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Functional amnesia: Definition, types, challenges and future directions
Abstract
The meaning of the term functional amnesia has undergone changes over time. Initially seen as the opposite of so-called "organic" amnesia, the use of the term functional amnesia shifted to designate amnes(t)ic disorders that occur without evidence of significant brain damage as detected by conventional structural brain imaging techniques and have an unsure etiology. Although several authors still use the terms psychogenic, dissociative or functional amnesia interchangeably, implicitly acknowledging that a number of functional amnesias have a psychological basis, there are subtle differences among these terminologies and their theoretical scaffolding. The term dissociative amnesia by definition designates a form of psychogenic amnesia underlain by the psychological mechanism of dissociation (DSM-IV-TR, 2000). Mirroring Janet's (1907) view of dissociation as ''an inability of the personal self to bind together the various mental components in an integrated whole under its control" (Janet, 1907, p.23), dissociative disorders are nowadays regarded in DSM-IV-TR (2000) as disturbances of the integrated organization of memory, perception, consciousness, identity or emotion, which are causally-bound to psychological trauma or stress. In contrast to the term dissociative amnesia, which carries an a priori specific theoretical load with it, the term psychogenic amnesia refers to amnes(t)ic disorders that are etiologically linked to a larger variety of psychological mechanisms. The concept of functional amnesia (Lundholm, 1932; Schultz, 1924) was suggested by De Renzi et al. (1997) as a "more suitable term to classify patients whose memory disorders cannot be traced back to organic or psychological causes" (p.788). Although several cases of functional amnesia were found to occur on background of psychological stress or trauma, alone or in combination with a co-occurring (mild) physical insult (such as a mild traumatic brain injury, mild electrocuting accident, mild physical injury), there are case-reports of functional amnesia where a clear-cut psychological etiological mechanism could not be identified. The lack of readily identifiable psychological factors in some cases of functional amnesia may have several explanations, as we will detail below. The memory impairment in functional amnesia is usually of a retrograde nature, but might at times be anterograde as well. The memory impairment does not occur in isolation, but it is often accompanied by impairments of executive functions, theory of mind functions, emotional processing, self-consciousness and mental time travelling.
Autobiographical amnesia is found in patients with focal or diffuse brain damage ("organic amnesia"), but also without overt brain damage (at least when measured with conventional brain imaging methods). This last condition is usually named dissociative amnesia at present, and was originally described as hysteria. Classically and traditionally, dissociative amnesia is seen as a disorder that causes retrograde amnesia in the autobiographical domain in the aftermath of incidents of major psychological stress or trauma. In the present study one of the probably largest published collections of patients (28) with psychogenically caused autobiographical amnesia, who were assessed with comprehensive neuropsychological tests, will be described and documented in order to identify variables which are central for the occurrence of dissociative amnesia. The presented cases demonstrate that autobiographical amnesia without direct brain damage can have very mixed clinical presentations, causes and consequences. The described cases of psychogenic amnesia are clustered according to a number of manifestations and features, which include a reduced effort to perform cognitively at a normal level, a forensic background, anterograde (instead of retrograde) autobiographical amnesia, the fugue condition, concurrent somatic diseases, and their appearance in childhood and youth. It is concluded that autobiographical amnesia of a psychogenic origin may occur within a variety of symptom pictures. For all patients, it probably serves a protective function by offering them a mechanism to exit a life situation which appears to them unmanageable or adverse.
