Addressing Hxstorical Amnesia: Proactively Combating Hxstorical Amnesia as a Means of Healing in Higher Education

In a political context characterized by the desire to “Make America Great Again,” the romanticization of the past and the erasure of narratives of marginalized communities affect how students experience and navigate higher education. Institutions of higher education were built on systems of colonization and imperialism and continue to benefit from the legacy of domination and subordination; this hxstory shapes student learning. The authors introduce hxstorical amnesia, its effects on student development, and methods of actively combating hxstorical amnesia in higher education. The authors explore ways to heal from hxstorical amnesia through community-care, cogenerative dialogues, and Sentipensante Pedagogy. By discussing the contemporary impacts of hxstorical amnesia on higher education and student learning, the authors hope to (re)write the narrative of higher education to underline the importance of the hxstories of marginalized communities

Neuropsychological Generation of Source Amnesia: An Episodic Memory Disorder of the Frontal Brain

Source amnesia is an explicit memory (declarative) disorder, particularly episodic, where source or contextual information concerning facts is severely distorted and/or unable to be recalled. This paper reviews the literature on source amnesia, including memory distrust syndrome, and its accepted correlation with the medial diencephalic system and the temporal lobes, and the suggested linkage between the frontal lobes, including special interest with the prefrontal cortex. Posthypnotic induction was the first presentation of source amnesia identified in the literature. The Wisconsin Cart Sorting Test (WCST), Positron Emission Topography (PET), Phonemic Verbal Fluency Test, Stroop Color Word Interference Test, and explicit and implicit memory tests are defined and linked to empirical research on amnesiacs

Transient epileptic amnesia: an emerging late-onset epileptic syndrome.

Transient epileptic amnesia (TEA) is a distinct neurologic condition occurring in late-middle/old age and presenting with amnesic attacks of epileptic nature and interictal memory disturbances. For many years this condition has been associated with the nonepileptic condition of transient global amnesia (TGA) and still today is poorly recognized by clinicians. Despite the clinical and laboratory findings that distinguish TEA from TGA, differential diagnosis may be difficult in the individual patient. Every effort must be employed for an early diagnosis, since antiepileptic treatment may readily control both ictal episodes and memory disturbances

Effect of scopolamine-based amnesia on the number of astrocytes in the rat's hippocampus

As neuron-astrocyte interactions play a crucial role in the adult brain, it is thought that astrocytes support learning and memory through specific mechanisms. In this study, the effect of scopolamine based amnesia on the number of astrocytes in rats' hippocampus was studied. Adult male albino Wistar rats were bilaterally cannulated into the CA1 region and animals received saline or different doses of scopolamine (0.5, 1 and 2 mg/ rat, intra - CA1), immediately after training. Then all the rats were sacrificed and coronal sections were taken from the dorsal hippocampal formation of the right cerebral hemispheres and stained with PTAH. The area densities of the astrocytes in dentate gyrus were measured and compared in the all groups (p < 0.05). Data showed that post-training scopolamine (0.5, 1 and 2 μg/rat, intra-CA1) dose-dependently reduced the step-through latency in the inhibitory avoidance task, showing scopolamineinduced amnesia. Also we found different response of astrocytes in different subfields of hippocampal formation. In dentate gyrus the number of astrocytes was increased, but in other areas scopolamine can decreased the density of astrocytes. We concluded that scopolamine can cause amnesia and this phenomenon can have an effect on astrocyte numbers in the rats hippocampal formation

Acute-onset amnesia: transient global amnesia and other causes

Acute-onset amnesia is a dramatic neurological presentation that can cause considerable concern to both patient and clinician. The patient typically presents with an inability to not only retain new memories but also access previously acquired memories, suggesting disturbance of hippocampal function. Transient global amnesia (TGA) is most common cause of acute-onset amnesia and is characterized by a profound anterograde and retrograde amnesia that typically lasts for <24 hours. Whilst the presentation of TGA is strikingly stereotypical, it can be challenging to distinguish between TGA and other similar differential diagnoses (including posterior circulation strokes, transient epileptic amnesia, psychogenic amnesia, post-traumatic amnesia, and toxic/drug-related amnesia). In this article, we describe the general approach to the acutely amnesic patient; summarise the clinical and neuropsychological differences between the potential causes; and provide practical recommendations to aid diagnosis and management of acute amnesia. Regardless of cause and the dramatic presentation, the prognosis of non-ischaemic acute-onset amnesia is generally favourable

