ライフサイエンスコーパス: amnesia

1 forgotten, a phenomenon known as 'infantile amnesia'.

2 plicit, recently formed memories (retrograde amnesia).

3 vestigator to be vaccine related (keratitis; amnesia).

4 uired before the damage occurred (retrograde amnesia).

5 that it is rapidly forgotten (inattentional amnesia).

6 first examination of the default network in amnesia.

7 n of complex objects in individuals with MTL amnesia.

8 in bilateral diencephalic lesion and severe amnesia.

9 l retrograde amnesia' in transient epileptic amnesia.

10 epilepsy can manifest itself in episodes of amnesia.

11 eficits in patients with transient epileptic amnesia.

12 addressed the area of malingered retrograde amnesia.

13 ECT in efficacy and resulted in less severe amnesia.

14 nding the malingering paradigm to retrograde amnesia.

15 thalamic nuclei at the heart of diencephalic amnesia.

16 uced more severe retrograde than anterograde amnesia.

17 Damage of this nature may account for dense amnesia.

18 ociated with both retrograde and anterograde amnesia.

19 episode' predisposing to later psychological amnesia.

20 ociated with both retrograde and anterograde amnesia.

21 onsolidation, a disruption of which leads to amnesia.

22 his is not true for ALF and autobiographical amnesia.

23 er anisomycin, attenuated anisomycin-induced amnesia.

24 parently by inducing selective immunological amnesia.

25 d related medial temporal lobe structures in amnesia.

26 same lesions produced devastating retrograde amnesia.

27 om presentation, or even present solely with amnesia.

28 ation in the rehabilitation of patients with amnesia.

29 e of these was affected by midazolam-induced amnesia.

30 ia and a 1-30 d temporally graded retrograde amnesia.

31 etermine the nature and extent of retrograde amnesia.

32 in human clinical cases and animal models of amnesia.

33 een the memory impairments in MT versus ACoA amnesia.

34 spared delay EBCC previously observed in MT amnesia.

35 indicating that they had a dense retrograde amnesia.

36 hours after memory reactivation produced no amnesia.

37 onset was correlated with greater levels of amnesia.

38 lso observed in patients with post-traumatic amnesia.

39 mGluR5 after training rescues the infantile amnesia.

40 h mechanisms underlie infantile memories and amnesia.

41 nsolidation is held to result in a permanent amnesia.

42 tion, and more feelings of disembodiment and amnesia.

43 y but may be left with permanent anterograde amnesia.

44 plicit) and repetition priming (implicit) in amnesia.

45 ts that illuminates the paradox of infantile amnesia.

46 ithout stable contacts yielded immunological amnesia.

47 have contributed to his extensive retrograde amnesia.

48 nesia involve the same mechanisms as organic amnesia?

49 s impaired and what is spared in anterograde amnesia?

50 reported less than 24 hours of posttraumatic amnesia (37 reported >/= 24 hours), and 111 of 117 of th

51 c features (insomnia 89.7%, confusion 65.5%, amnesia 55.6%, hallucinations 51.9%), dysautonomia (hype

52 a (79.2%), nausea (75.5%), headache (60.4%), amnesia (58.5%), and >5% weight loss (52.8%).

53 rst year of life can result in developmental amnesia, a disorder characterized by markedly impaired e

54 pt occurrence of severe anterograde episodic amnesia accompanied by repetitive questioning, has been

55 ings support the contention that anterograde amnesia affects learning that depends on building novel

56 tures, except to the extent that anterograde amnesia affects performance.

57 Retrograde amnesia after an associative learning task can be induce

58 Observations of temporally graded retrograde amnesia after hippocampal damage suggest that the hippoc

59 ngs indicate that amygdala-based anterograde amnesia after hypoxia/reoxygenation is sustained by IL-1

60 Cases of amnesia after unilateral temporal lobectomy illustrate t

61 ed the subiculum produced marked anterograde amnesia and a 1-30 d temporally graded retrograde amnesi

62 ically and demonstrate empirically that both amnesia and also transient negative moods can be associa

63 f consciousness or evidence of posttraumatic amnesia and an emergency department Glasgow Coma Scale s

64 ecognition is consistently impaired in human amnesia and animal models thereof.

