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This paper reports a reassessment of published literature on the question of whether retrograde amnesia data from patients with severe trauma supports the idea that there is ongoing consolidation of long-lasting memories. That is, memory consolidation continues for decades with older memories being increasingly consolidated, and, thus, more protected from forgetting. Our analysis was limited to patients with specific traumas rather than neurodegenerative conditions that can be complicated by the additional presence of significant anterograde amnesia. These constraints were used because trauma patients have a definitive start to their amnesia allowing comparison of their memories before this event, unlike when there is an undefined amnesia onset. Our results revealed that the standard account of retrograde amnesia only fits part of the data, with more than half not conforming to this account. Specifically, damage to different brain areas was associated with different patterns of retrograde amnesia. Those cases where the standard retrograde amnesia account was held tended to involve damage to the hippocampus and temporal lobes, as expected. Future directions to better understand the influence of retrograde amnesia and memory consolidation are suggested.

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BACKGROUND: Time to reorientation after electroconvulsive therapy (ECT) has been shown to predict retrograde amnesia and is a useful measure for monitoring patients over the acute treatment course. This study investigated the effects of treatment, clinical and demographic factors on the recovery of orientation after ECT. METHODS: Data from 555 ECT patients across two different clinical CARE Network sites were analysed. The main outcome variable was recovery of orientation on the 10-Item Orientation Questionnaire assessed after every ECT treatment. A linear mixed-effects repeated measures model was used to predict the recovery of orientation across the ECT course based on multiple factors, including age, gender, electrode montage, ECT number and frequency, diagnosis, and baseline cognitive impairment. RESULTS: Type of ECT demonstrated a significant effect (F(2, 2341) = 48.414, p = 0.000): individuals who received right unilateral (RUL) ultrabrief ECT or bifrontal ECT had higher orientation scores compared to those who received RUL brief pulse ECT. Older age groups and female patients had lower orientation scores. Baseline global cognitive functioning significantly influenced orientation scores (F(3, 2339) = 43.597, p = 0.000), with individuals with no or mild cognitive impairment exhibiting higher scores. LIMITATIONS: The study involved a retrospective analysis of de-identified data, which may have introduced inherent biases with missing data. CONCLUSIONS: This large-scale retrospective, real-world study showed that recovery of orientation after ECT was most affected by ECT type, though age, gender, and baseline level cognitive impairment also affected outcomes. These findings can inform the interpretation of post ECT orientation scores, facilitating its monitoring and optimisation of patient outcomes.

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OBJECTIVE: To describe a case of Post-Treatment Lyme Disease Syndrome (PTLDS) with an atypical cognitive profile. METHOD: A 41-year-old PTLDS patient underwent comprehensive neuropsychological testing and psychological assessment. RESULTS: The patient exhibited impaired intensive attention but preserved selective attention. Executive functions were normal. Short-term and anterograde memory were intact, while retrograde and semantic memory were significantly impaired. The patient also experienced identity loss, specific phobias, dissociative symptoms, and depressed mood. CONCLUSIONS: Severe episodic-autobiographical and retrograde semantic amnesia was consistent with some reports of dissociative amnesia. Loss of identity and phobias were also highly suggestive of a psychogenic mechanism underlying amnesia.

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Transient global amnesia (TGA) is an uncommon neurologic disorder that consists of a sudden and temporary loss of memory, both present and past. Its causes and risk factors are not well known. We describe a case of a 58-year-old woman who was brought to the emergency department (ED) with sudden onset loss of memory and disorientation after a dive in the ocean. She presented memory deficits with incapacity to retain new memories and amnesia for the previous 24 hours. All exams ordered were normal, including computed tomography of the brain and laboratory analysis. After six hours of close monitoring in the ED, she gradually started to retain short-term memories and was discharged after 48 hours with no memory or other deficits. The diagnosis of TGA was made based on the clinical presentation and the patient's rapid improvement. Follow-up neurology consultation and further testing did not demonstrate any evidence to exclude this diagnosis. Further research is needed on this topic to allow the identification of risk factors and causes to prevent it.

