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What is anterograde amnesia and what symptoms does it have?

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When we talk about someone suffering from amnesia, we automatically think of a person who does not remember her past. There is another type, anterograde amnesia, which consists of the inability to form new memories.

This memory problem usually goes hand in hand with retrograde amnesia, that of past episodes, but it is not always linked. It is, therefore, a form of independent amnesia with its own altered causes and mechanisms.

Causes of anterograde amnesia

The causes that cause brain injuries can be very diverse: head injuries, hypoxia, herpetic encephalitis or vascular problems. The lesion that causes the purest antegrade amnesia is the lesion of the anterior thalamus, usually of vascular origin.

In addition, it is possible to lose pyramidal cells in the bilateral hippocampus due to lack of oxygen or some blow to the the skull, causing amnesia that may be pure, or may occur in conjunction with other types of amnesia.

What is the problem in this type of amnesia?

Roughly speaking, patients with antegrade amnesia cannot learn new information. They are unable to long-term retain a name, a new face, or learn some kind of game that they were previously unfamiliar with.

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They have no perception problems, and they have a good working memory. These patients can remember new information and work with it for a short period of time, but they are unable to retain and remember it after a few hours. It is as if the new information, once it is no longer present, disappears.

We know that in order to store information in memory, a coding and storage process needs to occur. Science, curious by nature, wonders exactly at what point in this process individuals with anterograde amnesia fail. Here are the most used hypotheses.

1. Coding problems

There are hypotheses that support that it is a problem of coding. The brain, although it receives sensory stimuli, has difficulty giving them meaning and extracting which are the most important characteristics.

For example, patients with Korsakoff syndrome have trouble learning apple-cheese word pairs. Normally, this learning is facilitated because both things share a characteristic, but the Korsakoffs are unable to establish this relationship. However, this explanation is weak and does not seem the most fundamental.

2. Consolidation problems

Another hypothesis suggests that the biological processes responsible for transporting the encoded information and storing it are damaged.. Thus, although the subject can process the information and work with it in the moment, he is unable to save it for later.

For example, a group of football players was taken who, 30 seconds after suffering a concussion, were asked what had happened. The players were able to explain the order of events well, but as the time each time they were able to remember fewer events, showing that the memory had not been consolidated.

This theory does not provide an answer, however, as to why the loss of these memories due to non-consolidation is gradual.

3. Contextual information problems

From this hypothesis People with anterograde amnesia are said to lose the ability to store contextual information. Although they can remember specific words, they are not able to relate them to anything. For this reason, when they are asked to repeat the words they have heard before, by not relating these words to any previous situation, they are unable to retrieve them.

This hypothesis presents problems, such as that the deficit in context coding is closely related to damage to the temporal lobe, and those patients who do not have it damaged may have anterograde amnesia without a contextual deficit specific.

4. Accelerated forgetfulness

The fourth possibility says that memory processing and storage is intact, the problem is that new information is forgotten very quickly. However, it is a hypothesis that has contradictory scientific support that has not been able to be replicated.

5. Recovery issues

This way of understanding anterograde amnesia is subdivided into two hypotheses. The hypothesis of "pure" dysfunction in recovery says that there will be difficulties in accessing information learned regardless of how it was learned. The other hypothesis postulates that, since information retrieval depends a lot on how it has been learned, the amnesiac has problems accessing the memory for an initial problem in the coding.

In summary, the different theories point to a problem in the acquisition and consolidation of information, with a more subtle effect on the recovery processes. The exact explanation as to why this acquisition problem occurs remains up in the air. One of the possible explanations may be that the brain of the amnesic patient is unable to relate different types of information, such as contextual information.
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