Conflict versus consolidation of memory traces to explain "retrograde amnesia" produced by ECS.
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A case is presented of a 2-week onset of acute retrograde amnesia as initial presentation, caused by presumed cancer. While acute retrograde amnesia has been reported in the literature, a report linked to cancer has not previously been published. An 82-year-old Caucasian woman presented to the emergency department, with 3-day history of increasing confusion and mild frontal headaches. Until 2 weeks previously she had been living on her own and coping with her activities of daily life. She believed very firmly that she was living with her husband in the house in which they lived in over 30 years ago. A magnetic resonance imaging scan demonstrated a lesion extending from cortex anteriorly to the right basal ganglia posteriorly. Postgadolinium enhancement was consistent with a diagnosis of a primary or secondary neoplasm. In some patients, cognitive behaviour changes or amnesia is the sole presenting feature of a serious underlying pathology. A lesion in either the temporal or frontal lobe can lead to this presentation. A family conference was convened and there was decision to take a conservative approach and not to investigate further. She was discharged to the care of her daughter and died 3 months later without return of her memory.
OBJECTIVE: Substantial progress has been made in identifying how the treatment parameters used in ECT impact on cognitive side effects. However, there is limited information regarding individual differences in vulnerability to these side effects. The authors examined patients' pretreatment global cognitive status and postictal orientation recovery time as potential predictors of the magnitude of retrograde amnesia for autobiographical memories after ECT. METHOD: Seventy-one inpatients with major depressive disorder were randomly assigned to four ECT conditions that varied in electrode placement (right unilateral versus bilateral) and stimulus dosage (low versus high intensity). Orientation recovery time was assessed at virtually every session during the course of ECT. Global cognitive status was assessed with the modified Mini-Mental State examination before treatment, during the week after termination of treatment, and 2 months after treatment ended. Retrograde amnesia was assessed at these same time points with the Autobiographical Memory Interview. RESULTS: Pre-ECT global cognitive status and the duration of postictal disorientation were strong predictors of the magnitude of retrograde amnesia in the week after the course of ECT and at 2-month follow-up. In general, these relationships were maintained regardless of technical parameters in the administration of the ECT. CONCLUSIONS: Patients who manifest global cognitive impairment before treatment and patients who experience prolonged disorientation in the acute postictal period may be the most vulnerable to persistent retrograde amnesia for autobiographical information.
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Our earlier retrospective study presented a formula relating lengths of retrograde amnesia to length of post-traumatic amnesia (PTA) and length of time since injury (Crovitz, Horn and Daniel, 1983). The earlier study derived the formula from 27 cases with retrograde amnesia. The present study adds another 75 cases, and we discuss similarities and differences between the two samples.
Rats deprived of water were placed, for 4-minute sessions, into a chamber containing a hole in one wall. After several sessions the number of times these rats explored the hole markedly decreased. Rats given access to water at the hole for a brief period explored the hole more frequently than controls, when they were tested later. This increase in hole explorations was abolished when the water reinforcement was followed by electro-convulsive shock but not when followed by foot shock.
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The retrograde amnesia of patients with memory loss related to rupture and surgical repair of anterior communicating artery (ACoA) aneurysms is compared with the retrograde amnesia of temporal amnesic patients and nonamnesic control participants. Two tests which focus on popular culture but which differ according to extent of news exposure and the cognitive processes necessary for task performance were used to measure retrograde memory. ACoA patients demonstrated more significant retrograde memory problems than did nonamnesic controls; however, the severity and pattern of their memory loss was less severe than that seen in association with temporal amnesia. Different factors influenced the remote memory loss of respective groups: ACoA patients' problems were related to impaired lexical retrieval whereas temporal amnesic patients had problems secondary to both retrieval and storage deficits.
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Patients with mild to moderate Alzheimer's disease and normal controls were tested on two retrograde memory tests, one based on public events, and the other querying autobiographical memory. On both tests, patients showed strong decrements as compared to normal controls, pointing to retrograde amnesia. Evidence for a gradient in retrograde amnesia was conflicted, with analyses of variance revealing no gradient beyond the most recent period, and more sensitive analyses pointing to shallow Ribot gradients on both tests. A literature review shows that this is the case in most published studies. In autobiographical remote memory patients generated many incorrect answers, a tendency correlated with the number of false alarms on an anterograde memory test administered several months earlier. This suggests a stable, possibly executive, factor underlying memory errors.
Two experiments examined the extent to which retrograde amnesia (RA) is attenuated by prior learning experiences. In Experiment 1, rats initially received either passive avoidance training in a step-through apparatus, exposure to the apparatus, or noncontingent footshock. When training on a second but different passive avoidance task was followed by hypothermia treatment, RA was obtained only in the latter two groups. In Experiment 2, one-way active avoidance training, yoked noncontingent shocks, or apparatus exposure constituted the initial experience. Subsequent step-down passive avoidance training and amnestic treatment resulted in memory loss for the prior apparatus exposure group, but not for either of the preshocked conditions. These experiments demonstrate that certain types of prior aversive experience can substantially modify the magnitude of RA, and, in conjunction with other familiarization studies, emphasize a paradox for interpretations of RA based solely upon CNS disruption. The possibility that hypothermia treatment serves as an important contextual or encoding cue necessary for memory retrieval was considered. It was suggested that prior experience may block RA by enabling rats to differentiate training and treatment conditions.
Retrograde amnesia (RA) was studied in patients with Huntington's disease (HD) or Alzheimer's disease (AD) using an updated version of the remote memory battery originally developed by Albert, Butters and Levin. Regardless of whether remote memory was measured by unaided recall or cued recall, HD patients exhibited deficits that were equally severe across decades. RA was more severe in AD than in HD patients and the AD patients recalled significantly more items from the 1940s and 50s than from the 60s, 70s or 80s. The AD patients also displayed dysnomia, while the HD patients did not. Naming difficulties appeared to contribute to the poor overall performance of the AD patients, but did not account for the temporal gradient of their RA. These findings, like recent reports focusing on these patients' ability to learn new information and to search semantic memory, indicate that the processes underlying AD and HD patients' memory failures are distinct.
Subseizure electrical stimulation of the amygdala produced retrograde amnesia for a visual discrimination shock-motivated task. Animals pretreated with the alpha-adrenergic antagonist phenoxybenzamine, or the beta-adrenergic antagonist propranolol, did not develop amnesia. The findings indicate that adrenergic antagonists attenuate amnesia produced by amygdala stimulation for visual discrimination training. These results are consistent with previous evidence indicating that adrenergic antagonists attenuate the amnesias produced by a variety of agents, and thus, suggest that adrenergic mechanisms may be involved in the production of retrograde amnesia.
Temporal evolution of internal memory states in a terrestrial mollusk, Limax flavus, was studied using cooling-induced retrograde amnesia. The slug was conditioned to avoid carrot odor by temporally correlated presentation of carrot juice and a bitter-taste stimulus of quinidine sulfate. We could induce retrograde amnesia by cooling of the conditioned slug immediately after the training trial. Thus, we studied the memory states in the slug using the retrograde amnesia according to strategies used in the studies of memory states in mammals or insects. In the early process of memory acquisition, at least two distinctive memory states were observed, short-term memory and long-term memory (LTM). For LTM, two states were also observed. One was a reactivated state of LTM, which was sensitive to the cooling used to induce the amnesia. The other was a so-called resting state of LTM, which was insensitive to cooling. A few days after memory acquisition, further evolution was observed in that the amnesia could not be induced even if the memory trace was reactivated. The results obtained in Limax flavus was comparable with those obtained in a variety of animals.
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