Emotion-induced retrograde amnesia and trait anxiety

Emotional arousal can both enhance and impair memory. Considering that both emotional memory and trait anxiety (TA) have been associated with adrenergic activity, the authors investigated whether there is an association between 2 opposite emotional memory biases and the TA. The authors used a procedure recently put forward by B. A. Strange, R. Hurlemann, and R. J. Dolan (2003) to elicit an emotion-induced retrograde amnesia (ERA) coupled to an emotional memory enhancement (EME). The authors contrasted the association between these emotional memory biases and the TA in several conditions involving different levels of encoding and types of recall. The results presented here indicated a significant interaction of the TA with EME and ERA and the dependency of these biases on the consciously controlled use of memory.     

The fractionation of retrograde amnesia

This single case study describes our investigations of the retrograde memory deficit of a patient who became severely and selectively amnesic after an encephalitic illness. On clinical assessment his retrograde deficit for both personal and public events appeared to encompass his entire adult life. However, he retained knowledge of words introduced into the vocabulary during the retrograde period. The experimental investigation documented his inability to recall, recognize, and place in temporal order the names and faces of famous people for all time periods sampled. By contrast, his recall of either a famous face or a famous name was significantly facilitated by the verbal cue of the person's first name and initial of the surname (i.e., Margaret T...). His performance on a test of "familiarity" that required him to select the famous name or the famous face from two distractors (unknown) was within normal limits. It is argued that names and faces of famous people are represented in more than one system: both in a vocabulary-like fact memory system that is preserved and also in a congnitively mediated schemata that in this case is functionally inoperative.     

Focal retrograde amnesia and the episodic-semantic distinction

This article reports a review of focal retrograde amnesia (FRA), or the phenomenon of organically based severe memory loss restricted to retrograde, or pretraumatic, memory. Cases of FRA are classified according to the type of memory loss: episodic, semantic, or both. A few different clusters of the disorder were identified. Lesions to either the anterior temporal lobes or the posterior/visual cortex can result in an FRA that devastates retrograde episodic memory, while having smaller effects on semantic memory. A number of left-hemisphere patients have FRA confined to semantic memory. There are several additional examples of FRA following minor cerebral trauma that disrupts either episodic memory alone or both episodic and semantic memory that are not accompanied by evidence of structural brain lesions. We discuss these different profiles of FRA and their implications for the understanding of memory retrieval.     

Mental shock can produce retrograde amnesia

Subjects in three experiments saw a short film of a mentally shocking event in which a young boy is violently shot in the face. Compared to other subjects who saw a nonviolent version of the same film, those who saw the mentally shocking version showed poorer retention of the details of the film. Retention was poorer whether measured by recognition or recall. Furthermore, impaired memory occurred only when the event was mentally upsetting, and not when it was merely unexpected but not upsetting. These results suggest that mentally shocking episodes may disrupt the lingering processing necessary for full storage of information in memory.     

Stability of long temporal gradients of retrograde amnesia in mice

Mice were given a single training trial and then received a series of four electroconvulsive shocks (ECS), 1 h apart, at one of several times after training (1-180 days). Retention was then tested at one of three times after ECS: 7, 14, or 28 days. Control animals that received sham treatment exhibited gradual forgetting with increasing training-retention intervals. Mice given ECS exhibited temporally graded retrograde amnesia, which affected memories acquired up to about 14 days before treatment. The retrograde amnesia was relatively stable, maintaining its temporally graded appearance for at least 28 days after ECS. Some recovery may have occurred in the case of memories acquired 7 days or longer before ECS, but memories acquired only 1 or 5 days before ECS did not recover. These findings extend the parallel between experimental amnesia in laboratory animals and human amnesia.     

Substance p reversal of electroconvulsive shock and cycloheximide-induced retrograde amnesia

Subcutaneous post-trial administration of the neuropeptide substance P was found to reverse the amnestic effects of both electroconvulsive shock and cycloheximide. Substance P was observed to reverse the amnestic effects of cycloheximide in both C57B1/6J and heterogeneous strain (HS) mice. Substance P was found to reverse the amnestic effects of electroconvulsive seizures in C57B1/6J animals. Peripheral injections of substance P were also found to facilitate the retention of a single-trial passive avoidance habit in animals of both genotypes, provided a weak footshock was used during training.     