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BACKGROUND: A progressive decrease in spontaneous locomotion with repeated exposure to a novel environment has been assessed using both within and between-session measures. While both are well-established and reliable measurements, neither are useful alone as methods to concurrently assess treatment effects on acquisition and retention of habituation. NEW METHOD: We report a behavioral method that measures habituation by combining the within and between measurements of locomotion. We used a 30 min session divided into 6 five min blocks. In the first novel environment session activity was maximal in the first 5 min block but was reduced to a low level by the sixth block, indicative of within-session habituation. Using 8 daily sessions, we showed that this terminal block low level of activity progressed incrementally to the first block to achieve complete habituation. RESULTS/COMPARISON WITH EXISTING METHODS: Within-session activity across sessions was used to identify different stages of between session habituation. It was then possible to assess drug treatment effects from partial to complete habituation, so that treatment effects on retention of the previously acquired partial habituation, expressed as a reversion to an earlier within session habituation pattern (retrograde amnesia assessment), as well as the effects on new learning by the failure in subsequent sessions to acquire complete between-session habituation (anterograde amnesia assessment). CONCLUSIONS: The use of spontaneous motor activity to assess learning and memory effects provides the opportunity to assess direct treatment effects on behavior and motor activity in contrast to many learning and memory models.

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The participation of DNA methylation processes in the mechanisms of anterograde and retrograde amnesia caused by impaired reconsolidation of conditioned food aversion memory by NMDA glutamate receptor antagonists or serotonin receptor antagonists, respectively, were studied on grape snails. Anterograde amnesia was characterized by impaired formation of long-term memory during repeated learning. Administration of a DNA methyltransferase (DNMT) inhibitor to amnestic animals resulted in accelerated formation of long-term memory during 1 day of repetitive training vs 3 days during initial training. In serotonin-dependent retrograde amnesia, repeated learning without DNMT inhibitor administration or after inhibitor injections led to the formation of long-term memory. The dynamics of memory formation was similar in both cases and did not differ from that during the initial training: the memory was formed within 3 days of training. Thus, epigenetic processes of DNA methylation are selectively involved in the mechanisms of anterograde amnesia, but do not participate in the mechanisms of retrograde amnesia.

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Is retrograde amnesia associated with an ability to know who we are and imagine what we will be like in the future? To answer this question, we had S.G., a patient with focal retrograde amnesia following hypoxia, two brain-damaged (control) patients with no retrograde memory deficits, and healthy controls judge whether each of a series of trait adjectives was descriptive of their present self, future self, another person, and that person in the future, and later recognize studied traits among distractors. Healthy controls and control patients were more accurate in recognizing self-related compared to other-related traits, a phenomenon known as the self-reference effect (SRE). This held for both present and future self-views. By contrast, no evidence of (present or future) SRE was observed in SG, who concomitantly showed reduced certainty about his personality traits. These findings indicate that retrograde amnesia can weaken the self-schema and preclude its instantiation during self-related processing.

