"This looks like a movie": a case report of post-surgical amnesia.

A 52-year-old male patient with a background of adaptive personality disorder was admitted for mitral valve repair and cardiac ablation for atrial fibrillation. He suffered intraoperative complications with severe mitral insufficiency that suffered ischemia.. Post-operatively, he demonstrated acute loss of retrograde autobiographical memory, prosopagnosia and a loss of public semantic memory. His CT scan was normal and MRI was not possible due to intra-cardiac leads. An initial diagnosis of hypoxic-ischemic encephalopathy was considered. A neuropsychological examination undertaken 20 days after his surgery showed a severe alteration of retrograde autobiographical memory, marked alteration of semantic knowledge and prosopagnosia. He demonstrated an average performance in tasks measuring constructional praxis, visuospatial ability, and executive functions. 34 days after surgery, and after a short nap, the patient "returns" to the day before admission and consequently recovers his memory. Repeat neuropsychological assessment demonstrated performance within the normal range across all previously tested domains. This sudden recovery of memory, together with a normal MRI, led to a rethinking of the diagnosis of dissociative amnesia. This case illustrates the long-standing discussion about the organic or functional origin of some memory disorders, in which, despite advances in neuroimaging techniques, it is still difficult to know their etiology .

Mechanism of seizure-induced retrograde amnesia.

Seizures cause retrograde amnesia, but underlying mechanisms are poorly understood. We tested whether seizure activated neuronal circuits overlap with spatial memory engram and whether seizures saturate LTP in engram cells. A seizure caused retrograde amnesia for spatial memory task. Spatial learning and a seizure caused cFos expression and synaptic plasticity overlapping set of neurons in the CA1 of the hippocampus. Recordings from learning-labeled CA1 pyramidal neurons showed potentiated synapses. Seizure-tagged neurons were also more excitable with larger rectifying excitatory postsynaptic currents than surrounding unlabeled neurons. These neurons had enlarged dendritic spines and saturated LTP. A seizure immediately after learning, reset the memory engram. Seizures cause retrograde amnesia through shared ensembles and mechanisms.

Neuropsychological and neuropathological observations of a long-studied case of memory impairment.

We report neuropsychological and neuropathological findings for a patient (A.B.), who developed memory impairment after a cardiac arrest at age 39. A.B. was a clinical psychologist who, although unable to return to work, was an active participant in our neuropsychological studies for 24 y. He exhibited a moderately severe and circumscribed impairment in the formation of long-term, declarative memory (anterograde amnesia), together with temporally graded retrograde amnesia covering ∼5 y prior to the cardiac arrest. More remote memory for both facts and autobiographical events was intact. His neuropathology was extensive and involved the medial temporal lobe, the diencephalon, cerebral cortex, basal ganglia, and cerebellum. In the hippocampal formation, there was substantial cell loss in the CA1 and CA3 fields, the hilus of the dentate gyrus (with sparing of granule cells), and the entorhinal cortex. There was also cell loss in the CA2 field, but some remnants remained. The amygdala demonstrated substantial neuronal loss, particularly in its deep nuclei. In the thalamus, there was damage and atrophy of the anterior nuclear complex, the mediodorsal nucleus, and the pulvinar. There was also loss of cells in the medial and lateral mammillary nuclei in the hypothalamus. We suggest that the neuropathology resulted from two separate factors: the initial cardiac arrest (and respiratory distress) and the recurrent seizures that followed, which led to additional damage characteristic of temporal lobe epilepsy.

Parallel pathways of seizure generalization.

