Functional Amnesia

The Brittle Mind
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Le Pèlerin by René Magritte
Source: www.medicinaepersona.org [17]

Functional amnesia is an amnesic disorder, characterized by the lack of a direct biological and/or psychological mechanism of causation[1]. As a heterogeneous type of infirmity of mind and memory, functional amnesia covers a wide variety of phenotypes. The disorder usually presents itself as a type of retrograde amnesia, however can also be anterograde, usually specifically targeting episodic-autobiographical memory[1]. The loss of memory is either confined to a distinct timeframe or encompasses one’s entire autobiographical memory[1]. Both chronic as well as acute cases have been identified[1].

Even though this variety of amnesia has been recognized since the start of 19th century by the likes of Pierre Janet, not a lot of empirical scientific research has been done on the matter. For this reason a lot of the current knowledge still relies on clinical descriptions[6]. There are however a handful of scientists who have done a fair amount of research on this topic, yet interest in the field does not seems to extend beyond these few. A consequence of this is that a review of the research will present the same reoccurring names, keeping the pool of information somewhat homogeneous.

In the literature functional amnesia is mainly also known as dissociative or psychogenic amnesia, though there are slight differences in the theories underlying these terms[1]. There has been a lot of debate as to which is the most appropriate terminology for the disorder, which speaks to the general disagreement among academia regarding the etiology and mechanism of the disorder[8]. For the purposes of this page, the three terms will be discussed in conjunction to allow for a complete overview of the topic.

A Heterogeneous Disorder

Amnesia

Amnesia is an impairment of the mind characterized by the loss of memory. In terms of the nature of memory impairment, a common distinction is made between two types. Retrograde amnesia consists of the loss of previous memories, while anterograde amnesia is characterized by the failure to form new memories[2]. In some cases both types will co-occur. Amnesia can arise due to a variety of factors such as neurological trauma, the effects of substance abuse or psychological mechanisms[2]. In the past these causative factors were subdivided in two main categories: organic and inorganic causes of amnesia. The neat division between organic and inorganic amnesia has recently been debated however, as some types of amnesia do not fit in to just one of these distinct categories[3].

Dissociative Amnesia, Psychogenic Amnesia and Functional Amnesia

Functional, dissociative and psychogenic amnesia are all quite similar in nature and are often used interchangeably[1]. Some scientists however make a distinction between the three based on their underlying theories of causation[1]. Overall, the amnesia in this disorder usually specifically targets the episodic-autobiographical memory[1]

Amnesia
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Source: mentalhealthy.co.uk [18]
  • Dissociative Amnesia

Dissociative amnesia is the most specific terminology of the three. This amnesia is defined as psychogenic, as it usually is not tied to any neurobiological traumatic damage. The gaps in memory that arise due to the amnesia are thought to be related to stressful and/or traumatic life-events[1][5][7]; thus by extension the terminology is mostly applied to cases of retrograde amnesia[6]. Classified as a dissociative disorder in the DSM-IV, the psychological mechanism of causation is thought to be dissociation[1][6]. A further distinction is made by some to attend to whether the dissociation arises consciously or unconsciously, the former being 'factitious' or 'exaggerated' amnesia, and the latter 'hysterical' amnesia[8].

  • Psychogenic Amnesia

With regards to psychogenic amnesia, there seems to be some inconsistency in the way it is defined. Some sources such as the DMS IV refer to it as an older terminology for dissociative amnesia, while others distinguish it from the former as a more general type of amnesia[8]. In these cases the etiology of the amnesia is not necessarily dissociation, but can be a variety of other psychological mechanisms. This term encompasses both anterograde as well as retrograde amnesia[8].

  • Functional Amnesia

Finally, functional amnesia is the most general terminology of the three. Whereas dissociative and psychogenic amnesia are only termed to arise as a result of psychological mechanisms, functional amnesia is flexible enough to also encompass cases in which biology might be at play. For example, functional amnesia may be diagnosed in patients with mild brain injuries. In these cases the amnesia is termed to be functional (as opposed to organic) because the amnesia is thought to be disproportionate or not necessarily tied to the neurological damage[1]. In other words, while acknowledging physical trauma as a potential contributing factor to the amnesia, the neurobiological damage is not sufficient to explain the memory impairment on its own. It is assumed that there is more at play than the biology, such as a variety of deleterious psychological mechanisms [1]. Because of this interplay between biology and psychology, functional amnesia speaks to the limitations of the concrete established distinction between organic and inorganic amnesia[3]. 

