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Declarative information:

Declarative memory can be broken down into semantic memory and episodic memory. Semantic memory being that of facts and episodic memory being that of memory related to events.

While a patient with amnesia might have a loss of declarative memory, this loss might vary in severity as well as the declarative information that it affects  may vary depending on many factors. For example, LSJ was a patient that had retrograde declarative memory loss as the result of bilateral medial temporal lobe damage, but she was still able to remember how to perform some declarative skills. She was able to remember how to read music and the techniques used in art. She had preserved skill-related declarative memory for some things even though she had deficits in other declarative memory tasks. She even scored higher on skill-related declarative memory than the control in watercolor techniques, a technique that she used in her professional career before she acquired amnesia (source 3)

Semantic Information:

The loss of semantic information in amnesia is most closely related with damage to the medial temporal lobe (source 5) or to the neocortex (source 7)

Some patients with anterograde amnesia can still acquire some semantic information, even though it might be more difficult and might remain rather unrelated to more general knowledge. H.M. could accurately draw a floor plan of the home in which he lived after surgery, even though he had not lived there in years. There is evidence that the hippocampus and the medial temporal lobe may help to consolidate semantic memories but then they are more correlated with the neocortex. While legions of the hippocampus normally lead to the loss of episodic memory, if there is any effect on semantic memory it is more varied and usually doesn’t last for as long. (source 7)

Episodic Information:

One  reason that patients could not form new episodic memories is likely because the CA1 region of the hippocampus was a lesion, and thus the hippocampus could not make connections to the cortex. After an ischemic episode, an interruption of blood flow to the brain, following surgery, an MRI of patient R.B. showed his hippocampus to be intact except for a specific lesion restricted to the CA1 pyramidal cells.[1][better source needed] In one instance transient global amnesia was caused by a hippocampal CA1 lesion. While this case was a temporary case of amnesia it still shows the importance of the CA1 region of the hippocampus in memory. (source 6). Episodic memory loss is most likely to occur when there has been damage to the hippocampus. There is evidence that when there is damage to the medial temporal lobe that there is loss of autobiographical episodic memory, but that episodic memory is not affected to the same extent. (source 7)

Non-declarative information

Some retrograde and anterograde amnesiacs are capable of non-declarative memory, including implicit learning and procedural learning. For example, some patients show improvement on the pseudorandom sequences experiment as healthy people do. Therefore, procedural learning can proceed independently of the brain system required for declarative memory. Some patients with amnesia were able to remember skills that they had learned without being able coconsciously recall where they had learned that information. For, example they may learn to do a task and then be able to perform the task later without any recollection of learning the task. (source #1) According to fMRI studies, the acquisition of procedural memories activates the basal ganglia, the premotor cortex and the supplementary motor area, regions which are not normally associated with the formation of declarative memories. This type of dissociation between declarative and procedural memory can also be found in patients with diencephalic amnesia such as Korsakoff's syndrome. Another example demonstrated by some patients, such as K.C. and H.M, who have medial temporal damage and anterograde amnesia, still have perceptual priming. Priming was accomplished in many different experiments of amnesia and was found that the patients can be primed, they have no conscious recall of the event, but the response is there. (source 8) Those patients did well in the word fragment completion test. [1][better source needed] There is some evidence that non-declarative memory can be held onto in the form of motor skills. (source3) This idea was disputed though because it is argued that motor skills require both declarative and non-declarative information. (source 3).

Anterograde amnesia is the inability to create new memories due to brain damage, while long-term memories from before the event remain intact. The brain damage can be caused by the effects of long-term alcoholism, severe malnutrition, stroke, head trauma, encephalitis, surgery, Wernicke–Korsakoff syndrome, cerebrovascular events, anoxia or other trauma.[15] The two brain regions related with this condition are medial temporal lobe and medial diencephalon. (source 10) Anterograde amnesia cannot be treated with pharmacological methods due to neuronal loss.[16] However, treatment exists in educating patients to define their daily routines and after several steps they begin to benefit from their procedural memory. Procedural memory can be intact even when other forms of memory is not, although not always the case. (source 9) Likewise, social and emotional support is critical to improving quality of life for anterograde amnesia sufferers.[16] Fentanyl use by opioid users has been identified as a potential cause in a cluster of cases that occurred in Boston, MA.[17]

Retrograde amnesia is inability to recall memories before onset of amnesia. One may be able to encode new memories after the incident. Retrograde is usually caused by head trauma or brain damage to parts of the brain besides the hippocampus. The hippocampus is responsible for encoding new memory. Episodic memory is more likely to be affected than semantic memory. The damage is usually caused by head trauma, cerebrovascular accident, stroke, tumor, hypoxia, encephalitis, or chronic alcoholism. People suffering from retrograde amnesia are more likely to remember general knowledge rather than specifics. Recent memories are less likely to be recovered, but older memories will be easier to recall due to strengthening over time.[18][better source needed] Retrograde amnesia is usually temporary and can be treated by exposing them to memories from the loss.[19][better source needed] Another type of consolidation (process by which memories become stable in the brain) occurs over much longer periods of time/days, weeks, months and years and likely involves transfer of information from the hippocampus to more permanent storage site in the cortex. The operation of this longer-term consolidation process is seen in the retrograde amnesia of patients with hippocampal damage who can recall memories from childhood relatively normally, but are impaired when recalling experiences that occurred just a few years prior to the time they became amnesic. (Kirwan et al.,2008) In the case of LSJ, her case shows that retrograde amnesia can affect many different parts of knowledge. LSJ wasn’t able to remember things from her child or adult life. She wasn’t able to remember things that most people pick up in everyday life such as logos or the names of common songs. (source 3)