Generalized convulsive status epilepticus is a life-threatening emergency, because recurrent convulsions can cause death or injury. A common form of generalized convulsive status epilepticus is of focal onset. The neuronal circuits activated during seizure spread from the hippocampus, a frequent site of seizure origin, to the bilateral motor cortex, which mediates convulsive seizures, have not been delineated. Status epilepticus was initiated by electrical stimulation of the hippocampus. Neurons transiently activated during seizures were labelled with tdTomato and then imaged following brain slice clearing. Hippocampus was active throughout the episode of status epilepticus. Neuronal activation was observed in hippocampus parahippocampal structures: subiculum, entorhinal cortex and perirhinal cortex, septum, and olfactory system in the initial phase status epilepticus. The tdTomato-labelled neurons occupied larger volumes of the brain as seizures progressed and at the peak of status epilepticus, motor and somatosensory cortex, retrosplenial cortex, and insular cortex also contained tdTomato-labelled neurons. In addition, motor thalamic nuclei such as anterior and ventromedial, midline, reticular, and posterior thalamic nuclei were also activated. Furthermore, circuits proposed to be crucial for systems consolidation of memory: entorhinal cortex, retrosplenial cortex, cingulate gyrus, midline thalamic nuclei and prefrontal cortex were intensely active during periods of generalized tonic-clonic seizures. As the episode of status epilepticus waned, smaller volume of brain was activated. These studies suggested that seizure spread could have occurred via canonical thalamocortical pathway and many cortical structures involved in memory consolidation. These studies may help explain retrograde amnesia following seizures.

Hippocampal Damage Causes Retrograde Amnesia and Slower Acquisition of a Cue-Place Discrimination in a Concurrent Cue-Place Water Task in Rats.

Explanations of memory-guided navigation in rodents typically suggest that cue- and place-based navigations are independent aspects of behavior and neurobiology. The results of many experiments show that hippocampal damage causes both anterograde and retrograde amnesia (AA; RA) for place memory, but only RA for cue memory. In the present experiments, we used a concurrent cue-place water task (CWT) to study the effects of hippocampal damage before or after training on cue- and place-guided navigation, and how cue and place memory interact in damaged and control rats. We found that damaging the hippocampus before training caused a delay in the expression of cue-place navigation strategies relative to intact control animals; surprisingly, place navigation strategies emerged following pre-training hippocampal damage. With additional training, both control and damaged rats used local cues to navigate in the CWT. Damaged animals also show minor impairments in latency to navigate to the correct cue following a cue contingency reversal. By contrast to these anterograde effects, damage made after training causes RA for cue choice accuracy and latency to navigate to the correct cue. In addition, the extent of hippocampal damage predicted impairments in choice accuracy when lesions were made after training. These data extend previous work on the role of the hippocampus in cue and place memory-guided navigation, and show that the hippocampus plays an important role in both aspects of memory and navigation when present during the learning experience.

Retrosplenial cortex damage produces retrograde and anterograde context amnesia using strong fear conditioning procedures.

Contextual fear conditioning relies upon a network of cortical and subcortical structures, including the hippocampus and the retrosplenial cortex (RSC). However, the contribution of the hippocampus is parameter-dependent. For example, with "weak" training procedures, lesions of the hippocampus produce both retrograde and anterograde context amnesia. However, with "strong" training procedures (e.g., more trials and/or higher levels of footshock), lesions of the hippocampus produce retrograde context amnesia but not anterograde amnesia (Wiltgen et al., 2006). Likewise, prior studies have shown that with weak training, RSC lesions produce both retrograde and anterograde context amnesia (Keene & Bucci, 2008). The purpose of the current study was to examine the effects of RSC damage on contextual fear conditioning following strong training. In Experiment 1, lesions of the RSC resulted in both retrograde and anterograde context amnesia following strong training using the same unsignaled fear conditioning procedures described by Wiltgen et al. (2006). In Experiment 2, using a signaled fear conditioning procedure, we replicated these effects on context memory observing both retrograde and anterograde context amnesia. In contrast, there were no lesion effects on tone-fear memory. Thus, unlike lesions of the hippocampus, lesions of RSC produce both retrograde and anterograde context amnesia even when rats undergo strong fear conditioning. These findings suggest that the RSC has an essential role in contextual fear conditioning and that other systems or pathways are unable to compensate for the loss of RSC function.

Retrograde Autobiographical Memory From PTA Emergence to Six-Month Follow-Up in Moderate to Severe Traumatic Brain Injury.