The presence of head injury is not a prerequisite for diagnosis of functional amnesia however[1]; neither is the identification of a specific psychological mechanism of causation. Overall, functional amnesia is a flexible term which allows for a lot of heterogeneity in how and to what extent it presents itself. For this reason, the term has been suggested by some as the most viable terminology to grasp the complexity of this type of amnesia; in addition, seeing as it transcends the outdated organic versus inorganic dichotomy, it allows for communication between psychiatry and neurobiology[1]. 

Regardless of the exact mechanism of causation, imaging techniques have identified definite neurological changes associated with the amnesia[1]. 

Phenotypes

The DSM IV categorizes dissociative amnesia according to Pierre Janet’s general classification of amnesia types: localized, systematized, generalized, continuous[6]. A patient with localized amnesia is unable to remember anything over a distinct period of time; this can encompass seconds, minutes or even years, such as in cases of chronic abuse[6]. A distinct type of localized amnesia, selective amnesia, is diagnosed when the patient can remember some but not all events occurring over a specific timeframe[6]. An example of this is a case in which the patient has witnessed a murder and remembers the events leading up to the crime, but cannot remember the actual act taking place[6].

Systematized amnesia is perhaps the most common type, and presents itself when the patient fails to recall memories pertaining to a specific information category, such as a specific person or a specific place[6]. Finally, generalized amnesia is the most rare and severe type of amnesia; it is characterized by the loss of memory of one’s entire life and thus also one’s sense of identity[6].

In addition, the American Psychological Association (APA) terms dissociative amnesia as characteristic of the other dissociative disorders (dissociative fugue and dissociative identity disorder (DID)) as well as a diagnostic prerequisite for post-traumatic stress disorder (PTSD), acute stress disorder and somatization disorder[6].

Finally functional amnesia can either be retrograde, anterograde or both in conjunction [2]. In addition, while the amnesia usually targets episodic-autobiographical memory, semantic memory can also be effected [2]

Etiology and Theoretical Frameworks

Biological Theories

Because dissociative and psychogenic amnesia are defined as medically unrelated, this section is devoted to functional amnesia, which does not negate the possible contribution of biology in certain cases.

There is a possibility that in cases with functional amnesia where mild traumatic injury has occurred, neurobiology might be contributing to the amnesia[1][11]. These cases remain distinct from those in which the head trauma has direct causal links to the amnesia, shown through neuroimaging techniques. 

There is still some uncertainty regarding to what extent or how the mild damage can contribute to the onset of memory impairment in cases of functional amnesia. The issue lies in the seemingly normal results of neuroimaging tests after mild head injuries. Though on a macro level everything might seem in order, it is possible that the damage is so slight that it cannot be grasped by the tests. For instance multifocal diffuse axonal damage may occur after mild head traumatic injuries, and go unnoticed during imaging tests because of their microscopic size[4]; Diffusion Tensor Imaging studies (DTI) can in some cases show (temporary) changes in the white matter[1]. Disregarding the size of the damage, it can nonetheless have deleterious effects as a result such as executive dysfunctions and defective conscious mnemonic processing[1] [4]. For instance, research has shown that acutely measured lower DLPFC (Dorsolateral Prefrontal Cortex) white matter Fractional Anisotropy (FA) in patients having suffered a mTBI (mild Traumatic Brain Injury) were a good indicator of cognitive deficiency[4]. In addition, some mild head injuries show alterations in the volume of structures linked to mnemonic processing, of which the amygdala and hippocampus are of prime importance[1].

Yet these changes are once again not enough to explain the amnesia entirely. It is thought that in these cases there is a complex interaction between the biological damage and deleterious psychological mechanisms[1][11]. 

Psychological Theories

There are a variety of psychological mechanisms that have been identified as possible causes or contributors to the emergence of functional amnesia. The following are some of the most important ones:

The Psychological Stress model:
Severe stress is thought to both possibly effect the retrieval of episodic-autobiographical memories as well as memory consolidation[1] (see Neurobiology). The memory impairments are thought to be triggered by traumatic and/or stressful life experiences; usually these are ongoing experiences, stretched out over a certain timeframe, originating during childhood or young adulthood[1]. There is however no clear-cut formula resulting in functional amnesia. The amnesia arises due to a complex interaction between psychological environment and predispositions of the individual[1]. Research has shown that dissociation is an empirically supported defense mechanism in face of extreme emotional trauma and stress[10]. This is can be done both consciously as well as unconsciously[8]. The dissociation is thought to function to protect the subjective experience of integrity of self-identity. Dissociation as a coping mechanism is believed to allow for effected patients to continue to function within their environment without knowledge of the stressful events[16].