Retrograde amnesia is described as condition which can occur after direct brain damage, but which occurs more frequently as a result of a psychiatric illness. In order to understand the amnesic condition, content-based divisions of memory are defined. The measurement of retrograde memory is discussed and the dichotomy between “organic” and “psychogenic” retrograde amnesia is questioned. Briefly, brain damage-related etiologies of retrograde amnesia are mentioned. The major portion of the review is devoted to dissociative amnesia (also named psychogenic or functional amnesia) and to the discussion of an overlap between psychogenic and “brain organic” forms of amnesia. The “inability of access hypothesis” is proposed to account for most of both the organic and psychogenic (dissociative) patients with primarily retrograde amnesia. Questions such as why recovery from retrograde amnesia can occur in retrograde (dissociative) amnesia, and why long-term new learning of episodic-autobiographic episodes is possible, are addressed. It is concluded that research on retrograde amnesia research is still in its infancy, as the neural correlates of memory storage are still unknown. It is argued that the recollection of episodic-autobiographic episodes most likely involves frontotemporal regions of the right hemisphere, a region which appears to be hypometabolic in patients with dissociative amnesia.
Im klinisch-neurowissenschaftlichen Bereich wird Vergessen meist mit Amnesie gleichgesetzt, wobei der Terminus „Amnesie“ vielfältige Bedeutung haben kann: Er kann sowohl den vollständigen Verlust der eigenen Erinnerung meinen („retrograde Amnesie“) als auch das Fehlen von Erinnerung an bestimmte Ereignisse, bestimmte Lebensepochen, bestimmtes Material etc. als auch die Unfähigkeit, sich neues Material bleibend anzueignen (anterograde Amnesie). Entsprechend vielfältig sind die mit Amnesien verbundenen Störungsbilder: großflächige Hirnschäden, die zu Demenzen führen, distinkte Hirnschäden, die mit anterograden (und teilweise auch mit retrograden) Amnesien verbunden sind, und funktionelle oder dissoziative Amnesien, die teilweise reversibel sind und deswegen auch als mnestisches Blockadesyndrom bezeichnet werden. Gerade dieser letzte – psychogene – Bereich ist schon seit Sigmund Freud mit vergessensnahen Phänomenen wie Verdrängen, Täuschen, Fehlerinnerungen haben oder Nicht-vergessen-Können verbunden. Alle diese Phänomene werden – auch anhand von Beispielsfällen und eigenen Daten – diskutiert.
During the past years brain imaging techniques like positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) became more and more important for gaining new insights into processes of and circuits for memory encoding and retrieval. These findings also had a great impact on a better understanding of memory dysfunctions and their underlying brain mechanisms. In the present review, data on memory dysfunctions are analyzed separately according to whether they are of an organic, or a psychiatric psychogenic etiology. Studies examining patients with various forms of amnesia and dementia, for whom functional brain imaging data were available, indicate early functional brain changes. These early changes differ from subsequent structural brain changes and therefore support the clinical and diagnostic use of functional brain imaging techniques in memory disturbances. Furthermore, research outcomes from patients suffering from psychogenic amnesias (dissociative amnesias) and psychogenic fugue conditions are summarized. Finally, differences and similarities between organic amnesia and psychogenic amnesia are discussed with regard to the present literature and exemplified with two single cases from our lab.
The authors examined whether perception of emotional stimuli is normal in amnesia and whether emotional arousal has the same enhancing effect on memory in amnesic patients as it has in healthy controls. Forty standardized color pictures were presented while participants rated each picture according to emotional intensity (arousal) and pleasantness (valence). An immediate free-recall test was given for the pictures, followed by a yes-no recognition test. Arousal and valence ratings were highly similar among the amnesic patients and controls. Emotional arousal (regardless of valence) enhanced both recall and recognition of the pictures, and this enhancement was proportional for amnesic patients and controls. Results suggest that emotional perception and the enhancing effect of emotional arousal on memory are intact in amnesia. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Abstract A 34-year-old man without a past history of any psychiatric or neurological disorder developed severe anterograde amnesia following a psychological trauma. Initial assessment of neuropsychological functions 3 months after the psychological trauma indicated severe memory deficits for acquiring new information in both verbal and visual modalities with widespread cognitive deficits in attention, executive functions, and intellectual ability. Importantly, working and remote memory were intact. The case illustrates that psychogenic anterograde amnesia might be associated with a wider range of cognitive deficits. Possible neurobiological explanations are discussed to explain large cognitive impairments associated with anterograde psychogenic amnesia.
