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 hage in infants at increased risk of abusive head trauma.

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

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

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

7 and management of children with minor blunt head trauma.

8 risk of intracranial injury following minor head trauma.

9 fective in lowering the incidence of abusive head trauma.

10 progressive neuronal injury after stroke and head trauma.

11 anism of avoidable neuronal injury following head trauma.

12 Three patients had predisposing head trauma.

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

14 ly present for medical care after sustaining head trauma.

15 al outcome after focal cerebral ischemia and head trauma.

16 tive cytokine produced in response to severe head trauma.

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

18 dentate gyrus 1 week after fluid percussion head trauma.

19 ation hardware, and general neurosurgery and head trauma.

20 eath was listed as cerebrovascular stroke or head trauma.

21 disease incidence cases without a history of head trauma.

22 of neurological disorders such as stroke and head trauma.

23 rachnoid bleeds in infants who have suffered head trauma.

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

25 aluation as a neuroprotectant for stroke and head trauma.

26 of intracranial hypertension as a result of head trauma.

27 A 12% mortality was experienced after head trauma.

28 known to contribute to neuronal damage from head trauma.

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

30 The effect was particularly strong for mild head trauma.

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

32 dichotomized based on likelihood of abusive head trauma.

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

34 hild was acting abnormally after minor blunt head trauma.

35 o our institution for possible nonaccidental head trauma.

36 emorrhages are an important sequela of fatal head trauma.

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

38 A history of LOC after minor blunt head trauma.

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

40 department evaluation of children with blunt head trauma.

41 ecrease morbidity and mortality from abusive head trauma.

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

43 ense of smell in people undergoing recurrent head traumas.

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

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

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

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

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

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

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

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

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

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

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

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

56 ,412 children aged 0 to 18 years with blunt head trauma and Glasgow Coma Scale scores of 14 and 15 e

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

58 Head trauma and hematuria were the most prominent featur

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

90 Severe head trauma causes widespread neuronal shear injuries an

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

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

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

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

95 entifying cherry hemorrhages may aid abusive head trauma diagnosis.

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

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

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

99 Head trauma from abuse, including shaken baby syndrome,

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

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

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

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

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

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

106 Donors with head trauma had numerically more quantitated proteinuria

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

125 Head trauma leading to concussion and electroconvulsive

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

144 Survivor abusive head trauma pathology demonstrates unique, irreversible

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

160 Stroke and head trauma stimulate proliferation of endogenous neural

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

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

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

164 Head trauma subjects without TBI have an elevated risk o

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

166 Both abusive head trauma survivor cases demonstrated severe optic ner

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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