OBJECTIVE: The overwhelming focus of research on memory following traumatic brain injury (TBI) has been on anterograde amnesia, and very little attention has been paid to retrograde amnesia. There is evidence to suggest that retrograde autobiographical memory deficits exist after severe TBI, although there have been no prospective studies of autobiographical memory in a representative sample of moderate to severe cases recruited from hospital admissions. METHODS: The purpose of the present study was to report changes in autobiographical memory performance among a group of patients soon after emergence from posttraumatic amnesia (PTA) and at the 6-month follow-up compared with a healthy control (HC) group. The authors also examined associations with anterograde memory function and community integration to assist in understanding the functional impact of autobiographical memory deficits and potential underlying mechanisms. The Autobiographical Memory Interview and the Rey Auditory Verbal Learning Test were used as measures of retrograde and anterograde memory, respectively, and the Community Integration Questionnaire was used as a measure of functional outcome in the TBI group. RESULTS: The results demonstrated that both personal semantic and episodic autobiographical memory scores were impaired following emergence from PTA and at the 6-month follow-up. Only subtle differences emerged in change over time in different injury severity groups. Recent retrograde memory function was associated with anterograde memory performance, which supports some degree of overlap in underlying mechanisms. CONCLUSIONS: The findings suggest that autobiographical memory deficits are prevalent following moderate to severe TBI and warrant consideration in rehabilitation.

Isolated Fornix Infarction with Damage to the Limbic System as a Cause of Persistent Amnesia: A Case Report.

BACKGROUND The fornix is a white matter tract bundle that acts as the major output of the hippocampus and is an important component of the Papez circuit. We present an instructive imaging case of sudden onset of persistent amnesia due to selective ischemic damage of the anterior fornix. CASE REPORT A 54-year-old Japanese male came to our attention for a sudden onset of retrograde amnesia, associated with severe anterograde amnesia. The brain magnetic resonance imaging demonstrated a bright diffusion restriction, which was associated with swollen fornices bilaterally. His symptoms gradually improved, but episodic memory impairment still persisted after 1 month. The coronal T1-weighted MPRAGE (magnetization-prepared rapid acquisition with gradient echo) sequence clearly showed disruption of the left anterior fornix. Diffusion tensor tracking showed decrease in the density of entire fiber tracts on the Papez circuit as well as location of the left fornix. CONCLUSIONS When dealing with sudden, persistent amnesia associated with small fornix infarction, it is prudent to consider the possibility of tract damage along with limbic system damage using MPRAGE sequence.

Retrograde Personal Semantic Memory During Post-Traumatic Amnesia and Following Emergence.

OBJECTIVES: Anecdotal reports suggest that following traumatic brain injury (TBI) retrograde memories are initially impaired and recover in order of remoteness. However, there has been limited empirical research investigating whether a negative gradient in retrograde amnesia-relative preservation of remote over recent memory-exists during post-traumatic amnesia (PTA) compared with the acute phase post-emergence. This study used a repeated-measures design to examine the pattern of personal semantic (PS) memory performance during PTA and within two weeks of emergence to improve understanding of the nature of the memory deficit during PTA and its relationship with recovery. METHODS: Twenty patients with moderate-severe TBI and 20 healthy controls (HCs) were administered the Personal Semantic Schedule of the Autobiographical Memory Interview. The TBI group was assessed once during PTA and post-emergence. Analysis of variance was used to compare the gradient across lifetime periods during PTA relative to post-emergence, and between groups. RESULTS: PS memory was significantly lower during PTA than post-emergence from PTA, with no relative preservation of remote memories. The TBI group was still impaired relative to HCs following emergence from PTA. Lower overall PS memory scores during PTA were associated with increased days to emerge from PTA post-interview. CONCLUSIONS: These results suggest a global impairment in PS memory across lifetime periods particularly during PTA, but still present within 2 weeks of emergence from PTA. PS memory performance may be sensitive to the diffuse nature of TBI and may, therefore, function as a clinically valuable indicator of the likely time to emerge from PTA. (JINS, 2018, 24, 1064-1072).

