It is proposed that a regular facet of anterograde amnesia is damage to part of an extended hippocampal system that consists of the hippocampus, the fornix, the mammillary bodies, and the anterior thalamic nuclei (Mayes & Downes, 1997). This instigates deficit in the recall of episodic information. The film illustrates that Lucy’s head injury impaired a part of her brain, although details are not explicitly explained. In a review published in the Medical Journal in 2004, According to clinical neuropsychologist Sallie Baxendale (2004), “it bears no relation to any known neurological or psychiatric condition”. Although dysfunctions in different brain regions can result in anterograde amnesia, the contribution of individual structures and their relationships still remains a matter of uncertainty and debate (Mayes & Downes, 1997). The failure to resolve this central issue is partly due to lack of amnesic subjects with specific patterns of pathology. It may also be due to the complexity of the relationships between those regions contributing to amnesia.Anterograde amnesia “diminishes between ECT treatments and accumulates across treatments” (Squire & Chace, 1975). It is difficult to identify exactly the point at which new learning ability reaches normal levels. Patients with anterograde amnesia following bilateral ECT in a number of studies seem to have recovered by 6 months after treatment and there is no good evidence that new learning ability is still deficient at this time.
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