Henry Molaison, formerly known as H.M., changed the way people thought of memory. The case was first reported in a paper by William Beecher Scoville and Brenda Milner in 1957.[43] He was a patient who suffered from severe epilepsy attributed to a bicycle accident at the age of nine. Physicians were unable to control his seizures with drugs, so the neurosurgeon Scoville tried a new approach involving brain surgery. He removed his medial temporal lobe bilaterally by doing a temporal lobectomy. His epilepsy did improve, but Molaison lost the ability to form new long-term memories (anterograde amnesia). He exhibited normal short-term memory ability. If he was given a list of words, he would forget them in about a minute's time. In fact, he would forget that he was even given a list in the first place.[44] However, H.M.’s working and short-term memory seemed to be intact. He had a normal digit span and could hold a conversation that didn’t require him to recall past parts of the conversation. (source 4) Once Molaison stopped thinking about the lists he was unable to recall them again from long term memory. This gave researchers evidence that short-term and long-term memory are in fact two different processes.[45] Even though he forgot about the lists, he was still able to learn things through his implicit memory. The psychologists would ask him to draw something on a piece of paper, but to look at the paper using a mirror. Though he could never remember ever doing that task, he would improve after doing it over and over again. This showed the psychologists that he was learning and remembering things unconsciously.[46] In some studies it was found that H.M.’s perceptual learning was intact and that his other cognitive skills were working appropriately. It was also found that some people with declarative information amnesia are able to be primed.(source 4)

Studies were completed consistently throughout Molaison's lifetime to discover more about amnesia.[1] Researchers did a 14-year follow-up study on Molaison. They studied him for a period of two weeks to learn more about his amnesia. After 14 years, Molaison still could not recall things that had happened since his surgery. However, he could still remember things that had happened prior to the operation. Researchers also found that, when asked, Molaison could answer questions about national or international events, but he could not remember his own personal memories.[44] After his death Molaison donated his brain to science, where they were able to discover the areas of the brain that had the lesions which caused his amnesia, particularly the medial temporal lobe.[45] This case study provided important insight to the areas of the brain that are affected in anterograde amnesia, as well as how amnesia works.

H.M.’s case showed us that memory processes are consolidated into different parts of the brain and that short-term and working memory are not usually impaired in cases of amnesia. (source 4)

Clive Wearing

Another famous historical case of amnesia was that of Clive Wearing. Clive Wearing was a conductor and musician that contracted herpes simplex virus. This virus affected the hippocampal regions of the brain. Because of this damage, Wearing was unable to remember information for more than a few moments. (source #2) Wearing’s non-declarative memory was still functioning but his declarative memory was impaired. To him, he felt that he had just come to consciousness for the first time every time he was unable to hold onto information. This case also can be used as evidence that there are different memory systems for declarative and non-declarative memory. This case was more evidence that the hippocampus is an important part of the brain in remembering past events and that declarative and non-declarative memories have different processes in different parts of the brain.

Sources to add:

1:Butters, N., & Delis, D. C. (1995). Clinical assessment of memory disorders in amnesia and dementia. Annual Review of Psychology, 46(1), 493. https://doi-org.byui.idm.oclc.org/10.1146/annurev.ps.46.020195.002425

2:Kopelman, M. (2015). Precious Memories. Biologist, 62(5), 16–19.

3:Gregory, E., McCloskey, M., Ovans, Z., & Landau, B. (2016). Declarative memory and skill-related knowledge: Evidence from a case study of amnesia and implications for theories of memory. Cognitive Neuropsychology, 33(3/4), 220–240. https://doi-org.byui.idm.oclc.org/10.1080/02643294.2016.1172478

5: Buckner, R. L. (2000). Neural origins of “I remember.” Nature Neuroscience, 3(11), 1068. https://doi-org.byui.idm.oclc.org/10.1038/80569

4: What hm taught us

6: Hiroshi Yokota, Kazuhiro Yokoyama, & Satoru Iwasaki. (2015). Transient global amnesia with intracranial vertebral artery dissection and hippocampal CA1 lesion. Neurology India, 63(4), 604–605. https://doi-org.byui.idm.oclc.org/10.4103/0028-3886.162077

7: Rosenbaum, R. S., Moscovitch, M., Foster, J. K., Schnyer, D. M., Fuqiang Gao, Kovacevic, N., Verfaellie, M., Black, S. E., & Levine, B. (2008). Patterns of Autobiographical Memory Loss in Medial-Temporal Lobe Amnesic Patients. Journal of Cognitive Neuroscience, 20(8), 1490–1506. https://doi-org.byui.idm.oclc.org/10.1162/jocn.2008.20105

8: Hamann, S. B., & Squire, L. R. (1997). Intact priming for novel perceptual representations in amnesia. Journal of Cognitive Neuroscience, 9(6), 699. https://doi-org.byui.idm.oclc.org/10.1162/jocn.1997.9.6.699

9: van der Hart, O., & Nijenhuis, E. (2001). Generalized dissociative amnesia: episodic, semantic and procedural memories lost and found*. Australian & New Zealand Journal of Psychiatry, 35(5), 589–600. https://doi-org.byui.idm.oclc.org/10.1080/0004867010060506

10: Buckley, M. (2005). The role of the perirhinal cortex and hippocampus in learning, memory, and perception. Quarterly Journal of Experimental Psychology: Section B, 58(3/4), 246–268. https://doi-org.byui.idm.oclc.org/10.1080/02724990444000186