Retrograde Amnesia

Retrograde amnesia is an inability to remember events from the period before the onset of amnesia. It refers to loss of information acquired before the onset of the brain damage, in other words.

This memory gap can range from a few minutes to decades. There is however, a temporal gradient to the loss, in that newer memories are more likely to be lost than older ones (e.g., Kolb & Whishaw, 2003).

In patients with amnesia caused by HSE (Herpes Simplex Encephalitis) it has been found that the medial temporal region also tends to be the main site of lesions (Damasio et al., 1985), though the lesions are usually more extensive and involve most of the temporal cortex. Similar lesions are found in the early stages of Alzheimer’s disease (West et al., 1994), though in the later stages of this progressive condition there are more extensive lesions, extending into the forebrain at first and later affecting many areas of the brain.

The other main area of the brain where lesions tend to produce amnesia is the dicenphalon, a region which includes the thalamus and mamillary bodies. These are the areas which are damaged in most Korsakoff patients, though their lesions may be quite diffuse and frequently also include lesions of the frontal cortex (Victor et al., 1989).

In fact the lesions found in two cases of the same amnesic aetiology are by no means always identical. For example, some Korsakoff patients have frontal lesions whilst others do not. However, most amnesics are found to have lesions in either the temporal lobes or the diencephalon, and the characteristics and symptoms of their amnesia will be determined by the location of their lesions rather than by their actual cause. It is therefore quite possible for two Korsakoff patients to have quite different amnesic symptoms, and it is equally possible for two amnesic patients to have similar amnesic symptoms despite having different aetiologies.

It may seem rather surprising that there are two different areas of the brain (i.e. temporal lobes and diencephalon) where lesions can produce severe amnesia, and that damage to either one of these areas alone can cause amnesia without damage to the other. It seems highly unlikely that these two brain areas both have the same function, and a more likely explanation s that they probably work together in some way so that both areas are vital to intact memory function. One hypothesis based on known connections and lesion outcomes is that the hippocampus is probably responsible for creating new memories for storage elsewhere in the temporal lobes. Parts of the diencephalon may be important in processing and retrieving memories from these storage sites, which could explain why both hippocampal and diencephalic lesions are capable of causing amnesia.