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Amnesia
Published in Alexander R. Toftness, Incredible Consequences of Brain Injury, 2023
Can a person who loses memories due to retrograde amnesia get them back? The answer is yes, they can relearn the forgotten details, but no, they won't be likely to recover forgotten memories. People typically do not recover the episodic nature of the lost memories which leaves behind a residual unfamiliarity with their own lives (e.g., Fujiwara et al., 2008; Sellal et al., 2002). That is, the emotions, sights, and sounds typically can no longer be re-experienced as part of the memory, leaving behind only the semantic facts.
The Neurologic Disorders in Film
Published in Eelco F. M. Wijdicks, Neurocinema—The Sequel, 2022
Two types of amnesia occur after traumatic head injury. Anterograde amnesia is typically impaired new learning and forgetting. Retrograde amnesia involves deficits in memory storage or retrieval. Psychogenic (functional) amnesia is not restricted to a single event (usually hours before the event) but involves a large part of the past. (It often affects young people.) This memory deficit may last for years. These patients are unable to recall information before the onset of the event, but anterograde memory is intact. Many may have a sudden loss of the ability to read, write, or use the telephone.
Return to Play Following Brain Injury
Published in Mark R. Lovell, Ruben J. Echemendia, Jeffrey T. Barth, Michael W. Collins, Traumatic Brain Injury in Sports, 2020
Ruben J. Echemendia, Robert C. Cantu
Although variously described by different investigators, PTA as core ingredients include impaired orientation, i.e., retrograde amnesia and anterograde amnesia (Shores; Levin, O’Donnell et al. 1979; Daniel, Crovitz et al. 1987; Geffen, Encel et al. 1991). Recently, some investigators have suggested that PTA might better be called post traumatic confusional state (Benson, Gardner et al., 1976; Alexander, 1982; Barth, 1989; Katz, 1992). Post-traumatic amnesia may be divided into two types; retrograde defined by Cartlidge and Shaw (Cartlidge, 1981) as a “partial or total loss of the ability to recall events that have occurred during the period immediately preceding brain injury.” The duration of retrograde amnesia usually progressively decreases.
Systems consolidation and fear memory generalisation as a potential target for trauma-related disorders
Published in The World Journal of Biological Psychiatry, 2022
Lizeth K. Pedraza, Rodrigo O. Sierra, Lucas de Oliveira Alvares
Extensive research with animal models also corroborates these results since recent, but not remote memory, is affected by hippocampal lesion (Winocur 1990; Anagnostaras et al. 1999; Maviel et al. 2004). For instance, electrolytic lesions or pharmacological inactivation of the dorsal hippocampus impairs memory for contextual fear conditioning (CFC) when performed recently after training, but not in remote timepoints (Kim and Fanselow 1992; Winocur et al. 2005; Lee et al. 2016). This pattern of temporally retrograde amnesia has been consistently described in different studies (Anagnostaras et al. 1999, Winocur 1990; Winocur et al. 2001; Maviel et al. 2004), and suggest a decreasing involvement of hippocampal activity in memory retrieval over time. Based on these reports, different theories have been formulated pointing out the role of hippocampal/cortical interactions supporting memory.
Experiences that challenge self-identity following traumatic brain injury: a meta-synthesis of qualitative research
Published in Disability and Rehabilitation, 2021
Darrelle Villa, Hilary Causer, Gerard A. Riley
TBI can result in profound changes to physical, cognitive, emotional, and behavioural functioning [3,5]. Physical changes, such as changes in gait, voice or body shape, can result in people with acquired brain injuries (ABIs) including TBI being less recognisable to themselves and others [6]. Retrograde amnesia can result in loss of access to an accurate self-history on which to base conceptualisations of a continuous self [6]. Cognitive changes (such as changes in memory, attention and concentration, planning and problem-solving and inhibition), emotional changes (including depression, anxiety and ability to regulate mood), and behavioural changes are frequently identified in judgements of personality change [6,7] which are common following TBI [8]. Any one of these changes can influence reintegration into society and the ability to fulfil self-defining roles in relation to living independently, work, intimate relationships and parenting [3,9,10]. Unsurprisingly then, experiences of identity change and crisis are commonly reported by people with acquired ABI including TBI [6]. The concept of identity change has been used to refer to disruption in the continuity of a person’s subjective sense of who they are post-injury and is considered to be a key feature of TBI [3,5,11–14].
Valentin Magnan and Sergey Korsakov: French and Russian pioneers in the study of alcohol abuse
Published in Journal of the History of the Neurosciences, 2018
Toward the end of the nineteenth and the beginning of the twentieth century, the main alcohol-related neurological syndromes were outlined: Wernicke encephalopathy (Wernicke, 1881), Korsakov syndrome (Korsakov, 1887b), and Marchiafava-Bignami disease (Marchiafava & Bignami, 1903). Wernicke’s encephalopathy, also called Wernicke’s disease, refers to the presence of neurological symptoms caused by biochemical lesions of the central nervous system after exhaustion of B-vitamin reserves, in particular vitamin B1, thiamine. Classically, German neurologist Karl Wernicke (1848–1905) encephalopathy is characterized by the triad ophthalmoplegia, ataxia, and confusion. Korsakov’s syndrome is a manifestation of Wernicke’s encephalopathy. The major symptoms are anterograde amnesia, retrograde amnesia, confabulation, minimal content in communication, lack of insight, and apathy. Finally, Marchiafava-Bignami disease (MBD) is a rare condition characterized by demyelination of the corpus callosum.