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Background: The identification of different factors affecting anesthesia and physiological changes during anesthesia can be effective in improving the quality of anesthesia. Midazolam is a benzodiazepine that has been used for many years for sedation under anesthesia. Stress is also an important factor affecting memory and other physiological changes, such as blood pressure and heart rate. Objectives: his study aimed to investigate the effects of stress on retrograde and anterograde amnesia among patients undergoing general anesthesia. Methods: This multi-center, parallel, stratified, randomized controlled trial was performed on patients undergoing non-emergency abdominal laparotomy. The patients were divided into high- and low-stress groups according to the Amsterdam Preoperative Anxiety and Information Scale. Then, both groups were randomly divided into three subgroups receiving 0, 0.02, or 0.04 mg/kg of midazolam. Recall cards were shown to patients at 4 minutes, 2 minutes, and immediately before injection to determine retrograde amnesia and at 2 minutes, 4 minutes, and 6 minutes after injection to determine anterograde amnesia. Hemodynamic changes were recorded during intubation. The chi-square and multiple regression tests were used to analyze the data. Results: Midazolam injection was associated with the development of anterograde amnesia in all groups (P < 0.05); however, it had no effect on the development of retrograde amnesia (P < 0.05). Midazolam could decrease the systolic and diastolic blood pressure and heart rate during intubation (P < 0.05). Stress also caused retrograde amnesia in patients (P < 0.05); nevertheless, it had no effect on anterograde amnesia (P > 0.05). Stress and midazolam injection could not affect the oxygen levels during intubation. Conclusions: The results showed that midazolam injection could induce anterograde amnesia, hypotension, and heart rate; nonetheless, it had no effect on retrograde amnesia. Stress was associated with retrograde amnesia and increased heart rate; however, it was not associated with anterograde amnesia.

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One-trial appetitive learning developed from one-trial passive avoidance learning as a standard test of retrograde amnesia. It consists of one learning trial followed by a retention test, in which physiological manipulations are presented. As in passive avoidance learning, food- or water-deprived rats or mice finding food or water inside an enclosure are vulnerable to the retrograde amnesia produced by electroconvulsive shock treatment or the injection of various drugs. In one-trial taste or odor learning conducted in rats, birds, snails, bees, and fruit flies, there is an association between a food item or odorant and contextual stimuli or the unconditioned stimulus of Pavlovian conditioning. The odor-related task in bees was sensitive to protein synthesis inhibition as well as cholinergic receptor blockade, both analogous to results found on the passive avoidance response in rodents, while the task in fruit flies was sensitive to genetic modifications and aging, as seen in the passive avoidance response of genetically modified and aged rodents. These results provide converging evidence of interspecies similarities underlying the neurochemical basis of learning.

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Here, we examined mechanisms that affect retrograde memory in amnestic mild cognitive impairment (a-MCI) as a function of longitudinal clinical outcome. 8 a-MCI who converted to Alzheimer's dementia (AD) during the subsequent 3-year follow-up (converter a-MCI) and 10 a-MCI who remained clinically stable during the same period (stable a-MCI) were compared at the baseline evaluation (i.e., when they were diagnosed as a-MCI) using a remote memory questionnaire for public events that allows disentangling the differential contribution of storage and retrieval mechanisms to performance accuracy. Results suggest that deficits in remote memory are primarily explained by impaired retrieval abilities in stable a-MCI and by impaired storage in converter-to-AD a-MCI. This distinction between retrograde amnesia due to defective trace utilisation in stable a-MCI and trace storage in converter a-MCI is consistent with the temporal unfolding of declining anterograde memory over the course of disease progression to AD.

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This article discusses the possibility of practitioners who mistake organic memory loss for dissociative amnesia. It starts with the case of a young man with complete retrograde amnesia due to a traumatic head injury. Because he did not show any gross neurological abnormalities, a neurologist thought his amnesia had a psychological origin. An extensive neuropsychological examination revealed that the man did have an organic reason for his amnesia. Next, the existence of dissociative memory loss as well as isolated organic retrograde amnesia is considered. While cases of organic memory loss are well-documented, there is hardly any evidence for dissociative amnesia. It is argued that organic memory loss might be mistakenly taken for dissociative amnesia. In line with the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders, practitioners are advised to rule out the possibility of organic memory loss, before diagnosing a patient with dissociative amnesia.

