Dissociative amnesia

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Dissociative amnesia
Other namesPsychogenic amnesia
Brain-imaging data.jpg
Brain-imaging data from two patients with dissociative amnesia
Specialty Psychiatry
Symptoms Memory loss [1]

Dissociative amnesia or psychogenic amnesia is a dissociative disorder "characterized by retrospectively reported memory gaps. These gaps involve an inability to recall personal information, usually of a traumatic or stressful nature." [1] In a change from the DSM-IV to the DSM-5, dissociative fugue is now subsumed under dissociative amnesia. [2]

Contents

Dissociative amnesia was previously known as psychogenic amnesia, a memory disorder, which was characterized by sudden retrograde episodic memory loss, said to occur for a period of time ranging from hours to years to decades. [3]

The atypical clinical syndrome of the memory disorder (as opposed to organic amnesia) is that a person with psychogenic amnesia is profoundly unable to remember personal information about themselves; there is a lack of conscious self-knowledge which affects even simple self-knowledge, such as who they are. [4] Psychogenic amnesia is distinguished from organic amnesia in that it is supposed to result from a nonorganic cause: no structural brain damage should be evident but some form of psychological stress should precipitate the amnesia. [5] Psychogenic amnesia as a memory disorder is controversial. [6]

Definition

Psychogenic amnesia is the presence of retrograde amnesia (the inability to retrieve stored memories leading up to the onset of amnesia), and an absence of anterograde amnesia (the inability to form new long term memories). [7] [8] [9] Access to episodic memory can be impeded, [3] while the degree of impairment to short term memory, semantic memory and procedural memory is thought to vary among cases. [4] If other memory processes are affected, they are usually much less severely affected than retrograde autobiographical memory, which is taken as the hallmark of psychogenic amnesia. [4] However the wide variability of memory impairment among cases of psychogenic amnesia raises questions as to its true neuropsychological criteria, as despite intense study of a wide range of cases there is little consensus of which memory deficits are specific to psychogenic amnesia. [6]

Past literature [4] has suggested psychogenic amnesia can be 'situation-specific' or 'global-transient', the former referring to memory loss for a particular incident, and the latter relating to large retrograde amnesic gaps of up to many years in personal identity. [4] [10] The most commonly cited examples of global-transient psychogenic amnesia are 'fugue states', of which there is a sudden retrograde loss of autobiographical memory resulting in impairment of personal identity and usually accompanied by a period of wandering. [6] Suspected cases of psychogenic amnesia have been heavily reported throughout the literature since 1935 where it was reported by Abeles and Schilder. [11] There are many clinical anecdotes of psychogenic or dissociative amnesia attributed to stressors ranging from cases of child sexual abuse [12] to soldiers returning from combat. [1] [13]

Cause

The neurological cause of psychogenic amnesia is controversial. [4] [6] Even in cases of organic amnesia, where there is lesion or structural damage to the brain, caution must still be taken in defining causation, as only damage to areas of the brain crucial to memory processing is possible to result in memory impairment. [6] Organic causes of amnesia can be difficult to detect, and often both organic cause and psychological triggers can be entangled. [14] Failure to find an organic cause may result in the diagnosis that the amnesia is psychological, [15] however it is possible that some organic causes may fall below a threshold of detection, while other neurological ails are thought to be unequivocally organic (such as a migraine) even though no functional damage is evident. [6] Possible malingering must also be taken into account. [16] Some researchers [15] have cautioned against psychogenic amnesia becoming a "wastebasket" [15] diagnosis when organic amnesia is not apparent. Other researchers [16] have hastened to defend the notion of psychogenic amnesia and its right not to be dismissed as a clinical disorder. Diagnoses of psychogenic amnesia have dropped since agreement in the field of transient global amnesia, suggesting some over diagnosis at least. [15] Speculation also exists about psychogenic amnesia due to its similarities with 'pure retrograde amnesia', as both share similar retrograde loss of memory. [6] Also, although no functional damage or brain lesions are evident in the case of pure retrograde amnesia, unlike psychogenic amnesia it is not thought that purely psychological or 'psychogenic triggers' are relevant to pure retrograde amnesia. [6] Psychological triggers such as emotional stress are common in everyday life, yet pure retrograde amnesia is considered very rare. [6] Also the potential for organic damage to fall below threshold of being identified does not necessarily mean it is not present, and it is highly likely that both psychological factors and organic cause exist in pure retrograde amnesia. [6]