Previous results from research on individuals with Asperger syndrome (AS) suggest a diminished ability for recalling episodic autobiographical memory (AM). The primary aim of this study was to explore autobiographical memory in individuals with Asperger syndrome and specifically to investigate whether memories in those with AS are characterized by fewer episodic 'remembered' events (due to a deficit in autonoetic consciousness). A further aim was to examine whether such changes in AM might also be related to changes in identity, due to the close relationship between memory and the self and to the established differences in self-referential processes in AS. Eleven adults with AS and fifteen matched comparison participants were asked to recall autobiographical memories from three lifetime periods and for each memory to give either a remember response (autonoetic consciousness) or a know response (noetic consciousness). The pattern of results shows that AS participants recalled fewer memories and that these memories were more often rated as known, compared to the comparison group. AS participants also showed differences in reported identity, generating fewer social identity statements and more abstract, trait-linked identities. The data support the view that differences in both memory and reported personal identities in AS are characterized by a lack of specificity.
Psychogenic amnesia is a complex disorder characterised by a wide variety of symptoms. Consequently, in a number of cases it is difficult distinguish it from organic memory impairment. The present study reports a new case of global psychogenic amnesia compared with two patients with amnesia underlain by organic brain damage. Our aim was to identify features useful for distinguishing between psychogenic and organic forms of memory impairment. The findings show the usefulness of a multidimensional evaluation of clinical, neuroradiological, neuropsychological and psychopathological aspects, to provide convergent findings useful for differentiating the two forms of memory disorder.
Memory disturbances belong to the most common concomitants of various forms of brain damage. During the last years it became established that there are varying relations between certain forms and etiologies of brain damage and impaired versus preserved memory domains. Nevertheless the dominant view in brain research is that a measurable damage of neuronal tissue has to be present in cases with persisting forms of amnesia. This view is challenged by recent data on patients with minor brain or skull damage, other forms of traumatic influences on the body, or psychic alterations due to pure (aversive) environmental stimulation. The presently available reports on this principally psychogenic forms of amnesia are listed and discussed.
Memory is one of the most complex and important human brain functions. It can be subdivided along dimensions time (e.g., short and long-term-memory) or contents (e.g., episodic and semantic memory), and according to the stages of information processing (encoding, consolidation, storage, and retrieval of information). It is assumed that in different memory processes specific brain structures, so called ‘bottleneck structures’ (e.g., Markowitsch, 1995b), are primarily involved. Amnesic syndromes can therefore occur as a consequence of widespread brain damage, such as in Alzheimer’s disease, as well as after tiniest lesions or functional alterations of the brain.
Extensive neuropsychological testing is reported on two chronic patients with combined temporopolar and prefrontal damage, dominantly left-hemispheric, and, as control, one chronic patient with bi-hemispheric prefrontal damage. The principal finding is that combined temporofrontal damage, but not substantial prefrontal damage alone, results in marked retrograde memory deficits while leaving intelligence and new learning relatively unimpaired. Although their general world knowledge was good, the temporopolar patients demonstrated retrograde memory impairments on several tests of past events and faces of previously famous people. With respect to retrograde autobiographical memory, one of the temporopolar patients was severely impaired and the other was judged to be moderately impaired. The control patient appeared to be normal. These results, together with corresponding data from related single case and dynamic imaging studies, strongly support a crucial role of the temporofrontal junction area in the ecphory of old memories.
The focus of this article is the assessment and management of medically unexplained ('psychogenic') amnesia, which we classify here as global or situation specific. Other psychiatric causes for memory disorder and neurological conditions that could cause diagnostic confusion are briefly reviewed, as are forensic aspects of memory complaints. Finally, brain and physiological mechanisms potentially associated with psychogenic amnesia are discussed.
