ライフサイエンスコーパス: head trauma

1 children were included (n = 35 with abusive head trauma).

2 pact to the head (hereinafter referred to as head trauma).

3 department evaluation of children with blunt head trauma.

4 to minimize neuronal death after a stroke or head trauma.

5 hemorrhage (ICH) associated with stroke and head trauma.

6 get in management of bone response following head trauma.

7 hemia results from cardiac arrest, stroke or head trauma.

8 and management of children with minor blunt head trauma.

9 risk of intracranial injury following minor head trauma.

10 fective in lowering the incidence of abusive head trauma.

11 progressive neuronal injury after stroke and head trauma.

12 anism of avoidable neuronal injury following head trauma.

13 Three patients had predisposing head trauma.

14 presentations of this form of non-accidental head trauma.

15 ly present for medical care after sustaining head trauma.

16 al outcome after focal cerebral ischemia and head trauma.

17 tive cytokine produced in response to severe head trauma.

18 or longer) changes in the hippocampus after head trauma.

19 dentate gyrus 1 week after fluid percussion head trauma.

20 All donors died from severe head trauma.

21 eath was listed as cerebrovascular stroke or head trauma.

22 disease incidence cases without a history of head trauma.

23 of neurological disorders such as stroke and head trauma.

24 rachnoid bleeds in infants who have suffered head trauma.

25 s a genetic susceptibility to the effects of head trauma.

26 aluation as a neuroprotectant for stroke and head trauma.

27 of intracranial hypertension as a result of head trauma.

28 A 12% mortality was experienced after head trauma.

29 known to contribute to neuronal damage from head trauma.

30 ease were evaluated in rat brain cells after head trauma.

31 The effect was particularly strong for mild head trauma.

32 ntervals of 3, 10, 24 h, 3 and 10 days after head trauma.

33 inical Modification codes for both abuse and head trauma.

34 eping the immune system in balance following head trauma.

35 in samples with a low base rate of lifetime head trauma.

36 djusting for age, combat exposure, and blunt head trauma.

37 hage in infants at increased risk of abusive head trauma.

38 League (NHL) players are exposed to frequent head trauma.

39 f head computed tomography for patients with head trauma.

40 ne to developing intracranial bleeding after head trauma.

41 erate recovery in children who have suffered head trauma.

42 124 male military veterans with penetrating head trauma.

43 ecrease morbidity and mortality from abusive head trauma.

44 hat placed them at increased risk of abusive head trauma.

45 ation hardware, and general neurosurgery and head trauma.

46 dichotomized based on likelihood of abusive head trauma.

47 o history of loss of consciousness or direct head trauma.

48 with PTH-CH that developed within 7 days of head trauma.

49 hild was acting abnormally after minor blunt head trauma.

50 o our institution for possible nonaccidental head trauma.

51 emorrhages are an important sequela of fatal head trauma.

52 aining as a sign of axonal injury in abusive head trauma.

53 A history of LOC after minor blunt head trauma.

54 in patients with a baseline elevated ICP or head trauma.

55 ense of smell in people undergoing recurrent head traumas.

56 surgery (19 of 49 episodes [29%]) and remote head trauma (15 of 49 episodes [23%]).

57 ty (abusive head trauma, 25.7% vs nonabusive head trauma, 18.7%; hazard ratio, 1.758; p = 0.60).

58 ulated aORs were 2.15 (95% CI 1.72-2.70) for head trauma; 19.3 (95% CI 14.3-26.0) for neurosurgery; 4

59 nt of the brain was reduced in patients with head trauma (2.8 +/- 1.4 to 1.1 +/- 0.9 [SEM]) and in pa

60 here was no difference in mortality (abusive head trauma, 25.7% vs nonabusive head trauma, 18.7%; haz

61 s were more frequent among the subjects with head trauma (27.8%) than among the population controls (

62 Donor causes of death included head trauma (39.4%), cerebrovascular/stroke (25.8%), and

63 t common reason for requesting the study was head trauma (40.5%); only 15.6% of these studies showed

64 acranial hypertension in each group (abusive head trauma, 66.7% vs nonabusive head trauma, 69.0%).

