Amnesia Study

Amnesia, as an organic clinical disorder caused by brain damages, refers to permanent disturbance of declarative memory despite preserved cognitive functions (Markowitsch, 2001; Moscovitch, 2004). Patients with anterograde amnesia (AA) consistently show different degrees of impairment in forming declarative memory, with normal implicit and working memory. Studying amnesia provides insights on cognitive and biological mechanism underling memory, and a representative model is vital for understanding existing data and making predictions. Although researches on amnesia have progressed a lot since the famous case of H.M., a convincing and widely accepted model has yet to be established. One of the main debates concerning it is whether the major

Apart from the models themselves, external factors have also posed difficulties in determining whether one of them is better. Although declarative memory could be subdivided, the interdependent nature of the subcomponents makes it difficult to test them separately in a clean way. Furthermore, difficulty in making accurate predictions is also a barricade. To predict impairments from brain lesions, it is essential to localize the neural substrates of memory in the corresponding brain regions. However, the plasticity of brain and adoption of compensatory strategies make it difficult to map the impairments and preserved abilities in brain. In this essay, the associative model proposed by Squire and the dissociative model proposed by Aggleton and Brown (A&B) would be used to illustrate the difficulties in determining whether one of them better describes amnesia. It is argued that both of them are inconclusive in explaining all the of existing data. Moreover, the interdependent nature of subtypes within declarative memory and plasticity of brain make both of the models not testable or