Examined 25 consecutive psychogenic amnesia patients (aged 17–51 yrs) diagnosed with modified Diagnostic and Statistical Manual of Mental Disorders-III-Revised (DSM-III-R) criteria using an extensive clinical history, mental status examination, collateral interviews, neurological examination, EEG, intelligence testing, MMPI, and a dissociative experiences scale. In most cases the amnesia was selective, chronic, and not of sudden onset. There were multiple stressful psychological precipitants. There were many similarities to 50 patients with multiple personality disorder, providing further proof that dissociative disorders occur along a dissociative spectrum. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
In functional amnesia, there is an inhibition by a subconscious mechanism, which attacks, not directly the function of thinking again the past experience, but the specific striving which was at work relative to the experience on its occurrence. Such inhibition modifies the meaning of the experience, so as to make it appear strange, foreign, and without feeling of personal reference. The subject suffering from amnesia is able to think the event; if it is related to him, he grasps cognitively the story told, but this story is not experienced as something that has happened to him in the past or as a personal experience of his own. If the story of the event is told to him he will not spontaneously and voluntarily think of it, for the reason that there is no incentive for so doing, the event, by the inhibition referred to, having become indifferent to him. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Neuroimaging results from research into schizophrenic and affective disorders are reviewed and commented on, including methodological problems and pitfalls inherent in interpreting imaging data. The wealth and methodological diversity of neuroimaging data in all fields of psychiatry have led to an enormous amount of findings that cover both gross brain alterations and such minute focal changes as glial reductions in a single Brodmann area. Many of these findings tend to narrow the traditional gap between neurological and psychiatric approaches in defining a disease process.
While amnesia and other cognitive disturbances are usually caused by structural brain damage, there are a few instances in which environmental stress may induce neuronal death in memory-sensitive brain regions such as the hippocampus. Here we report on a patient who, after a single brief exposure to an event reminding him of a similar stressful event from his childhood, deteriorated immediately and persistently without manifesting structural, but manifesting functional, brain damage as measured by position emission tomography. This patient probably represents the first case in which a direct relation between a single psychic event and the occurrence of brain malfunctioning in cognition is documented by dynamic neuroimaging methods. Psychic shock may cause lasting reductions in brain metabolism with the consequence of severe intellectual malfunctioning.
Autobiographical-episodic memory is the conjunction of subjective time, autonoetic consciousness and the experiencing self. Understanding the neural correlates of autobiographical-episodic memory might therefore be essential for shedding light on the neurobiology underlying the experience of being an autonoetic self. In this contribution we illustrate the intimate relationship between autobiographical-episodic memory and self by reviewing the clinical and neuropsychological features and brain functional imaging correlates of psychogenic amnesia - a condition that is usually characterized by severely impaired retrograde memory functioning, in absence of structural brain damage as detected by standard imaging. We demonstrate that in this disorder the autobiographical-episodic memory deficits do not exist in isolation, but occur with impairments of the autonoetic self-consciousness, emotional processing, and theory of mind or executive functions. Furthermore functional and metabolic brain alterations involving regions that are agreed upon to exert crucial roles in memory processes were frequently found to accompany the psychogenic memory "loss".
Functional amnesia (FA) is characterized by an extensive retrograde memory loss in the absence of detectable structural brain damage. The two main hypotheses put forward to explain this disturbance involve a global retrieval deficit (affecting both pre- and post-onset memories) and a selective inability to explicitly retrieve pre-onset memories. Here, we extensively examined P.P., a patient with FA, with a view to obtaining additional insights into the cognitive and neural mechanisms underlying this disorder. In Experiments 1 and 2, post-onset memories were assessed using tasks focusing on the state of consciousness associated with their retrieval. Although subtle deficits in the ability to recollect post-onset personal events were detected, P.P.'s performances were normal when the encoding of the event was monitored in a laboratory setting. In Experiment 3, implicit recognition of pre-onset memories was tested using skin conductance responses. Results showed that P.P. responded implicitly to photographs of personal pre-onset events that were not explicitly recognized. In Experiment 4, designed to assess the patient's ability to suppress newly acquired information, P.P. suppressed more items than controls. Additionally, while no grey matter loss was evidenced with voxel-based morphometry, magnetic resonance spectroscopy and magnetization transfer imaging showed significant metabolic and structural changes within the white matter of the right prefrontal lobe. In conclusion, our results suggest that FA may result from a combination between two processes, a "hypo-retrieval" of pre-onset memories, tentatively due to white matter tract damage, and a "hyper-suppression" mechanism, concomitantly preventing the retrieval of pre-onset memories.
