Developmental amnesia, featured with severely impaired episodic memory and almost normal semantic memory, has been discovered to occur in children with hippocampal atrophy. This unique combination of characteristics seems to challenge the understanding that early loss of episodic memory may impede cognitive development and result in severe mental retardation. Although a few underlying mechanisms have been suggested, no computational model has been reported that is able to mimic the unique combination of characteristics. In this study, a cognitive system is presented, and developmental amnesia is demonstrated computationally in terms of impaired episodic recall, spared recognition and spared semantic learning. Impaired sequential/spatial learning ability of the hippocampus is suggested to be the cause of such amnesia. Simulation shows that impaired sequential leaning may only result in severe impairment of episodic recall, but affect neither recognition ability nor semantic learning. The spared semantic learning is inline with the view that semantic learning is largely associated with the consolidation of episodic memory, a process in which episodic memory may be mostly activated randomly, instead of sequentially. Furthermore, retrograded amnesia is also simulated, and the result and its mechanism are in agreement with most computational models of amnesia reported previously.
Declarative memory, or explicit memory, can be fractionated into episodic memory and semantic memory (Tulving, 1972). Episodic memory refers to personally based memories and semantic memory refers to the memory of factual knowledge. The loss of the capacity in retaining episodic memory leads to various amnesias, e.g., retrograde amnesia and anterograde amnesia. Neuropsychological analyses and functional imaging studies (e.g., Aggleton & Brown, 1999;Eichenbaum, 1992, Hodges & Carpenter, 1991;Zola et al. 1986) have broadly confirmed the link between declarative memory and the medial temporal lobe (MTL). The MTL consists of the hippocampus (including the CA fields, dentate gyrus and subiculum), and the adjacent entorhinal, perirhinal and parahippocampal cortices, and plays a critical role in both episodic memory retention and semantic memory acquisition through memory consolidation (see Eichenbaum, 2004). Many theoretical and computational models have been proposed to characterize the important role of the MTL in semantic learning via memory consolidation of episodic memory (e.g., Gluck & Myers, 1993;Hasselmo et al., 1996;Milner, 1989;Nadel et al., 2000;Squire et al., 1984;Treves & Rolls, 1992). Some of the models have simulated how a damaged hippocampus may affect the capacity of episodic memory, resulting in retrograde amnesia and/or anterograde amnesia, as well as, the failure of memory consolidation (e.g., Alvarez & Squire, 1994;McClelland et al., 1995;Meeter & Murre, 2005;Murre, 1996;O'Reilly & Rudy, 2000). Therefore, lesioned hippocampus may severely impair the acquisition of semantic memory since impaired episodic memory could result in the deficit of memory consolidation. This view is supported by empirical findings about patients with hippocampal amnesia who often show extreme difficulty in the acquisition of semantic knowledge (e.g., Gabrieli et al., 1988; The finding of developmental amnesia first reported by Vargha-Khadem et. al. (1997) provides a new twist to the understanding about the correlation between episodic memory and semantic memory.
Developmental amnesia is a rather atypical form of memory deficit that has been discovered to occur in children with hippocampal lesion. The patients studied by Vargha-Khadem et. al. had all suffered bilateral damage limited to the hippocampal formation at very early ages with sparing of surrounding cortical areas. Crucially, they all appeared to have profound lack of memory for the events of everyday life, but all developed normal levels of performance on tests of intelligence, language, and general knowledge. Subsequent studies of other developmental amnesic patients (e.g., Baddeley et al., 2001;Isaacs et al. 2003) confirmed the severely impaired episodic memory that is accompanied by intact capacity of semantic learning. The impairment of episodic memory in such patients is unique, and appears to only affect the capacity of recall, not of recognition. For example, Baddeley et al. (2001) reported a patient who appeared to lack the recollective phenomenological experience normally associated with episodic memory, but performed within the normal range on each of six recognition tests.
Early loss of episodic memory should impede cognitive development and result in severe mental retardation, based on the view that semantic memory largely results from the consolidation of episodic memory. This does not seem to be the case for patients with developmental amnesia. Vargha-Khadem et al. (1997) suggested that the unique characteristics of developmental amnesia could be explained based on the view that episodic memory is partially dissociated from semantic memory, and only episodic memory is fully dependent on the hippocampus. They also argued that recognition could be dissociated from recall memory, which was supported by evidence from hippocampectomized monkeys. Baddeley et al. (2001) further suggested that the recollective process of episodic memory is not necessary for either recognition or acquisition of semantic knowledge. On the other hand, Squire & Zola (1998) and Manns & Squire (1999) proposed a number of different explanations. One is that the early onset of damage in the patients may have led to some form of adaptation of semantic acquisition, and another is about the residual episodic memory observed in all such patients. They noted that the damage to episodic memory of the studied patients was not complete (i.e. patients had non-zero scores on recall tests and non-total atrophy in the hippocampus), and suggested this residual ability might be enough to explain their near normal semantic memory performance. While none of the proposed explanations has been commonly agreed on, no computational model has been reported to simulate the unique characteristics of impaired recall, spared recognition and semantic memory under any given underlying mechanism.
In this study, a cognitive and computational model is presented in which the impaired sequential learning
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