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Book 1, Chapter 2 Investigating memory: experimental and clinical investigations of remembering and forgetting runs to 40 pages and is one of the three chapters that are options on the first TMA.

Introduction re-introduces the encoding, storage and retrieval model of memory and points out that there are different types of memory which are considered in more detail throughout the rest of the chapter.

What types of memory are there? This begins by introducing the idea of remembering as a form of mental time-travel (Tulving, 2002) made up of a series of episodes and autobiographical events. There is a discinction between declarative memory (i.e. memory of events) and non-declarative memory (i.e. memory of processes). The episodic memory is linked to the hippocampus and medial temporal lode (MTL) (as evidenced through brain damage and observational/experimental studies). Memory malfunction: the evidence from neuropsychology and amnesia goes on to consider what happens when something goes wrong in particular examining the cases of Clive Wearing and Henry Molaison who, through losing the ability to lay down new memories, are essentially always living as though they had just woken up. Although in both cases their episodic memory is gone, they retain their procedural memory so CW can still play musical instruments. This anterograde inability to create new memories contrasts with retrograde amnesia which is the loss of memories previously laid down. The general lack of loss of semantic memory (i.e. language or intellectual impairments) implies a separation of these from episodic memory (Tulving, 1985). All cases are different as a consequence of the differing causes and different brain regions affected. Memory brain regions: the key role of the hippocampus begins by pointing out that since the damage to CW’s brain was to the hippocampus and since he both retained knowledge of events before the damage and was able to carry on normal conversations (thus retaining short term memory), these functions must take place outside the hippocampus (Milner). Moreover, he could still acquire new vocabulary and new semantic information (albeit inconsistently) (Corkin, 1984, 2002). Other damage in areas adjacent to the hippocampus points to these having an role in laying down long term memories (e.g. the fencing foil incident). Converging evidence for the role of the hippocampus in memory starts with Krebs (1989) study of birds that found those with larger hippocampuses were better at remembering where they stored food with Sherry and Hoshooley (2010) finding that it was largest at the times of year when chickadees stashed their food. O’Keef (1976) found that rats build an internal map of their enclosures using place cells and head cells which acted as direction indicators. Maquire (2000) found a similar effect in London cab drivers: the hippocampus increased in size with experience in the job (would this still apply now that GPSs are used?). Huppert and Piercy (1976, 1978) highlighted the difference between familiarity and recognition in their experient with Korsakoff patients: both normal and afflicted patients had very similar scores on familiarity but quite different ones on recognition of having seen the images the same day or the day before. Shimamura and Squire (1987) referred to this difference as source amnesia i.e. a difficulty of recalling when things happened. Korsakoff patients also exhibit confabulation, the remembering of things that didn’t happen (Moscovitch, 2002) which may be related to déja vu. Malfunctioning mental time travel: retrograde amnesia and the temporal gradient introduces the concept of retrograde amnesia i.e. the loss of memories predating the damage which tends to have a temporal gradient with earlier memories being more resilient. Consolidation theory (Squire, 1992), proposes that after a time in the hippocampus the memories are consolidated elsewhere. Takashima 2009) illustrated this and it has been shown through damage to the hippocampus largely affecting recent memories rather than distant ones (Squire, 1992). That said, there is a remineniscence bump in autobiographical memories around the teens and twenties. Autobiographical memories are difficult to test for accuracy and may have a social or family memory effect. Knowing what you don’t know you know: explicit versus implicit memory picks up the idea of explicit memory (what happened when) and implicit memory (procedural). For example, Henry Molaison (HM) could improve his performance on a motor task yet couldn’t remember practicing it. In the case of Parkinson’s this is reversed i.e. they have episodic memory but can’t learn new processes.

Testing memory: a few reflections starts off by noting that memories consist of events that have an item, a time and a place and that usually we will have some cue to trigger the recall. Laboratory tests are generally either free recall, cued recall or recognition tests. Standing (1973) showed that recognition is very easy to do. Huppert and Piercy (1976, 1978) suggested that it is the links between event and times is broken in amnesia i.e. it is in the reconstruction that the problem occurs. Notably, impaired familiarity with normal recollection doesn’t happen. Note that serial recall (recalling items in order) is harder than free recall for normal adults but the reverse applies in Altzeimers patients (Cherry, 2002). Familiarity versus recollection: neurological correlates notes developments in memory research on ageing with the latest (Tree and Perfect, 2004) indicating that it is the linking of source and item that is lost on ageing i.e. you’ll know something but not be able to relate it to when it happened. Thus Cohen and Faulkner (1989) found that there were difficulties in source based information.

Modelling memory introduces two different memory models. Model 1: Aggleton and Brown’s (1999) neural model of episodic memory posited that memory had system 1 that in the hippocampus/mammilliary bodies/thalmic regions that dealt with episodic information (explicit memory and recollection) and system 2 in the MTL which dealt with familiarity i.e. context free memory. Squire (2000) and others have argued that there is no functional difference and that the whole MTL is used in memory. It’s supported by Korsakoff patients who have pre-frontal cortex lesions and who do well on familiarity tests but poorly on others (Ranganath and Knight, 2003). Neuropsychological evidence for the two-system proposal underpinning recall and recognition is supplied by Mayes (2002) who had a patient with hippocampus damage performing well on recognition but poorly on recall. Neuropsychological evidence against the two-system proposal Chan (2002) had a similar patient who performed poorly on both recall and recognition as did Squire (2007). Davachi and and Wagner (2002) present fMRI evidence showing that there is always some hippocampus activity in memory. Model 2: Baddeley and Hitch’s working memory model took account of the recency effect in memory and proposed that all incoming information is held in short term memory before being transferred to longer term memory by way of a working memory (Short Term Storage, STS) which had a limited capacity. Baddeley and Hitch (1974) using a dual task experiment showed that working memory and STS weren’t the same thing. From this, they proposed that there were multiple STS areas (e.g. verbal, image). Baddeley (1975) showed that there was no difference in the number of short or long words that could be remembered but only if they were presented visually. Modes include audio, visual and spacial (Baddeley, 1980). An important part of this model is the central executive which Baddeley proposed as the mechanism by which focus, task switching and prioritisation was achieved. Alzeimer’s patients are unable to perform tasks concurently even when they are at an appropriate level of difficulty. Finally there is the episodic buffer which can hold around four parts of information (Allen, 2012) and enables us to remember a sentence when ordinarily we can only remember around two seconds of random words.

Reference: Kaye, H. and Tree, J. (2016). Investigating memory: experimental and clinical investigations of remembering and forgetting. In Ness, H., Kaye, H. and Stenner, P. (2016). Investigating Psychology 3. Milton Keynes: The Open University.

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