Anterograde amnesia is the loss of the ability to create new memories, leading to a partial or complete inability to recall the recent past, even though long-term memories from before the event which caused the amnesia to remain intact. Sufferers may, therefore, repeat comments or questions several times, for example, or fail to recognize people they met just minutes before.
|Did You Know?|
|Perhaps the most famous case of anterograde amnesia is that of the patient usually known just as “H.M.” (more recently identified as Henry Molaison), whose hippocampus was removed in brain surgery.|
He started as a patient of Scoville and Milner in 1957 and was still being studied up until his death in 2008.
Another remarkable case is that of “E.P.”, a severely amnesic patient who was, however, able to learn simple 3-word sentences.
The British musician Clive Wearing suffers from an acute and long-lasting case of both anterograde amnesia and retrograde amnesia.
Anterograde amnesia may be drug-induced (several benzodiazepines are known to have powerful amnesic effects, and alcohol intoxication also has a similar effect) or it may follow a traumatic brain injury or surgery in which there is damage to the hippocampus or medial temporal lobe of the brain, or an acute event such as a concussion, a heart attack, oxygen deprivation or an epileptic attack. Less commonly, it can also be caused by shock or an emotional disorder.
Research shows that anterograde amnesia results from a failure of memory encoding and storage. New information is processed normally, but almost immediately forgotten, never making it into the regions of the brain where long-term memories are stored. More specifically, in normal use, neurons in the mammillary bodies of the hypothalamus make connections with the thalamus, which in turn makes connections with the cortex of the brain, where long-term memories are stored. Anterograde amnesia can, therefore, result from damage to the hypothalamus and thalamus and the surrounding cortical structures, so that encoded memories are never stored since connections between hippocampus and cortex are disrupted.
Sufferers from anterograde amnesia usually only lose declarative memory (the recollection of facts), but they retain non-declarative or procedural memory (the learning of skills and habits). For instance, they may be able to remember or learn how to do things, such as talking on the phone or riding a bicycle, but they may not remember what they had eaten for lunch earlier that day. This was made clear in the early 20th Century by Édouard Claparède, who showed that, although anterograde amnesiacs were unable to remember meeting him on previous days they were still able to learn and remember some things (new tasks involving procedural memory). We now know that this is because procedural memory does not rely on the hippocampus and medial temporal lobe memory system in the same way as declarative memory.
Even more specifically, anterograde amnesia patients often lose only the episodic part of their declarative memory (that part which relates to autobiographical information with a temporal and/or spatial context), and not the semantic part (factual information, such as language, history, geography, etc, with autobiographical association).
When there is damage to just one side of the medial temporal lobe, the neuroplasticity of the brain (its ability to re-map its neural connections when necessary) can often allow the opportunity for normal, or near-normal, functioning for memories with time.
A more recent 2005 case in Germany has muddied the water somewhat, though. A dental patient, after receiving a routine root canal treatment, suddenly started exhibiting symptoms of anterograde amnesia, even though scans showed that his hippocampus was entirely intact and unaffected, and there was no evidence of his brain being affected by the anaesthetic. Furthermore, he could only retain new procedural memories for an hour or two, just about the time that the initial process of consolidation typically takes to “cement” a memory into place in the synapses. This consolidation process involves the production of new proteins to rebuild the synapses in the new shape, and that process seemed to have stopped working in this case, for no apparent reason.