65 r Irish family with autosomal dominant early amnesia and behavioural change or parkinsonism associate

66 rienced FBDS prior to the development of the amnesia and confusion that characterize LE.

67 required patients with medial temporal lobe amnesia and controls to remember three objects, location

68 anations of memory recovery after retrograde amnesia and critically challenges the traditional memory

69 unctional relationship between temporal lobe amnesia and diencephalic amnesia depends on determining

70 tatus or scientific validity of dissociative amnesia and dissociative identity disorder.

71 s into the pathophysiology of post-traumatic amnesia and evidence that memory impairment acutely afte

72 sses the assessment of malingered retrograde amnesia and evidences that a critical moment has been re

73 Evidence from studies of amnesia and functional imaging in humans suggest that th

74 nto the functional pathology of diencephalic amnesia and have implications for the aetiology of the p

75 l lines for grafting in conditions of severe amnesia and hippocampal damage following recovery from c

76 etomidate, and barbiturates produce profound amnesia and hypnosis, but weak immobility, by enhancing

77 emic circulation to the cerebral cortex (for amnesia and loss of consciousness) and to the spinal cor

78 nd cellular mechanisms underlying retrograde amnesia and memory.

79 In the past 60 years, the amnesia and other impairments exhibited by these patient

80 the two agents provide similar responses to amnesia and pain control.

81 t enables sleep and communication, with less amnesia and pain medication requirements, during mechani

82 nal activity reflecting hypnosis, analgesia, amnesia and reflex suppression seems to be emerging givi

83 eatment increased and prolonged sedation and amnesia and stabilized vital signs while significantly d

84 aintain a detailed narrative is preserved in amnesia and suggest that a common MTL mechanism supports

85 oint interrupts the ability of ZIP to induce amnesia and that ZIP's ability to induce amnesia is reen

86 neurotrophins, selectively rescued both the amnesia and the molecular impairments produced by glucoc

87 n injury were classified into post-traumatic amnesia and traumatic brain injury control groups, based

88 ith striking comprehension deficits but with amnesia and variable anomia, leading some to conclude th

89 eatment with DU-14 could reverse scopolamine amnesia and/or enhance spacial memory in the place, prob

90 loss (also known as dissociative/functional amnesia), and still fewer studies of outcome, or compari

91 bitor antibiotics are widely used to produce amnesia, and have been recognized to inhibit general or

92 d empirically, the recognition of analgesia, amnesia, and hypnosis as discrete elements comprising th

93 r effects (loss of consciousness, analgesia, amnesia, and immobility) remain an unsolved mystery.

94 azolam, an anesthetic that induces temporary amnesia, and once after an injection of saline.

95 itsch's and Kopelman's models of psychogenic amnesia, and with respect to Anderson's neuroimaging fin

96 tion task to test patient P01, who has dense amnesia, approximately 50% bilateral hippocampal volume

97 that the mnemonic symptoms of post-traumatic amnesia are caused by functional disconnection within th

98 Patients presenting with subacute amnesia are frequently seen in acute neurological practi

99 These cases of postoperative amnesia are further considered in the context of the cog

100 ion was found as performant as posttraumatic amnesia (area under the curve, 0.81; difference between

101 nced episodic memory impairments, suggesting amnesia as a critical diagnostic feature.

102 cortices) impairs new learning (anterograde amnesia) as well as memory for information that was acqu

103 e the difference in the extent of retrograde amnesia associated with hippocampal lesions and large MT

104 issociative hallucinations, and intermittent amnesia at delivery.

105 duced significant anterograde and retrograde amnesia at doses that did not impair performance process

106 In conclusion, severe amnesia at presentation in FTD is commoner than previous

107 A review of severe amnesia at presentation in patients with pathologically

108 ly, some behavioral cases (n = 5) had marked amnesia at presentation.

