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 uired before the damage occurred (retrograde amnesia).

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

5 h mechanisms underlie infantile memories and amnesia.

6 sponsible for diencephalic and temporal lobe amnesia.

7 lar constraints that ultimately give rise to amnesia.

8 nsolidation is held to result in a permanent amnesia.

9 tion, and more feelings of disembodiment and amnesia.

10 y but may be left with permanent anterograde amnesia.

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

12 ithout stable contacts yielded immunological amnesia.

13 have contributed to his extensive retrograde amnesia.

14 first examination of the default network in amnesia.

15 sed athletes with a loss of consciousness or amnesia.

16 n of complex objects in individuals with MTL amnesia.

17 in bilateral diencephalic lesion and severe amnesia.

18 l retrograde amnesia' in transient epileptic amnesia.

19 epilepsy can manifest itself in episodes of amnesia.

20 eficits in patients with transient epileptic amnesia.

21 addressed the area of malingered retrograde amnesia.

22 ECT in efficacy and resulted in less severe amnesia.

23 nding the malingering paradigm to retrograde amnesia.

24 a as a method of understanding the nature of amnesia.

25 thalamic nuclei at the heart of diencephalic amnesia.

26 uced more severe retrograde than anterograde amnesia.

27 Damage of this nature may account for dense amnesia.

28 ociated with both retrograde and anterograde amnesia.

29 ociated with both retrograde and anterograde amnesia.

30 onsolidation, a disruption of which leads to amnesia.

31 his is not true for ALF and autobiographical amnesia.

32 er anisomycin, attenuated anisomycin-induced amnesia.

33 ons why individuals may experience unethical amnesia.

34 d related medial temporal lobe structures in amnesia.

35 revented under anisomycin-induced retrograde amnesia.

36 same lesions produced devastating retrograde amnesia.

37 om presentation, or even present solely with amnesia.

38 ation in the rehabilitation of patients with amnesia.

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

40 26) cohorts and specific to lesions causing amnesia.

41 new information, and remote autobiographical amnesia.

42 temporal lobe epilepsy, or transient global amnesia.

43 t that incorporates > 95% of lesions causing amnesia.

44 parently by inducing selective immunological amnesia.

45 ts that illuminates the paradox of infantile amnesia.

46 rize semantic search deficits in hippocampal amnesia.

47 episode' predisposing to later psychological amnesia.

48 lso observed in patients with post-traumatic amnesia.

49 mGluR5 after training rescues the infantile amnesia.

50 ade it susceptible to reactivation-dependent amnesia.

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

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

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

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 diseases, type 2 diabetes mellitus, obesity, amnesia among other disorders.

62 uit using 53 case reports of strokes causing amnesia and a map of the human connectome (n = 1000).

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

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

65 lamic tract to model aspects of diencephalic amnesia and assessed the impact of these lesions on mult

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

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

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

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

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

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

76 mmon features: sensory blockade, immobility, amnesia and lack of awareness (unconsciousness).

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 ay explain the variability across studies of amnesia and speak to debates in memory neuroscience.

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

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

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

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

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

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

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 neuroscience but the neural underpinnings of amnesia are hotly debated.

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

102 protocol that purports to show recovery from amnesia as a method of understanding the nature of amnes

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

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

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

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

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

114 like memory formation, and that treating the amnesia by re-exposure to all trauma-related cues cures

115 f BM-LTM in a number of studies that induced amnesia by targeting memory maintenance or reconsolidati

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

117 K (Tolerance/Worry About Drinking/Eye-Opener/Amnesia/C[K]ut Down on Drinking), Drug Abuse Severity Te

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

119 Diencephalic amnesia can be as debilitating as the more commonly know

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

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

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

123 However, when unethical amnesia can serve as a justification for a future action

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

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

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

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

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

129 on or maintenance but abolished hPAC and the amnesia caused by the intrahippocampal administration of

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

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

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

133 Cognitively triggered amnesia constitutes an unrecognized forgetting process t

134 with focal bilateral hippocampal damage and amnesia could supply important evidence regarding these

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

136 MTL group exhibited an extensive retrograde amnesia covering decades.

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

138 , together with temporally graded retrograde amnesia covering ~5 y prior to the cardiac arrest.

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

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

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

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

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

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

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

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

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

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

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

150 with focal bilateral hippocampal damage and amnesia engaged in dreaming.

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

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

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

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

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

156 These studies may help explain retrograde amnesia following seizures.

157 Cases of amnesia following unilateral temporal lobe surgery are r

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

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

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

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

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

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

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

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

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

167 a relates to salient traumatic cues, partial amnesia for the traumatic context can also be observed.

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 gering windows of anterograde and retrograde amnesia in healthy people.

182 projections has consistently been linked to amnesia in humans and spatial memory deficits in animal

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

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

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

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

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

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

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

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

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

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

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 Here, we show in mice that contextual amnesia is causally involved in PTSD-like memory formati

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

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

204 This approach argues that if the amnesia is due to a retrieval failure, BM-LTM should rem

205 The literature strongly suggests that such amnesia is due to storage rather than retrieval impairme

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

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

208 ignal we detect, and demonstrate that immune-amnesia is largely undetectable in small populations wit

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

210 Unethical amnesia is observed when people do not remember or remem

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

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

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

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

215 Severe amnesia is usually observed following bilateral hippocam

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

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

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

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

220 Classic studies of amnesia led to characterizations of hippocampal function

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

222 ical, and molecular techniques in a relevant amnesia mouse model and primary hippocampal neuronal cul

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

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

225 Retrograde amnesia of learned associative memories is elicited by i

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

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

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

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

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

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

232 y in both time-delay and scopolamine-induced amnesia paradigms in the novel object and social recogni

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

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

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

236 Patients with hippocampal amnesia play a central role in memory neuroscience but t

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

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

239 Amnesia produced by protein synthesis inhibitors such as

240 We also demonstrate that the amnesia provoked by disrupting ORM reconsolidation throu

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

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

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

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

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

246 ationship between anterograde and retrograde amnesia remains unclear.

247 interferes with sensory processing to cause amnesia remains unclear.

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

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

250 neuroscience is determining whether cases of amnesia result from eradication of the memory trace (sto

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

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

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

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

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

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

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

258 >60 years, intoxication, headache, vomiting, amnesia, seizure, or trauma above the clavicle) had an L

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

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

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

262 f temporal lobe and diencephalic anterograde amnesia.SIGNIFICANCE STATEMENT It has long been conjectu

263 and 1970s involving three groups of patients-amnesia, split brain, and blindsight.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

278 f long-term, declarative memory (anterograde amnesia), together with temporally graded retrograde amn

279 r conceptualizing pharmacological control of amnesia, unconsciousness, and immobility.

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

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

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

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

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

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

286 f a 2- to 3-year duration of measles "immune-amnesia." We show that periodicity has a negligible effe

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

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

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

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

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

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

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

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

300 ing as the more commonly known temporal lobe amnesia, yet the precise contribution of diencephalic st