (

66 62-3.51) and the subset with isolated severe head injury (2.21; 1.62-3.03), with adjustment for age,

67 Seven years after head injury, 206/767 (27%) people had died.

68 ypes (7.3, 3.3-16.4; p<0.0001), and previous head injury (4.1, 2.1-8.1; p<0.0001).

69 including nonhead blunt injuries (43.2%) and head injuries (40.1%).

70 Head injuries (46.8% of patients) and extremity fracture

71 When compared with persons without a head injury, a statistically significant ALS risk elevat

72 omplaints among those undergoing CT included head injury, abdominal pain, and headache.

73 dler was brought to the hospital with severe head injury after being struck by a car.

74 m chloride) is appropriate for patients with head injury, alkalosis, or hyponatremia, but in large vo

75 disruption, cervical spine instability, and head injury all combine to increase tracheal intubation

76 INTERPRETATION: While head injury alone was not associated with PD risk, our d

77 Glucocorticoid administration early after head injury also has not been found to reduce the risk o

78 h severe alcohol withdrawal syndrome, severe head injury also predicted progression to delirium treme

79 onset PD was more likely to have sustained a head injury, although numbers were small.

80 tal lobe lesion group with focal penetrating head injuries and a non-head-injured control group for t

81 We included 534 patients with head injury and 827 control patients with other nonhead

82 ay reduce cellular oxygen delivery following head injury and attenuate the ability of the brain to in

83 nly complicates stroke and, less frequently, head injury and brain tumours.

84 Physical abuse is a leading cause of serious head injury and death in children aged 2 years or younge

85 at the time of admission to hospital after a head injury and followed up 7 years later.

86 le discusses the evaluation of children with head injury and how to make the distinction between acci

87 l field defect; the usual causes are stroke, head injury and intracranial tumours.

88 Individuals with both head injury and long Rep1 were diagnosed 4.9 years earli

89 because of possible links between repetitive head injury and neurodegenerative diseases.

90 ssion remains elevated for decades following head injury and seems to be highest in those who have ha

91 after taking into account deployment-related head injury and stress and depression symptoms.

92 In contrast to prior studies of head injury and stroke, we could not detect a relationsh

93 s is the largest study to date investigating head injury and subsequent mental illness.

94 udies investigating the relationship between head injury and subsequent psychiatric disorders often s

95 r determined that the infant had sustained a head injury and that the manner of death was a homicide,

96 Patients' perceptions of their head injury and their behavioural responses play importa

97 reported having been removed from play after head injury and was evident in individual players.

98 e emergency department within 48 hours after head injury and were considered to have an acute concuss

99 t debate focused on the diagnosis of abusive head injury and whether children with vitamin D deficien

100 tically ill trauma patients without isolated head injury and with an Injury Severity Score > or = 16

101 mmatory processes progress after the initial head injury and worsen with time.

102 l-related injuries (hip and other fractures, head injuries, and joint dislocations) and fall-related

103 l haemorrhage, alcohol poisoning and related head injury, and a completed suicide) and one in MoonLyt

104 luding posttraumatic stress disorder (PTSD), head injury, and alcohol abuse.

105 s include hearing loss, ototoxic medication, head injury, and depression.

106 ables, including smoking, other medications, head injury, and disease severity, had no material impac

107 were compared for patients with and without head injury, and for those treated in a neurosurgical ve

108 ing), hypotension, immediate surgery, severe head injury, and injury severity score.

109 and pulmonary embolism), multiorgan failure, head injury, and other.

110 combat exposure, depressive symptoms, prior head injury, and posttraumatic stress disorder (PTSD).

111 major cause of delayed neuronal death after head injury, and several major clinical trials in severe

112 re dealing with the neuropathology of infant head injury, and the question of whether diffuse traumat

113 ds in major trauma patients with and without head injury, and to establish the effect of neurosurgica

114 hospital shock, severity of limb amputation, head injury, and torso hemorrhage.

115 ere TBI has been documented, the majority of head injuries are mild, such as those that occur in athl

116 s for the management of patients with severe head injury are based on data showing that aggressive ma

117 verse perinatal events, febrile illness, and head injury are potentially preventable associated facto

118 ossibly because not all patients with severe head injury are treated in a neurosurgical centre.