After an infarction in the territory of the anterior perforating arteries, a 15-year-old, previously healthy, left-handed patient developed considerable verbal long term memory disturbances which could be followed up and tested for more than nine months. An extensive memory test battery was used to determine spared and impaired functions. The patient had remote memory disturbances with respect to personal events for the last 5 years and problems in all verbal task tested which required remembering items over time periods exceeding an hour. The patient was indistinguishable from control subjects on short-term memory tests and on a number of nonverbal learning and recognition tests. The crucial lesion for the observed deficits in the genu of the left internal capsule was assumed to have disrupted the anterior and inferior thalamic peduncles, fornix (column), stria terminalis, anterior commissure and the medial part of the globus pallidus. This infarct, therefore, most likely damaged traversing fibres which intercommunicate within the Papez circuit and the basolateral limbic circuit and which in part provide access to cortical memory representing areas.
The principal thalamic and hypothalamic structures implicated in mnemonic information processing are the mediodorsal nucleus of the thalamus, the pulvinar, anterior thalamus, and laterodorsal nucleus, the mamillary body, and the mamillothalamic tract and internal medullary lamina. Determining the contribution of an individual region in memory is quite difficult as it is nearly impossible to find a circumscribed damage of only one region. On the contrary, some illnesses affecting primarily the diencephalon, such as Korsakoff's disease, tend to involve several structures together. Furthermore, even when cases with similar circumscribed diencephalic damage can be found, these will not necessarily demonstrate the same outcome on the behavioral level. Therefore, the role or contribution of individual memory-related diencephalic structures has to be inferred by comparing a number of cases and by then extracting distinct features common to a given group. Such an approach revealed that the contributions of the two fiber systems mentioned above, mamillothalamic tract and internal medullary lamina, might be more important in processing information long-term than had been acknowledged previously and might be more important than that of the nuclear masses mentioned, especially of the mediodorsal thalamus. This outcome underlines the view that emphasizing interactions between brain regions rather than single static masses will provide a more realistic picture of how the nervous system acts in information processing.
We studied 11 patients with amnesia and personality change after surgical repair of ruptured anterior communicating artery ( ACoA ) aneurysm. CT and clinical evidence suggested that infarction in the territory of the ACoA was responsible for amnesia and personality change. The medial septal nuclei, the paraventricular nucleus of the anterior hypothalamus, and the medial forebrain bundle are the primary areas of potential interest in these cases. Gross infarction in the frontal lobes is not a requirement for the syndrome.
We report two cases of recovery from retrograde amnesia, which occurred almost suddenly, 1 year and 1 month from onset, respectively. Amnesia followed a left thalamic infarction in one patient and a mild head trauma in the other. Full and permanent recovery occurred within a short time after the spontaneous emergence to consciousness of a single autobiographical event, triggered by the specific experience of a very similar new event. Recovery was limited to retrograde amnesia, leaving unaffected the anterograde deficit present in one of the patients. The nature (psychogenic versus organic) of our patients' memory loss is commented upon in the light of a review of previously reported cases of retrograde amnesia. The transient defect of retrograde memory is discussed in terms of a reversible distortion of the neuronal 'patterned matrices' suggested by Gloor (Brain 1990; 113: 1673-94).