65 up (abusive head trauma, 66.7% vs nonabusive head trauma, 69.0%).

66 tated most frequently by infections (38.2%), head trauma (9%), or alcohol consumption (5.4%).

67 th decreased rates of computed tomography in head trauma (adjusted odds ratio [AOR], 0.76; 95% CI, 0.

68 Abusive head trauma (AHT) in children is often missed in medical

69 Abusive head trauma (AHT) is a dangerous form of child abuse tha

70 Abusive head trauma (AHT) is a serious condition, with an incide

71 Abusive head trauma (AHT) is the leading cause of infant death a

72 rvention may reduce the incidence of abusive head trauma (AHT) of infants and young children.

73 factors associated with mortality in abusive head trauma (AHT) owing to the severity of the diagnosis

74 ttern is the most common trigger for abusive head trauma (AHT).

75 Cox regression analysis adjusted for stroke, head trauma, alcohol abuse, and cancer showed 1-year, 2-

76 "Mild" head trauma also interfered with hippocampal neurodevelo

77 sser extent, they are known to develop after head trauma and brain inflammatory diseases.

78 ,412 children aged 0 to 18 years with blunt head trauma and Glasgow Coma Scale scores of 14 and 15 e

79 ildren younger than 2 years with minor blunt head trauma and guardian reports of the child acting abn

80 Head trauma and hematuria were the most prominent featur

81 nnection between early-life exposure to mild head trauma and late-life emergence of neurodegenerative

82 stablish a causal relationship between early head trauma and late-life neurodegeneration, emphasizing

83 ified in 10 patients included viral illness, head trauma and primary mood disorder.

84 imer's disease and to the poor outcome after head trauma and stroke associated with apoE4 in humans.

85 entral nervous system pathologies, including head trauma and stroke.

86 ispose of neurotoxic material generated from head trauma and to instruct the wound healing process.

87 eurological and histological outcome in both head trauma and transient focal cerebral ischemia.

88 to the emergency department with acute blunt head trauma and were examined with multidetector CT veno

89 Children with severe thrombocytopenia plus head trauma and/or hematuria appeared to be at particula

90 osis and is implicated in cerebral ischemia, head trauma, and age-related neurodegenerative diseases.

91 dical disorders, learning disability, severe head trauma, and alcohol or drug abuse were enrolled.

92 tracranial pressure, including inflammation, head trauma, and brain tumors.

93 exual abuse, physical child abuse, inflicted head trauma, and child abuse prevention.

94 of neurovascular regulation such as stroke, head trauma, and migraine.

95 dial infarction, drug overdose, nonoperative head trauma, and nonoperative multiple trauma.

96 ts without headache, coma triggered by minor head trauma, and slowly progressive cerebellar ataxia) w

97 nical evaluation of ACEA 1021 for stroke and head trauma, and suggests that glycine site antagonists

98 s have suggested that outcomes after abusive head trauma are less favorable than after other injury m

99 Stroke and head trauma are worldwide public health problems and lea

100 nts; DGF; donor age older than 35 years; and head trauma as a cause of initial injury (relative risk

101 ing sports today that have a similar risk of head trauma as high school football played in the 1950s.

102 tin use, supplement use, caffeine intake and head trauma, as well as occupational and environmental e

103 Symptomatic head trauma associated with American-style football (ASF

104 A and therefore eliminated the occurrence of head trauma associated with other preclinical stroke mod

105 ision rules can identify patients with minor head trauma at low risk of severe intracranial injuries.

106 children aged 0-2 years treated for abusive head trauma at our institute between 1997 and 2009 were

107 consequences of exposure to football-related head trauma at the high school level.

