Role of Hippocampus in Declarative Memory
The hippocampus is a structure of the medial temporal lobe; an area which has long been associated with declarative memory (episodic/autobiographical memory). Von Bechterew (1900), Gruntal (1947), Glees & Griffin (1952). In particular, Scoville’s (1954) famous case study of H.M. indicated the role of the medial temporal lobe in episodic memory after H.M. showed severe anterograde and moderate temporally graded retrograde amnesia (upto 7 years) following surgical bilateral removal of this area aimed at curing his epileptic seizures. The deficit was specific to declarative memory – e.g. H.M. could still learn new procedural skills (non-declarative).
(Hippocampus)
Subsequently, evidence emerged which pinpointed episodec memory loss to damage of the hippocampus. Milner (1974) concluded that severity of damage to the hippocampal formation in patients with medial temporal lobe resections correlated with severity of memory deficits. Rempel-Clower et al. (1996) showed patients with non-mechanical damage to the hippocampus and medial temporal lobe in three case studies who suffered severe memory loss following physiological damage to these areas. Post mortem examination revealed that damage was only evident in the hippocampus. Results on the patients word recognition tasks were good, however they were greatly impaired on recall tasks, implying that the role of the hippocampus may lie here (recall). Criticisms of this study are however that all three patients lived very unhealthy lifesyles with high co-morbidities (alcohol Kortakoffs?). Furthermore, damage to the hippocampus is far easier to detect than that of other areas due to it’s uniform structure. Therefore it cannot be assumed that damage was limited only to the hippocampus.
Animal models of human amnesia may be a more controlled method of investigation due to the ability to manipulate variables. Mishken et al. (1978) developed a ‘non-matching sample task’ in monkeys where identification of a novel object
(Hippocampus)
Subsequently, evidence emerged which pinpointed episodec memory loss to damage of the hippocampus. Milner (1974) concluded that severity of damage to the hippocampal formation in patients with medial temporal lobe resections correlated with severity of memory deficits. Rempel-Clower et al. (1996) showed patients with non-mechanical damage to the hippocampus and medial temporal lobe in three case studies who suffered severe memory loss following physiological damage to these areas. Post mortem examination revealed that damage was only evident in the hippocampus. Results on the patients word recognition tasks were good, however they were greatly impaired on recall tasks, implying that the role of the hippocampus may lie here (recall). Criticisms of this study are however that all three patients lived very unhealthy lifesyles with high co-morbidities (alcohol Kortakoffs?). Furthermore, damage to the hippocampus is far easier to detect than that of other areas due to it’s uniform structure. Therefore it cannot be assumed that damage was limited only to the hippocampus.
Animal models of human amnesia may be a more controlled method of investigation due to the ability to manipulate variables. Mishken et al. (1978) developed a ‘non-matching sample task’ in monkeys where identification of a novel object