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-hemisperic 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 Semantics|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]
References
- ↑ 1.0 1.1 1.2 1.3 Markowitsch HJ (2003). "Psychogenic amnesia". Neuroimage. 20 Suppl 1: S132–8. PMID 14597306.
- ↑ 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) - ↑ 3.0 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 7.0 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.
- ↑ 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.
- ↑ Kopelman MD (2002). "Disorders of memory". Brain. 125 (Pt 10): 2152–90. PMID 12244076. Retrieved 2008-04-05.