Motivated Forgetting:
The exaggeration or simulation of symptoms has also been identified as possible contributor to the onset of functional amnesia. It is thought that with time these mechanisms become reinforced, resulting in true amnesia[1]. A possible explanation for this is that through constant rehearsal, the feigned material becomes more integrated into the narrative of self, such that what was once fabricated has become an integral part of the person’s experience of self[1]. Conscious dissociation due to stress is an example of motivated forgetting[8].

Fantasy Proneness Model:
Not all agree with the psychological stress model and in fact some believe that people with functional amnesia are prone to creating false memories, confabulate and/or are highly suggestible[1]. In addition some have proposed that those who are prone to dissociation are more likely to have the hypnotisability trait[1]. Research however on this model has not been conclusive and recent work has shown that when controlling for fantasy proneness, trauma is still positively correlated with the emergence of the amnesia[10].

Socio-cognitive Mode of Functional Amnesia:
Research on DID has revealed that dissociative amnesia is thought to target meta-memory as opposed to objective memory. The former is thought to encompass one’s subjective stance on memory such as one’s feelings, knowledge and beliefs regarding memory[6]. This in turn is reflective of one’s sociocultural environment[1]. One specific example of this is “diagnosis threat” in which the patient’s beliefs about the nature of his or her head injury effect the results of cognitive tests and clinical descriptions of symptoms[1].

The Neurobiology of Functional Amnesia

Disconnection Syndrome

Functional amnesia has often been referred to as a disconnection syndrome, arising due to a disconnect between different brain regions, resulting in memory impairment[1]. The fronto-temporal regions have been identified as key in instagating the retrieval of stored autobiographical memories by the limbic structures[1]. A rupture in this tightly synchronized mechanism across brain structures may explain the onset of the amnesia[1].

Neurobiological Correlates of Functional Amnesia

Kikuchi et al., (2009)
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fMRI of patient with dissociative amnesia; repressed versus normal memory.
The imaging shows the greater activation of the pFC
and the greater deactivation of the left hippocampus during the experiment
when exposed to cues related to repressed memories. Adapted from[5]

Lesion studies have shown that emotionally tinted memories are processed through different pathways than other types of memories; the amygdala specifically seems to be of most importance[8]. In 2000 and 2002 a psychological stress model was proposed for psychogenic amnesia[8]. The frontal areas were identified as key in accommodating the retrieval of episodic - autobiographical memories[8]. The hypothesis is that severe stress can work both on the medial temporal diencephalic system as well as the frontal or executive areas of the brain. The former causes anterograde amnesia, as the stress can act such as to inhibit to consolidation of new memories[9]. The effect of stress on the frontal areas is thought to effect memory retrieval, thus possibly resulting in retrograde amnesia; this is considered to be the most likely pathway[9]. The stress on the frontal regions can result in executive overload, such that in the process of trying to inhibit traumatic memories from entering one's consciousness, the frontal regions end up inhibiting much more, repressing other episodic-autobiographic memory that is not necessarily traumatic in the process[1]. Functional amnesia is quite rare however, thus it is not just the stress that causes its onset, but an interaction between stress and genetic vulnerability and the degree of glucocorticoid release in response to the stress.[2]

Based on this hypothesized model, Kikuchi et al. found in their 2009 paper evidence for the role of the prefrontal cortex and the hippocampus in the mechanism behind involuntarily repressed memories in patients with dissociative amnesia[5]. By way of a remarkable experiment they were able to demonstrate higher activation states in the prefrontal cortex and lower activation states in the hippocampus associated with repressed memories[5]. From these results Kikuchi et al. hypothesized that the prefrontal cortex acted as “inhibitor”, deactivating the hippocampus, overall resulting in a memory retrieval deficit[5]. This experiment however did not prove causality between the two findings; more research would be needed to confirm this hypothesis. Nonetheless their results are of great importance, reinforcing this type of amnesia to be a veritable phenomenon.

Other research has also confirmed that there are neurobiological correlates of functional amnesia, though with somewhat different results than Kikuchi et al.[11]. Previously CT-scans and conventional MR imaging techniques had not found any structural changes associated with functional amnesia. However, Tramoni et al. were able to detect metabolic and structural changes on a microscopic scale in the white matter, using more advanced MR techniques such as Magnetization Transfer Ratio (MTR) or MR Spectroscopic Imaging (MRSI)[11]. Therefore they proposed in their conclusion that functional amnesia arises through a combination of "hypo-retrieval", reflected in the white matter damage in the frontal regions and "hyper-suppression"[11].