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It is well established that sleep deprivation after learning impairs hippocampal memory processes and can cause amnesia. It is unknown, however, whether sleep deprivation leads to the loss of information or merely the suboptimal storage of information that is difficult to retrieve. Here, we show that hippocampal object-location memories formed under sleep deprivation conditions can be successfully retrieved multiple days following training, using optogenetic dentate gyrus (DG) memory engram activation or treatment with the clinically approved phosphodiesterase 4 (PDE4) inhibitor roflumilast. Moreover, the combination of optogenetic DG memory engram activation and roflumilast treatment, 2 days following training and sleep deprivation, made the memory more persistently accessible for retrieval even several days later (i.e., without further optogenetic or pharmacological manipulation). Altogether, our studies in mice demonstrate that sleep deprivation does not necessarily cause memory loss but instead leads to the suboptimal storage of information that cannot be retrieved without drug treatment or optogenetic stimulation. Furthermore, our findings suggest that object-location memories, consolidated under sleep deprivation conditions and thought to be lost, can be made accessible again several days after the learning and sleep deprivation episode, using the clinically approved PDE4 inhibitor roflumilast.

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The objective of this research was to learn about the effects of music as a non-pharmacological therapeutic intervention applied to Alzheimer's disease. To this aim, we evaluated its results regarding symptomatology and caregiver burden. Methods: This systematic review followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) criteria. We searched Pubmed/Medline (NLM), Web of Science, Scopus, Cochrane and Google Scholar, including articles from 1 January 2011-20 July 2021, using the keywords "Alzheimer´s disease", "Music therapy", "Caregivers overload", "Amnesia retrograde" and "Clinical evolution". To select the articles our criteria included complete text availability, quantitative research of an experimental nature and studies which, at least, figured in SJR or in JCR. Results: We found a relationship between the application of music therapy in patients with Alzheimer's disease and an improvement regarding symptomatology, as it smoothed down the progress of the disease. Using music therapy in Alzheimer's patients also led to a decrease in caregivers' burden and an increase in their well-being. Conclusions: Our results showed the benefits of music therapy, as it improved both patients' symptomatology and caregivers' burden.

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Seizures cause retrograde amnesia. We have previously demonstrated that seizures erode recently formed memories through shared ensembles and mechanisms in the CA1 region of the hippocampus. Here, we tested whether seizure circuits overlap spatial memory circuits outside of the CA. Spatial memory is consolidated by the hippocampal-cortical coupling that are connected via multiple pathways. We tested whether a seizure invades structures involved in memory consolidation by using the activity reporter TRAP2 mice. T-maze alternation learning activated neurons in the dentate gyrus, mediodorsal thalamus, retrosplenial cortex, and medial prefrontal cortex. This spatial memory relies on the plasticity of the AMPA receptor GluA1 subunit. GluA1 knockout/TRAP2 mice did not learn to alternate, and structures interposed between the hippocampus and the cortex were not active. A seizure prevented the recall of alternation memory and activated memory-labeled structures. There was a widespread overlap between learning-activated ensembles and seizure-activated neurons, which likely contributes to retrograde amnesia.Significance StatementWe propose that seizures cause retrograde amnesia by engaging the circuits that participate in memory consolidation.

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Two important themes in Ivan Izquierdo's research each offered both answers and questions about the topic of memory formation and maintenance. The first theme provided evidence supporting the view that short- and long-term memory were distinct processes and could be selectively modulated by several treatments, with some affecting only short-term, others only affecting long-term memory, and still others affecting both. Over many years, Izquierdo's laboratory documented molecular responses across time after training obtaining results that showed differences as well as similarities in the biochemical changes during the first 1-2 h and the next 4-6 h after training, i.e., during the transition from short- to long-term memory. This work clarified the biological underpinnings of the memory processes. The second theme described waves of susceptibility of memory to enhancing and impairing treatments after time, a biphasic profile that contrasted with earlier monotonic decreases in the efficacy of memory modulating treatments as a function of time between training and treatment. Remarkably, these waves of susceptibility to modification were accompanied by biphasic changes in molecular measures at similar times after training. Remarkably, some of the molecular players exhibited persistent changes after training, with increases in levels lasting days following the training experience. These persistent molecular changes may reveal a biological basis for the dynamic nature of memories seen long after the initial memory is consolidated.

