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THE CASE OF K C. Contributions of a memory-impaired person to memory theory. By Daniel Moffatt. K C was born prematurely in 1951 and raised in a supportive family of two parents and four younger siblings in Toronto. His childhood development was reported as unremarkable. He experienced two head injuries in his youth, the first, a bale of hay falling on his head, and the second, a multi-vehicle collision. He suffered a third, and most severe, accident at age 30, after he crashed his motorcycle driving home from work, resulting in an emergency hospital presentation. Due to the severity of his condition, he was transferred to a larger specialty hospital where he underwent neurosurgery to remove a large left-sided subdural hematoma. His consciousness returned 72 hours post-accident, where he spent one month in the intensive care unit, followed by another six months in a rehabilitation unit. At initial presentation to the emergency department after his motorcycle crash, K C was unconscious, suffering from clonic seizures with dilated fixed pupils. Upon waking up in the intensive care unit, K C demonstrated a stuporous demeanor for the next five days, an altered level of consciousness rendering him only able to respond to simple commands, and at seven days post-trauma he was able to recognize his mothers face. Upon his transfer to a rehabilitation ward at one-month post trauma, K C was noted to be reading and conversing well, and began to recognize his friends faces. However, he still showed a slowed mentation, with right-sided paralysis, and right-sided homonymous hemianopia, a condition where half the visual field from each eye is lost. Once K C was discharged home, seven months post-trauma, the details of his memory difficulties became evident. He appeared unable to commit any new self-perspective information to memory, a form of anterograde amnesia which continues to present day, as details of personal occurrences continue to exist only in the present, vanishing from K C’s reality the moment his thoughts are directed elsewhere, for example he does not recall meeting a researcher who had visited his house on multiple occasions. He was also found to lack autonoetic consciousness, the ability to experience a vivid mental representation of a past memory or possible future event from a self-perspective. Friends of K C reported that he did not remember the details of events they had shared together, regardless of how meaningful the event was, such as the circumstances of when he was told about his own brothers’ death. Many years after the accident, K C has been able to acquire some personal knowledge of the events in his life pre-injury, however this is attributed to a semantic learning mechanism, where he understands that an event took place as if it had happened to someone else, rather than remembering the event from a self-perspective. Friends of K C also report a distinct change in his personality, as his previous extroverted, thrill-seeking character has changed to become a tranquil, soft-spoken individual. K C underwent thorough neuropsychological testing in both 1996 and 2003, with scores shown in Figure 1. His intellectual and non-mnemonic cognitive function was found to be mostly normal, obtaining Full-Scale, Performance, and Verbal IQ scores of 99 on the Wechsler Abbreviated Scale of Intelligence test in 2003, indicating average intelligence. His language functions were typically well preserved, showing no signs of aphasia on the Western Aphasia Battery test, and no difficulty in naming line drawings of objects on the Boston Naming Test in 1996. Visual impairments were apparent, with borderline tritan colour-blindness seen on the City University Color Vision Test, and difficulties with complex face-matching task that requires the synthesis of multiple visual features on the Facial Recognition Test. Anterograde memory function was found to be severely impaired, with K C showing significantly poor performance on the Wechsler Memory Scale Revised test, the California Verbal Learning Test. On the Warrington Recognition Memory Test for words and faces, K C scored under the 5th percentile for immediate recall, and under the 1st percentile for delayed recall. Retrograde memory function was also severely impaired, where he was unable to produce a single episode from his past that was distinct in time and place on the Autobiographical Memory Inventory test. K C’s physical exam is unremarkable, showing strength, bulk, tone, and reflexes are within normal limits, except for decreased dexterity in the right hand and a right extensor plantar response. Somatosensory function is normal, apart from a slight right-sided decrease temperature perception. Cerebellar function is normal, although gait is wide based due to osteoarthritis. He suffers mild vision loss in the right eye, and severe vision loss in the left eye as a result of glaucoma. K C underwent three MRI scans in 1990, 1996 and 2002, all of which showed similar results as seen in Figure 2 & 3, where the dark areas indicate tissue damage or death. There is a large posterior occipital–temporal infarction on the left hemisphere, involving the cuneous, lingual and parahippocampal gyri, likely resulting from posterior cerebral artery compression secondary to the increased intracranial pressure caused by the motorcycle accident. This is consistent with K C’s symptoms of impaired colour perception and complex facial matching, whilst preserving other visual functions such as reading and recognition of objects. There is also a smaller anterior lesion in K C’s frontal–parietal cortex, which is limited to the dorsolateral and pre-motor functional areas. This may account for his majority preservation of executive function, with small impairments in phonemic fluency and reduced strategic retrieval of recent and remote memories. The most substantial damage is located in K C’s medial temporal lobes, with pronounced necrosis and atrophy of the hippocampal formation, including the hippocampus, parahippocampus, and associated diencephalic and basal forebrain structures, spreading out into entorhinal and perirhinal cortices. This is theorised to be the cause of his profound impairment in autobiographical memory, as the affected areas are critical for explicit memory and learning. Additionally, damage to K C’s amygdala may account for his personality changes and subdued demeanour. His lateral temporal cortex and occipital structures appear unaffected, which may explain his preservation of semantic memory and implicit learning. The case of K C has played a fundamental role in our understanding of memory and its associated brain structures. After suffering significant head trauma from a motorcycle accident, K C presented with a lack of autonoetic consciousness, in addition to global anterograde amnesia and retrograde episodic amnesia. Neuropsychological testing and diagnostic imaging found substantial atrophy of his hippocampal formation, alongside changes to his amygdala, posterior occipital–temporal cortex, and anterior frontal–parietal cortex, which caused significant impairment of autobiographical memory, without impairing executive or intellectual function. This case challenged the notion that memory was a unified system, demonstrating that explicit and implicit memory can be selectively impaired. It also helped establish the importance of the hippocampal formation as related to learning and memory. This information is crucial for psychological research and the understanding of the human brain. Thank you for listening.