The case of a patient with above-average intelligence and educational background, high motivation, and an approximate IQ-MQ difference of 40 points is documented. The patient has been examined repeatedly for nearly a decade. Extensive neuroradiological material of his focal bilateral brain damage in the dorsal diencephalon is available. A widespread range of cognitive tests was used to investigate his actual performance on all relevant aspects of intelligence, attention, subjective memory, immediate retention, learning, skill and problem solving abilities, concept formation, cognitive flexibility, priming, constructional ability, retrograde memory, and long-term retention. The total of more than 50 tests included German-language forms of the revised Wechsler Memory Scale and of the Rivermead Behavioural Memory Test. The patient's short-term memory and attention were, in spite of his advanced years, average or well above average. He gave a number of examples of still intact skills and implicit memory abilities, though there was no uniformity in his performance on implicit memory tests (e.g., with respect to stored vs. new implicit information). He had no awareness of his severe anterograde and retrograde amnesia, documented over a large range of verbal and figural tests. Taken together, the results from our patient confirm the principal dichotomy between declarative and nondeclarative mnestic functions, but give evidence for some restrictions as well. They furthermore demonstrate that focal diencephalic damage may result in profound anterograde and selective retrograde amnesia, especially with respect to data-based material, and that disconnecting portions of the medial and basolateral limbic circuits has devastating consequences on memory.
In almost all cases of acute, sudden, persistent amnesia, the cause can be determined. Ischemic stroke, hypoglycemia, syncope, and seizure are the most likely causes.
In a clinical study, 2 elderly men are described in which sudden, permanent amnesia developed in the absence of a satisfactory explanation. In 1 case, a neuropathologic study disclosed Alzheimer disease; in the other, magnetic resonance imaging showed a temporal lobe abnormality bilaterally.
A man aged 80 years suddenly lost his memory of the previous 60 years. Neuropathologic study 5 years later showed the changes of Alzheimer disease. In the second case a disabling amnesia developed overnight in a man aged 70 years. There was no progression of the disabling amnesia in the next 15 years. Magnetic resonance imaging 10 years from the onset showed abnormality of the medial temporal lobe bilaterally.
In neither case was the amnesia satisfactorily explained. It is likely that rare cases of amnesia occur as the result of an unrecognized pathophysiologic process.
We report a long-term follow-up study of case JM, who demonstrated a focal retrograde amnesia (FRA) as a consequence of cerebral vasculitis. The present study showed that, several years post-onset, JM experienced considerable impairment in episodic retrograde memory, with normal anterograde autobiographical memory. Further investigations demonstrated that she showed no evidence of accelerated forgetting, unlike some other cases of FRA. Knowledge of people, pre- and post-illness, was also normal. Her ability to recall details of famous public events was good (though weaker for pre-illness events). JM's pattern of impairment is discussed in the context of other recent cases of FRA and developments in models of normal memory function.
Autobiographical memory relies on complex interactions between episodic memory contents, associated emotions and a sense of self-continuity over the course of one's life. This paper reports a study based upon the case of the patient NN who suffered from a complete loss of autobiographical memory and awareness of identity subsequent to a dissociative fugue. Neuropsychological, behavioral, and functional neuroimaging tests converged on the conclusion that NN suffered from a selective retrograde amnesia following an episode of dissociative fugue, during which he had lost explicit knowledge and vivid memory of his personal past. NN's loss of self-related memories was mirrored in neurobiological changes after the fugue whereas his semantic memory remained intact. Although NN still claimed to suffer from a stable loss of autobiographical, self-relevant memories 1 year after the fugue state, a proportionate improvement in underlying fronto-temporal neuronal networks was evident at this point in time. In spite of this improvement in neuronal activation, his anterograde visual memory had been decreased. It is posited that our data provide evidence for the important role of visual processing in autobiographical memory as well as for the efficiency of protective control mechanisms that constitute functional retrograde amnesia.