Amnesia pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Govindavarjhulla, M.B.B.S. [2]

Overview

Amnesia results from damage to different memory centers in the brain, such as the medial temporal lobe and the hippocampus, which are involved in acquiring and restoring memory.

Pathophysiology

Memory is disrupted by damage that may occur in different parts of the brain such as the medial temporal lobe, the hippocampus, the cortex and the frontal lobe. Injury to any of these areas may lead to specific disruptions in the processes of acquiring and recalling memories. For instance, damage to the medial temporal lobe and hippocampus can sharply reduce the ability to acquire new declarative memory whereas damage to the storage areas in the cortex can disrupt retrieval of old memories and interfere with the acquisition of new memories.

Anterograde Amnesia

Anterograde amnesia can result from damage to the hippocampus, fornix, or mammillary bodies, thus lending credence to the theory that these structures are primarily responsible for laying down long-term memories. However, the condition can also arise from damage to the basal forebrain (which produces acetylcholine) or a set of brain structures called the diencephalon.

Dissociative or Functional or Psychogenic Amnesia

There are three types of memory – sensory, short-term, and long-term memory. Sensory memory lasts up to hundreds of milliseconds and short-term memory lasts from seconds to minutes while anything else longer than short-term memory is considered to be a long-term memory.[1][2]

The information obtained from the peripheral nervous system (PNS) is processed in four stages -encoding, consolidating, storage, and retrieval.[1] During encoding, the limbic system is responsible for bottlenecking or filtering information obtained from the PNS. According to the type of information given, the duration of consolidating stage varies drastically. Majority of consolidated information gets stored in the cerebral cortical networks where the limbic system record episodic-autobiographical events. These stored episodic and semantic memories can be obtained by triggering the uncinate fascicle that interconnects the regions of the temporofrontal junction area.

Emotion seems to play an important role in memory processing in structures like the cingulated gyrus, the septal nuclei, and the amygdala that is primarily involved in emotional memories.[1][3] Functional imaging of normal patients reveal that right-hemispheric amygdala and ventral prefrontal regions are activated when they were retrieving autobiographical information and events. Additionally, the hippocampal region is known to be linked to recognizing faces. Researchers have found that emotional memories can be suppressed in non-mentally ill individuals via the prefrontal cortex in two stages - an initial suppression of the sensory aspects of the memory, followed by a suppression of the emotional aspect.[4] It has also been proposed that glucocorticoids can impair memory retrieval, though to date this has only been tested in rats.[5]

Traumas can interfere with several memory functions. Dr. Bessel van der Kolk divided these functional disturbances into four sets, traumatic amnesia, global memory impairment, dissociative processes and traumatic memories' sensorimotor organization. Traumatic amnesia involves the loss of remembering traumatic experiences. The younger the subject and the longer the traumatic event is, the greater the chance of significant amnesia. Global memory impairment makes it difficult for these subjects to construct an accurate account of their present and past history. Dissociation refers to memories being stored as fragments and not as unitary wholes. Not being able to integrate traumatic memories seems to be the main element which leads to PTSD. In the sensorimotor organization of traumatic memories, sensations are fragmented into different sensory components.[6]

Psychogenic amnesia is far from being completely understood and while several explanations have been proposed, none of them have been verified as the mechanism that fits all types of psychogenic amnesia. Different theories include:

  • Freudian psychology states that psychogenic amnesia is an act of self-preservation, an alternative to suicide.[7]
  • Cognitive point-of-view states that this disorder utilizes the body’s personal semantic belief system to repress unwanted memories from entering the consciousness by altering neuropeptides and neurotransmitters released during stressful events, affecting the formation and recall of memory.[7]
  • "Betrayal trauma theory suggests that psychogenic amnesia is an adaptive response to childhood abuse. When a parent or other powerful figure violates a fundamental ethic of human relationships, victims may need to remain unaware of the trauma not to reduce suffering but rather to promote survival. Amnesia enables the child to maintain an attachment with a figure vital to survival, development, and thriving. Analysis of evolutionary pressures, mental modules, social cognitions, and developmental needs suggests that the degree to which the most fundamental human ethics are violated can influence the nature, form, and processes of trauma and responses to trauma."[8]
  • Normal autobiographical memory processing is blocked by imbalance or altered release of stress hormones such as glucocorticoids and mineralocorticoids in the brain.[1][3] The regions of expanded limbic system in the right hemisphere are more vulnerable to stress and trauma, affecting the body's opioids, hormones, and neurotransmitters such as norepinephrine serotonin, and neuropeptide Y.[2] Increased levels of glucocorticoid and mineralocorticoid receptor density may affect the anterior temporal, orbitofrontal cortex, hippocampal, and amygdalar regions. These morphological changes may be caused by loss of regulation of gene expressions in those receptors along with inhibition of neurotrophic factors during chronic stress conditions.
  • Stress may directly affect the medial temporal/diencephalic system, inhibiting the retrieval of autobiographical memories and producing a loss of personal identity. Negative feedback produced by this system may dampen the patient's emotions, giving a perplexed or 'flat' appearance.[9]

