HM (patient)

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

## Contents

* 1 Overview
* 2 History
* 3 Insights into memory formation
* 4 HM's lifelong contribution to science
* 5 Related Chapters
* 6 External Links
* 7 References

## Overview[edit | edit source]

HM (also known as "H.M." and "Henry M.," born 1926 in Connecticut) is an anonymous memory-impaired patient who has been widely studied since the late 1950s and has been very important 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 studies brain injury to infer normal psychological function. He is still alive today and resides in a care institute located in Hartford, Connecticut, where he remains in ongoing investigation.[1] Audio-recordings from the 1990s of him talking to scientists were released in early 2007.

## History[edit | edit source]

HM suffered from intractable epilepsy that has been often--though inconclusively--attributed to a bicycle accident at the age of seven. He suffered from partial seizures for many years, and then several tonic-clonic seizures following his sixteenth birthday. In 1953, HM was referred to William Scoville, a surgeon at Hartford Hospital, for treatment.

Scoville localized HM's epilepsy to his medial temporal lobe (MTLs) and suggested surgical resection of the MTLs as a treatment. On September 1, 1953, Scoville removed parts of HM's medial temporal lobe on both sides of his brain. HM lost approximately two-thirds of his hippocampal formation, parahippocampal gyrus (all his entorhinal cortex was destroyed), and amygdala. His hippocampus appears entirely nonfunctional because the remaining 2 cm of hippocampal tissue appears atrophic and because the entire entorhinal (which forms the major sensory input to the hippocampus) was destroyed. Some of his anterolateral temporal cortex was also destroyed.

After the surgery he suffered from severe anterograde amnesia: although his short-term memory was intact, he could not commit new events to long-term memory. According to some scientists (e.g., Schmolck, Kensinger, Corkin, & Squire, 2002), HM is impaired in his ability to form new semantic knowledge but researchers argue over the extent of this impairment. He also suffered moderate retrograde amnesia, and could not remember most events in the 3-4 day period before surgery, and some events up to 11 years before, meaning that his amnesia was temporally graded. However, his ability to form long-term procedural memories was still intact; thus he could, as an example, learn new motor skills, despite not being able to remember learning them.

The case was first reported in a paper by Scoville and Brenda Milner in 1957.

## Insights into memory formation[edit | edit source]

HM has been important not only for the knowledge he has provided about memory impairment and amnesia, but also because his exact brain surgery has 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, he has provided vital information about brain pathology, and has helped form theories of normal memory function.

Particularly, that he seems to be able 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, that HM cannot create new long-term memories, but can recall long-term memories that existed well before his surgery suggests that encoding and retrieval of long-term memory information may also be mediated by distinct systems.

## HM's lifelong contribution to science[edit | edit source]

The study of the patient HM has revolutionized our understanding of the organization of human memory. It has provided broad evidence for the rejection of old theories, as well as 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.

Since the age of 10, the patient HM suffered from increasing epileptic seizures. Eventually the seizures became so intense and frequent that by the age of 27 his doctors suggested removing parts of the brain that were thought to be responsible for his disorder. In 1953, the surgeon Scoville performed brain surgery on HM's medial temporal lobes. Regarding the exact areas of surgery. Scoville & Milner (1957) noted: “bilateral medial temporal lobe resection was carried out, extending posteriorly for a distance of 8 cm from the midpoints of the tips of the temporal lobes, with the temporal horns constituting the lateral edges of resection” (p. 107). HM recovered from the operation, which eased his epileptic seizures to a manageable degree. However, the surgery had induced serious side-effects, which were first described by Scoville & Milner (1957) as “a complete loss of memory for events [...], together with a partial retrograde amnesia for the three years leading up to his operation” (p. 108). Furthermore, they found that “early memories are seemingly normal and there is no impairment of personality or general intelligence” (p. 108).