119 s) who presented within 48 hours of an acute head injury at 1 of 9 pediatric emergency departments wi

120 rticosteroid Randomisation After Significant Head Injury-basic and International Mission for Prognosi

121 Head injury between ages 11 and 15 years was the stronge

122 Four days after head injury, blood was sampled for arginine and fibrinog

123 to reproduce TAI in animal models of closed head injury, but in vitro stretch injury models reproduc

124 d with moderate to severe TBI or penetrating head injury, but other visual field deficits were preval

125 inoschisis can very rarely occur after crush head injury, but remain specific for shaken baby syndrom

126 Widely used models induce head injury by lateral fluid percussion, a controlled co

127 Head injury can also have long-term cognitive effects, b

128 e of APOE genotype in younger patients after head injury can be expressed as, at age <15 years, carri

129 decisions on the use of CT imaging for mild head injury can now be guided by a prediction rule for c

130 tudy, based on advantages of both the closed head injury (CHI) and controlled cortical impact (CCI) m

131 This review will examine mild closed head injury (CHI) and the current evidence on head compu

132 (ICD-9) codes denoting open (OHI) or closed head injury (CHI) in isolation or in combination with ot

133 ls have been developed to mimic human closed head injury (CHI).

134 controlled cortical impact (CCI), and closed head injury (CHI).

135 proteins in an experimental model of closed head injury (CHI).

136 gency Care Applied Research Network (PECARN) head injury cohort study included patients enrolled in 2

137 ified admissions to a Neurosurgical Unit for head injury, collected demographic and clinical data, de

138 lly placed tube entering the brain following head injury continue to occur, as do reports of esophage

139 tically ill trauma patients without isolated head injury contributes independently to in-hospital mor

140 The added risk of mental illness following head injury did not differ between individuals with and

141 cognitive stimulation and social activities, head injury, diet, and reproductive and oral health.

142 l (CI): 1.2, 8.1) and patients who had had a head injury during the past 10 years (OR = 3.2, 95 perce

143 neuromonitoring of patients following severe head injury during the period from 2001 to 2002.

144 lity monitoring of patients following severe head injury during the period of 2004-2005.

145 was only associated with greater severity of head injury during year 1.

146 lts underscore the importance of documenting head injuries even within the mild range as they may int

147 Group 1 included rats with head injury fed a standard enteral nutrition (Sondalis H

148 s HP, n = 10) and group 2 included rats with head injury fed the standard enteral nutrition plus argi

149 Importance: Head injury following explosions is common.

150 y of baseline CIWA-Ar score, age, and severe head injury for developing delirium tremens.

151 odel to simulate human repetitive concussive head injury for systematic study.

152 the practitioner must distinguish accidental head injury from abusive head injury.

153 Severe head injury (GCS = 3) triggered more prompt transfer, bu

154 ed a comparison cohort of patients with mild head injuries (Glasgow Coma Scale score 13-15) and calcu

155 f secondary generalized seizures, history of head injury, handedness and side of surgery.

156 he critical period for epileptogenesis after head injury has been better defined.

157 ials of seizure prophylaxis in children with head injury have not been conducted and are needed to co

158 ractures in the assessment of a patient with head injury, have shown excellent promise in recent stud

159 ing approach that first considers concurrent head injury, hemodynamic stability and the presence of p

160 stablish how long term outcome evolves after head injury (HI) and factors related to this, to inform

161 lable hemorrhage (e.g. isolated extremity or head injury), However, the latest recommendations are to

162 ivities of three clinical decision rules for head injuries in children were high when used as designe

163 e variations in care of patients with severe head injury in academic trauma centers across the United

164 Fifty-three cases of non-accidental head injury in children were subjected to detailed neuro

165 hirty-five MTBI patients evaluated for acute head injury in emergency departments of 3 LEVEL I trauma

166 Severe closed head injury in mice induced abundant MAC deposition in t

167 gow population, risk of death was high after head injury in months 1-2 (23 times), 3-12 (3 times) and

168 evidence suggests that patients with severe head injury in particular will benefit significantly fro

169 which suggest a particular vulnerability to head injury in the Alzheimer brain.

170 ment of neocortical epileptic seizures after head injury in the rat.

171 in the first and six subsequent years after head injury, in a prospectively identified cohort admitt

172 CS is a constellation of symptoms related to head injury including somatic symptoms, sleep dysregulat

173 The nature of the head injury, including observers' accounts, clinical and

174 Given the high population frequency of head injury, independent verification of these results i

175 roducts, crystalloid/12 hrs, presence of any head injury, injury severity score, and 12 hrs base defi

176 ampal A beta burden in a clinically relevant head injury/intervention model using mice expressing hum

177 Head injury is a causative factor in the development of

178 Head injury is an inconsistently reported risk factor fo

179 Bleeding head injury is associated with gastric stasis, a symptom

180 Mechanical stress producing head injury is associated with Parkinson's disease, sugg

181 ts recently admitted to hospital with severe head injury is well recognized, less is known about thei

182 ents with premorbid conditions (eg, previous head injury, learning difficulties, or behavioral proble

183 increased intracranial pressure; an initial head injury less than 10 days earlier; a core temperatur

184 ock/hypotension (49.4%), sepsis (39.4%), and head injury/major neurologic insult (35.2%).

