User:Dinosaurchicken03/Retrograde amnesia
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[edit]In neurology, retrograde amnesia (RA) is the inability to access memories or information from before an injury or disease onset occurred.[1] RA differs from a similar condition called anterograde amnesia (AA), which is in the inability to form new memories following injury or disease onset.[2] Although an individual can have both RA and AA at the same time, RA can also occur on its own; this 'pure' form of RA can be further divided into three types: focal, isolated, and pure RA.[3] RA negatively affects an individual's episodic, autobiographical, and declarative memory, but they can still form new memories because RA leaves procedural memory intact.[3] Depending on its severity, RA can result in either temporally-graded or more permanent memory loss.[3] However, memory loss usually follows Ribot's law, which states that individuals are more likely to lose recent memories than older memories.[4] Diagnosing RA generally requires using an Autobiographical Memory Interview (AMI) or observing brain structure using magnetic resonance imaging (MRI), a computed tomography scan (CT), or electroencephalography (EEG).[insert Reed, Squire Citation]
Temporally graded Retrograde Amnesia
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Memory loss in patients with temporally graded RA strongly follows Ribot's law, meaning that one will experience more memory loss for events closer to the injury or disease onset.[4] This type of RA is commonly triggered in individuals with Korsakoff syndrome due to a combination of effects from long-term alcohol use and Wernicke encephalopathy.[5] Debate has risen about why this temporal gradient forms in the first place. Initial theories proposed that the hippocampus and medial temporal lobe are not nearly as important for long-term memories compared to short-term memories.[3] As memory processing occurs in the brain, neocortical regions can directly communicate with each other over time and thus do not rely as heavily on the hippocampus for long-term memory storage.[3] Hence, if an individual experiences retrograde amnesia that damages the hippocampus, they will lose less long-term memories compared to short-term memories. This theory has been challenged by the multiple-trace theory, which claims that the brain develops a hippocampal trace each time a memory is retrieved.[3] Since more hippocampal traces are present for older memories, it is easier for older memories to remain intact when temporally graded RA occurs.[3]
Focal, Isolated, and Pure Retrograde Amnesia
[edit]An absence of anterograde amnesia (AA) characterizes pure forms of RA, which fall into three main categories: focal, isolated, and pure RA.[3] Slight differences in the use of these terms to describe a pure form of RA are summarized below:
| Focal RA | Isolated RA | Pure RA |
|---|---|---|
| Focal RA generally results from neurological problems like epilepsy and is characterized by memory loss prior to – but not after – injury or disease onset.[6] When an individual experiences focal RA, a combination of their episodic and semantic memories may be affected.[7] Take a case study of a middle-aged female, for instance, who experienced focal RA after significant head trauma.[7] Although she could be re-taught information from her past, these memories were not episodic, but rather, semantic.[7] With focal RA, the details of a patient's life prior to amnesia onset can be reintroduced, but they are unable to recall how they perceived the experience.[7] | Isolated RA is usually associated with a visible thalamic lesion.[8] Consistent with other forms of RA, the isolated form is marked by the inability to recall past information.[8] Take the case a middle-aged man coined JG, whose thalamic lesion expanded as he grew older.[8] This lesion growth induced his isolated RA, resulting in both autobiographical memory loss and the inability to recognize information from popular culture.[8] | Pure RA (PRA) is caused by a range of factors such as vascular diseases, encephalitis, and head injuries.[9] It is often confused with peritraumatic amnesia that may follow mild concussions, but the severity and duration of PRA differs from that of peritraumatic amnesia.[9] Current discussion in the neuropsychiatry literature centers on whether PRA is possibly psychogenic or solely organic in nature.[9] |
A pure form of RA is rare as most cases of RA co-occur with AA. A famous example is that of patient ML. The patient's MRI revealed damage to the right ventral frontal cortex and underlying white matter, including the uncinate fasciculus, a band of fibers previously thought to mediate retrieval of specific events from one's personal past.[10]
During consolidation, the hippocampus acts as an intermediate tool that quickly stores new information until it is transferred to the neocortex for the long-term. The temporal lobe, which holds the hippocampus, entorhinal, perirhinal and parahippocampal cortices, has a reciprocal connection with the neocortex.[11] The temporal lobe is temporarily needed when consolidating new information; as the learning becomes stronger, the neocortex becomes more independent of the temporal lobe.[11]
Studies on specific cases demonstrate how particular impaired areas of the hippocampus are associated with the severity of RA. Damage can be limited to the CA1 field of the hippocampus, causing very limited RA for about one to two years.[11] More extensive damage limited to the hippocampus causes temporally graded amnesia for 15 to 25 years.[11] Another study suggests that large medial temporal lobe lesions, that extend laterally to include other regions, produce more extensive RA, covering 40 to 50 years.[11] These findings suggest that density of RA becomes more severe and long-term as the damage extends beyond the hippocampus to surrounding structures.
