In many cases of acute dissociative amnesia, the psychosocial environment out of which the amnesia develops is massively conflictual, with the patient experiencing intolerable emotions of shame, guilt, despair, rage, and desperation. These usually result from conflicts over unacceptable urges or impulses, such as intense sexual, suicidal, or violent compulsions.

Betrayal trauma attempts to explain amnesia by the intensity of trauma and by the extent that a negative event represents a betrayal by a trusted, needed other. This betrayal is thought to influence the way in which the event is processed and remembered. Information about the abuse is not linked to mental mechanisms that control attachment and attachment behavior.

The classic disorder is an overt, florid, dramatic clinical disturbance that frequently results in the patient being brought quickly to medical attention specifically for symptoms related to the dissociative disorder. It is frequently found in those who have experienced extreme acute trauma. It also commonly develops, however, in the context of profound intrapsychic conflict or emotional stress. Patients may present with intercurrent somatoform or conversion symptoms, alterations in consciousness, depersonalization, derealization, trance states, spontaneous age regression, and even ongoing anterograde dissociative amnesia. Depression and suicidal ideation are reported in many cases. No single personality profile or antecedent history is consistently reported in these patients, although a prior personal or family history of somatoform or dissociative symptoms has been shown to predispose individuals to develop acute amnesia during traumatic circumstances. Many of these patients have histories of prior adult or childhood abuse or trauma. In wartime cases, as in other forms of combat-related posttraumatic disorders, the most important variable in the development of dissociative symptoms, however, appears to be the intensity of combat.

These patients frequently come to treatment for a variety of symptoms, such as depression or mood swings, substance abuse, sleep disturbances, somatoform symptoms, anxiety and panic, suicidal or self-mutilating impulses and acts, violent outbursts, eating problems, and interpersonal problems. Self-mutilation and violent behavior in these patients may also be accompanied by amnesia. Amnesia may also occur for flashbacks or behavioral reexperiencing episodes related to trauma.

The DSM-IV-TR diagnostic criteria for dissociative amnesia specify that the disturbance must be “too extensive to be explained by normal forgetfulness.” Furthermore, nonpathological forms of amnesia have been described, such as infantile and childhood amnesia, amnesia for sleep and dreaming, and hypnotic amnesia.

In patients with dementia, organic amnestic disorders, and delirium, the memory loss for personal information is embedded in a far more extensive set of cognitive, language, attentional, behavioral, and memory problems. Loss of memory for personal identity is usually not found without evidence of a marked disturbance in many domains of cognitive function. Causes of organic amnestic disorders include Korsakoff’s psychosis, cerebral vascular accident, postoperative amnesia, postinfectious amnesia, anoxic amnesia, and transient global amnesia. Electroconvulsive therapy (ECT) may also cause a marked temporary amnesia, as well as persistent memory problems in some cases. Here, however, memory loss for autobiographical experience is unrelated to traumatic or overwhelming experiences and seems to involve many different types of personal experience, most commonly that occurring just before or during the ECT treatments.

In posttraumatic amnesia caused by brain injury, there is usually a history of a clear-cut physical trauma, a period of unconsciousness or amnesia or both, and objective clinical evidence of brain injury.

In most seizure cases, the clinical presentation differs significantly from that of dissociative amnesia, with clear-cut ictal events and sequelae. Patients with pseudoepileptic seizures may also have dissociative symptoms, such as amnesia and an antecedent history of psychological trauma. Rarely, patients with recurrent complex partial seizures present with ongoing bizarre behavior, memory problems, irritability, or violence, leading to a differential diagnostic puzzle. In some of these cases, the diagnosis can only be clarified by telemetry or ambulatory electroencephalographic (EEG) monitoring.

A variety of substances and intoxicants have been implicated in the production of amnesia.

Transient global amnesia can be mistaken for a dissociative amnesia, especially because stressful life events may precede either disorder. In transient global amnesia, however, there is the sudden onset of complete anterograde amnesia and learning abilities; pronounced retrograde amnesia; preservation of memory for personal identity; anxious awareness of memory loss with repeated, often perseverative, questioning; overall normal behavior; lack of gross neurological abnormalities in most cases; and rapid return of baseline cognitive function, with a persistent short retrograde amnesia. The patient usually is older than 50 years of age and shows risk factors for cerebrovascular disease, although epilepsy and migraine have been etiologically implicated in some cases.

