Abstract
Amnesia is a condition characterized by memory loss or inability to form new memories that can be caused by organic or functional factors. Organic factors that cause amnesia include brain injuries from physical trauma or medical condition. Functional factors are psychological responses to traumatic events or internal conflicts. Although the cause of amnesia is clear when memory is impaired by organic factors, the role of physiological processes in dissociative amnesia is still controversial. This paper aims to provide an overview of amnesia and the physiological processes that can explain how functional factors affect the brain and impair memory recovery.
Keywords: amnesia, dissociative amnesia, memory, physiology
Introduction
Amnesia is condition in which a person experiences a partial or complete inability to recall previous memories or form new memories. The inability to form new memories is referred to as anterograde amnesia, which usually occurs after a traumatic brain injury that impairs the processing of short-term memory and its storage in long-term memory. The inability to recall previous memories is referred to as retrograde amnesia. Physical injuries are a common cause of retrograde amnesia, but psychological trauma can also lead to memory repression or fugue states, in which case the condition is referred to as dissociative amnesia. The exact prevalence of amnesia is unknown because some types of amnesia can be undetected (e.g., dissociative amnesia) or temporary (e.g. drug-induced amnesia, fugue amnesia, and transient global amnesia), and amnesia is sometimes considered a symptom of a neurodegenerative disease (e.g., Alzheimer’s disease or Wernicke-Korsakoff syndrome). The two main types of causes that can lead to amnesia are organic and functional causes.
Organic causes are related to medical conditions. For example, some forms of malnourishment, such as thiamine deficiency, can lead to memory loss. Other organic causes of amnesia are usually related to brain injuries, and there are several medical conditions that can cause brain damage that leads to memory loss. Examples include brain infections, seizures, traumatic brain injury, altered cerebral blood flow, brain tumors, and lack of oxygen delivery to the brain cells.
Functional causes are psychological factors that result in dissociative amnesia, which is characterized by repressing memories, self-identity impairment, or forgetting episodic information (Arzy et al., 2011). Events that are experienced or witnessed by the individual, such as abuse, abandonment, or death, are usually considered the main causes of dissociative amnesia. Memory loss in these cases can be limited to specific stressful or traumatic events, but the psychological reactions to traumatic events can make years worth of memory inaccessible. Aside from environmental factors, internal conflicts can also lead to the onset of dissociative amnesia. For example, feelings of guilt, interpersonal issues, and deviant personal behaviors that are not resolved can lead to denial and the suppression of relevant memories. A person may not be able to recall a certain memory because of its association with painful emotional experiences, but repressed memories still exist and can affect behavioral reactions to external stimuli.
Although functional factors can result in severe memory repression or fugue states, dissociative amnesia is currently a controversial topic. According to the American Psychological Association (APA; 2013), dissociative amnesia is characterized by the inability to recall autobiographical memory that is severe to the extent that it cannot be explained by forgetfulness, but it can be diagnosed only when medical conditions are ruled out. A variety of medical examinations can be conducted to perform a differential diagnosis and eliminate organic causes of amnesia. Magnetic resonance imaging (MRI) is used to assess potential structural causes of amnesia. Electroencephalography (EEG) needs to be conducted to eliminate seizure-related amnesia. Drug tests using blood or urine are conducted to test the patient for illicit substances that can alter brain functions and cause memory loss.
This definition of dissociative amnesia indicates that only episodic and autobiographical memory is impaired whereas other systems remain functional. Because of this limited effect of dissociative amnesia on a person’s memory and the supposed absence of physiological factors, some professionals consider that the existence of repressed memories in dissociative amnesia is feigned and should be disputed. However, it is not possible to completely separate biological factors from psychological factors because the causality in their relationship is not one-directional. Biological processes can affect psychological factors, but psychological factors also have an impact on biological processes. Therefore, even though the current definition of dissociative amnesia excludes any influence of biological factors on memory recovery impairment, there has to be a physiological explanation as to why dissociative amnesia occurs.
Method
A literature search was conducted on MEDLINE and ScienceDirect databases using the search phrase “functional amnesia physiology” and applying filters to return only articles published within the past 3 years (2011 to present). The searches were repeated with terms “dissociative,” “traumatic,” and “psychogenic” to substitute the term “functional” because those terms are sometimes used interchangeably. Articles that discussed amnesia as a component in patients diagnosed with posttraumatic stress disorder (PTSD), traumatic brain injury, or neurodegenerative disease were excluded.