Childhood Amnesia

Since Miles first officially documented childhood amnesia as a psychological phenomenon, many theories of its causes and character have been developed. Some of the most notable are described here to aid in understanding what childhood amnesia may be. It is worth noting that many of these theories are highly controversial and the true nature of childhood amnesia is still being debated.

Freud’s Trauma Explanation

Sigmund Freud’s theories of psychosexual development are highly intertwined with childhood experiences, and Freud’s explanation of childhood amnesia is one of the most controversial. In what is now published as The Standard Edition of the Complete Psychological Works of Sigmund Freud, Freud theorized that childhood amnesia is the result of the mind’s attempt to repress memories of traumatic events that, according to Freud, necessarily occur in the psychosexual development of every child. This would lead to the repression of the majority of the first years of life (Gleitman, et al., 2004). Some evidence has been found that could support the repression theory. In one study, high school and college students were asked to recall the nature of their earliest memory. In the first phase, high school students were found to have much later earliest retrievable memories, many of which featured traumatic events. In a retest several months later, 42% of the high school students reported a different earliest memory, and many of these new memories were markedly less traumatic than the ones they had recalled the first time (Kihlstrom, et al., 1982). At the same time, Freudian theory, including his explanation for childhood amnesia, has been severely criticized. One criticism is actually about the evidence, often anecdotal rather than purely scientific, and said to frequently permit multiple interpretations (Gleitman, et al., 2004). Criticism specifically of the Kihlstrom experiment includes the observation that no part of the study actually involved children, but rather adolescents and young adults (Bauer, 2004).

Physical Development Explanation

Another often-cited explanation of childhood amnesia is that the infant’s mind is not mentally mature enough to create long-lasting autobiographical memories. In particular, it is not until the age 3 or 4 that toddlers have a mature hippocampus and prefrontal cortex. These regions of the brain are known to be associated with the formation of autobiographical memories of the type notably missing from adult recollection of early childhood (Gleitman, 2004; Newcombe, et al., 2000).

Language Explanation

The incomplete development of language in young children may be a cause of childhood amnesia in that infants do not have the language capacity to encode autobiographical memories in a manner that their language-based adult selves can interpret correctly. Indeed, the typical schedule of language development seems to support this theory. Babies of one year old tend to be limited to one word utterances, and childhood amnesia predicts that adults have very few, if any, memories of this time. By the age of three, however, children are capable of two or three word phrases, and by age five their speech already resembles adult speech. This language development seems to very much correspond to childhood amnesia because it is around the age of three to four that is the time of most adults’ earliest recallable memory (Gleitman, et al., 2004).

Emotion Explanation

One explanation notes the connections between the emotion or amygdala-governed memory pathway and the autobiographical or hippocampus- governed pathway. While these two memory systems do have much independence, it is also known that emotions and the amygdala play a role in the encoding of memories typically associated with the hippocampus (Phelps, 2004). Knowing this, it has been suggested that the differences between the emotions experienced by infants and adults may be a cause of childhood amnesia (West, et al., 1999). One problem with this explanation, however, is that one of the most widely proclaimed examples of emotion influencing memory, the "flashbulb memory" mechanism, may not exist at all. If so, it would be unlikely for emotion and memory to be so intertwined as to cause an inability to recall the first several years of memories (McCloskey, et al., 1988).

Context Explanation

The difference in perspective that children and adults experience of the world may be a cause of childhood amnesia. For children, their physical perception of objects and their understanding of people and events are very different from the world of the adult. Moreover, an infant’s basic understanding of the universe, like object permanence or occlusion effects, is not innate at birth. This leads to a disparity in retrieval cues used by the adult and those used by the infant, who will encode memories without many of these principles that are ingrained in the mind of the adult trying to recollect. This different context could lead to the inability of the adult to remember his earliest years at all (Gleitman, et al., 2004). For example, one study showed that an infant’s development of a theory of mind is linked to his ability to form episodic memories. The conclusion was that the context explanation may be justified, especially since infants develop the ability to perceive the world as adults do around the age of 3 to 5, when many people also have their earliest retrievable memory (Perner, et al., 1995).