HM's general condition has been described as heavy anterograde amnesia, as well as temporally graded retrograde amnesia (Smith & Kosslyn, 2007). HM is highly unable to form new long-term memories of new events or new semantic knowledge –- he basically lives in the past (Corkin, 2002). Since HM did not show any memory impairment before the surgery, the removal of the medial temporal lobes can be held responsible for his memory disorder. Consequently, the medial temporal lobes can be assumed to be a major component involved in the formation of semantic and episodic long-term memories (cf. medial temporal lobes described as a convergence zone for episodic encoding in Smith & Kosslyn, 2007). Further evidence for this assumption has been gained by studies of other patients with lesions of their medial temporal lobe structures (cf. Kolb & Whishaw, 1996; Scoville & Milner, 1957).

Despite of his amnesic symptoms, HM performs quite normal in tests of intellectual ability and shows largely intact language abilities indicating that some memory functions (e.g., short-term stores, stores for words, phonemes etc.) were not impaired by the surgery (Smith & Kosslyn, 2007; Corkin, 2002). HM is able to remember information over short intervals of time. This has been tested in a working memory experiment involving the recall of previously presented numbers; in fact, his performance is not worse than that of control subjects (Smith & Kosslyn, 2007). This finding provides evidence that working memory does not rely on medial temporal structures. It further supports the general distinction between short-term and long-term stores of memory (Kolb & Whishaw, 1996). HM's largely intact language abilities provide evidence that language production and comprehension, as well as lexical memory, are independent of the medial temporal structures (Corkin, 2002).

In addition to his intact working memory and intellectual abilities, studies of HM's ability to acquire new motor skills demonstrated preserved motor learning (Corkin, 2002). In a study conducted by Milner in the early 1960s, HM acquired the new skill of drawing a figure by looking at its reflection in a mirror (Corkin, 2002). Further evidence for intact motor learning was provided in a study carried out by Corkin (1968). In this study, HM was tested on three different motor learning tasks and HM demonstrated full motor learning abilities in all three tasks. HM's ability to learn certain problem-solving procedures has also been shown with the Tower of Hanoi task (Kolb & Whishaw, 1996). Experiments involving repetition priming underscored HM's ability to acquire implicit (non-conscious) memories, in contrast to his inability to acquire new explicit semantic and episodic memories (Corkin, 2002). These findings provide evidence that memory of skills and repetition priming rely on different neural structures than memories of episodes and facts; whereas procedural memory and repetition priming do not rely on the medial temporal structures removed in HM, semantic and episodic memory do (cf. Corkin, 1984). The dissociation of HM's implicit and explicit learning abilities along their underlying neural structures has served as an important contribution to our understanding of human memory: Long-term memories are not unitary and can be differentiated as being either declarative and non-declarative (Smith & Kosslyn, 2007).

According to Corkin (2002), studies of HM's memory abilities have also provided insights regarding the neural structures responsible for spatial memory and processing of spatial information. Despite his general inability to form new episodic or factual long-term memories, as well as his heavy impairment on certain spatial memory tests, HM was able to draw a quite detailed map of the topographical layout of his residence. This finding is remarkable since HM had moved to the house five years after his surgery and hence, given his severe anterograde amnesia and insights from other cases, the common expectation was that the acquisition of topographical memories would have been impaired as well. Corkin (2002) hypothesized that HM “was able to construct a cognitive map of the spatial layout of his house as the result of daily locomotion from room to room” (p. 156). Regarding the underlying neural structures, Corkin (2002) argues that HM's ability to acquire the floor plan is due to partly intact structures of his spatial processing network (e.g. the posterior part of his parahippocampal gyrus). In addition to his topographical memory, HM showed some learning in a picture memorization-recognition task, as well as in a famous faces recognition test, but in the latter only when he was provided with a phonemic cue. HM's positive performance in the picture recognition task might be due to spared parts of his ventral perirhinal cortex. Furthermore, Corkin (2002) argues that despite HM's general ability to form new declarative memories, he seems to be able to acquire small and impoverished pieces of information regarding public life (e.g., cued retrieval of celebrities names). These findings underscore the importance of HM's spared extrahippocampal sites in semantic and recognition memory and enhance our understanding of the interrelations between the different medial temporal lobe structures. HM's heavy impairment in certain spatial tasks provides further evidence for the association of the hippocampus with spatial memory (Kolb & Whishaw, 1996).

