Patient N.A.

Last updated
Patient N.A.
Born (1938-07-09) July 9, 1938 (age 85)
Known forpatient of anterograde amnesia

Patient N.A. (born July 9th, 1938) was (is?) an American man, who developed anterograde amnesia as a result of an 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]

Contents

Patient N.A.’s accident happened when he was 22 years old (1960). A fencing foil went up his nose and injured his brain. This resulted in severe anterograde amnesia, especially for verbal material, as well as impaired eye movements. His cognitive abilities remained intact. [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

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

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 past memories, having no retrograde amnesia. [4]

Neuropathology

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

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

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

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]

Related Research Articles

<span class="mw-page-title-main">Thalamus</span> Structure within the brain

The thalamus is a large mass of gray matter on the lateral walls of the third ventricle forming the dorsal part of the diencephalon. Nerve fibers project out of the thalamus to the cerebral cortex in all directions, known as the thalamocortical radiations, allowing hub-like exchanges of information. It has several functions, such as the relaying of sensory and motor signals to the cerebral cortex and the regulation of consciousness, sleep, and alertness.

<span class="mw-page-title-main">Wernicke–Korsakoff syndrome</span> Combined presence of Wernickes encephalopathy (WE) and Korsakoffs syndrome

Wernicke-Korsakoff syndrome (WKS) is the combined presence of Wernicke encephalopathy (WE) and Korsakoff syndrome. Due to the close relationship between these two disorders, people with either are usually diagnosed with WKS as a single syndrome. It mainly causes vision changes, ataxia and impaired memory.

<span class="mw-page-title-main">Korsakoff syndrome</span> Mental illness caused by a lack of thiamine in the brain

Korsakoff syndrome (KS) is a disorder of the central nervous system characterized by amnesia, deficits in explicit memory, and confabulation. This neurological disorder is caused by a deficiency of thiamine (vitamin B1) in the brain, and it is typically associated with and exacerbated by the prolonged, excessive ingestion of alcohol. Korsakoff syndrome is often accompanied by Wernicke encephalopathy; this combination is called Wernicke–Korsakoff syndrome.

<span class="mw-page-title-main">Henry Molaison</span> American memory disorder patient

Henry Gustav Molaison, 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.

<span class="mw-page-title-main">Temporal lobe</span> One of the four lobes of the mammalian brain

The temporal lobe is one of the four major lobes of the cerebral cortex in the brain of mammals. The temporal lobe is located beneath the lateral fissure on both cerebral hemispheres of the mammalian brain.

<span class="mw-page-title-main">Mammillary body</span> Part of the limbic system

The mammillary bodies are a pair of small round bodies, located on the undersurface of the brain that, as part of the diencephalon, form part of the limbic system. They are located at the ends of the anterior arches of the fornix. They consist of two groups of nuclei, the medial mammillary nuclei and the lateral mammillary nuclei.

In neurology, anterograde amnesia is the inability to create new memories after an event that caused amnesia, leading to a partial or complete inability to recall the recent past, while long-term memories from before the event remain intact. This is in contrast to retrograde amnesia, where memories created prior to the event are lost while new memories can still be created. Both can occur together in the same patient. To a large degree, anterograde amnesia remains a mysterious ailment because the precise mechanism of storing memories is not yet well understood, although it is known that the regions of the brain involved are certain sites in the temporal cortex, especially in the hippocampus and nearby subcortical regions.

<span class="mw-page-title-main">Fornix (neuroanatomy)</span> Bundle of nerve fibers in the brain

The fornix is a C-shaped bundle of nerve fibers in the brain that acts as the major output tract of the hippocampus. The fornix also carries some afferent fibers to the hippocampus from structures in the diencephalon and basal forebrain. The fornix is part of the limbic system. While its exact function and importance in the physiology of the brain are still not entirely clear, it has been demonstrated in humans that surgical transection—the cutting of the fornix along its body—can cause memory loss. There is some debate over what type of memory is affected by this damage, but it has been found to most closely correlate with recall memory rather than recognition memory. This means that damage to the fornix can cause difficulty in recalling long-term information such as details of past events, but it has little effect on the ability to recognize objects or familiar situations.