Comparison with organic amnesia

Psychogenic amnesia is supposed to differ from organic amnesia in a number of ways; one being that unlike organic amnesia, psychogenic amnesia is thought to occur when no structural damage to the brain or brain lesion is evident. [17] Psychological triggers are instead considered as preceding psychogenic amnesia, [16] and indeed many anecdotal case studies which are cited as evidence of psychogenic amnesia hail from traumatic experiences [12] such as World War II. [13] As aforementioned however, an etiology of psychogenic amnesia is controversial [4] as causation is not always clear, [17] and both elements of psychological stress and organic amnesia may be present among cases. [6] Often, but not necessarily, a premorbid history of psychiatric illness such as depression is thought to be present in conjunction to triggers of psychological stress. [4] Lack of psychological evidence precipitating amnesia does not mean there is not any, for example trauma during childhood has even been cited as triggering amnesia later in life, [3] but such an argument runs the risk of psychogenic amnesia becoming an umbrella term for any amnesia of which there is no apparent organic cause. [15] Due to organic amnesia often being difficult to detect, [17] defining between organic and psychogenic amnesia is not easy [16] and often context of precipitating experiences are considered (for example, if there has been drug abuse) as well as the symptomology the patient presents with. [17] Psychogenic amnesia is supposed to differ from organic amnesia qualitatively [4] in that retrograde loss of autobiographical memory while semantic memory remains intact is said to be specific of psychogenic amnesia. [3] [4] Another difference that has been cited between organic and psychogenic amnesia is the temporal gradient of retrograde loss of autobiographical memory. [4] The temporal gradient of loss in most cases of organic amnesia is said to be steepest at its most recent premorbid period, whereas for psychogenic amnesia the temporal gradient of retrograde autobiographical memory loss is said to be quite consistently flat. [4] Although there is much literature on psychogenic amnesia as dissimilar to organic amnesia, the distinction between neurological and psychological features is often difficult to discern and remains controversial. [18] [19] [20]

Diagnosis

Brain activity can be assessed functionally for psychogenic amnesia using imaging techniques such as fMRI, PET and EEG, in accordance with clinical data. [6] Some research has suggested that organic and psychogenic amnesia to some extent share the involvement of the same structures of the temporo-frontal region in the brain. [7] It has been suggested that deficits in episodic memory may be attributable to dysfunction in the limbic system, [21] while self-identity deficits have been suggested as attributable to functional changes related to the posterior parietal cortex. [3] To reiterate however, care must be taken when attempting to define causation as only ad hoc reasoning about the aetiology of psychogenic amnesia is possible, which means cause and consequence can be infeasible to untangle. [15]

Treatments

Because psychogenic amnesia is defined by its lack of physical damage to the brain, [15] treatment by physical methods is difficult. [6] Nonetheless, distinguishing between organic and dissociative memory loss has been described as an essential first-step in effective treatments. [1] Treatments in the past have attempted to alleve psychogenic amnesia by treating the mind itself, as guided by theories which range from notions such as 'betrayal theory' to account for memory loss attributed to protracted abuse by caregivers [22] to the amnesia as a form of self-punishment in a Freudian sense, with the obliteration of personal identity as an alternative to suicide. [23]

Treatment attempts often have revolved around trying to discover what traumatic event had caused the amnesia, and drugs such as intravenously administered barbiturates (often thought of as 'truth serum') were popular as treatment for psychogenic amnesia during World War II; benzodiazepines may have been substituted later. [13] 'Truth serum' drugs were thought to work by making a painful memory more tolerable when expressed through relieving the strength of an emotion attached to a memory. [24] Under the influence of these 'truth' drugs the patient would more readily talk about what had occurred to them. [13] However, information elicited from patients under the influence of drugs such as barbiturates would be a mixture of truth and fantasy, and was thus not regarded as scientific in gathering accurate evidence for past events. [13] Often treatment was aimed at treating the patient as a whole, and probably varied in practice in different places. [13] Hypnosis was also popular as a means for gaining information from people about their past experiences, but like 'truth' drugs really only served to lower the threshold of suggestibility so that the patient would speak easily but not necessarily truthfully. [25] If no motive for the amnesia was immediately apparent, deeper motives were usually sought by questioning the patient more intensely, often in conjunction with hypnosis and 'truth' drugs. [23] In many cases, however, patients were found to spontaneously recover from their amnesia on their own accord so no treatment was required. [13] [23]

Controversy

It has been argued by critics of the concept of repressed memories that dissociative amnesia is merely a rebranding of the repressed memory concept. [26]

Dissociative amnesia is a common fictional plot device in many films, books and other media. Examples include William Shakespeare's King Lear , who experienced amnesia and madness following a betrayal by his daughters; [27] and the title character Nina in Nicolas Dalayrac's 1786 opera. [27] Sunny, the title character in Omocat's Omori, is suspected of having dissociative amnesia becoming a hikikomori after accidentally killing his older sister. [28]

See also

Related Research Articles

<span class="mw-page-title-main">Dissociative fugue</span> Dissociative disorder

Dissociative fugue, formerly called a fugue state or psychogenic fugue, is a rare psychiatric phenomenon characterized by reversible amnesia for one's identity in conjunction with unexpected wandering or travel. This is sometimes accompanied by the establishment of a new identity and the inability to recall personal information prior to the presentation of symptoms. Dissociative fugue is a mental and behavioral disorder that is classified variously as a dissociative disorder, a conversion disorder, and a somatic symptom disorder. It is a facet of dissociative amnesia, according to the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5).

