The world’s second most famous amnesiac patient

10 May

We all know the story of H.M.; the ill-fated young man who underwent an experimental procedure to cure his epilepsy in 1953. Although the procedure successfully cured his epilepsy, it also left him unable to form any new, lasting memories from that time up until his death in 2008 at the age of 82 (with the exception of a very limited learning capacity in some experimental tests).

After spending over 50 years as the subject of intense scientific research, H.M. (or Henry Molaison as he later became known) is widely regarded as the most famous amnesiac patient in history. In fact, interest in Henry’s condition has continued since his death. Researchers in The Brain Observatory in San Diego are continuing to work with Henry’s brain, which has been sliced into 4,201 fine sections for further analysis and exploration.

A woman walks past a display of a brain slice of patient H.M. in the Massachusetts Institute of Technology Museum. (Xinhua/Reuters Photo).

A woman walks past a display of a brain slice of patient H.M. in the Massachusetts Institute of Technology Museum. (Xinhua/Reuters Photo).

But now, for the first time, an international team of researchers have described in detail the case of another amnesiac patient, E.P., who they suggest provides some surprising findings concerning how our memory system functions, and how this system breaks down.

Like H.M., E.P. suffered dramatic memory loss (following a viral encephalitis infection) which lasted 16 years, until his death (also in 2008). Unlike H.M., however, E.P.’s capacity to learn any new information was “absolutely zero”. This indicates that H.M.’s small residual learning ability was likely due to the sparing of some key learning-related brain tissue, and not due to the popular suggestion that an alternative learning mechanism exists within the brain.

EP Brain

Comparative stained sections of a healthy brain (top) and of patient E.P., showing significant damage in the medial temporal lobe. E.g. EC: entorhinal cortex, PRC: perirhinal cortex. Credited to UCSD.

The case of E.P. is also unique in that his retrograde amnesia was profound, extending back 40 to 50 years before the onset of illness. In most cases of amnesia, impairment for memories formed long ago is limited, as these memories should theoretically be well-established. It is probable that the extent of E.P.’s retrograde amnesia was due to the devastating loss of brain tissue he suffered, which included the medial temporal lobe, amygdala, hippocampus, and others. Since his death, E.P.’s brain has also been processed by researchers at The Brain Observatory. (See here for more info.)

So, when we think about amnesia, let’s not forget E.P. – a man described as “a 6-foot-2, 192-pound affable fellow with a fascination for computers and a sense of humour” (Squire, 2000), and the second most famous amnesia patient in the history of neuroscience.

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