185 recent changes in recommended CPP levels for head injury management across populations of patients wi

186 the effect of APOE genotype on outcome after head injury may be expressed through the processes of re

187 results suggest that mild-to-moderate closed head injury may increase PD risk decades later.

188 These data support the notion that head injury may increase the risk of ALS.

189 ot associated with PD risk, our data suggest head injury may initiate and/or accelerate neurodegenera

190 mpact (CCI) models, we developed a bilateral head injury model in mice.

191 Using a closed-head injury model of TBI in mice, we showed by MRI scans

192 ove functional recovery after TBI, a new rat head injury model was developed, in which a computer-con

193 cal diagnostic capability to a sophisticated head injury model, such as facilitating head impact sens

194 Head injury models are important tools to study concussi

195 nd Corticoid Randomisation After Significant Head injury models.

196 s in a group of survivors of moderate-severe head injury (n = 31).

197 f death since 1989 than did patients without head injury (n=154,231).

198 Patients with head injury (n=22,216) had a ten-fold higher mortality a

199 cide attempt (n=4), suicidal ideation (n=3), head injury (n=3), and aspiration pneumonia (n=3).

200 In patients with closed head injury, neither the administration of erythropoieti

201 ontaneous and miniature IPSC frequency after head injury; no concurrent change in paired-pulse ratio

202 as found for participants with more than one head injury (odds ratio (OR) = 3.1, 95 percent confidenc

203 ed group was 18.5% vs 13.4% in those with no head injury (odds ratio = 1.54, 95% confidence interval

204 with head injuries vs 8.5% of those without head injury (odds ratio = 1.63, 95% confidence interval

205 confidence interval [CI]: 3.8, 83.4), severe head injury (odds ratio, 3.2; 95% CI: 1.5, 7.1), high-en

206 ildren and adolescents (aged <18 years) with head injuries of any severity who presented to the emerg

207 hip between combat exposure, PTSD, and prior head injuries on cortical thickness (Monte Carlo correct

208 as well as in humans subjected to repetitive head injury, one may conclude that the presence of eleva

209 Those with isolated severe head injury or on chronic dialysis were excluded.

210 amine this, six patients with amnesia due to head injury or stroke and six normal controls heard list

211 lated, it was assumed to be the product of a head injury or toxic exposure.

212 ated risk of ALS among persons with previous head injuries (OR = 1.7, 95 percent CI: 1.3, 2.2).

213 potension (OR 1.44, 95% CI1.29-1.59), severe head injury (OR 1.34, 95% CI 1.17-1.54), and patients un

214 edictors of cumulative 1-year mortality were head injury (OR, 2.65; 95% CI, 1.24-5.67; P = .03) and l

215 manifest as skin injuries, skeletal trauma, head injury, or many other forms.

216 , death due to uncontrolled bleeding, severe head injury, or the development of multiple organ dysfun

217 ossible involvement of the gut microbiota in head injury outcomes.

218 , apoE acts directly or in concert with age, head injury, oxidative stress, ischemia, inflammation, a

219 Risk increased further with a subsequent head injury (p trend = 0.022) and with head injuries req

220 neuroprotective, compatible with the care of head injury patients, and conveniently implemented.

221 neuroprotective, compatible with the care of head injury patients, and conveniently implemented.

222 ation in both animal models of TBI and human head injury patients.

223 term neurological and psychiatric changes in head injury patients.

224 intervention among a cohort of 11,770 blunt head injury patients.

225 of future clinical trial in severe traumatic head-injury patients.

226 tnam veterans with predominantly penetrating head injury (PHI) suffered more than 30 years ago.

227 945 and were hospitalized at that time for a head injury, pneumonia, or laceration, puncture, or inci

228 2305 (33%) of patients with severe head injury (presenting between 1996 and 2003) were trea

229 Controls with a history of head injury prior to study entry were excluded.

230 nd Corticoid Randomisation after Significant Head injury prognostic models for prediction of outcome

231 nd Corticoid Randomisation After Significant Head injury prognostic models predict outcome after trau

232 he Corticoid Randomisation After Significant Head injury prognostic models show good generalizability

233 Head injuries related to increased cortical thickness in

234 genes are closely linked to the pathology of head injury-related disorder and AD.

235 death rate after admission to hospital with head injury remains high for at least 7 years, and is pa

236 Head injury remains the most common cause of death in ch

237 wever, neither the severity nor frequency of head injury required to trigger adverse behavioral outco

238 quent head injury (p trend = 0.022) and with head injuries requiring hospitalization.

239 In the area of minor head injury, research has focused on implementation of v

240 f anxiety or depression, pesticide exposure, head injury, rural living, beta-blockers, farming occupa

241 analysis (King's Outcome Scale for Childhood Head Injury score < 5a) in the development cohort.