108 5 years with a primary diagnosis of abusive head trauma between January 1, 2006, and December 31, 20

109 Common predisposing factors include closed head trauma, blood pressure alterations, history of pitu

110 ave a disproportionally severe outcome after head trauma, but the underlying mechanisms are unclear.

111 h NHL players with less frequent exposure to head trauma (C-F and C-P cohorts).

112 logic findings present in victims of abusive head trauma can also be seen in shaken adults.

113 Although diagnosing head trauma can be difficult in the absence of a history

114 oduced by experimental status epilepticus or head trauma can be replicated by focal interneuron loss

115 valuation in infants and young children with head trauma can help clinicians determine the likelihood

116 cale scores </=8, without gunshot or abusive head trauma, cardiac arrest, or Glasgow coma scale score

117 uality RetCam images of 21 eyes from abusive head trauma cases with varying degrees of retinal hemorr

118 ar folds could only be identified in abusive head trauma cases.

119 of a defense strategy in high-stakes abusive head trauma cases.

120 Sixty eyes were identified as "abusive head trauma" (cases), 46 as "alternative cause" (control

121 ever, whether a single episode of concussive head trauma causes a persistent increase in neuronal exc

122 model, we demonstrate that exposure to mild head trauma causes neurodegenerative conditions that eme

123 Severe head trauma causes widespread neuronal shear injuries an

124 her elucidate the association of exposure to head trauma, clinical features, and the development of p

125 In the abusive head trauma cohort, 67 (26.5%) of 252 children had evalu

126 and involved more retinal layers in abusive head trauma compared to controls (OR 2.7, CI 1.7-4.4; P

127 y, brain injuries, closed head injury, blunt head trauma, concussion, attention deficit disorders, AD

128 Participants who reported more symptomatic head trauma, defined as the total number of impacts to t

129 All 9 had abusive head trauma diagnosable with nonocular findings.

130 entifying cherry hemorrhages may aid abusive head trauma diagnosis.

131 ing corporal punishment or mandating abusive head trauma education to parents of newborns.

132 ldren younger than 18 years with minor blunt head trauma evaluated in 25 emergency departments.

133 ermine the relationships between measures of head trauma exposure and other potential modifiers and c

134 enalty minutes were both used as proxies for head trauma exposure.

135 Head trauma from abuse, including shaken baby syndrome,

136 ors that differentiate children with abusive head trauma from those with traumatic brain injury from

137 Adults with apparently minor head trauma (Glasgow Coma Scale [GCS] scores >/=13 who a

138 ecember 31, 2010, with severe TBI (ie, blunt head trauma, Glasgow Coma Scale score of <9, and abnorma

139 In the abusive head trauma group, positive beta-APP and ubiquitin immun

140 Abusive head trauma had a higher prevalence of seizures during r

141 e, multicenter series, children with abusive head trauma had differences in prehospital and in-hospit

142 Donors with head trauma had numerically more quantitated proteinuria

143 Information on abusive head trauma has been published in large amounts in the p

144 While the linear effects of head trauma have been extensively modeled, less is known

145 ve telephone clinical assessments (including head trauma history) with informants were performed blin

146 vous system are elevated, such as stroke and head trauma, homocysteine's neurotoxic (agonist) attribu

147 Minor head trauma (HT) is one of the most common causes of hos

148 ocysteinaemia, depression, stress, diabetes, head trauma, hypertension in midlife and orthostatic hyp

149 acerebral hemorrhage (ICH) caused by stroke, head trauma, hypertension, and a wide spectrum of disord

150 Causes of death were head trauma in 10 donors, intracranial bleed in 24, and

151 INTERPRETATION: Head trauma in adolescence, particularly if repeated, is

152 itive to the long-term impact of symptomatic head trauma in former professional ASF players and other

153 story, it is important to consider inflicted head trauma in infants and young children presenting wit

154 and simultaneous fractures, dislocations, or head trauma in inpatient or outpatient claims.

155 ren, female predominance was seen in abusive head trauma in our cohort.