Patients with dissociative identity disorder can present with acute forms of amnesia and fugue episodes. These patients, however, are characterized by a plethora of symptoms, only some of which are usually found in patients with dissociative amnesia. With respect to amnesia, most patients with dissociative identity disorder and those with dissociative disorder NOS with dissociative identity disorder features report multiple forms of complex amnesia, including recurrent blackouts, fugues, unexplained possessions, and fluctuations in skills, habits, and knowledge.

Most forms of dissociative amnesia are best conceptualized as part of a group of trauma spectrum disorders that includes acute stress disorder, PTSD, and somatization disorder. Many patients with dissociative amnesia meet full or partial diagnostic criteria for acute stress disorder, PTSD, or somatization disorder or a combination of these. Amnesia is a criterion symptom of each of the latter disorders. DSM-IV-TR stipulates that, to be diagnosed, the dissociative amnesia must be distinct from the course of acute stress disorder, PTSD, or somatization disorder. In practice, clinical judgment usually determines whether the extent of the amnesia warrants a separate dissociative diagnosis.

No absolute way exists to differentiate dissociative amnesia from factitious or malingered amnesia. Malingerers have been noted to continue their deception even during hypnotically or barbiturate-facilitated interviews. A patient who presents to psychiatric attention asking to recover repressed memories as a chief complaint most likely has a factitious disorder or has been subject to suggestive influences. Most of these individuals actually do not describe bona fide amnesia when carefully questioned, but are often insistent that they must have been abused in childhood to explain their unhappiness or life dysfunction.

Little is known about the clinical course of dissociative amnesia. Acute dissociative amnesia frequently spontaneously resolves once the person is removed to safety from traumatic or overwhelming circumstances. At the other extreme, some patients do develop chronic forms of generalized, continuous, or severe localized amnesia and are profoundly disabled and require high levels of social support, such as nursing home placement or intensive family caretaking. Clinicians should try to restore patients’ lost memories to consciousness as soon as possible; otherwise, the repressed memory may form a nucleus in the unconscious mind around which future amnestic episodes may develop.

Cognitive therapy may have specific benefits for individuals with trauma disorders. Identifying the specific cognitive distortions that are based in the trauma may provide an entrée into autobiographical memory for which the patient experiences amnesia. As the patient becomes able to correct cognitive distortions, particularly about the meaning of prior trauma, more-detailed recall of traumatic events may occur.

Hypnosis can be used in a number of ways in the treatment of dissociative amnesia. In particular, hypnotic interventions can be used to contain, modulate, and titrate the intensity of symptoms; to facilitate controlled recall of dissociated memories; to provide support and ego strengthening for the patient; and, finally, to promote working through and integration of dissociated material.

In addition, the patient can be taught self-hypnosis to apply containment and calming techniques in his or her everyday life. Successful use of containment techniques, whether hypnotically facilitated or not, also increases the patient’s sense that he or she can more effectively be in control of alternations between intrusive symptoms and amnesia.

No known pharmacotherapy exists for dissociative amnesia other than pharmacologically facilitated interviews. A variety of agents have been used for this purpose, including sodium amobarbital, thiopental (Pentothal), oral benzodiazepines, and amphetamines.

Pharmacologically facilitated interviews are used primarily in working with acute amnesias and conversion reactions, among other indications, in general hospital medical and psychiatric services. This procedure is also occasionally useful in refractory cases of chronic dissociative amnesia when patients are unresponsive to other interventions. The material uncovered in a pharmacologically facilitated interview needs to be processed by the patient in his or her usual conscious state.

Time-limited and longer-term group psychotherapies have been reported to be helpful for combat veterans with PTSD and for survivors of childhood abuse. During group sessions, patients may recover memories for which they have had amnesia. Supportive interventions by the group members or the group therapist, or both, may facilitate integration and mastery of the dissociated material.

Traditional psychodynamic formulations have emphasized the disintegration of the ego or have viewed depersonalization as an affective response in defense of the ego. These explanations stress the role of overwhelming painful experiences or conflictual impulses as triggering events.

A substantial proportion, typically one third to one half, of patients in clinical depersonalization case series report histories of significant trauma. Several studies of accident victims find as much as 60 percent of those with a life-threatening experience report at least transient depersonalization during the event or immediately thereafter. Military training studies find that symptoms of depersonalization and derealization are commonly evoked by stress and fatigue and are inversely related to performance.