Retrograde vs anterograde amnesia grated11/11/2023 M.’s memory impairment was restricted to declarative memory, or conscious memory for facts and events. He could keep information in his short-term, or working, memory, but when his attention turned to something else, that information was lost for good. He could not remember a conversation he had a few minutes prior or recognize the face of someone who had visited him that same day. could not remember any event that occurred since his surgery, including highly significant ones, such as the death of his father. was unable to learn new information, a memory impairment called anterograde amnesia. From the time of his surgery until his death in 2008, H. with a profound and permanent memory deficit. M.’s seizures and his general intelligence was preserved, the surgery left H. Although the surgery was successful in reducing H. The medial temporal lobes encompass the hippocampus and surrounding cortical tissue. suffered from severe epilepsy, and in 1953, he underwent surgery to have both of his medial temporal lobes removed to relieve his epileptic seizures. The most widely studied amnesic patient was known by his initials H. Unfortunately, this portrayal of amnesia is not very accurate. After some period of time (or another blow to the head), their memories come flooding back to them. Typically, in these fictionalized portrayals of amnesia, a character suffers some type of blow to the head and suddenly has no idea who they are and can no longer recognize their family or remember any events from their past. Most of us have had exposure to the concept of amnesia through popular movies and television. Ĭlearly, remembering everything would be maladaptive, but what would it be like to remember nothing? We will now consider a profound form of forgetting called amnesia that is distinct from more ordinary forms of forgetting. Patients with damage to the temporal lobes may experience anterograde amnesia and/or retrograde amnesia. Whether the condition is heterogeneous, involves a deficit in slow consolidation, disruption of unconsolidated memories, or blockage of maintenance or disruption of insufficiently rehearsed memories whether or not these have been slowly consolidated is discussed.\)įigure 19. Her long-term amnesia may have been caused by anterior temporal neocortex damage, possibly in association with her epileptic seizures. JL's remote memory was preserved for information first encountered in either the pre- or post-morbid period provided the information had received sufficient rehearsal over long periods of time. She also showed a retrograde amnesia, which appeared to be milder than her remote post-morbid memory deficit. Her recall and recognition was clearly impaired after a three-week delay. This problem may have been caused by JL's right-sided perirhinal and orbitofrontal cortex damage. The one exception was the patient's relatively greater impairment at difficult visual recognition tests for which verbalization may not have been an effective strategy. Her memory also seemed well preserved for at least 30 minutes following encoding. Apart from her memory impairments, JL's cognitive functions, including high-level visual perception, attention, semantic memory and executive functions were well preserved. Epilepsy developed within two years of JL's injury. The hippocampus appeared to be intact bilaterally. Her injury caused bilateral anterior temporal neocortex damage that was more extensive on the left and right-sided damage to the perirhinal and orbitofrontal cortices. A patient, JL, who has this condition following a closed-head injury, is described in detail. The precise neural and functional deficits that underlie this condition are unknown. Long-term amnesia is a slowly developing form of anterograde amnesia accompanied by retrograde amnesia of variable severity (Kapur, 1996 1997) often associated with damage to the anterior temporal neocortex and epileptic seizures.
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