Intraventricular extension of an aneurysmal subarachnoid hemorrhage is an independent predictor of a worse functional outcome.

OBJECTIVE: The objective of this study is to determine the impact of intraventricular hemorrhage (IVH) on the cognitive prognosis of subarachnoid hemorrhage (SAH) due to ruptured cerebral aneurysm, independent of the presence of intraparenchymal hemorrhage, hydrocephalus or vasospasm. PATIENT AND METHODS: A Retrospective review of a prospectively collected database of patients with aneurysmal SAH from July 2009 to November 2016 was performed. Patients were included if they had a saccular aneurysm with a Hunt-Hess grade (HHG) 1-3. Those who underwent craniectomy/clipping and those with vasospasm were excluded. Patients with IVH were grouped into 5 groups depending on the blood distribution in the ventricles. Functional outcomes studied were modified Rankin score (mRS) 0-2, cognitive impairment and memory impairment, and the presence of amnesia to the event. A univariate followed by a multivariate analysis ware performed. RESULTS: A total of 443 patients were identified and 124 patients met the criterion. There were no significant differences in the proportion of patients with mRS of 0-2 between patients with IVH and those without IVH but with EVD (external ventricular drain). There was a higher proportion of cognitive deficits in patients with IVH (71.95%), compared to those without (31.58%; p = 0.01). Patients with IVH had a higher rate of anterograde amnesia (100% vs. 4.3% p < 0.0001), lower rate of mRS 0-2 (78% vs 100% p < 0.001), and higher rate of cognitive impairment (71.9% vs. 13% p < 0.0001) compared with those who did not require an EVD. Grade 3 and grade 4 were shown to have lower rate of patients with mRS 0-2 and a higher rate of cognitive impairment. In multivariate analysis, independent predictors of cognitive and memory impairment were increasing HHG (OR = 155.33; P < 0.01), ACOM/A1/ACA/anterior choroidal aneurysms, (OR = 5.24; P = 0.04), increasing Fischer scale (OR = 6.93; P = 0.01), and increasing IVH grade (OR = 6.9; P = 0.01). Only worse HHG (OR = 2704.22; P = 0.01) and IVH grade 2-4 were associated (perfect predictor, OR cannot be extracted) with anterograde amnesia. CONCLUSION: IVH is an independent prognosticator of SAH cognitive outcomes. The effect of IVH drainage and other intraventricular therapies on SAH course is an attractive topic for further investigation.

I'm shocked: informed consent in ECT and the phenomenological-self.

This paper argues that phenomenological insights regarding selfhood are relevant to the informed consent process in the treatment of depression using electro-convulsive therapy (ECT). One of the most significant side-effects associated with ECT is retrograde amnesia. Unfortunately, the current informed consent model does not adequately appreciate the full extent in which memory loss disturbs lived-experience. Through the philosophy of Merleau-Ponty, it is possible to appreciate the way in which memory loss affects a person's self-experience, with emphasis given to one's pre-reflective and embodied, relationship with things in the world. This paper aims to demonstrate that proper informed consent should acknowledge the extent to which repeated ECT treatments affect a patient's sense self.

Validation of the 10-Item Orientation Questionnaire: A New Tool for Monitoring Post-Electroconvulsive Therapy Disorientation.

OBJECTIVES: Assessment of post-electroconvulsive therapy (ECT) disorientation at a single time point after ECT treatment may prove an effective and clinically useful method for monitoring the severity of disorientation and predicting ECT-induced retrograde amnesia. In this study, we aimed to validate a novel instrument (10-Item Orientation Questionnaire) developed to assess the level of disorientation after ECT. METHODS: Twenty-four depressed inpatients who were prescribed an acute course of ECT were administered the 10-Item Orientation Questionnaire at 30 minutes after ECT and had time to reorientation assessed at 3 time points after ECT (10, 30, and 60 minutes) at ECT treatments 1 to 3. The association between average performance of the 10-Item Orientation Questionnaire across the acute ECT course and retrograde amnesia at post-ECT was examined using the Autobiographical Memory Interview-Short Form. RESULTS: Mean performance on the 10-Item Orientation Questionnaire across treatments 1 to 3 was moderately correlated with average time to reorientation (r = -0.52, P = 0.02, n = 20). Across the acute ECT course, poorer performance on the 10-Item Orientation Questionnaire was associated with greater retrograde amnesia at post-ECT (r = 0.53, P = 0.03, n = 16). CONCLUSIONS: The 10-Item Orientation Questionnaire when administered at 30 minutes after ECT is sensitive for detecting patients with slow recovery of orientation after ECT. Use of this instrument therefore has potential for improving routine patient monitoring in clinical practice and identifying patients at increased risk of retrograde memory adverse effects following treatment.