109 The authors' search for an animal model of amnesia, based on ablations aimed at the hippocampal for

110 of one's unethical acts over time "unethical amnesia." Because of unethical amnesia, people are more

111 x damage is sufficient to induce anterograde amnesia but also support the validity of recent animal t

112 h follow-up, patients had reduced retrograde amnesia, but continued to show deficits in recalling the

113 on amongst patients with transient epileptic amnesia, but have been reported in other forms of epilep

114 mpairment reported in cases of developmental amnesia, but they are also clinically relevant given tha

115 ological treatments for medial temporal lobe amnesia, but various rehabilitative techniques may be us

116 ine produce analgesia, but weak hypnosis and amnesia, by inhibiting glutamate and nicotinic receptors

117 we show that this reconsolidation-associated amnesia can be achieved 48 h after formation of the orig

118 es has emphasized that malingered retrograde amnesia can be identified with relevant assessment metho

119 be formed without protein synthesis and that amnesia can be induced by drugs that do not affect prote

120 y in early childhood, but this developmental amnesia can have debilitating consequences, both at home

121 especially large learning rate: People with amnesia can learn quickly and happy people slowly.

122 es following hippocampal damage (anterograde amnesia) can be overcome with sufficient training.

123 tients with bilateral hippocampal damage and amnesia cannot construct novel or future scenes/events h

124 s unwanted side effects, including sedation, amnesia, cardiorespiratory depression, and anticonvulsiv

125 europsychological findings in 53 psychogenic amnesia cases (ratio of 3:1, males:females), in comparis

126 rrent investigation, human participants with amnesia categorized pictures of objects at study and the

127 al cortex, this recovery is impaired and the amnesia caused by the structural lesion is more severe.

128 sychological deficits emerged: the selective amnesia characteristic of the MCI phase was joined next

129 e (MTL) lesions typically produce retrograde amnesia characterized by the disproportionate loss of re

130 CA1s of a-FMHis-treated rats that displayed amnesia compared with in the control group.

131 Cognitively triggered amnesia constitutes an unrecognized forgetting process t

132 roup exhibited temporally limited retrograde amnesia covering approximately 5 years.

133 MTL group exhibited an extensive retrograde amnesia covering decades.

134 learning facts and events and had retrograde amnesia covering several decades.

135 sociative memory, patients in post-traumatic amnesia demonstrated impairments in information processi

136 tween temporal lobe amnesia and diencephalic amnesia depends on determining the role of the fornix, t

137 How anterograde amnesia develops or resolves remains elusive, but a link

138 ed level of overall awareness as a marker of amnesia did not differ between groups (p = .653).

139 temporal lobe, diencephalic and frontal lobe amnesias differ?

140 ls under protein synthesis inhibitor-induced amnesia, direct optogenetic activation of these cells re

141 of consciousness or period of posttraumatic amnesia) do not correlate with persistent concussion sym

142 Thus, amnesia does not appear immediately after training but d

143 To examine this, six patients with amnesia due to head injury or stroke and six normal cont

144 on (phase 1) and compared with posttraumatic amnesia duration and the initial Glasgow Coma Scale scor

145 patients, and by achieving greater levels of amnesia during FOB.

146 t include frequent focal seizures, prominent amnesia, dysautonomia, neuromyotonia and neuropathic pai

147 While most accounts of diencephalic amnesia emphasize the functional importance of the hippo

148 Molaison (H.M.), an epileptic patient whose amnesia ensued unexpectedly following a bilateral surgic

149 Midazolam provides rapid and reliable amnesia, even when administered for low levels of sedati

150 (v) Can retrograde amnesia ever be "isolated"?

151 BI must be demonstrable, and other causes of amnesia excluded.

152 amnesia; (iii) psychogenic focal retrograde amnesia following a minor neurological episode; and (iv)

153 The distinct temporal properties for amnesia following anisomycin injections into the hippoca

154 using a select group of patients with severe amnesia following circumscribed bilateral damage to the

155 Cases of amnesia following unilateral temporal lobe surgery are r

156 n hippocampal slices from R(AB) mice and the amnesia for context fear conditioning seen in R(AB) mice

157 ing selective hippocampal damage: retrograde amnesia for episodic memories is temporally limited or e

158 Bilateral ECT caused more marked amnesia for events and details than RUL ECT, and especia

159 s also exhibit temporally limited retrograde amnesia for factual information from the several years p

