Patient N.A.
 | This article may require copy editing for grammar, style, cohesion, tone, or spelling. (September 2023) |
Patient N.A. | |
|---|---|
| Born | July 9, 1938 |
| Known for | patient of anterograde amnesia |
Patient N.A. (born July 9th, 1938) was an American man who developed anterograde amnesia as a result of a fencing accident. He was a patient studied by Larry Squire, a professor of psychiatry, neuroscience and psychology at the University of California. The cause of his amnesia was found to be a thalamic lesion extending to the hypothalamus. Damage to the temporal cortex was also found and thought to be a result of an exploratory surgery.[1]
In 1960, when Patient N.A. was 22 years old, a fencing foil went up his nose and injured his brain. This resulted in severe anterograde amnesia, especially for verbal memory, as well as impaired eye movements. His other cognitive abilities remained inaffected.[1]
Since the accident, N.A. attended examinations in MIT laboratories and received home visits. Later, his case was studied and described by Larry Squire. CT scans and MRI findings revealed a large diencephalic lesion, involving left thalamus, hypothalamus, floor of the third ventricle and mammillary bodies. Damage of the right temporal lobe was also found, possibly due to an operation N.A. underwent.[2]
The accident
[edit]In 1960, N.A.’s brain was damaged by a miniature fencing foil. At the time he was 22 years old. With the help of magnetic resonance imaging (MRI) researchers found 26 years later the three areas that got damaged. N.A.´s injuries were studied by the neurologist Larry Squire and played an important role in the development of theories that explain the link between brain function and memory.[1]
Symptoms
[edit]N.A. exhibited symptoms of severe anterograde amnesia, being unable to form any new verbal memories.[3]
His nonverbal memory was less affected, as were most of his mental faculties including his perception, vigilance and memories, having no retrograde amnesia.[4]
Neuropathology
[edit]Patient N.A. underwent multiple neuroimaging studies using Computed Tomography (CT) and Magnetic Resonance Imaging.[2] His first CT was conducted in 1977, followed by another examination in 1983. In both examinations, N.A.'s brain abnormalities included a hypodense region in the left thalamus. In the 1983 examinations, an enlarged right temporal horn of the lateral ventricle was found.[2] Four magnetic resonance imaging studies were conducted on N.A., from 1986 to 1987. Diencephalic abnormalities were found including damage to the left thalamus extending anteroposteriorly into brain nuclei. Patient N.A.'s brain damage probably disrupted the mammillothalamic tract and postcommissural fornix. The posterior hypothalamus was disrupted and the mammillaries were missing in both brain hemispheres.[5] His right anterior temporal lobe was damaged.[2]
Neurologists' interpretations of NA's symptoms
[edit]Due to his injuries three major areas of the brain were damaged, leading to his severe amnesia. Other studies concerning amnesia suggested that when amnesia occurs, it is usually followed by a temporary retrograde amnesia,[6] thus distinguishing between a brief retrograde amnesia and a substantial impairment of the patient's cognitive functions.[7] Based on this information, doctors inferred that amnesia is a result of the conjointly damaged diencephalic structures, such as the internal medullary lamina, the intralaminar nuclei, the mediodorsal nucleus, and the mammillothalamic tract.[2]
At first, after undergoing a series of CT scans, it was assumed that the region of the mediodorsal nucleus was affected by a left thalamic lesion. After further investigations using magnetic resonance imaging it was shown that his lesion was more extended. According to the tests he underwent, he suffered from a memory impairment related mostly to verbal material rather than the nonverbal one;[1] however it was difficult to understand what damaged area was responsible for this effect.[1]
The damage in the mammillary nuclei itself was not related to the type of memory impairment that the patient N.A suffered from but rather influencing it through the combination with the damage that occurred in the thalamic structures.[1]
Contribution to science
[edit]The case of patient N.A provided valuable insights into the organization of memory systems in the brain and the role of the hippocampus in episodic memory formation. It has contributed significantly to our understanding of the brain’s memory processes and the distinction between different memory systems.[1]
Additionally, the study of patient N.A. has contributed to research on amnesia, especially anterograde amnesia. It gave an insight on the underlying structures and processes of amnesia. The case of N.A. helped to determine the causes of anterograde amnesia and proved that amnesia can be caused by damaging multiple diencephalic structures.[1]
Patient N.A. was subject of many studies and examinations since his accident.[1] Researcher Larry Ryan Squire did multiple studies with patient N.A.[6]
Cued recall
[edit]Cued recall tests done to test memory on patient N.A. and other patients suffering from Korsakoff syndrome or amnesia caused by ECT treatment found that these patients generally do not have the advantage of using category cues.[6] Several trials did show an increased advantage of patient N.A. using cues compared to Korsakoff patients. Therefore patient N.A. also helped to examine differences in different forms of amnesia.[6]
References
[edit]- ^ a b c d e f g h i Squire, Larry R.; Amaral, David G.; Zola-Morgan, Stuart; Kritchevsky, Mark; Press, Gary (July 1989). "Description of brain injury in the amnesic patient N.A. Based on magnetic resonance imaging". Experimental Neurology. 105 (1): 23–35. doi:10.1016/0014-4886(89)90168-4. PMID 2744126.
- ^ a b c d e Mair, Robert G.; Miller, Rikki L.A.; Wormwood, Benjamin A.; Francoeur, Miranda J.; Onos, Kristen D.; Gibson., Brett M. (July 2015). "The neurobiology of thalamic amnesia: Contributions of medial thalamus and prefrontal cortex to delayed conditional discrimination". Neuroscience & Biobehavioral Reviews. 54: 161–174. doi:10.1016/j.neubiorev.2015.01.011. PMID 25616180.
- ^ Ramos, Gabriel Bortoli; Lopes, Cesar Castelo Branco; Comerlatti, Luiz Roberto; Studart-Neto, Adalberto; Silva, Guilherme Diogo (November 2022). "Letter to the Editor: Is it time to expand the clinical spectrum of transient global amnesia?". Journal of the Neurological Sciences. 442: 120449. doi:10.1016/j.jns.2022.120449. PMID 36272269.
- ^ (2018, August 23) Who is Patient NA? Brain Stuff. https://brainstuff.org/blog/who-is-patient-na
- ^ Purves, Dale; Augustine, George J.; Fitzpatrick, David; Katz, Lawrence C.; LaMantia, Anthony-Samuel; McNamara, James O.; Williams, S. Mark, eds. (2001). "Sleep and Wakefulness". Neuroscience (2nd ed.). Sinauer Associates. ISBN 978-0-87893-742-4.
- ^ a b c d Squire, Larry R.; Douglas Wetzel, C.; Slater, Pamela C. (1978). "Anterograde amnesia following ect: An analysis of the beneficial effects of partial information". Neuropsychologia. 16 (3): 339–348. doi:10.1016/0028-3932(78)90027-1. PMID 703948.
- ^ Cohen, Neal J.; Squire, Larry R. (January 1981). "Retrograde amnesia and remote memory impairment". Neuropsychologia. 19 (3): 337–356. doi:10.1016/0028-3932(81)90064-6. PMID 7266827.
