Amnesia is partial or total inability to recall past experiences or inability to store new memories after the causative event. It may result from traumatic brain injury, degeneration, metabolic disorders, seizures, 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 the following:
- Registration (taking in new information)
- Encoding (forming associations, time stamps, and other processes necessary for 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
- Sense-specific: Amnesia for events processed by one sense—eg, visual memory
Amnesia may be
- Transient (as occurs after brain trauma)
- Fixed (as occurs after a serious event such as encephalitis, global ischemia, or cardiac arrest)
- Progressive (as occurs with degenerative dementias, such as Alzheimer disease)
Memory deficits more commonly involve facts (declarative memory) and, less commonly, skills (procedural memory).
Etiology of Amnesias
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 following are critical:
- Hippocampal gyri
- Nuclei of the basal forebrain
- Mediodorsal thalamic nuclei
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.
Amnesia may be caused by
- Thiamin deficiency (by causing Wernicke encephalopathy or Korsakoff psychosis) in patients with chronic alcohol abuse or severe undernutrition
- Traumatic brain injury
- Global brain anoxia or ischemia
- Embolic occlusion at the top of the basilar artery, causing ischemia in the anterior medial temporal lobes
- Degenerative dementias such as Alzheimer disease
- Various drug intoxications (eg, chronic solvent sniffing, amphotericin B or lithium toxicity)
- Hypothalamic tumors
- Psychologic trauma or stress
Wernicke-Korsakoff syndrome is a form of amnesia that combines Wernicke encephalopathy and Korsakoff psychosis.
Posttraumatic amnesias for the periods immediately before and after concussion or moderate or severe head trauma seem to result from medial temporal lobe injury. Moderate or severe trauma may affect larger areas of memory storage and recall, as can many diffuse cerebral disorders that cause dementia.
Psychologic disturbances of memory (as occurs in dissociative amnesia) result from extreme psychologic trauma or stress.
Age-associated memory impairment (benign senescent forgetfulness) refers to the memory loss that occurs with normal aging. People with benign senescent forgetfulness gradually develop noticeable problems with memory, often first for names, then for events, and occasionally for spatial relationships. Benign senescent forgetfulness has no proven relationship to dementia, although some similarities are hard to overlook.
Amnestic mild cognitive impairment (amnestic MCI) may be present in people who have a subjective memory problem, who do worse on objective memory tests, but who otherwise have intact cognition and daily function. People with amnestic MCI are more likely to develop Alzheimer disease than age-matched people without memory problems.
Diagnosis of Amnesias
- Bedside neurologic testing
- Neuropsychologic testing
Simple bedside tests (eg, 3-item recall, location of objects previously hidden in the room) and formal neuropsychologic 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 of Amnesias
- Treatment directed at the cause
Any underlying disorder or psychologic cause of amnesia must be treated. However, some patients with acute amnesia improve spontaneously. Certain disorders that cause amnesia (eg, Alzheimer disease, Korsakoff psychosis, herpes encephalitis) can be treated; however, treatment of the underlying disorder may or may not lessen the amnesia.
Cholinergic drugs (eg, donepezil) may improve memory slightly and temporarily in patients with Alzheimer disease; these drugs are often also tried when another dementia is the cause. Otherwise, no specific measures can hasten recovery or improve the outcome.
Key Points about Amnesias
- Amnesias have various causes, including traumatic brain injury, degenerative dementias, metabolic disorders, seizures, and psychologic trauma or stress.
- Diagnose amnesia clinically using bedside tests (eg, 3-item recall) or formal tests (eg, word list learning tests).
- Treat the cause of amnesia.
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