160 s differential presentation are unknown, but amnesia for loss of consciousness may be the underlying

161 Cognitive impairment does not explain the amnesia for loss of consciousness seen in fallers with c

162 ups (5.1 vs. 5.4 s; p = 0.42), but witnessed amnesia for loss of consciousness was more frequent in f

163 cated that damage to this structure produced amnesia for newly acquired memories but did not affect t

164 ciated with severe episodic but not semantic amnesia for postmorbid autobiographical events that was

165 sion could be as performant as posttraumatic amnesia for predicting traumatic brain injury recovery,

166 ensory intrusive hypermnesia and declarative amnesia for the same traumatic event.

167 damage produces temporally graded retrograde amnesia for the social transmission of a food preference

168 n contrast, research with offenders claiming amnesia for their crimes has emphasized that malingered

169 me periods, whereas the two focal retrograde amnesia groups showed a 'reversed' temporal gradient wit

170 By contrast, the two focal retrograde amnesia groups showed less improvement and continued to

171 d Rule (>/=65 years; >/=2 vomiting episodes, amnesia >30 minutes, pedestrian struck, ejected from veh

172 vely studied, whereas research on retrograde amnesia has tended to focus upon functional and organic

173 nduced blackouts (ie, periods of anterograde amnesia) have received limited recent research attention

174 Recent studies in patients with amnesia, however, have shown that performance on declara

175 distinct clinical profiles appear to induce amnesia, hypnosis, and immobility via different molecula

176 station of seizures is recurrent episodes of amnesia; (ii) accelerated long-term forgetting, in which

177 fugue state; (ii) fugue-to-focal retrograde amnesia; (iii) psychogenic focal retrograde amnesia foll

178 s in a profound temporally graded retrograde amnesia, implying that it is necessary for memory acquis

179 rodents and monkeys, and result in profound amnesia in adult humans.

180 ealed robust default network connectivity in amnesia in cortical default network regions such as medi

181 in recent discussion: studies of retrograde amnesia in memory-impaired patients who have well-charac

182 demonstrated this reconsolidation associated amnesia in nonhuman animals, the evidence for its occurr

183 ne (DU-14) could reverse scopolamine induced amnesia in rats in a passive avoidance memory paradigm.

184 , it has been uncertain whether the observed amnesia in the early stages of AD is due to disrupted en

185 itation, we use two case studies of citation amnesia in the field of hypothetical carbon allotropes t

186 Before amyloid plaque deposition, the amnesia in these mice is age-dependent, which correlates

187 nduce a cellular state of enforced oncogenic amnesia in which, only upon oncogene inactivation, the t

188 ence for the occurrence of 'focal retrograde amnesia' in transient epileptic amnesia.

189 iated with epilepsy: (i) transient epileptic amnesia, in which the sole or main manifestation of seiz

190 OGCs 1 month after training did not produce amnesia, indicating that adult-generated OGCs play a tim

191 First, we demonstrate that the amnesia induced by blockade of reconsolidation does not

192 (vi) Does psychogenic amnesia involve the same mechanisms as organic amnesia?

193 mited or extensive and ungraded; anterograde amnesia involves both recollective and familiarity proce

194 Transient epileptic amnesia is a distinctive syndrome of temporal lobe epile

195 Transient epileptic amnesia is a form of temporal lobe epilepsy in which suf

196 Malingered anterograde amnesia is a phenomenon that has been exhaustively studi

197 lex perceptual-motor skills in patients with amnesia is a robust phenomenon, and that it can be demon

198 Clinically, post-traumatic amnesia is an important predictor of functional outcome.

199 Transient epileptic amnesia is an under-recognized but treatable cause of tr

200 his review supports the idea that contextual amnesia is at the core of PTSD and its persistence and t

201 Although this amnesia is considered as a critical etiological factor o

202 Hippocampal amnesia is defined by deficits in the binding of relatio

203 It has been suggested that infantile amnesia is due to the underdevelopment of the infant bra

204 polymorphism, an emotion-induced retrograde amnesia is expressed solely in the presence of the short

205 tance, the pathophysiology of post-traumatic amnesia is not understood.