Utility of Retrograde Amnesia Assessment Alone, Compared with Anterograde Amnesia Assessment in Determining Recovery After Traumatic Brain Injury: Prospective Cohort Study.

BACKGROUND: Posttraumatic amnesia (PTA) after traumatic brain injury (TBI) comprises anterograde amnesia (AA), disorientation, and retrograde amnesia (RA). However, RA is often neither assessed nor emphasized. A recent study demonstrated that although AA and disorientation were both present in non-TBI inpatients uniformly taking opioids, RA was absent. This suggests potentially significant utility with RA assessment alone since opioids are commonly prescribed post TBI. METHODS: We compared RA recovery with AA recovery in a prospective cohort post TBI. The Galveston Orientation and Amnesia Test (GOAT) represented a crude test for PTA (GOAT <75). AA was primarily assessed using the Westmead PTA Scale, and RA was assessed using the GOAT. All patients were prescribed oxycodone. RESULTS: Results were obtained (n = 31). While RA recovery coincided with a GOAT recovery in 19/31 (61%), AA recovery coincided with GOAT recovery in only 6/31 (19%), (χ2 = 11.5, P < 0.001). RA recovery preceded AA recovery in 15/31 (48%), while AA recovery preceded RA recovery in 7/31 (23%) (χ2 = 8.6, P = 0.003). Where RA recovery less frequently followed AA recovery, temporal lobe contusions were more frequent. RA recovery preceded/coincided with AA recovery in 100% of those who recovered when AA was defined as ×3 consecutive 12/12 scores (as is current widespread practice). AA recovery typically followed RA recovery with minimal delay. CONCLUSIONS: In the presence of potential in-hospital confounders including opioids, RA recovered significantly sooner after TBI than AA and was predictive of imminent AA recovery. RA assessment alone therefore had significant and novel utility in post-TBI assessment. RA assessment should be routinely recorded in all PTA assessment. Given its simplicity and resilience to common confounders, RA assessment should also be incorporated into the Glasgow Coma Scale.

Ethyl-acetate fraction of Trichilia catigua restores long-term retrograde memory and reduces oxidative stress and inflammation after global cerebral ischemia in rats.

We originally reported that an ethyl-acetate fraction (EAF) of Trichilia catigua prevented the impairment of water maze learning and hippocampal neurodegeneration after transient global cerebral (TGCI) in mice. We extended that previous study by evaluating whether T. catigua (i) prevents the loss of long-term retrograde memory assessed in the aversive radial maze (AvRM), (ii) confers hippocampal and cortical neuroprotection, and (iii) mitigates oxidative stress and neuroinflammation in rats that are subjected to the four vessel occlusion (4-VO) model of TGCI. In the first experiment, naive rats were trained in the AvRM and then subjected to TGCI. The EAF was administered orally 30min before and 1h after TGCI, and administration continued once per day for 7days post-ischemia. In the second experiment, the EAF was administered 30min before and 1h after TGCI, and protein carbonylation and myeloperoxidase (MPO) activity were assayed 24h and 5days later, respectively. Retrograde memory performance was assessed 8, 15, and 21days post-ischemia. Ischemia caused persistent retrograde amnesia, and this effect was prevented by T. catigua. This memory protection (or preservation) persisted even after the treatment was discontinued, despite the absence of histological neuroprotection. Protein carbonyl group content and MPO activity increased around 43% and 100%, respectively, after TGCI, which were abolished by the EAF of T. catigua. The administration of EAF did not coincide with the days of memory testing. The data indicate that antioxidant and/or antiinflammatory actions in the early phase of ischemia/reperfusion contribute to the long-term antiamnesic effect of T. catigua.