In neurology, retrograde amnesia (RA) is the inability to access memories or information from before an injury or disease occurred. RA differs from a similar condition called anterograde amnesia (AA), which is the inability to form new memories following injury or disease onset. Although an individual can have both RA and AA at the same time, RA can also occur on its own; this 'pure' form of RA can be further divided into three types: focal, isolated, and pure RA. RA negatively affects an individual's episodic, autobiographical, and declarative memory, but they can still form new memories because RA leaves procedural memory intact. Depending on its severity, RA can result in either temporally graded or more permanent memory loss. However, memory loss usually follows Ribot's law, which states that individuals are more likely to lose recent memories than older memories. Diagnosing RA generally requires using an Autobiographical Memory Interview (AMI) and observing brain structure through magnetic resonance imaging (MRI), a computed tomography scan (CT), or electroencephalography (EEG).

<span class="mw-page-title-main">Papez circuit</span> Neural circuit

The Papez circuit, or medial limbic circuit, is a neural circuit for the control of emotional expression. In 1937, James Papez proposed that the circuit connecting the hypothalamus to the limbic lobe was the basis for emotional experiences. Paul D. MacLean reconceptualized Papez's proposal and coined the term limbic system. MacLean redefined the circuit as the "visceral brain" which consisted of the limbic lobe and its major connections in the forebrain – hypothalamus, amygdala, and septum. Over time, the concept of a forebrain circuit for the control of emotional expression has been modified to include the prefrontal cortex.

Memory disorders are the result of damage to neuroanatomical structures that hinders the storage, retention and recollection of memories. Memory disorders can be progressive, including Alzheimer's disease, or they can be immediate including disorders resulting from head injury.

The mammillothalamic tract is an efferent pathway of the mammillary body which projects to the anterior nuclei of thalamus. It consists of heavily myelinated fibres. It is part of a brain circuit involved in spatial memory.

Ribot's law of retrograde amnesia was hypothesized in 1881 by Théodule Ribot. It states that there is a time gradient in retrograde amnesia, so that recent memories are more likely to be lost than the more remote memories. Not all patients with retrograde amnesia report the symptoms of Ribot's law.

<span class="mw-page-title-main">Medial dorsal nucleus</span>

The medial dorsal nucleus is a large nucleus in the thalamus.

Kent Cochrane, also known as Patient K.C., was a widely studied Canadian memory disorder patient who has been used as a case study in over 20 neuropsychology papers over the span of 25 years. In 1981, Cochrane was involved in a motorcycle accident that left him with severe anterograde amnesia, as well as temporally graded retrograde amnesia. Like other amnesic patients, Cochrane had his semantic memory intact, but lacked episodic memory with respect to his entire past. As a case study, Cochrane has been linked to the breakdown of the single-memory single-locus hypothesis regarding amnesia, which states that an individual memory is localized to a single location in the brain.

The trisynaptic circuit or trisynaptic loop is a relay of synaptic transmission in the hippocampus. The circuit was initially described by the neuroanatomist Santiago Ramon y Cajal, in the early twentieth century, using the Golgi staining method. After the discovery of the trisynaptic circuit, a series of research has been conducted to determine the mechanisms driving this circuit. Today, research is focused on how this loop interacts with other parts of the brain, and how it influences human physiology and behaviour. For example, it has been shown that disruptions within the trisynaptic circuit lead to behavioural changes in rodent and feline models.

Retrospective memory is the memory of people, words, and events encountered or experienced in the past. It includes all other types of memory including episodic, semantic and procedural. It can be either implicit or explicit. In contrast, prospective memory involves remembering something or remembering to do something after a delay, such as buying groceries on the way home from work. However, it is very closely linked to retrospective memory, since certain aspects of retrospective memory are required for prospective memory.

Amnesia is a deficit in memory caused by brain damage or brain diseases, but it can also be temporarily caused by the use of various sedative and hypnotic drugs. The memory can be either wholly or partially lost due to the extent of damage that is caused.

Semantic amnesia is a type of amnesia that affects semantic memory and is primarily manifested through difficulties with language use and acquisition, recall of facts and general knowledge. A patient with semantic amnesia would have damage to the temporal lobe.

Vascular thalamic amnesia occurs when the thalamus is affected by Korsakoff's syndrome or damaged by lacunar infarcts or hemorrhages. Another common cause for damage to the thalamus that may contribute to the development of amnesia is a stroke. It involves a loss of memory and a shift in behaviors and attitudes that are associated with various behavioral disorders.

References

  1. 1 2 3 4 5 6 7 8 9 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.
  2. 1 2 3 4 5 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.
  3. ↑ 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.
  4. ↑ (2018, August 23) Who is Patient NA? Brain Stuff. https://brainstuff.org/blog/who-is-patient-na
  5. ↑ 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.
  6. 1 2 3 4 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.
  7. ↑ 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.
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