206 uce amnesia and that ZIP's ability to induce amnesia is reengaged only 45 h after retrieval.

207 Consequently, the literature on psychogenic amnesia is somewhat fragmented and offers little prognos

208 Posttraumatic amnesia is superior to the initial Glasgow Coma Scale sc

209 Retrograde amnesia is the most persistent cognitive adverse effect

210 s from typical Alzheimer-type dementia where amnesia is the primary deficit.

211 Severe amnesia is usually observed following bilateral hippocam

212 C COMMENTARY ON THIS ARTICLE: Post-traumatic amnesia is very common immediately after traumatic brain

213 el manner, that one deficit underlying their amnesias is vulnerability to retroactive interference.

214 r factual knowledge (from 11-30 years before amnesia) is intact.

215 call results in a non-recoverable retrograde amnesia, known as reconsolidation blockade.

216 am was found to cause a greater incidence of amnesia lasting up to 30 minutes when compared to placeb

217 Classic studies of amnesia led to characterizations of hippocampal function

218 ment with an OT antagonist produced a social amnesia-like effect in Oxt+/+ mice.

219 novo protein synthesis and that experimental amnesia may not result from a disruption of memory conso

220 ologic programs inducing a state of cellular amnesia, not only inducing relentless cellular prolifera

221 ore, the results demonstrate that retrograde amnesia occurs as a result of subcortical damage only if

222 Retrograde amnesia of learned associative memories is elicited by i

223 , giving rise to recurrent, brief attacks of amnesia, often occurring on waking.

224 cular, we examined the pattern of retrograde amnesia on an assessment of autobiographical memory (the

225 n shortly after memory reactivation produces amnesia on later tests, regardless of whether reactivati

226 ening should be considered in families where amnesia or atypical parkinsonism coexists with behaviour

227 A prior head injury with amnesia or loss of consciousness was associated with an

228 lunt head trauma with loss of consciousness, amnesia, or disorientation and a Glasgow Coma Scale scor

229 s prevent memory restabilization and produce amnesia, others have shown that GluN2B-selective NMDAR a

230 In conclusion, the outcome in psychogenic amnesia, particularly those characterized by fugue, is b

231 me "unethical amnesia." Because of unethical amnesia, people are more likely to act dishonestly repea

232 s an experience learned during the infantile amnesia period is stored as a latent memory trace for a

233 ns the pattern of recognition and priming in amnesia primarily as a reduction in the strength of a si

234 red release of neurotransmitters may mediate amnesia produced by anisomycin and, further, raise impor

235 wed that the effect is not due to retrograde amnesia produced by LiCl, and (c) confirmed that memorie

236 Amnesia produced by protein synthesis inhibitors such as

237 Retrospective assessment of post-traumatic amnesia (PTA) must take into account factors other than

238 ild-to-moderate TBI (52% with post-traumatic amnesia (PTA)</=24 hours), but including some with sever

239 A rodent model of diencephalic amnesia, pyrithiamine-induced thiamine deficiency (PTD),

240 We propose that infantile amnesia reflects a developmental critical period during

241 s for the severe memory loss in diencephalic amnesia remain unknown.

242 ationship between anterograde and retrograde amnesia remains unclear.

243 interferes with sensory processing to cause amnesia remains unclear.

244 processes, such as benzodiazepine-associated amnesia, remains unexplored.

245 ticipants (87.1%) who reported posttraumatic amnesia reported less than 24 hours of posttraumatic amn

246 We showed in rats that the amnesia resulting from systemic, intracerebroventricular

247 It is currently believed that ACoA amnesia results from basal forebrain damage that disrupt

248 We propose that amnesia results from memory integration of the internal

249 ntegrated within the initial memory and that amnesia results from the absence of this state at testin

250 ng co-occurring items is tested, hippocampal amnesia results in a deficit even at very short lags.

