Título: Henry Molaison
Seção: Biography
Background: Henry Gustav Molaison (February 26, 1926 - December 2, 2008), known widely as H.M., was an American memory disorder patient 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. H.M. was widely studied from late 1957 until his death in 2008. 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.

Conteúdo: Henry Molaison was born on February 26, 1926, and experienced intractable epilepsy that has sometimes been attributed to a bicycle accident at the age of seven. (This accident was initially reported to have occurred at age nine, but was corrected by the patient's mother at a later stage.) He had partial seizures for many years, and then several tonic-clonic seizures following his 16th birthday. In 1953, he was referred to William Beecher Scoville, a neurosurgeon at Hartford Hospital, for treatment.  Scoville localized Molaison's epilepsy to his left and right medial temporal lobes (MTLs) and suggested surgical resection of the MTLs as a treatment. On September 1, 1953, at the age of 27, Molaison's bilateral medial temporal lobe resection included the removal of the hippocampal formation and adjacent structures, including most of the amygdaloid complex and entorhinal cortex. His hippocampi appeared entirely nonfunctional because the remaining 2 cm of hippocampal tissue appeared to have atrophied and because the entire entorhinal cortex, which forms the major sensory input to the hippocampus, was destroyed. Some of his anterolateral temporal cortex was also destroyed.  After the surgery, which was partially successful in its primary goal of controlling his epilepsy, 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 h

user: Where was Molaison born?

assistant: CANNOTANSWER

user: When did he first learn he had epilepsy?

assistant: He had partial seizures for many years, and then several tonic-clonic seizures following his 16th birthday.

user: Did he go to University?

assistant: CANNOTANSWER

user: What was something interesting from the article?

assistant: After the surgery, which was partially successful in its primary goal of controlling his epilepsy,

user: What happened after the surgery?

assistant: Molaison developed severe anterograde amnesia:

user: What are the symptoms of that?

assistant: although his working memory and procedural memory were intact, he could not commit new events to his explicit memory.

user: How did he cope with that?

assistant: However, his ability to form long-term procedural memories was intact; thus he could, for example, learn new motor skills, despite not being able to remember learning them.