by Saul McLeod published 2011
Anterograde amnesia refers to loss of memory for events after an incident – often such cases are examples of what are known as pure amnesiacs. Therefore, a person can’t store new information in their short term memory.
Patients with anterograde amnesia quite often show normal memory for events prior to the incident responsible for the memory deficit but have severely impaired ability to recall information about events occurring after the incident.
Whereas with retrograde amnesia there is almost always a gradual restoration of most of the lost information, with anterograde amnesia there is quite often no such recovery and patients are left with a permanent and debilitating condition. The case which led to the discovery of the condition of anterograde amnesia is that of H.M. (Milner et al 1968).
Anterograde amnesia can be caused by a number of potential factors, such as brain surgery, e.g. HM, or alcohol, e.g. Korsakoffs syndrome.
H.M. had brain surgery in 1953 when he was 27 yrs. old. The surgery involved removal of part of the brain known as the hippocampus to alleviate the severe symptoms of epilepsy. Although the surgery controlled the epileptic seizures H.M. suffered serious and debilitating memory impairment as a side effect.
His short-term memory was normal but he was completely unable to transfer any new information into his long-term memory. He showed almost no knowledge of current affairs because he forgot any news item as soon as he had read about it; he knew nothing of recent family events including moving house and the death of his father.
Despite being able to remember people he had known long ago he was never able to store information about new people he encountered and they remained forever complete strangers to him.
In many respects H.M. seemed cognitively 'normal' as he was able to learn and remember perceptual and motor skills although he needed reminding of what he was able to do.
This case and others illustrate the highly selective nature of the problems of anterograde amnesia following brain damage. There is no general deterioration of memory function but specific deficits in which some abilities such as learning new information are severely impaired whilst others, including language and memory span are quite normal.
In 1889 Sergei Korsakoff, a Russian physician described a severe memory disorder due to brain damage. The most obvious symptom of what became known as Korsakoffs syndrome is a severe anterograde amnesia where the patients appears to be unable to form any new memories but can still remember some old ones (i.e. short term memory is impaired).
Korsakoff s syndrome usually, although not always, results from a thiamine (vitamin Bl) deficiency after years of alcohol abuse. Alcoholics often have a poor diet because they get sufficient calories from their alcohol intake, thus their vitamin intake from food is very low.
In addition to the problem of taking in few vitamins alcohol also interferes with the absorption of thiamine in the intestines. Very occasionally Korsakoffs syndrome can also result from infusions of glucose given to people suffering from severe malnutrition.
Many patients go through an acute phase, known as Wernicke's encephalopathy, during which they suffer from impairments of movement and emotional and cognitive functioning. In the chronic phase that follows the primary symptom is amnesia, primarily anterograde but also retrograde.
The brain damage in Korsakoff syndrome appears to be widespread with loss of nerve cells often occurring in several regions of the brain including the thalamus, cerebellum, cerebral cortex and frontal lobe. Interestingly, patients who have suffered frontal lobe damage due to-injury often encounter the same problem solving difficulties experienced by Korsakoff patients.
Milner, B., Corkin, S., et al. (1968). Further Analysis of Hippocampal Amnesic Syndrome - 14-Year Follow-up Study of HM. Neuropsychologia, 215-230.
McLeod, S. A. (2011). . Retrieved from