Amnesia is partial or total inability to recall past experiences. It may result from traumatic brain injury, degeneration, metabolic disorders, seizure disorders, or psychologic disturbances. Diagnosis is clinical but often includes neuropsychologic testing and brain imaging (eg, CT, MRI). Treatment is directed at the cause.

Processing of memories involves registration (taking in new information), encoding (forming associations, time stamps, and other processes necessary for retrieval), and retrieval. Deficits in any of these steps can cause amnesia. Amnesia, by definition, results from impairment of memory functions, not impairment of other functions (eg, attention, motivation, reasoning, language), which may cause similar symptoms.

Amnesia can be classified as follows:

• Retrograde: Amnesia for events before the causative event
• Anterograde: Inability to store new memories after the causative event
• Global: Amnesia for information related to all senses and past times
• Sense-specific: Amnesia for events processed by one sense—eg, an agnosia

Amnesia may be transient (as occurs after brain trauma), fixed (as occurs after a serious event such as encephalitis, global ischemia, or cardiac arrest), or progressive (as occurs with degenerative dementias, such as Alzheimer's disease).

Memory deficits more commonly involve facts (declarative memory) and, less commonly, skills (procedural memory).

Etiology

Amnesia can result from diffuse cerebral impairment, bilateral lesions, or multifocal injuries that impair memory-storage areas in the cerebral hemispheres. Predominant pathways for declarative memory are located along the medial parahippocampal region and hippocampus as well as in the inferomedial temporal lobes, orbital surface of the frontal lobes (basal forebrain), and diencephalon (which contains the thalamus and hypothalamus). Of these structures, the hippocampal gyri, hypothalamus, nuclei of the basal forebrain, and dorsomedial thalamic nuclei are critical. The amygdaloid nucleus contributes emotional amplifications to memory. The thalamic intralaminar nuclei and brain stem reticular formation stimulate the imprinting of memories. Bilateral damage to the mediodorsal nuclei of the thalamus severely impairs recent memory and the ability to form new memories; the most common causes are

• Thiamin deficiency
• Hypothalamic tumors
• Vertebrobasilar ischemia

Other causes of amnesia include the following:

• Bilateral damage to the medial temporal lobes (especially the hippocampus)
• Degenerative dementias
• Severe brain trauma
• Global brain anoxia or ischemia
• Alcoholic-nutritional disorders (eg, Wernicke's encephalopathy, Korsakoff's psychosis—see Drug Use and Dependence: Wernicke's Encephalopathy and see Drug Use and Dependence: Korsakoff's Psychosis)
• Various drug intoxications (eg, chronic solvent sniffing, amphotericin BSome Trade Names
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  or lithiumSome Trade Names
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  toxicity)

Posttraumatic amnesias for the periods immediately before and after concussion or more severe head trauma seem to result from medial temporal lobe injury. More severe injuries may affect larger areas of memory storage and recall, as can many diffuse cerebral disorders that cause dementia.

Psychologic disturbances of memory result from extreme psychologic trauma or stress (see Dissociative Disorders: Dissociative Amnesia).

With aging, many people gradually develop noticeable problems with memory, often first for names, then for events, and occasionally for spatial relationships. This widely experienced so-called benign senescent forgetfulness has no proven relationship to dementia, although some similarities are hard to overlook. People who have a subjective memory problem, who do worse on objective memory tests, but who otherwise have intact cognition and daily function may have amnestic mild cognitive impairment (amnestic MCI). People with amnestic MCI are more likely to develop Alzheimer's disease than age-matched people without memory problems.

Diagnosis

• Bedside testing

Simple bedside tests (eg, 3-item recall, location of objects previously hidden in the room) and formal tests (eg, word list learning tests such as the California Verbal Learning Test and the Buschke Selective Reminding Test) can help identify verbal memory loss. Assessment of nonverbal memory is more difficult but may include recall of visual designs or a series of tones. Clinical findings usually suggest causes and any necessary tests.

Treatment

• Treatment directed at the cause

Any underlying disorder or psychologic cause must be treated. However, some patients with acute amnesia improve spontaneously. Certain disorders that cause amnesia (eg, Alzheimer's disease, Korsakoff's psychosis, herpes encephalitis) can be treated; however, treatment of the underlying disorder may or may not lessen the amnesia. If it does not, no specific measures can hasten recovery or improve the outcome.

Transient Global Amnesia

Transient global amnesia is disturbed memory typically caused by vascular or ischemic lesions in the brain. Diagnosis is primarily clinical but includes laboratory tests and CT, MRI, or both to evaluate central circulation. The amnesia typically remits spontaneously but may recur. There is no specific treatment, but underlying abnormalities are corrected.

Transient global amnesia is typically caused by ischemia (eg, due to atherosclerosis, thrombosis, or thromboembolism) that transiently affects the posteromedial thalamus or hippocampus bilaterally, but this amnesia can be caused by seizure activity or migraines.

A distinct benign form of transient global amnesia can follow excessive alcohol ingestion, moderately large sedative doses of barbiturates, use of several illicit drugs, or sometimes relatively small doses of benzodiazepines (especially midazolamSome Trade Names
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and triazolamSome Trade Names
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).

Symptoms and Signs

Patients present with acute global amnesic confusion that usually lasts 6 to 12 h but may last from 30 min to 24 h (rarely). Patients have a retrograde memory deficit that can extend back for several years; they are often disoriented to time and place but usually not to personal identity. Anterograde memory is less disturbed. Many patients are anxious or agitated and may repeatedly ask questions about transpiring events. Language function, attention, visual-spatial skills, and social skills are retained. Impairments gradually resolve as the episode subsides.

The benign transient amnesia after substance ingestion is distinct because it is selectively retrograde (ie, for events during and preceding intoxication), relates specifically to drug-accompanied events, does not cause confusion (once acute intoxication resolves), and recurs only if similar amounts of the same drug are ingested.

Diagnosis

• Primarily clinical evaluation
• Brain imaging

Diagnosis is primarily clinical. Neurologic examination typically does not detect any abnormalities other than disturbed memory. Brain ischemia must be ruled out (see Stroke (CVA): Diagnosis). Laboratory tests should include CBC, coagulation tests, and evaluation for hypercoagulable states. CT, MRI, or both, with or without angiographic protocols, are done. EEG usually shows nonspecific abnormalities and is unnecessary unless a seizure is suspected or episodes recur.

Prognosis

Prognosis is good. Symptoms typically last < 24 h. As the disorder resolves, the amnesia lessens, but memory for events during the attack may be lost. Usually, episodes do not recur, unless the cause is seizures or migraines. Overall lifetime recurrence rate is about 5 to 25%.

Treatment

No specific treatment is indicated. However, underlying ischemia (see Stroke (CVA): Treatment) or seizure (see Seizure Disorders: Prognosis) should be treated.

Last full review/revision September 2008 by Alexander Auchus, MD

Content last modified February 2012