Another contribution of HM to our understanding of human memory regards the neural structures of the memory consolidation process, which is responsible for forming stable long-term memories (Eysenck & Keane, 2005). HM displayed a temporally graded retrograde amnesia in the way that he “could still recall childhood memories, but he had difficulty remembering events that happened during the years immediately preceding the surgery” (Smith & Kosslyn, 2007, p. 214). His old memories were not impaired, whereas the ones relatively close to the surgery were. This is evidence that the older childhood memories do not rely on the medial temporal lobe, whereas the younger long-term memories seem to do so (Smith & Kosslyn, 2007). The medial temporal structures, which were removed in the surgery, are hypothesized to be involved in the consolidation of memories in the way that “interactions between the medial temporal lobe and various lateral cortical regions are thought to store memories outside the medial temporal lobes by slowly forming direct links between the cortical representations of the experience” (Smith & Kosslyn, 2007, p. 214).

## Related Chapters[edit | edit source]

* Amnesia
* Cognitive neuropsychology
* Phineas Gage
* Memory
* Clive Wearing
* Cenn Fáelad mac Aillila

## External Links[edit | edit source]

* The Day His World Stood Still \- Article on HM from Brain Connection
* H.M.'s Brain and the History of Memory \- NPR Piece on HM

## References[edit | edit source]

1. ↑ Henry M. Right Now (2006), retrieved August 5, 2006.

* W. B. Scoville & Brenda Milner (1957). "Loss of recent memory after bilateral hippocampal lesions" (PDF). Journal of Neurology, Neurosurgery and Psychiatry. 20: 11&ndash, 21. PMID 10678523.
* S. Corkin (2002). "What's new with the amnesic patient H.M.?" (PDF). Nature Reviews Neuroscience. 3 (2): 153&ndash, 160.
* H. Schmolck, E.A. Kensinger, S. Corkin, & L. Squire (2002). "Semantic knowledge in Patient H.M. and other patients with bilateral medial and lateral temporal lobe lesions" (PDF). Hippocampus. 12: 520&ndash, 533.CS1 maint: Multiple names: authors list (link)
* S. Corkin (1984). "Lasting consequences of bilateral medial temporal lobectomy: Clinical course and experimental findings in H.M.". Seminars in Neurology (4): 249&ndash, 259.
* S. Corkin, D. G. Amaral, R. G. González, K. A. Johnson, & B. T. Hyman (1997). "H. M.'s medial temporal lobe lesion: Findings from magnetic resonance imaging". The Journal of Neuroscience (17): 3964&ndash, 3979.CS1 maint: Multiple names: authors list (link)
* S. Corkin (1968). "Acquisition of motor skill after bilateral medial temporal-lobe excision". Neuropsychologia (6): 255&ndash, 265.
* M. W. Eysenck, and M. T. Keane (2005). Cognitive Psychology: A Student’s Handbook (5th edition ed.). Hove, UK: Psychology Press.CS1 maint: Extra text (link)
* E. E. Smith and S. M. Kosslyn (2007). Cognitive Psychology: Mind and Brain (1st edition ed.). Upper Saddle River, NJ: Pearson/Prentice Hall.CS1 maint: Extra text (link)
* B. Kolb and I. Q. Whishaw, I. Q. (1996). Fundamentals of human neuropsychology (4th edition ed.). New York, NY: W. H. Freeman.CS1 maint: Extra text (link)
* Philip J. Hilts. Memory's Ghost. ISBN 0-684-82356-X. Provides further discussion of the author's meetings with HM.

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