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 вЂ" 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 пÑ" 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 produces a reward. Mechanical lesioning of the medial temporal lobe targeting the hippocampus resulted in impaired performance with increasing delay between encoding and recall. This supports the role of the hippocampus in recognition memory, however it is not clear how selective damage was to the hippocampus. Several researchers have since used ibotenic acid to more selectively destroy the hippocampus in monkeys (e.g. Zola et al. 2000). Essentially, it has been reported that as a lesion becomes more and more specific to the hippocampus, the effect (symptoms) of the lesion becomes weaker; these findings are of course very bad news for the hippocampalcentric view of declarative memory. (i.e. obvious that other areas involved).

In a review by Aggleton & Brwon (2001) the entorhinal and perirhinal cortices alone were said to have as large an effect on episodic memory as hippocampal damage. The perirhinal cortex in particular was particularly associated with recognition memory; agreeing with a similar finding by Squire & Zola (1996). This review also suggested that tests on monkeys and humans rely on different types of recognition and they inferred from evidence generated by these that the hippocampus may support episodic based recognition whereas the perirhinal and entorhinal cortices support familiarity based recognition.

Studies in humans however contradict in part the view emerging from animal studies that the hippocampus alone is not responsible for episodic memory. Zola-Morgan’s (1982) study of R.B. and Rempel-Clover et al.’s (1996) study which also included other patients with damage specific to the hippocampus concluded that severity of impairment is dependant on extent of damage with the hippocampus and that damage to this area alone is sufficient to cause temporally graded retrograde amnesia. The advantage of these studies is in their ecological validity and human relevance. However, limitations also lie here; with the uncertainty of how specific damage actually was to the hippocampus. In addition, it is difficult to make empirical statements based on a small amount of qualitative data.

In a more quantitative study of human memory impairment, Di Paola et al. (2007?)conducted fMRI scans of 18 Alzheimer’s disease and 18 control subjects and found that performance on episodic memory delayed recall tests covaried with grey matter volume in the entorhinal cortex; supporting its role in episodic