Chapter 7
Summary
- Organic amnesia is caused by brain damage, usually affecting the temporal lobes, hippocampus and anterior thalamic nuclei.
- Such brain lesions may arise from a variety of different causes, such as Alzheimer’s disease, Korsakoff syndrome, herpes simplex encephalitis, strokes and tumours.
- Organic amnesia is characterised by an impairment of long-term memory, but the short-term working memory usually remains intact.
- Most amnesics suffer from anterograde amnesia, so that they have difficulty in learning new information from the time period subsequent to onset.
- Many amnesics also suffer from retrograde amnesia, in which memories are also lost from the period preceding onset. However, the retrograde impairment may be fairly limited, and memories for earlier time periods such as childhood often remain intact.
- The anterograde and retrograde components of amnesia appear to be fairly independent of one another, so that their relative severity can vary considerably from patient to patient. In rare cases either retrograde or anterograde amnesia may occur in isolation.
- Most amnesics suffer a severe impairment of conscious declarative and explicit memory processes such as event and context recollection, but there is usually no impairment of non-declarative and implicit memory processes such as motor skill learning, priming and familiarity judgements.
- In addition to the amnesias which are characteristic of the organic amnesic syndrome, memory impairment may also be caused by other factors, such as ageing, concussion, ECT and psychogenic causes. However, these impairments tend to have their own distinct characteristics, and differ somewhat from the pattern of organic amnesic symptoms.
- Although brain lesions are usually irreversible, many rehabilitation strategies have been devised to help organic amnesics to cope with their memory impairment.
Glossary
Alzheimer’s disease (AD) A degenerative brain disorder usually (but not always) afflicting the elderly, which first appears as an impairment of memory but later develops into a more general dementia.
Amnesia A pathological impairment of memory function.
Anterograde amnesia (AA) Impaired memory for events which have occurred since the onset of the disorder (contrasts with retrograde amnesia).
Confabulation The reporting of memories which are incorrect and apparently fabricated, but which the patient believes to be true.
Declarative memory Memory which can be reported in a deliberate and conscious way (contrasts with procedural memory).
Diencephalon A brain structure which includes the thalamus and hypothalamus. Parts of the diencephalon are involved in processing and retrieving memories, and damage to these structures can cause amnesia.
Electroconvulsive therapy (ECT) A treatment used to alleviate depression which involves passing an electric current through the front of the patient’s head.
Extended hippocampal complex A system of interconnected structures within the brain, incorporating the hippocampus, anterior thalamus and mammillary bodies, which is involved in the encoding and storage of new memory traces.
Herpes simplex encephalitis (HSE) A virus infection of the brain, which in some cases leaves the patient severely amnesic.
Hippocampus A structure lying within the temporal lobes, which is involved in the creation of new memories. Hippocampal lesions usually cause impairment of memory, especially the storage of new memories.
Korsakoff’s syndrome A brain disease which usually results from chronic alcoholism, and which is mainly characterised by a memory impairment.
Organic amnesia An impairment of memory function caused by physical damage to the brain.
Procedural memory Memory which can be demonstrated by performing some skilled procedure such as a motor task, but which the subject is not necessarily able to report consciously (contrasts with declarative memory).
Psychogenic amnesia A memory impairment of psychological origin.
Rehabilitation Strategies used to help patients to cope with an impairment or disability, enabling them to function as effectively as possible within the limitations created by the impairment.
Retrograde amnesia (RA) Impaired memory for events which occurred prior to the onset of amnesia (contrasts with anterograde amnesia).
Amnesia
Main structures of the limbic system
Reading List
Aggleton, J. P. (2008). Understanding anterograde amnesia: Disconnections and hidden lesions. Quarterly Journal of Experimental Psychology,61, 1441–1471.
http://www.tandfonline.com/doi/abs/10.1080/17470210802215335
Baddeley, A. D., Kopelman, M. D., & Wilson, B. A. (2004). The Essential Handbook of Memory Disorders for Clinicians. Chichester, UK: John Wiley.
Campbell, R., & Conway, M. A. (1995). Broken Memories. Oxford: Blackwell.
Graf, P., Squire, L. R., & Mandler, G. (1984). The information that amnesic patients do not forget. Journal of Experimental Psychology: Learning, Memory, and Cognition, 10, 164–178.
http://psycnet.apa.org/journals/xlm/10/1/164/
Moscovitch, M., Nadel, L., Winocur, G., Gilboa, A., & Rosenbaum, R. S. (2006). The cognitive neuroscience of remote episodic, semantic and spatial memory. Current Opinion in Neurobiology, 16( 2), 179–190. http://www.sciencedirect.com/science/article/pii/S0959438806000389
Murray, L. J., & Ranganath, C. (2007). Dorsolateral prefrontal cortex contributes to successful relational memory encoding. Journal of Neuroscience, 27(20): 5515–5522.
http://www.jneurosci.org/content/27/20/5515
Wilson, B. A., Gracey, F., Evans, J. J., & Bateman, A. (2009). Neuropsychological Rehabilitation: Theory, Models, Therapy and Outcome. Cambridge: Cambridge University Press.
Weblinks
Memory systems
http://thebrain.mcgill.ca/flash/a/a_07/a_07_p/a_07_p_tra/a_07_p_tra.html#3
Anatomy of memory
http://www.exploratorium.edu/memory/braindissection/index.html