Results
Current research suggests that memory consolidation and information processing occur mainly in the hippocampus (Blake, Boccia, Krawczyk, & Baratti, 2013). The hippocampus proper processes episodic memories while the surrounding structures are responsible for processing semantic memories. If psychological factors are the main reason for the inability to recall those memories, there needs to be functional change in the brain physiology that affects the hippocampus and other neural structures that would lead to the inability to recall certain memories.
The psychological stress model offers several explanations that could clarify the role of physiological processes in the onset of both anterograde and retrograde cases of functional amnesia. Although anterograde functional amnesia is rare, it is possible that the increase of stress hormones during stressful situations creates a consolidating deficit either by impacting brain structures and functions associated with memory consolidation or by affecting the wake-sleep cycle, which enhances memory consolidation (Staniloiu & Markowitsch, 2012). If a person experiences retrograde functional amnesia the psychological stress model explains that the sensitivity of the limbic network involved in information processing is susceptible to traumatic environmental factors. Upon exposure to traumatic events, those structures can result in morphological and functional changes in those regions that lead to a memory retrieval blockade (Staniloiu & Markowitsch, 2012).
A common objection to the legitimacy of dissociative amnesia is the fact that declarative memory in affected individuals usually stays intact, but current concepts of memory processing suggest that such an outcome is possible. In healthy individuals, memory retrieval occurs through the interaction of three neural networks, which include the activating brain stem structures, neocortical structures, and the limbic network (Staniloiu & Markowitsch, 2012). The neocortical structures are critical for recalling facts and events. The limbic network provides emotional context for the information stored in the neocortical structures. However, it is important to understand the distribution of memories within these systems to understand why functional amnesia occurs. Tulving’s serial, parallel, independent (SPI) model explains that memory encoding is serial, but the brain can store it in different systems and its retrieval is independent of the system that encoded the information (Staniloiu & Markowitsch, 2012). Therefore, it is possible that a person will be able to store new information and retrieve some previous memories if amnesia affects only specific memory storage structures.
Given the fact that the understanding of the physiological processes involved in memory consolidation and retrieval has been well researched, current research aims to develop a solution for memory reconsolidation in amnesia patients by targeting the hippocampus with pharmacological agents to facilitate memory reconsolidation in amnesia. Blake et al. (2013) found that the administration of choline bitrate via intra-dorsal-hippocampal injections improved memory recovery in mice, so the authors suggested that altering physiological processes involved in memory reconsolidation is a viable strategy for assisting individual in recovering. Although research in this field still relies on the animal model and can only make rough estimates of the implications of the same treatment in human subjects, the ability to reconsolidate memories could facilitate the recovery process in many amnesia patients.
Until the use of pharmacological agents for memory reconsolidation is tested in clinical trials, there are three main treatment strategies that can be used to address amnesia if its symptoms persist. The first strategy is to establish a coping strategy for affected patients to help them accept their condition and improve their memory skills. The second strategy is to address underlying conditions that can lead to amnesia. For example, thiamin deficiency or substance abuse can be addressed through proper nutritional plans and psychological interventions. The third strategy is to engage in psychotherapy. This approach is used specifically in cases of dissociative memory to address the issues responsible for the repression of memories, but therapists need to be cautious when treating affected patients because it is important to distinguish between repressed memories and motivated forgetting in order to correctly identify underlying issues.
Discussion
Functional and organic factors are two established causes of amnesia, but organic amnesia appears to be an acceptable concept to researchers than functional amnesia. As the name suggests, organic causes are associated with physical injuries (e.g., blow to the head) or medical conditions that cause brain injury, but functional factors are abstract and often times cannot be measured objectively because perceptions of stress or trauma levels are always subjective. However, it would be wrong to assume that functional amnesia is characterized by a complete absence of physiological factors. It has long been known that physiological reactions during stress can affect the hippocampus, amygdala, and other regions of the brain (Staniloiu & Markowitsch, 2012). Neuropeptides and neurotransmitters that are released during stressful events are responsible for affecting those regions and modulating memory functions. Consequently, a person will experience memory repression or long-term alterations in cases of severe psychological trauma.
