ライフサイエンスコーパス: head injury

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

2 abilities that are particularly sensitive to head injury.

3 uld modulate bacterial invasion in rats with head injury.

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

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

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

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

8 ative capability in patients after traumatic head injury.

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

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

11 tical and hippocampal cell populations after head injury.

12 ions evolve following relatively mild closed head injury.

13 ortant role in managing patients with severe head injury.

14 ative effect in the treatment of significant head injury.

15 ed prehospital care for patients with severe head injury.

16 portant strategy in the management of severe head injury.

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

18 neurosurgical care on mortality after severe head injury.

19 elivered greater benefit to patients without head injury.

20 4.0 (PedsQL-4.0) at 4, 8, and 12 weeks after head injury.

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

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

23 attainable for treatment of human accidental head injury.

24 n determining treatment strategies for acute head injury.

25 fective treatment of cognitive deficits post head injury.

26 oss populations of patients with significant head injury.

27 e distinction between accidental and abusive head injury.

28 serious sequelae may increase with repeated head injury.

29 tinguish accidental head injury from abusive head injury.

30 influence patient outcome following a severe head injury.

31 of depression increased with severity of the head injury.

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

33 tetanic stimulation in the hippocampus after head injury.

34 formed on anesthetized mice following closed head injury.

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

36 bution of abnormalities in focal and diffuse head injury.

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

38 of depressive illness 50 years after closed head injury.

39 manner in infants and children after severe head injury.

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

41 odegenerative conditions, such as stroke and head injury.

42 t be explained by a history of alcoholism or head injury.

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

44 orrhages in potential cases of nonaccidental head injury.

45 clinical symptoms with a medical history of head injury.

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

47 outcome observed in patients after a single head injury.

48 ric disorders following hospital contact for head injury.

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

50 tested interaction between Rep1 genotype and head injury.

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

52 isrupted among DMN key structures after mild head injury.

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

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

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

56 e importance of protecting young people from head injuries.

57 stablish the presence and severity of closed head injuries.

58 nsive care units that care for children with head injuries.

59 mon comorbidity of stroke and other bleeding head injuries.

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

61 137 children and adolescents attending with head injuries.

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

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

64 he starting gate (35.1%), including 29.5% of head injuries, 39.8% of arm/hand injuries, and 52.0% of

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

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

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

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

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

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

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

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

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

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

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

76 d as a screening test in patients with minor head injury, although the results are often normal.

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

78 Of these, 35 had sustained a blunt head injury and 14 some type of acute non-traumatic brai

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

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

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

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

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

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

85 Head injury and infectious agents are environmental fact

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

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

88 In this regard, severe traumatic head injury and refractory status epilepticus are useful

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

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

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

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

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

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

95 relation (P = 0.008) between the severity of head injury and the N-acetylaspartate/choline ratio.

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 ths or less, all of whom died from inflicted head injuries, and 14 control infants who died of other

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

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

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

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

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

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

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

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

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 aline administration to children with closed head injury appears to be a promising therapy for contro

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 In patients with severe head injuries, brain damage occurs not only from the pri

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

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

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

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

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

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

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

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

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

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

134 ls have been developed to mimic human 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 most of the changes seen after severe human head injury, except for the early fall in p(tiO(2)), fur

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

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

150 Importance: Head injury following explosions is common.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

166 al injury is an uncommon sequel of inflicted head injury in children.

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

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

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

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

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

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

173 stological abnormality in cases of inflicted head injury in the very young is diffuse hypoxic brain d

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

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

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

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

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

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

180 Head injury is a causative factor in the development of

181 Head injury is an inconsistently reported risk factor fo

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

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

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

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

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

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

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

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

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

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

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

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

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

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

196 nd Corticoid Randomisation After Significant Head injury models.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

224 945 and were hospitalized at that time for a head injury, pneumonia, or laceration, puncture, or inci

225 2305 (33%) of patients with severe head injury (presenting between 1996 and 2003) were trea

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

227 Controlled NHBDs had catastrophic head injury, prognosis for no meaningful recovery, decis

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

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

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

231 There were 37 infants, age at head injury ranging from 20 days to 9 months, and 16 chi

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

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

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

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

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

237 Most head injuries resulted from being thrown from the horse

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

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

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

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

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

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

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

245 -appearing white matter which correlate with head injury severity, and that this may provide a pathol

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

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

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

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

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

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

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

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

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

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

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

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

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

259 For the evaluation of patients with minor head injury, the use of CT can be safely limited to thos

260 .3%; after excluding brain death from severe head injury, there were 6.4% misclassifications.

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

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

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

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

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

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

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

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

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

270 Head injury was associated with a higher risk of schizop

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

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

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

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

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

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

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

278 Severe/isolated head injuries were excluded.

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

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

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

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

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

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

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

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

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

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

289 ould be used to identify patients with minor head injury who do not need to undergo CT.

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

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

292 n only two children, both of whom had severe head injuries with multiple skull fractures.

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