156 veloped a new model of repetitive rotational head trauma in rodents and demonstrated acute and prolon

157 hift in injury patterns favoring more severe head trauma in the DCR cohort.

158 h cortical and hippocampal damage induced by head trauma in the rat.

159 only occurred in donors who suffered severe head trauma in this cohort, which may be a predisposing

160 scriptional response of the meninges to mild head trauma in youth and aging.

161 Mild head trauma, including concussion, can lead to chronic b

162 ISR emerges as a promising avenue to combat head trauma-induced chronic cognitive deficits.

163 that a single episode of experimental closed head trauma induces long-lasting alterations in the hipp

164 Brain injury, as occurs in stroke or head trauma, induces a dramatic increase in levels of tu

165 Repetitive head trauma is a risk factor for Alzheimer's disease and

166 rch in the management of children with minor head trauma is actively evolving.

167 Here, we demonstrate that severe head trauma is associated with a marked loss (41%) of hi

168 he neural level, olfactory impairment due to head trauma is best characterized by heightened response

169 of zinc chelators for neuroprotection after head trauma is considered.

170 ementias associated with aging or repetitive head trauma is rising.

171 Abusive head trauma is the leading cause of death from physical

172 Head trauma leading to concussion and electroconvulsive

173 In 194 patients with penetrating head trauma, lesion damage to this network correlated wi

174 hs suggest that children with severe abusive head trauma may benefit from therapies including invasiv

175 ious concussive and repetitive subconcussive head trauma may underlie the reduced F0 encoding in athl

176 ic lateral sclerosis (ALS) and that repeated head trauma might have contributed to this increase.

177 In patients with blunt head trauma, multidetector CT venographic evaluation sho

178 neurotoxicity has been implicated in stroke, head trauma, multiple sclerosis and neurodegenerative di

179 after closed-head injury, particularly mild head trauma, must include consideration of the effect of

180 ospital emergency room in 1999 with an acute head trauma (n = 737) were followed up until February 20

181 e, has been described in ischemic stroke and head trauma, no information exists regarding their possi

182 orthodromically evoked [K+]o elevation after head trauma occurred in association with a greater popul

183 to investigate the long-term effects of mild head trauma on brain structure and function, as well as

184 We sought to determine the impact of abusive head trauma on mortality and identify factors that diffe

185 All patients had a confirmed history of head trauma or brain surgery with altered consciousness

186 Infants were assigned to abusive head trauma or control groups, according to published cr

187 ury is clearly evident whether the injury is head trauma or ischemia, or whether the measurements wer

188 histaminergic tone may improve arousal after head trauma or other conditions.

189 therapy for cerebral edema in patients with head trauma or postoperative edema.

190 lso associated with poor outcome after acute head trauma or stroke.

191 pressure experienced in left heart failure, head trauma, or high altitude can lead to endothelial ba

192 alformation, intracranial venous thrombosis, head trauma, or tumour; haemorrhagic transformation with

193 , and donor cause of death other than closed head trauma (P = .04).

194 Missing the diagnosis of abusive head trauma, particularly in its mild form, is common an

195 Survivor abusive head trauma pathology demonstrates unique, irreversible

196 ation in therapies and outcome for pediatric head trauma patients by patient characteristics and by p

197 r risk for developing Alzheimer's disease in head trauma patients.

198 ior hypothalamus, has never been examined in head trauma patients.

199 ad computed tomography (HCT) after pediatric head trauma (PHT); however, quantitative data are lackin

200 ld of child maltreatment, addressing abusive head trauma, physical abuse, sexual abuse, and global is

201 We next found that head trauma potentiates BACE1 elevation in GGA3-null mic

202 Children with minor blunt head trauma presenting to the emergency department with

203 focusing on home visiting programs, abusive head trauma primary prevention, parent training programs

204 Episodes of prolonged seizures or head trauma produce chronic hippocampal network hyperexc

205 concentration was observed in patients with head trauma (r2 = .91, p = .03), and postoperative edema

206 e in memory function, were down-regulated in head trauma-related disorders.