Various existing models have established the possibility of psychological factors influencing memory-related processes in the brain, so it is possible to confirm that physiological processes are altered in people with dissociative amnesia. However, the exact physiological mechanisms leading to dissociative amnesia are unclear because there are many factors that can affect brain structures. For example, increased glucocorticoid levels were associated with dissociative amnesia and could explain why alterations in the limbic structures caused by stress or trauma occur rapidly in some individuals (Staniloiu & Markowitsch, 2012). While some theories focus on the alterations in the limbic system as the physiological changes associated with dissociative amnesia, Arzy et al. (2010) found altered activations in the left posterior parietal cortex that could explain why self-identity and episodic memory deficits occur. Although there is evidence that both organic and functional factors contribute to dissociative amnesia, the exact structures involved in the process and their interactions are not yet clarified.
However, dissociative amnesia will probably remain a controversial topic because there are instances of amnesia simulations that need to be distinguished from real cases of dissociative amnesia. Imaging studies showed a clear distinction between prefrontal brain activity patterns in people who engage in motivated forgetting or cognitive avoidance and those who actually experience dissociative amnesia (Staniloiu & Markowitsch, 2012). Motivated forgetting and cognitive avoidance are conscious mechanisms at first, but they eventually become unconscious as the individual achieves self-deception. The individual eventually manages to block real memories and/or believe in false memories, and their symptoms and beliefs become a coherent narrative. Therefore, without conducting brain imaging assessments, it is difficult to distinguish between accurate and false cases of dissociative amnesia even when extensive psychological assessments are used to corroborate data.
Although dissociative amnesia is associated with dysfunctions of neural networks involved in memory, the topic will probably remain controversial because opinions are not always based on evidence. Previous researchers established that forgetting in functional amnesia is a cultural symptom, and many contemporary psychologists still hold that belief even though it has been disproved through cross-cultural studies (Staniloiu & Markowitsch, 2012). Likewise, it is now known that only episodic memory can be affected because memory retrieval occurs through multiple structures and is independent of encoding structures. However, those findings were made possible by the fact that the understanding of physiological processes involved in memory has improved. Because it was previously believed that it would be impossible to lose the ability to recall only one type of memory, it is possible that similar misconceptions about the legitimacy of dissociative amnesia still exist today.
One of the biggest challenges contemporary researchers face when investigating amnesia is the inability to distinguish between recall and consolidation mechanisms when investigating underlying processes responsible for the onset of amnesia. That challenge exists because the process of memory consolidation is a continuous process that takes several years and is never final as the brain receives new input and the hippocampus needs to consistently perform memory re-consolidations (Staniloiu & Markowitsch, 2012). That would explain why severe alterations in the hippocampus can result in both anterograde and retrograde amnesia that can last anywhere between 15 and 25 years before spontaneous recovery occurs (Wible, 2013).
Future research needs to develop a methodology that can allow researchers to distinguish between retrieval and consolidation in order to develop an accurate explanation of the processes involved in the development of amnesia. Studies on dissociative amnesia should also focus more on the biopsychosocial model to would explain how functional factors interact with physiological factors in the onset of functional amnesia. It is expected that potential recovery strategies targeting brain regions responsible for manipulating and storing memory, such as the hippocampus, will continue to develop. Although those studies are still in early phases, they show promising results in animal models and could be applied to human subjects in the future.
In summary, the organic and functional causes of amnesia used to be differentiated, but current theories suggest that psychological factors can influence brain structures and their functions. That is why it is not possible to disregard the role of organic factors in the development of functional amnesia.
References
American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders. (5th ed.). Arlington, VA: American Psychiatric Publishing.
Arzy, S., Collette, S., Wissmeyer, M., Lazeyras, F., Kaplan, P. W., & Blanke, O. (2011). Psychogenic amnesia and self‐identity: A multimodal functional investigation. European Journal of Neurology, 18(12), 1422-1425.
Blake, M. G., Boccia, M. M., Krawczyk, M. C., & Baratti, C. M. (2013). Hippocampal α7-nicotinic cholinergic receptors modulate memory reconsolidation: A potential strategy for recovery from amnesia. Neurobiology of Learning and Memory, 106, 193-203.
Staniloiu, A., & Markowitsch, H. J. (2012). Towards solving the riddle of forgetting in functional amnesia: Recent advances and current opinions. Frontiers in Psychology, 3. doi:10.3389/fpsyg.2012.00403
Wible, C. G. (2013). Hippocampal physiology, structure and function and the neuroscience of schizophrenia: A unified account of declarative memory deficits, working memory deficits and schizophrenic symptoms. Behavioral Sciences, 3(2), 298-315.
