Amnesia
Memory loss from brain damage, disease, or trauma.
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Amnesia is a deficit in memory caused by brain damage, brain diseases, or the temporary use of sedative and hypnotic drugs. It involves the partial or total loss of memory, with two main types: retrograde amnesia (inability to recall information acquired before a particular date) and anterograde amnesia (inability to transfer new information from short-term to long-term store). Other recognized forms include transient global amnesia, dissociative amnesia, childhood amnesia, and post-traumatic amnesia. The term derives from Ancient Greek, meaning 'without memory.'
The condition is typically linked to damage in the medial temporal lobe, particularly the CA1 region of the hippocampus, as well as areas of the diencephalon. Recent research has also correlated a deficiency in the RbAp48 protein with memory loss, as observed in mice with damaged memory. Despite profound impairments, individuals with amnesia often retain the ability to recall immediate information and can form new procedural knowledge.
Priming, both perceptual and conceptual, can assist in learning fresh non-declarative knowledge. Patients also preserve substantial intellectual, linguistic, and social skills, even when they cannot recall specific information from prior learning episodes. Declarative memory—comprising semantic memory (facts) and episodic memory (events)—can be affected to varying degrees. For instance, one patient with bilateral medial temporal lobe damage retained skill-related declarative memory for techniques like reading music and watercolor painting, which she had used professionally before acquiring amnesia.
Episodic memory loss is most likely with hippocampal damage, while semantic information loss correlates more closely with damage to the medial temporal lobe or neocortex. Some patients with anterograde amnesia can still acquire semantic information, though it may remain isolated from general knowledge. Non-declarative memory, including implicit and procedural learning, often remains intact, as seen in patients who improve on pseudorandom sequence experiments similarly to healthy individuals.
Quick Facts
- Field
- Psychiatry, neurology
Facts from the source article.
Lore & Background
Amnesia is a memory deficit resulting from brain damage, brain diseases, or the temporary use of sedative and hypnotic drugs. Memory loss may be partial or complete, depending on the extent of injury. The condition primarily involves two main types: retrograde amnesia, which is the inability to recall information acquired before a specific date (such as an accident or operation), with memory loss potentially spanning decades or only a few months; and anterograde amnesia, which prevents the transfer of new information from short-term to long-term storage, making it impossible to remember things for extended periods.
These types can occur together. Other recognized forms include transient global amnesia, a sudden temporary loss; dissociative amnesia, linked to emotional stress and involving the inability to recall personal experiences; childhood amnesia, a common early-life memory loss; and post-traumatic amnesia, following head injury with confusion and memory impairment around the trauma. Amnesia is typically associated with damage to the medial temporal lobe, especially the CA1 region of the hippocampus, and also with damage to the diencephalon.
A deficiency of the RbAp48 protein has been correlated with memory loss in studies. Individuals retain immediate recall and can form new procedural knowledge, as well as benefit from priming to learn non-declarative information. Despite profound impairments in recalling specific prior learning episodes, they maintain substantial intellectual, linguistic, and social skills.
Reader's Guide
Amnesia is significant as a condition that reveals the neural basis of memory. The distinction between retrograde and anterograde amnesia has helped map memory functions to specific brain regions, such as the hippocampus and medial temporal lobe.
Case studies of patients like H.M. and R.B. have demonstrated that damage to the CA1 region of the hippocampus impairs episodic memory formation while sparing some semantic and procedural learning. The condition also highlights the dissociation between declarative and non-declarative memory, as amnesiacs can acquire skills and show priming without conscious recall. Understanding amnesia has informed treatments for memory disorders and deepened knowledge of how memory is consolidated and stored.
Frequently Asked Questions
Which brain structures are most critical to Amnesia?
The medial temporal lobe—especially the hippocampus and its CA1 subregion—along with the diencephalon, are the key areas whose damage or dysfunction produces amnestic symptoms. A deficiency in the protein RbAp48 has also been linked to memory-formation failures in these circuits.
What are the most common causes of Amnesia?
Head trauma, psychologically traumatic events, and progressive neurodegenerative conditions such as Alzheimer's disease are the leading triggers. Short-term amnestic episodes can also follow the use of certain sedative or hypnotic drugs.
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Sources
Compiled from Wikipedia and the sources listed below. Text from Wikipedia is available under CC BY-SA 4.0; this entry is adapted from it.
- Wikipedia: Amnesia (CC BY-SA 4.0).
- Word definitions: the Codexery glossary, each quoted from its Wikipedia article.
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