207 These results suggest that following head trauma, released galectin-3 may act as an alarmin,

208 mography scans for children with minor blunt head trauma resulting in potentially harmful radiation e

209 fter 40 days because of mechanical fall with head trauma resulting in subdural hematoma with no assoc

210 essing epidemiology, physical abuse, abusive head trauma, sexual abuse, sequelae, and prevention.

211 Individuals were excluded for history of head trauma, significant substance abuse, and medical co

212 Environmental insults, including mild head trauma, significantly increase the risk of neurodeg

213 Patients with a history of stroke, burn, head trauma, spinal cord injury, or joint replacement we

214 Stroke and head trauma stimulate proliferation of endogenous neural

215 pressive craniectomy is often required after head trauma, stroke, or cranial bleeding to control subs

216 However, head trauma, stroke, status epilepticus and other pathol

217 findings that are characteristic of abusive head trauma--subdural hemorrhages, optic nerve sheath he

218 Head trauma subjects without TBI have an elevated risk o

219 investigating the long-term effects of mild head trauma, suggest an increased vulnerability to brain

220 There was no history of head trauma, surgery, drug therapy, smoking, or alcohol

221 Both abusive head trauma survivor cases demonstrated severe optic ner

222 rnative cause" (controls), and 4 as "abusive head trauma survivor".

223 en on T2*-weighted MRI in patients following head trauma that have previously been considered a marke

224 Among patients with apparent minor head trauma, the absence of any of the features of the C

225 In patients with head trauma, the beneficial effect of hypertonic saline

226 ce of compressive deformations in most blunt head trauma, this information is critically important fo

227 rs in the cortex after a latent period after head trauma; this delay has been attributed to the desta

228 reated in 25 emergency departments for blunt head trauma, traumatic brain injury was identified on CT

229 drome associated with repetitive exposure to head trauma: traumatic encephalopathy syndrome.

230 function and the influences of etiology (eg, head trauma, upper respiratory infection), sex, age, smo

231 ases in the dentate gyrus after experimental head trauma, using a combination of whole-cell recording

232 spinal canal subdural hemorrhage in abusive head trauma versus that in accidental trauma.

233 ces of spinal subdural hemorrhage in abusive head trauma versus those in accidental trauma was statis

234 tion is often compromised by such factors as head trauma, viruses, and toxic agents, the olfactory ep

235 ention) among the 23,079 patients with minor head trauma was 7.1% (95% CI, 6.8%-7.4%) and the prevale

236 The DNA fragmentation induced after severe head trauma was accompanied by an increase in the activi

237 Abusive head trauma was more likely to be unrecognized in very y

238 Symptomatic head trauma was not correlated with average stride times

239 all patients with an admitting diagnosis of head trauma were included (n = 477).

240 Abusive head trauma were more likely to 1) be transported from h

241 PK organs were younger, more often died from head trauma, were less often female, and more often blac

242 APP and ubiquitin with a high OR for abusive head trauma when compared to controls.

243 This is most evident with regards to abusive head trauma, wherein both lay and scientific press chall

244 for ophthalmic findings in suspected abusive head trauma, which has excellent interobserver and intra

245 teen patients with acute stroke and two with head trauma who had undergone intraarterial or intraveno

246 to the emergency department following acute head trauma who received a head CT were enrolled within

247 nt in more than 60% of children with abusive head trauma who underwent thoracolumbar imaging in this

248 nger than 18 years presenting within 24 h of head trauma with Glasgow Coma Scale scores of 14-15 in 2

249 whether they had experienced an MMTBI (blunt head trauma with loss of consciousness, amnesia, or diso

250 Head trauma with or without traumatic brain injury (TBI)

251 t is not known why long-term mortality after head trauma without traumatic brain injury is elevated.

252 We hypothesized that ASF-related symptomatic head trauma would predict worse gait performance, partic