242 f mortality after discharge included maximum head injury score on Abbreviated Injury Score scale (HR,

243 Patients with a head Injury Severity Score of 3 or greater, an out-of-st

244 poor outcome and in developing the Relative Head Injury Severity Score, which can assess severity of

245 type and intent of injury, injury severity, head injury severity, and Charlson Comorbidity Index.

246 echanism of injury, overall injury severity, head injury severity, and comorbid conditions.

247 Standards for management of severe closed head injury should help to establish a foundation for ro

248 umatic epilepsy in an animal model of impact head injury, showing a striking similarity to the enduri

249 index, dementia, depression, alcohol abuse, head injury, smoking, body mass index, and vision and he

250 significant, particularly in the presence of head injury, spine injury, mechanical ventilation, high

251 When the data were analysed by median age at head injury, statistically significant patterns of age-r

252 ractivity to challenges including subsequent head injury, stress, or induction of a peripheral immune

253 Medical contact for head injury, stroke, epilepsy, polyneuropathy, diseases

254 e sample of combat veterans from the Vietnam Head Injury Study, which is a prospective, long-term fol

255 lar when we excluded those with a history of head injury, substance abuse, or clinical depression.

256 Conversely, large head injuries that left eyes intact increased eye progen

257 ces of a clinically relevant model of closed head injury, the lateral fluid percussion injury (FPI),

258 multisystem blunt trauma, particularly with head injury, the most recent experimental data have begu

259 niocervical junction is vulnerable in infant head injury, the neuropathology being that of stretch in

260 Two days after head injury, the rats received a single enteral bolus of

261 .3%; after excluding brain death from severe head injury, there were 6.4% misclassifications.

262 patients with isolated extremity, thermal or head injury, they should be limited in conditions with p

263 oblems associated with torture and traumatic head injury (THI).

264 evice that can be used to inflict controlled head injury to flies, resulting in physiological respons

265 d by a weight drop model to produce a closed head injury to mice and the effect of inhaled nitric oxi

266 Closed head injury to the developing rat brain causes an acute

267 (CPPopt) for patients after severe traumatic head injury, using continuous monitoring of cerebrovascu

268 n was detected in 11.2% of the veterans with head injuries vs 8.5% of those without head injury (odds

269 Cumulative 1-year mortality in NCTPs with a head injury was 51.1% and increased to 73.2% if the Inju

270 Repeated head injury was a risk factor for death in the MHI group

271 t neurological symptoms, a history of a past head injury was actually more common in our psychogenic

272 Head injury was associated with a higher risk of schizop

273 A further control group admitted with a non-head injury was in addition matched for duration of hosp

274 Overall, ever having experienced a head injury was nonsignificantly associated with a highe

275 Overall, head injury was not significantly associated with PD (po

276 In 65 patients with abnormal GCS (38%), no head injury was recorded.

277 The authors examined whether head injury was related to ALS risk in a case-control st

278 However, head injury was strongly associated with PD in those wit

279 a controlled cortical impact (CCI) model of head injury, we show a large increase in the expression

280 Severe/isolated head injuries were excluded.

281 terans with (n = 520) and without (n = 1198) head injuries were interviewed in 1996-1997 for their li

282 ull cohort and a subset with isolated severe head injury were evaluated.

283 Veterans with head injury were more likely to report major depression

284 Male Sprague-Dawley rats with head injury were randomized into two groups.

285 o the Wessex Neurological Centre with severe head injury were selected for the study.

286 The primary causes of death after head injury were the same as those in the general popula

287 extual variables (alcohol use and deployment head injury) were significantly related to neuropsycholo

288 In contrast to clinical head injury, which reflects a complex multi-factorial di

289 Among 15162 children with GCS 13 to 15 head injuries who received head computed tomographic ima

290 ars of age with coma after sustaining closed head injuries who were randomly assigned to be treated w

291 ietin, n = 102; placebo, n = 98) with closed head injury who were unable to follow commands and were

292 genotyped for Rep1 and interviewed regarding head injuries with loss of consciousness or concussion p

293 For participants who had had multiple head injuries with the latest occurring in the past 10 y

294 and modification of epileptic seizures after head injury with a cooling protocol that is neuroprotect

295 and modification of epileptic seizures after head injury with a cooling protocol that is neuroprotect

296 AIS > or = 3 (OR 1.92; 95% CI 1.64 to 2.26), head injury with AIS > or = 3 (OR 1.24; 95% CI 1.05 to 1

297 A prior head injury with amnesia or loss of consciousness was as

298 s not responsible for mortality in rats with head injury with infectious complications and reduced th

299 ased mortality rate for patients with severe head injury, with no significant difference in functiona

300 the emergency department with concussion and head injury within the previous 48 hours had modest disc