Treatment

"Mysterious Amnesia Case" on CBS News
Source: CBS channel on youtube, August 22 2009 [19]

Little empirical research has been done on the effectiveness of treatments, therefore our knowledge is largely limited to general outcomes of clinical case studies. Psychoanalysis has been a popular means of treating functional amnesia, especially in the past[12]. The goal during the therapy sessions was to reveal repressed memories, evoking catharsis and thus alleviating the amnesia. Along these lines, hypnotherapy, such as ego-strengthening, have also been used to strengthen the coping capabilities of patients in the hope of decreasing the experienced menace of the repressed memories and thus relieving the memory impairment[12][15]. The issue with both these methods, however, is the possibility of creating false memories in lieu of alleviating the amnesia[12].

Other types of therapy include systematic relaxation therapy or the use of Guided Imagery Therapy. These techniques place the patient in a safe therapeutic environment in which they are promoted and taught to relax their minds. Imagery,specifically, can function to desensitize the patients to experienced threat[12]. Suggestive psychotherapy can also be used to trigger lost memories[12].

During therapy sessions barbiturates such as sodium thiopental or amobarbital have been used to depress cortical activity in patients, such as to inhibit repression and recover memory[5][12][13]. While these drugs have proven to be effective in certain cases, in the case of amobarbital specifically, there is the danger of respiratory depression[13]. In contrast, Benzodiazepines which also have been used in therapy, carry a lesser risk for respiratory depression and are generally considered to be somewhat safer than barbiturates[13]. Their effectiveness is thought to result from their ability to increase GABA-activity, thus inhibiting cortical activity, alleviating the memory block as a result [12]. In a case study the administration of Lorazepam during therapeutic interviews resulted in the recovery of memory in two patients with dissociative amnesia. The drug put the patients in a hypnotic/sleepy state which aided their interaction with the interviewer, resulting in recovery[13]. It is of note to mention that, somewhat paradoxically, research has shown that administration of Lorazepam can lead to explicit memory impairment on memory tests[14]. Yet, this need not discount the research supporting its therapeutic effect on functional amnesia. In fact, due to its hypnotic and sedative effect, it may result in both inhibition of explicit recall, as well as relaxation of the mind such that it no longer represses the lost memories. Overall, the effectiveness of these drugs reinforces Kikuchi et al.’s findings regarding the overactivity of the pFC in patients with the disorder[5].

Previously it was thought that functional amnesia was reversible, however more and more research aided by imaging techniques has shown that in some cases the impairment is permanent. In some cases this has even been coupled with executive deterioration[1]. Functional Amnesia is a very serious disorder as it usually deeply affects the sense of self and personal identity, especially in cases where whole years’ worth of memory are lost[2]. For this reason, in cases where memory is lost indefinitely, it is important that the patient learns to cope with his or her impairment in a supportive environment. The discovery of self is often promoted through re-immersion or education of former life narratives[12].

Controversy

Ever since it was first described in the 19th century, the validity of this disorder has been debated due to a lack of absolute etiology[11]. While it is a rare type of amnesia, clear-cut empirical evidence has been found supporting its existence and neurobiological basis. Yet many scientists still believe that this is not a real phenomenon. Some have even described it as an "illness-simulating behavior"[12].

Getting an exact number on the occurrence of functional amnesia has proven to be quite hard, though generally it agreed that it is quite rare. Some think that it is underdiagnosed, especially in cases where it is comorbid with disorders, or when the symptoms are mild[1]. One of the key barriers in determining the epidemiology of functional amnesia has been the difficulty in determining whether the amnesia is real or feigned in potential cases[11]. In addition, there has been some dispute on whether functional amnesia is a culture-specific phenomenon arising more in certain cultures than others[1].

Bibliography
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3. Markowitsch H. and Staniloiu, A.The impairment of recollection in functional amnesic states. Cortex. 1-17, (2012).
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11. Tramoni, E., et al. Hypo- retrieval and hyper-suppression mechanisms in functional amnesia. Neuropsychologia. 47, 611–624, (2009).
12. Brandt, J. and Van Gorp, W. G. Functional ("Psychogenic") Amnesia. Semin Neurol. 26:3, 331 -340, (2006).
13. Lee, S., Park, S. and Park, S. Use of Lorazepam in Drug-Assisted Interviews: Two Cases of Dissociative Amnesia. Psychiatry Investig. 8, 377-380 , (2011).
14. Soo-ampon, S., et al. . Effects of word frequency on recall memory following lorazepam, alcohol, and lorazepam alcohol interaction in healthy volunteers. Psychopharmacology, 176, 420-425, (2004).
15. Iglesias, A. and Iglesias, A. Diagnosis and Hypnotic Treatment of an Unusual Case of Hysterical Amnesia. Am J Clin Hypn. 52:2, 123-131, (2009).
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19. CBS Healthwatch. (22 August 2009). Mysterious Amnesia Case. [Television Broadcast]. New York City, New York: CBS.

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