Capgras delusion or Capgras syndrome is a psychiatric disorder in which a person holds a delusion that a friend, spouse, parent, another close family member, or pet has been replaced by an identical impostor. It is named after Joseph Capgras (1873–1950), the French psychiatrist who first described the disorder.

<span class="mw-page-title-main">Korsakoff syndrome</span> Mental illness caused by a lack of thiamine in the brain

Korsakoff syndrome (KS) is a disorder of the central nervous system characterized by amnesia, deficits in explicit memory, and confabulation. This neurological disorder is caused by a deficiency of thiamine (vitamin B1) in the brain, and it is typically associated with and exacerbated by the prolonged, excessive ingestion of alcohol. Korsakoff syndrome is often accompanied by Wernicke encephalopathy; this combination is called Wernicke–Korsakoff syndrome.

Dissociation is a concept that has been developed over time and which concerns a wide array of experiences, ranging from a mild emotional detachment from the immediate surroundings, to a more severe disconnection from physical and emotional experiences. The major characteristic of all dissociative phenomena involves a detachment from reality, rather than a false perception of reality as in psychosis.

In neurology, anterograde amnesia is the inability to create new memories after an event that caused amnesia, leading to a partial or complete inability to recall the recent past, while long-term memories from before the event remain intact. This is in contrast to retrograde amnesia, where memories created prior to the event are lost while new memories can still be created. Both can occur together in the same patient. To a large degree, anterograde amnesia remains a mysterious ailment because the precise mechanism of storing memories is not yet well understood, although it is known that the regions of the brain involved are certain sites in the temporal cortex, especially in the hippocampus and nearby subcortical regions.

<span class="mw-page-title-main">Conversion disorder</span> Diagnostic category used in some psychiatric classification systems

Conversion disorder (CD), or functional neurologic symptom disorder, is a diagnostic category used in some psychiatric classification systems. It is sometimes applied to patients who present with neurological symptoms, such as numbness, blindness, paralysis, or fits, which are not consistent with a well-established organic cause, which cause significant distress, and can be traced back to a psychological trigger. It is thought that these symptoms arise in response to stressful situations affecting a patient's mental health or an ongoing mental health condition such as depression. Conversion disorder was retained in DSM-5, but given the subtitle functional neurological symptom disorder. The new criteria cover the same range of symptoms, but remove the requirements for a psychological stressor to be present and for feigning to be disproved. The ICD-10 classifies conversion disorder as a dissociative disorder, and the ICD-11 as a dissociative disorder with unspecified neurological symptoms. However, the DSM-IV classifies conversion disorder as a somatoform disorder.

In neurology, retrograde amnesia (RA) is the inability to access memories or information from before an injury or disease occurred. RA differs from a similar condition called anterograde amnesia (AA), which is the inability to form new memories following injury or disease onset. Although an individual can have both RA and AA at the same time, RA can also occur on its own; this 'pure' form of RA can be further divided into three types: focal, isolated, and pure RA. RA negatively affects an individual's episodic, autobiographical, and declarative memory, but they can still form new memories because RA leaves procedural memory intact. Depending on its severity, RA can result in either temporally graded or more permanent memory loss. However, memory loss usually follows Ribot's law, which states that individuals are more likely to lose recent memories than older memories. Diagnosing RA generally requires using an Autobiographical Memory Interview (AMI) and observing brain structure through magnetic resonance imaging (MRI), a computed tomography scan (CT), or electroencephalography (EEG).

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<span class="mw-page-title-main">Transient global amnesia</span> Temporary disruption of short-term memory

Transient global amnesia (TGA) is a neurological disorder whose key defining characteristic is a temporary but almost total disruption of short-term memory with a range of problems accessing older memories. A person in a state of TGA exhibits no other signs of impaired cognitive functioning but recalls only the last few moments of consciousness, as well as possibly a few deeply encoded facts of the individual's past, such as their childhood, family, or home perhaps.