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Transient global amnesia (TGA) is a syndrome characterized by a loss of anterograde memory with a less prominent loss in retrograde episodic memory that resolves within 24 hours or less. In this report, we present a rare case of a 62-year-old male who presented to the emergency department with sudden onset confusion and memory loss. Prior to this, the patient had no significant medical or psychiatric history. Magnetic resonance imaging (MRI) and computerized tomography (CT) showed a normal presentation, and a neurology consultation ruled out any organic brain abnormalities. After ruling out all other potential causes, diagnosis of transient global amnesia was made. We present this case highlighting the importance of ruling out other acutely morbid conditions when addressing TGA, guidance on timing of imaging, as well as offering insight on other etiologies of this condition.

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Recent research has assessed pupil size during past thinking in patients with retrograde amnesia. Building on this research, we assessed pupil size during future thinking in a retrograde amnesia patient. To this end, we measured pupil size during past and future thinking in L, a 19-year-old, right-handed man free of neurological/psychiatric disorders except for retrograde amnesia that occurred after an episode of fugue. During a past thinking condition, we invited L to retrieve retrograde events (i.e., events that occurred before amnesia) and anterograde events (i.e., events that occurred after amnesia). During a future thinking condition, we invited him to imagine events that might occur the following week, the following month, and in the new year. Past and future thinking occurred while L's pupil size was monitored with eye-tracking glasses. L demonstrated higher specificity during future than during past thinking. Critically, the results demonstrated a larger pupil size during future than during past thinking. The larger pupil size during future thinking observed in L can be attributed to the high cognitive load involved in future thinking. Our study not only demonstrates preserved future thinking in a patient with dissociative retrograde amnesia, but also shows that pupillometry can be used for the physiological assessment of future thinking in retrograde amnesia patients.

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The hippocampus (HPC) may compete with other memory systems when establishing a representation, a process termed overshadowing. However, this overshadowing may be mitigated by repeated learning episodes, making a memory resistant to post-training hippocampal damage. In the current study, we examined this overshadowing process for a hippocampal-dependent visual discrimination memory in rats. In Experiment 1, male rats were trained to criterion (80% accuracy on two consecutive days) on a visual discrimination and then given 50 additional trials distributed over 5 days or 10 weeks. Regardless of this additional learning, extensive damage to the HPC caused retrograde amnesia for the visual discrimination, suggesting that the memory remained hippocampal-dependent. In Experiment 2, rats received hippocampal damage before learning and required approximately twice as many trials to acquire the visual discrimination as control rats, suggesting that, when the overshadowing or competition is removed, the non-hippocampal memory systems only slowly acquires the discrimination. In Experiment 3, increasing the additional learning beyond criterion by 230 trials, the amount needed in Experiment 2 to train the non-hippocampal systems in absence of competition, successfully prevented the retrograde amnesic effects of post-training hippocampal damage. Combined, the findings suggest that a visual discrimination memory trace can be strengthened in non-hippocampal systems with overtraining and become independent of the HPC.

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There is an extreme dearth of empirical studies assessing the neuropsychiatric outcome of non-fatal hanging that indicates little attention to the area has been paid. We aimed to report the memory disturbances of 14 cases after an immediate non-fatal hanging attempt. We conducted the study from August 2020 to June 2021 and collected data from 14 hospitalized patients after an immediate non-fatal hanging attempt. We conducted series of clinical examinations to assess the memory disturbance and recorded it. Among the 14 cases, four (28.8%) were males and the rest ten (71.2%) were females. The mean age of the cases was 25.28 ± 8.19 years ranging from 15-40 years. All the cases had retrograde amnesia while six (42.9%) had both anterograde and retrograde amnesia. The current pilot study reported the distribution of memory disturbances among fourteen cases of non-fatal hanging that adds preliminary findings to the under-researched area and warrants further empirical studies to generalize the study results.