Syndromes of retrograde amnesia: a conceptual and empirical synthesis

This article attempts a synthesis of the range of disorders that have been subsumed under the rubric of retrograde amnesia. At a functional level, it is possible to make distinctions between various forms of retrograde amnesia, including a distinction between episodic amnesia for personally experienced events and semantic retrograde amnesia for components of knowledge, such as those relating to people and events. At an anatomical level, discrete lesions to limbic-diencephalic structures usually result in a limited degree of retrograde amnesia. Marked episodic or marked semantic retrograde amnesia is usually associated with significant involvement of cortical and neocortical structures. Retrograde amnesia is a functionally heterogeneous rather than a unitary phenomenon. Discontinuities and dissociations found in published studies point to the potential fractionation of retrograde amnesia into component disorders, each with its own neural profile.     

H.M., word knowledge, and aging: support for a new theory of long-term retrograde amnesia

This study develops a new theory of long-term retrograde amnesia that encompasses episodic and semantic memory, including word knowledge. Under the theory, retrograde amnesia in both normal individuals and hippocampal amnesics reflects transmission deficits caused by aging, nonrecent use of connections, and infrequent use of connections over the life span. However, transmission deficits cause severe and irreversible retrograde amnesia only in amnesics who (unlike normal persons) cannot readily form new connections to replace nonfunctioning ones. The results of this study are consistent with this theory: For low-frequency but not high-frequency words, a famous "hippocampal amnesic" (H.M.) at age 71 performed worse than memory-normal control participants in a lexical decision experiment and a meaning-definition task (e.g., What does squander mean?). Also as predicted, H.M.'s lexical decision performance declined dramatically between ages 57 and 71 for low-frequency words, but was age-invariant for high-frequency words.     

The retrieval hypothesis as an explanation of induced retrograde amnesia

The present experiment tested the hypothesis that retrograde induced amnesia is due to retrieval failure and anterograde induced amnesia to encoding failure by providing recall cues which were expected to eliminate retrograde amnesia but worsen or have no effect on anterograde amnesia. The 80 subjects received auditory presentation of 10 lists, each composed of 15 four-letter words presented at a rate of 2s/item at 75 dB in a free-recall task, followed by a 72 s recall period. The amnesia-producing event was an outstanding item in serial position 8 presented at 115 dB (about the intensity of a loud shout) on half the lists. During the first half of the recall period subjects free-recalled, but during the last half they were given a list of the first (single cue) or the first two (double cue) letters of each word, to be used as aids to recall. To demonstrate induced amnesia, lists containing a loud item were compared to those not containing one. First half free recall performance indicated that large retrograde and anterograde effects were present for both cue conditions. Second half cued recall performance indicated that in the double cue condition retrograde amnesia disappeared and anterograde amnesia became larger. Cueing had much smaller effects in the single cue condition.     

Anterograde and retrograde amnesia of place discrimination in retrosplenial cortex and hippocampal lesioned rats

Retrograde and anterograde amnesic effects of excitotoxic lesions of the rat retrosplenial cortex (RS) and hippocampus (HPC) were investigated. To test retrograde amnesia, rats were trained with two-arm place discrimination in a radial maze 4 wk and 1 d before surgery with a different arm pair, respectively. In the retention test 1 wk after surgery, both lesion groups showed temporally ungraded retrograde amnesia. To test anterograde amnesia, animals were trained after surgery to discriminate three arm pairs successively within a day, and then after interposition of 1- to 4-wk intervals, one of these pairs, respectively, was tested for retention. RS-lesioned rats could acquire these pairs of place discriminations rapidly but showed a retention interval-dependent impairment in the retention test. Conversely, HPC-lesioned rats took more sessions to acquire these pairs than did the control group, and their retention was approximately 70% of correct performance regardless of retention interval. Results suggest that RS and HPC have different roles in spatial memory and that RS is important for remote memory process.