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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,
often including neuropsychologic testing and brain imaging (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 can be classified as retrograde (for events before the cause), anterograde (inability to store new memories after the cause), global (for information related to all senses and past times), and sense-specific (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).
Pathophysiology
and 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 occur along the medial parahippocampal region and hippocampus as well as in the inferomedial temporal lobes, orbital surface of the frontal lobes, and diencephalon. Of these, 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 activated brain stem reticular formation stimulate the imprinting of memories. Bilateral damage to the medial and dorsal thalamus and to the brain stem reticular formation and adrenergic system severely impairs recent memory and the ability to form new memories; the most common causes are thiamin deficiency, hypothalamic tumors, and ischemia. Bilateral damage to the medial temporal lobes, especially the hippocampus, can cause semipermanent declarative amnesia.
Severe, irreversible memory loss is most commonly caused by degenerative dementias, severe brain trauma, brain anoxia or ischemia, alcoholic-nutritional disorders (eg, Wernicke's encephalopathy, Korsakoff's psychosis—see Drug Use and Dependence: Wernicke's Encephalopathy), and various drug intoxications (eg, chronic solvent sniffing, amphotericin B or lithium 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 perform 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
and Treatment
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 hence the necessary tests.
Any underlying disorder or psychologic cause (see Dissociative Disorders: Prognosis) 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 caused by central vascular or
ischemic lesions. 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 transient ischemia (eg, atherosclerosis, thrombosis, thromboembolic disease) affecting the posteromedial thalamus or hippocampus bilaterally, but it 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 midazolam and triazolam ).
Symptoms,
Signs, and Diagnosis
Patients present with acute global amnesic confusion that lasts from as little as 30 to 60 min to ≥ 12 h. 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. Smaller disturbances occur in anterograde memory. 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. Usually, episodes do not recur, except when the cause is seizures or migraines.
The benign transient amnesia (blackout) 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 is primarily clinical. Neurologic examination typically does not detect any abnormalities other than disturbed memory.
Prognosis
and Treatment
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. Lifetime recurrence rate is about 5 to 25%.
Evaluation to rule out central ischemia (eg, due to stroke, thrombosis, or thromboembolic disease) is required (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 is done. EEG may show nonspecific abnormalities and hence is unnecessary unless a seizure is suspected or episodes recur.
No specific treatment is indicated. However, underlying ischemia (see Stroke (CVA): Treatment) or seizure (see Seizure Disorders: Prognosis) should be treated accordingly.
Last full review/revision November 2005
Content last modified November 2005
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