Amnesia is an impairment of episodic memory, or memory for personally experienced events (autobiographical memory). This is a component of long-term (as opposed to working) memory, which is distinct from memory for facts (semantic memory), in that episodic memory is unique to the individual whereas semantic memory encompasses knowledge held in common by members of a cultural or linguistic group. Episodic memory generally accords with the lay perception of memory, although many complaints of "poor memory" represent faulty attentional mechanisms rather than true amnesia. A precise clinical definition for amnesia has not been demarcated, perhaps reflecting the heterogeneity of the syndrome.

Amnesia may be retrograde (for events already experienced) or anterograde (for newly experienced events). Retrograde amnesia may show a temporal gradient, with distant events being better recalled than more recent ones, relating to the duration of anterograde amnesia.

Amnesia may be acute and transient or chronic and persistent. In a pure amnesic syndrome, intelligence and attention are normal and skill acquisition (procedural memory) is preserved. Amnesia may occur as one feature of more widespread cognitive impairments (e.g., in Alzheimer’s disease).

Various psychometric tests of episodic memory are available. These include the Wechsler Memory Score (WMS-R), the Recognition Memory Test which has both verbal (words) and visual (faces) subdivisions, the Rey Auditory Verbal Learning Test (immediate and delayed free recall of a random word list), and the Rey-Osterreith Complex Figure (nonverbal memory). Retrograde memory may be assessed with a structured Autobiographical Memory Interview and with the Famous Faces Test. Poor spontaneous recall, for example of a word list, despite an adequate learning curve, may be due to a defect in either storage or retrieval. This may be further probed with cues: if this improves recall, then a disorder of retrieval is responsible; if cueing leads to no improvement, or false-positive responses are equal or greater than true positives, then a learning defect (true amnesia) is the cause.

The neuroanatomical substrate of episodic memory is a distributed system in the medial temporal lobe and diencephalon surrounding the third ventricle (the circuit of Papez) comprising the entorhinal area of the parahippocampal gyrus, perforant and alvear pathways, hippocampus, fimbria and fornix, mammillary bodies, mammillothalamic tract, anterior thalamic nuclei, internal capsule, cingulate gyrus, and cingulum. Basal forebrain structures (septal nucleus, diagonal band nucleus of Broca, nucleus basalis of Meynert) are also involved.

Classification of amnesic syndromes into subtypes has been proposed, since lesions in different areas produce different deficits reflecting functional subdivision within the system; thus left temporal lesions produce problems in the verbal domain, right sided lesions affect non-verbal/visual memory. A distinction between medial temporal pathology (e.g., hippocampus), leading to difficulty encoding new memories (anterograde amnesia and temporally limited retrograde amnesia), and diencephalic pathology (e.g., Korsakoff ’s syndrome), which causes difficulty retrieving previously acquired memories (extensive retrograde amnesia) with diminished insight and a tendency to confabulation, has been suggested, but overlap may occur. A frontal amnesia has also been suggested, although impaired attentional mechanisms may contribute. Functional imaging studies suggest medial temporal lobe activation is required for encoding with additional prefrontal activation with "deep" processing; medial temporal and prefrontal activation are also seen with retrieval.

Many causes of amnesia are recognized, including:

  • Acute/transient:
    • Closed head injury
      Transient global amnesia
      Transient epileptic amnesia
      Transient semantic amnesia (very rare)
  • Chronic/persistent:
    • Alzheimer’s disease (may show isolated amnesia in early disease)
      Sequela of herpes simplex encephalitis
      Limbic encephalitis (paraneoplastic or nonparaneoplastic)
      Hypoxic brain injury
      Temporal lobectomy (bilateral; or unilateral with previous contralateral injury, usually birth asphyxia)
      Bilateral posterior cerebral artery occlusion
      Korsakoff ’s syndrome
      Bilateral thalamic infarction
      Third ventricle tumor, cyst
      Focal retrograde amnesia (rare)

Few of the chronic persistent causes of amnesia are amenable to specific treatment. Plasma exchange or intravenous immunoglobulin therapy may be helpful in nonparaneoplastic limbic encephalitis associated with autoantibodies directed against voltage-gated potassium channels.
Functional or psychogenic amnesia may involve failure to recall basic autobiographical details, such as name and address. Reversal of the usual temporal gradient of memory loss may be observed (but this may also be the case in the syndrome of focal retrograde amnesia).


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Cross References

Confabulation; Dementia