Henry Molaison

Henry Gustav Molaison (February 26, 1926 – December 2, 2008), known widely as H.M., was an American who had a bilateral medial temporal lobectomy to surgically resect the anterior two thirds of his hippocampi, parahippocampal cortices, entorhinal cortices, piriform cortices, and amygdalae in an attempt to cure his epilepsy.

Although the surgery was partially successful in controlling his epilepsy, a severe side effect was that he became unable to form new memories.

A childhood bicycle accident is often advanced as the likely cause of H.M.'s epilepsy.

H.M. began to have minor seizures at age 10; from 16 years of age, the seizures became major.

Despite high doses of anticonvulsant medication, H.M.'s seizures were incapacitating.

When he was 27, H.M. was offered an experimental procedure by neurosurgeon W. B. Scoville.

Previously Scoville had only ever performed the surgery on psychotic patients.

Henry Molaison was born on February 26, 1926, in Manchester, Connecticut, and experienced intractable epilepsy that has sometimes been attributed to a bicycle accident at the age of seven.

The surgery took place in 1953 and H.M. was widely studied from late 1957 until his death in 2008.

He resided in a care institute in Windsor Locks, Connecticut, where he was the subject of ongoing investigation.

His case played an important role in the development of theories that explain the link between brain function and memory, and in the development of cognitive neuropsychology, a branch of psychology that aims to understand how the structure and function of the brain relates to specific psychological processes.

In 1953, Molaison was referred to William Beecher Scoville, a neurosurgeon at Hartford Hospital.

Scoville localized his epilepsy to the left and right medial temporal lobes (MTLs) and suggested their surgical resection.

On September 1, 1953, Scoville removed Molaison's medial temporal lobes on both hemispheres including the hippocampi and most of the amygdalae and entorhinal cortex, the major sensory input to the hippocampi.

His hippocampi appeared entirely nonfunctional because the remaining 2 cm of hippocampal tissue appeared to have atrophied and some of his anterolateral temporal cortex was also destroyed.

After the surgery, which was partially successful in controlling his seizures, Molaison developed severe anterograde amnesia: although his working memory and procedural memory were intact, he could not commit new events to his explicit memory.

According to some scientists, he was impaired in his ability to form new semantic knowledge.

Researchers argue over the extent of this impairment.

He also had moderate retrograde amnesia, and could not remember most events in the one- to two-year period before surgery, nor some events up to 11 years before, meaning that his amnesia was temporally graded.

He was able to fill in answers to clues that referred to pre-1953 knowledge.

For post-1953 information he was able to modify old memories with new information.

For instance, he could add a memory about Jonas Salk by modifying his memory of polio.

Molaison was influential not only for the knowledge he provided about memory impairment and amnesia, but also because it was thought his exact brain surgery allowed a good understanding of how particular areas of the brain may be linked to specific processes hypothesized to occur in memory formation.

In this way, his case was taken to provide information about brain pathology, and helped to form theories of normal memory function.

In particular, his apparent ability to complete tasks that require recall from short-term memory and procedural memory but not long-term episodic memory suggests that recall from these memory systems may be mediated, at least in part, by different areas of the brain.

Similarly, his ability to recall long-term memories that existed well before his surgery, but inability to create new long-term memories, suggests that encoding and retrieval of long-term memory information may also be mediated by distinct systems.

His case was first reported by Scoville and Brenda Milner in 1957, who referred to him by "H.M."

His full name was not revealed to the wider public until after his death.

While researchers had told him of the significance of his condition and of his renown within the world of neurological research, he was unable to internalize such facts as memories.

Near the end of his life, Molaison regularly filled in crossword puzzles.

Nevertheless, imaging of Molaison's brain in the late 1990s revealed the extent of damage was more widespread than previous theories had accounted for, making it very hard to identify any one particular region or even isolated set of regions that were responsible for HM's deficits.

The study of Molaison revolutionized the understanding of the organization of human memory.

It has provided broad evidence for the rejection of old theories and the formation of new theories on human memory, in particular about its processes and the underlying neural structures (cf. Kolb & Whishaw, 1996).

In the following, some of the major insights are outlined.

Molaison's brain was the subject of an anatomical study funded by the Dana Foundation and the National Science Foundation.

Molaison's brain was kept at University of California, San Diego where it was sliced into histological sections on December 4, 2009.

It was later moved to the MIND Institute at UC Davis.

The brain atlas constructed was made publicly available in 2014.

He had minor or partial seizures for many years, and then major or tonic-clonic seizures following his 16th birthday.

He worked for a time on an assembly line but, by the age of 27, he had become so incapacitated by his seizures, despite high doses of anticonvulsant medication, that he could not work nor lead a normal life.