<span class="mw-page-title-main">Organic brain syndrome</span> Disorder of mental function whose cause is alleged to be known as physiological

Organic brain syndrome, also known as organic brain disease, organic brain damage, organic brain disorder, organic mental syndrome, or organic mental disorder, refers to any syndrome or disorder of mental function whose cause is alleged to be known as organic (physiologic) rather than purely of the mind. These names are older and nearly obsolete general terms from psychiatry, referring to many physical disorders that cause impaired mental function. They are meant to exclude psychiatric disorders. Originally, the term was created to distinguish physical causes of mental impairment from psychiatric disorders, but during the era when this distinction was drawn, not enough was known about brain science for this cause-based classification to be more than educated guesswork labeled with misplaced certainty, which is why it has been deemphasized in current medicine. While mental or behavioural abnormalities related to the dysfunction can be permanent, treating the disease early may prevent permanent damage in addition to fully restoring mental functions. An organic cause to brain dysfunction is suspected when there is no indication of a clearly defined psychiatric or "inorganic" cause, such as a mood disorder.

Classified as a "conversion disorder" by the DSM-IV, a psychogenic disease is a condition in which mental stressors cause physical symptoms matching other disorders. The manifestation of physical symptoms without biologically identifiable cause results from disruptions in normal brain function due to psychological stress. During a psychogenic episode, neuroimaging has shown that neural circuits affecting functions such as emotion, executive functioning, perception, movement, and volition are inhibited. These disruptions become strong enough to prevent the brain from voluntarily allowing certain actions. When the brain is unable to signal to the body to perform an action voluntarily, physical symptoms of a disorder arise. Examples of diseases that are deemed to be psychogenic in origin include psychogenic seizures, psychogenic polydipsia, psychogenic tremor, and psychogenic pain.

Post-traumatic amnesia (PTA) is a state of confusion that occurs immediately following a traumatic brain injury (TBI) in which the injured person is disoriented and unable to remember events that occur after the injury. The person may be unable to state their name, where they are, and what time it is. When continuous memory returns, PTA is considered to have resolved. While PTA lasts, new events cannot be stored in the memory. About a third of patients with mild head injury are reported to have "islands of memory", in which the patient can recall only some events. During PTA, the patient's consciousness is "clouded". Because PTA involves confusion in addition to the memory loss typical of amnesia, the term "post-traumatic confusional state" has been proposed as an alternative.

Transient epileptic amnesia (TEA) is a rare but probably underdiagnosed neurological condition which manifests as relatively brief and generally recurring episodes of amnesia caused by underlying temporal lobe epilepsy. Though descriptions of the condition are based on fewer than 100 cases published in the medical literature, and the largest single study to date included 50 people with TEA, TEA offers considerable theoretical significance as competing theories of human memory attempt to reconcile its implications.

<span class="mw-page-title-main">Neurological disorder</span> Any disorder of the nervous system

A neurological disorder is any disorder of the nervous system. Structural, biochemical or electrical abnormalities in the brain, spinal cord or other nerves can result in a range of symptoms. Examples of symptoms include paralysis, muscle weakness, poor coordination, loss of sensation, seizures, confusion, pain, tauopathies, and altered levels of consciousness. There are many recognized neurological disorders, some relatively common, but many rare. They may be assessed by neurological examination, and studied and treated within the specialties of neurology and clinical neuropsychology.

Amnesia is a deficit in memory caused by brain damage or brain diseases, but it can also be temporarily caused by the use of various sedative and hypnotic drugs. The memory can be either wholly or partially lost due to the extent of damage that is caused.

Motivated forgetting is a theorized psychological behavior in which people may forget unwanted memories, either consciously or unconsciously. It is an example of defence mechanism, since these are unconscious or conscious coping techniques used to reduce anxiety arising from unacceptable or potentially harmful impulses thus it can be a defence mechanism in some ways. Defence mechanisms are not to be confused with conscious coping strategies.

In psychology, confabulation is a memory error consisting of the production of fabricated, distorted, or misinterpreted memories about oneself or the world. It is generally associated with certain types of brain damage or a specific subset of dementias. While still an area of ongoing research, the basal forebrain is implicated in the phenomenon of confabulation. People who confabulate present with incorrect memories ranging from subtle inaccuracies to surreal fabrications, and may include confusion or distortion in the temporal framing of memories. In general, they are very confident about their recollections, even when challenged with contradictory evidence.

Functional neurologic disorder or functional neurological disorder (FND) is a condition in which patients experience neurological symptoms such as weakness, movement disorders, sensory symptoms, and blackouts. As a functional disorder, there is by definition no known disease process affecting the structure of the body, yet the person experiences symptoms relating to their body function. Symptoms of functional neurological disorders are clinically recognisable, but are not categorically associated with a definable organic disease.

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