Acute Onset Vascular Dementia with Bi-Thalamic Infarct in an HIV-Positive Subject.

BACKGROUND Bi-thalamic infarctions are rare and marked by clinical polymorphism. Their association with HIV has never been reported. CASE REPORT We report a 51-year-old right-handed man with no medical history, who presented an acute onset vascular dementia associated with an antero-retrograde amnesia, a word-finding difficulty, and a dysexecutive syndrome. The CT scan was normal. Brain MRI revealed a paramedian and bi-thalamic infarction, evoking an occlusion of the Percheron artery. The electrocardiogram, transthoracic and transesophageal cardiac ultrasound, and Doppler echo of cervical arteries gave normal results. The biological work-up revealed a positive serology to HIV1. The patient was lost to follow-up and was reported dead 2 months later from an unknown cause. CONCLUSIONS This case illustrates the need to perform an HIV serology in the presence of a bi-thalamic infarction with no obvious cause, particularly in a young subject.

[Doctor, will I get my memory back? Electroconvulsive therapy and cognitive side-effects in daily practice]. / Dokter, komt mijn geheugen terug? Elektroconvulsietherapie en cognitieve bijwerkingen in de praktijk.

BACKGROUND: Patients undergoing or about to undergo electroconvulsive therapy (ECT) are often afraid they will experience negative cognitive side-effects. AIM: To answer questions that patients and referring clinicians often ask about cognitive problems that can result from ECT. METHOD: To discuss, on the basis of clinical perception and literature, the cognitive problems resulting from ECT. RESULTS: The cognitive problems resulting from ect are threefold: short-term postictal confusion (immediately after the treatment), anterograde amnesia and retrograde amnesia. A patient affected by anterograde amnesia, is temporarily less able to remember what he or she has experienced over a period of three months after treatment. The brain of a patient with retrograde amnesia is unable to retrieve or remember information or procedures 'saved' before the treatment took place. More specifically the patient with retrograde amnesia has three main types of problems: semantic memory problems (relating to facts), episodic memory problems (no longer able to retrieve memories concerning non-personal events), and procedural memory problems (no longer able to operate various devices). It is difficult to predict which patients will experience cognitive problems as a result from ect and to what extent. However, the problems are not intensified by maintenance treatment. Factual and autobiographical memory problems following ect-induced retrograde amnesia seems to have a more permanent character. According to the Dutch guidelines for ECT, cognitive side-effects need to be monitored. If patients are monitored before and after ect, they can be given a more targeted psycho-education and eventually a more targeted training course. CONCLUSION: We conclude that in clinical practice increasing attention is being given to ECT-related cognitive side-effects. Clearly, however, more consideration needs to be given to inter-individual variability. Cognitive monitoring is advisable because the course of the side-effects of ect must be followed and evaluated.

Dissociative amnesia: Disproportionate retrograde amnesia, stressful experiences and neurological circumstances.

Dissociative amnesias have been reported in neurological episodes mild enough to not cause any visible lesions on morphological examination. Disproportionate retrograde amnesia with or without identity loss happens in the context of psychological trauma (known or not). In metabolic imaging studies, some authors have reported functional alterations, particularly in the bilateral hippocampus, right temporal regions and inferolateral prefrontal cortex, despite normal morphological imaging. To avoid the presumption of an organic, psychogenic or mixed origin for such changes, De Renzi et al. suggested the term 'functional amnesia' to describe the condition. Patients have sometimes recovered during events similar to those preceding the amnesia in either a spectacular fashion or never. Also, in some cases, distraction or sedation may trigger the start of recovery. During psychotherapy, one patient remembered seeing a car on fire when he was a boy, and his amnesia started when his house was on fire. This suggests control by the frontal cortex, with repression blocking amnesic traces in the new emotional and biological context.