Keeping an eye on the truth: Pupil size, recognition memory and malingering

Background: Estimates of the incidence of malingering in patient populations vary from 1 to 12%, rising to ∼25% in patients seeking financial compensation. Malingering is particularly difficult to detect when patients feign poor performance on neuropsychological tests (see Hutchinson, 2001). One strategy to detect malingering has been to identify psychophysiological markers associated with deception. Tardif, Barry, Fox and Johnstone (2000) used electroencephalogram (EEG) recording to measure event related potentials (ERPs) during a standard recognition memory test. Previous research has documented an ERP “old/new effect” – late positive parietal ERPs are larger when participants view old, learned words compared to new words during recognition. Tardif et al. reasoned that if this effect is not under conscious control, then it should be equally detectable in people feigning amnesia as in participants performing to their best ability. As predicted, they found no difference in the magnitude and topography of the old/new ERP effect between participants who were asked to feign amnesia whilst performing the test and those asked to perform to their best ability. Whilst this approach shows some promise, EEG is comparatively time consuming and expensive. Previous research has shown that during recognition memory tests, participants' pupils dilate more when they view old items compared to new items (Otero, Weeks, and Hutton, 2006; Vo et al., 2008). This pupil “old/new effect” may present a simpler means by which to establish whether participants are feigning amnesia. Method: We used video-based oculography to compare changes in pupil size during a recognition memory test when participants were given standard recognition memory instructions, instructions to feign amnesia and instructions to report all items as new. Due to constant fluctuation in pupil size over time, and variation between individuals, a pupil dilation ratio (PDR) was calculated that represented the maximum pupil size during the trial as a proportion of the maximum during baseline. Results: Participants' pupils dilated more to old items compared to new items under all three instruction conditions (F(1.25) = 47.02, MSE < 0.001, p < .001, ηp2 = .65). There were no significant differences between baseline pupil size (F(1.63,40.76) = 1.90, p = .17, ns). Conclusions: The finding that under standard recognition memory instructions, participants' relative increase in pupil size is greater when they view old items compared to new items replicates previous research documenting the pupil old/new effect. That the effect persists, even when participants give erroneous responses during recognition, suggests that the “pupil old/new effect” is not under conscious control and may therefore have potential use in clinical settings as a simple means with which to detect whether patients are feigning amnesia

A single-system model predicts recognition memory and repetition priming in amnesia

We challenge the claim that there are distinct neural systems for explicit and implicit memory by demonstrating that a formal single-system model predicts the pattern of recognition memory (explicit) and repetition priming (implicit) in amnesia. In the current investigation, human participants with amnesia categorized pictures of objects at study and then, at test, identified fragmented versions of studied (old) and nonstudied (new) objects (providing a measure of priming), and made a recognition memory judgment (old vs new) for each object. Numerous results in the amnesic patients were predicted in advance by the single-system model, as follows: (1) deficits in recognition memory and priming were evident relative to a control group; (2) items judged as old were identified at greater levels of fragmentation than items judged new, regardless of whether the items were actually old or new; and (3) the magnitude of the priming effect (the identification advantage for old vs new items) overall was greater than that of items judged new. Model evidence measures also favored the single-system model over two formal multiple-systems models. The findings support the single-system model, which explains the pattern of recognition and priming in amnesia primarily as a reduction in the strength of a single dimension of memory strength, rather than a selective explicit memory system deficit

Retrograde amnesia for semantic information in Alzheimer's disease

Patients with mild to moderate Alzheimer's disease and normal controls were tested on a retrograde amnesia test with semantic content (Neologism and Vocabulary Test, or NVT), consisting of neologisms to be defined. Patients showed a decrement as compared to normal controls, pointing to retrograde amnesia within semantic memory. No evidence for a gradient within this amnesia was found, although one was present on an autobiographic test of retrograde amnesia that had a wider time scale. Several explanations for these results are presented, including one that suggests that extended retrograde amnesia and semantic memory deficits are in fact one and the same defici

Amnesia for violent crime among young offenders

Amnesia for the perpetration of violent offences is an important issue in medico-legal proceedings. Previous studies of amnesia have mainly relied on selected groups of unconvicted offenders, which raises the question of how reliable the findings are. The purpose of this study was to examine the prevalence and phenomenological qualities of amnesia in violent offenders. In semi-structured interviews with 105 young offenders convicted of serious violence, 20 (19%) reported partial amnesia for their offence and only one (1%) reported complete amnesia. Amnesia was associated with high alcohol intake, emotional ties to the victim, and cognitive processing during the assault. Complete amnesia for violent crime appears to be less frequent than suggested by previous reports using unconvicted samples. The findings have implications for the clinical assessment of claimed amnesia for violent crime and are potentially of medico-legal significance