Blackout (Alcohol Related Amnesia)

Various studies have proven links between general alcohol consumption and its effects on memory creation.[10] Particularly, these studies had shown that associations made between words and objects when intoxicated are less easily recalled than associations made when not intoxicated. Later blackout-specific studies have indicated that alcohol specifically impairs the brain's ability to take short-term memories and experiences and transfer them to long-term memory.[11] This was shown by the ability to recall associations made while intoxicated being affected over time; it is strongly indicated that memories can be easily recalled for 2-3 minutes before the permanent inability to recall them in the future. Blackouts are quite often associated with the consumption of large amounts of alcohol, however surveys of drinkers who have experienced blackouts have indicated that blacking out is not directly related to the amount of alcohol consumed. Respondents reported they frequently recalled having "had drunk as much or more without memory loss," compared to instances of blacking out.[12] Subsequent research has indicated that blackouts are most likely caused by a rapid increase in a person's blood-alcohol concentration. One study, in particular, resulted in subjects being stratified easily into two groups, those who consumed alcohol very quickly, and blacked out, and those who did not black out by drinking alcohol slowly, despite being extremely intoxicated by the end of the study.[13] Hence, in order to prevent a blackout, alcohol should not be consumed in large gulps, and should most likely not be drunk on an empty stomach.

References

  1. 1.0 1.1 1.2 1.3 Markowitsch HJ (2003). "Psychogenic amnesia". Neuroimage. 20 Suppl 1: S132–8. PMID 14597306.
  2. 2.0 2.1 Reinhold, N (2006). "Functional neuroimaging in memory and memory disturbances". Current Medical Imaging Reviews. 2 (1): 35–57. doi:10.2174/157340506775541668. Retrieved 2007-12-05. Unknown parameter |coauthors= ignored (help)
  3. 3.0 3.1 Yang JC, Jeong GW, Lee MS; et al. (2005). "Functional MR imaging of psychogenic amnesia: a case report". Korean J Radiol. 6 (3): 196–9. PMID 16145296.
  4. Depue BE, Curran T, Banich MT (2007). "Prefrontal regions orchestrate suppression of emotional memories via a two-phase process". Science. 317 (5835): 215–9. doi:10.1126/science.1139560. PMID 17626877.
  5. Roozendaal B, de Quervain DJ, Schelling G, McGaugh JL (2004). "A systemically administered beta-adrenoceptor antagonist blocks corticosterone-induced impairment of contextual memory retrieval in rats". Neurobiol Learn Mem. 81 (2): 150–4. doi:10.1016/j.nlm.2003.10.001. PMID 14990235.
  6. van der Kolk BA, Fisler R (1995). "Dissociation and the fragmentary nature of traumatic memories: overview and exploratory study". J Trauma Stress. 8 (4): 505–25. PMID 8564271. Retrieved 2008-03-22.
  7. 7.0 7.1 Brandt J, Van Gorp WG (2006). "Functional ("psychogenic") amnesia". Semin Neurol. 26 (3): 331–40. doi:10.1055/s-2006-945519. PMID 16791779.
  8. Freyd, J. (1994). "Betrayal Trauma: Traumatic Amnesia as an Adaptive Response to Childhood Abuse". Ethics & Behavior. 4 (4): 307–330. doi:10.1207/s15327019eb0404_1. Retrieved 2008-01-13.
  9. Kopelman MD (2002). "Disorders of memory". Brain. 125 (Pt 10): 2152–90. PMID 12244076. Retrieved 2008-04-05.
  10. PARKER, E.S.; BIRNBAUM, I.M.; AND NOBLE, E.P. Alcohol and memory: Storage and state dependency. Journal of Verbal Learning and Verbal Behaviour 15:691-702, 1976.
  11. ACHESON, S.; STEIN, R.; AND SWARTZWELDER, H.S. Impairment of semantic and figural memory by acute ethanol: Age-dependent effects. Alcoholism: Clinical and Experimental Research 22:1437-1442, 1998.
  12. GOODWIN, D.W; CRANE, J.B.; AND GUZE, S.B. Alcoholic "blackouts": A review and clinical study of 100 alcoholics. American Journal of Psychiatry 126:191-198, 1969.
  13. RYBACK, R.S. Alcohol amnesia: Observations in seven drinking inpatient alcoholics. Quarterly Journal of Studies on Alcohol 31:616-632, 1970.



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