Diagnosis
[edit]Since RA affects people's memories to different degrees, testing is required to fully diagnose RA; these tests, however, are inherently limited if a patient's previous neuropathological medical history is unknown.[12] As a result, some clinicians diagnose RA by testing patients about factual knowledge, such as current public events.[12] This testing is limited because people's knowledge about current events varies.[12] Furthermore, these tests must be adjusted to account for the time period that a patient is alive, which affects the amount of detail included in the questions asked.[13] Since some information obtained from this testing is subjective, it is difficult to verify how accurately memories are recalled; this difficulty is especially true for memories from the distant past.[12]
To avoid the previous issues, many researchers test for RA using the Autobiographical Memory Interview (AMI).[12][14] The AMI asks patients targeted questions about three different time parts of their life: childhood, early adult life, and recent life.[12] For each period of that individual's life, researchers ask questions that require the patient to use either their autobiographical or semantic memory.[14] Through the AMI, researchers can understand the types of memories affected, as well as the degree of a patient's RA.[12] AMI can be used in conjunction with functional brain imaging techniques like magnetic resonance imaging (MRI), computed tomography scans (CT) and electroencephalography (EEG).[15] These techniques can be used to detect brain damage that contributes to RA.[15]
References
[edit]- ^ Hunkin, N (1995). "Focal retrograde amnesia following closed head injury: A case study and theoretical account". Neuropsychologia. 33 (4): 509–523. doi:10.1016/0028-3932(94)00136-D.
- ^ Lafleche, Ginette; Verfaellie, Mieke (2017), Kreutzer, Jeffrey; DeLuca, John; Caplan, Bruce (eds.), "Anterograde Amnesia", Encyclopedia of Clinical Neuropsychology, Cham: Springer International Publishing, pp. 1–5, doi:10.1007/978-3-319-56782-2_1106-2, ISBN 978-3-319-56782-2, retrieved 2023-03-28
- ^ a b c d e f g h Lafleche, Ginette; Verfaellie, Mieke (2011), Kreutzer, Jeffrey S.; DeLuca, John; Caplan, Bruce (eds.), "Retrograde Amnesia", Encyclopedia of Clinical Neuropsychology, New York, NY: Springer, pp. 2167–2170, doi:10.1007/978-0-387-79948-3_1152, ISBN 978-0-387-79948-3, retrieved 2023-03-28
- ^ a b Wixted, John T. (2004-02-01). "The Psychology and Neuroscience of Forgetting". Annual Review of Psychology. 55 (1): 235–269. doi:10.1146/annurev.psych.55.090902.141555. ISSN 0066-4308.
- ^ "The three amnesias", Textbook of Clinical Neuropsychology, Taylor & Francis, pp. 749–762, 2016-02-26, ISBN 978-1-315-53751-1, retrieved 2023-03-28
- ^ Sehm, Bernhard; Frisch, Stefan; Thöne-Otto, Angelika; Horstmann, Annette; Villringer, Arno; Obrig, Hellmuth (2011-10-19). de Beeck, Hans P. Op (ed.). "Focal Retrograde Amnesia: Voxel-Based Morphometry Findings in a Case without MRI Lesions". PLoS ONE. 6 (10): e26538. doi:10.1371/journal.pone.0026538. ISSN 1932-6203. PMC 3197527. PMID 22028902.
{{cite journal}}: CS1 maint: PMC format (link) CS1 maint: unflagged free DOI (link) - ^ a b c d Wheeler, Mark A.; Mcmillan, Corey T. (2001-03-01). "Focal retrograde amnesia and the episodic—semantic distinction". Cognitive, Affective, & Behavioral Neuroscience. 1 (1): 22–36. doi:10.3758/CABN.1.1.22. ISSN 1531-135X.
- ^ a b c d Miller, L. A., Caine, D., Harding, A., Thompson, E. J., Large, M., & Watson, J. D. G. (2001). "Right medial thalamic lesion causes isolated retrograde amnesia", Neuropsychologia, 39, 1037–46.
- ^ a b c Lucchelli, F.; Muggia, S.; Spinnler, H. (1998). "The Syndrome of Pure Retrograde Amnesia". Cognitive Neuropsychiatry. 3 (2): 91–118. doi:10.1080/135468098396189. Retrieved 19 March 2019.
- ^ Levine, B., Black, S. E., Cabeza, R., Sinden, M., Mcintosh, A. R., Toth, J. P., Tulving, E., & Stuss, D. T. (1998). "Episodic memory and the self in a case of isolated retrograde amnesia", Brain, 121(10), 1951–73. doi:10.1093/brain/121.10.1951
- ^ a b c d e Squire, L. R., & Alvarez, P. (1995). "Retrograde amnesia and memory consolidation: A neurobiological perspective", Current Opinion in Neurobiology, 5(2), 169–77. doi:10.1016/0959-4388(95)80023-9
- ^ a b c d e f g Reed JM, Squire LR (May 1998). "Retrograde amnesia for facts and events: findings from four new cases". The Journal of Neuroscience : The Official Journal of the Society for Neuroscience. 18 (10): 3943–54. doi:10.1523/JNEUROSCI.18-10-03943.1998. PMC 6793126. PMID 9570821.
- ^ Baddeley A, Eysenck MW, Anderson MC (2015). Memory. New York: Psychology Press. pp. 444–48.
- ^ a b Kopelman, M. D.; Wilson, B. A.; Baddeley, A. D. (1989). "The autobiographical memory interview: A new assessment of autobiographical and personal semantic memory in amnesic patients". Journal of Clinical and Experimental Neuropsychology. 11 (5): 724–744. doi:10.1080/01688638908400928. ISSN 0168-8634.
- ^ a b "Functional Brain Imaging". Ontario Health Technology Assessment Series. 6 (22): 1–79. 2006-12-01. ISSN 1915-7398. PMC 3379170. PMID 23074493.