251 The finding that patients with amnesia retain the ability to learn certain procedural s

252 injury state, involving tests for continuing amnesia, risk promoting recall of events suggested by th

253 ases of the central nervous system including amnesia, schizophrenia, depression, Alzheimer disease, a

254 >60 years, intoxication, headache, vomiting, amnesia, seizure, or trauma above the clavicle) had an L

255 s) developed prominent psychiatric symptoms, amnesia, seizures, frequent dyskinesias, autonomic dysfu

256 Patients in post-traumatic amnesia showed abnormal functional connectivity between

257 Patients with post-traumatic amnesia showed evidence of widespread traumatic axonal i

258 Based on amnesia studies, that hypothesis states that active (i.e

259 s of neuropathology in cases of diencephalic amnesia such as Wernicke Korsakoff Syndrome (WKS), there

260 aneurysm rupture can lead to an anterograde amnesia syndrome similar to that observed after damage t

261 Transient epileptic amnesia (TEA) is a recently recognised form of epilepsy

262 viously in patients with transient epileptic amnesia (TEA), to date there have been no detailed studi

263 avy drinking can also cause mild anterograde amnesias, temporary cognitive deficits, sleep problems,

264 The Morris water maze (MWM) retrograde amnesia test was conducted on day 12 post-CCI and showed

265 ary diagnosis of seizure or transient global amnesia (TGA) served as control groups.

266 Transient global amnesia (TGA), an abrupt occurrence of severe anterograd

267 effect is an example of preserved memory in amnesia that does not easily fit into the categories of

268 In clinical cases of amnesia that followed bilateral excisions of medial temp

269 ronal lactate transporter MCT2 also leads to amnesia that is unaffected by either L-lactate or glucos

270 sia undoubtedly induces unresponsiveness and amnesia, the extent to which it causes unconsciousness i

271 Infantile amnesia, the inability of adults to recollect early epis

272 w coma scale or the length of post-traumatic amnesia, the increase in the choline/creatine ratio was

273 ning HPC lesions result in temporally graded amnesia, the precise HPC circuits and mechanisms involve

274 onal experience from memory in patients with amnesia, the reliability of specific emotional deficits

275 investigated the ability of individuals with amnesia to acquire referential labels across a series of

276 However, time courses for the onset of amnesia vary substantially after treatment with protein

277 This anisomycin-induced amnesia was abolished after cotreatment with JNKs select

278 Finally, resolution of anterograde amnesia was improved by both caffeine and by targeted A1

279 Amnesia was site specific and was not due to auditory st

280 erations underlying PTSD-related hypermnesia/amnesia, we describe a recent animal model mimicking in

281 during learning in patients with hippocampal amnesia, we investigated whether this task would be effe

282 Changes in default network connectivity in amnesia were largely restricted to the MTL subsystem, pr

283 In this study, individuals with ACoA amnesia were shown to be impaired at delay EBCC compared

284 s) that are now assumed to cause anterograde amnesia when damaged in humans.

285 performance processes, produced anterograde amnesia when given before training.

286 Furthermore, 7-NI produced retrograde amnesia when given immediately following training while

287 reater degree of anterograde than retrograde amnesia, whereas damage to discrete regions of cortex le

288 brain afferents results in dense anterograde amnesia, whereas the role of the perirhinal cortex in le

289 ed long-term forgetting and autobiographical amnesia, which are invisible to standard memory tests, h

290 summary, a distinct form of autobiographical amnesia, which is characterized by loss of experiential

291 boxylate transporter 4 (MCT4) or MCT1 causes amnesia, which, like LTP impairment, is rescued by L-lac

292 ppocampal dysfunction results in anterograde amnesia while sparing recollection of old, schema-based

293 r, some patients with hippocampal damage and amnesia who retain the ability to construct novel scenes

294 h selective bilateral hippocampal damage and amnesia, who cannot imagine spatially coherent scenes, d

295 Despite the evidence that individuals with amnesia whose damage includes the hippocampus show alter

296 ractionist) approach to the investigation of amnesia will be advocated.

297 use of the method, we compare a person with amnesia with normal controls and we compare people with

298 We assessed retrograde amnesia with the Autobiographical Memory Interview (AMI)

299 we tested the hypothesis that subjects with amnesia would be able to learn and retain a broad range

300 g the most potent drugs that cause temporary amnesia, yet the effects of inhalational anesthesia on h