IMPLICIT MEMORY AND AMNESIA Amnesic patients can still learn in - TopicsExpress



          

IMPLICIT MEMORY AND AMNESIA Amnesic patients can still learn in some ways. Procedural learning (such as learning a motor sequence) is intact and they can learn artificial grammar (Gazzaniga et al., 1998). In fact, people with intact brains can learn artificial grammar without explicit awareness of the rules. Fairly recently, a form of implicit memory known as priming has received widespread study in cognitive psychology (Schacter, 1987). Typically, participants view some words in an incidental learning task and are later asked to14 complete an independent word fragment test. Implicit memory is reflected by facilitated completion of words that participants were pre-exposed to, without an awareness that the pre-exposed words were relevant to the current test. One of the problems with such research is knowing whether some explicit memory is contaminating the results (Rugg, 1995). Amnesic patients are ideal for this sort of testing because they have no explicit memory for being pre-exposed at all. They show the same level of priming memory as do normal healthy participants, yet if given a recognition or recall test for the pre-exposed words, perform far worse than their counterparts. Their priming performance is dissociated from recall and recognition (Schacter, 1995). Similar dissociations have been observed within normal participants as a function of the instructions given during pre-exposure. While recognition has been found to be improved by generating rather than simply viewing words (a deeper level of processing), perceptual priming has shown the opposite effect (Roediger, 1990). It seems that seeing the word is important for priming to occur. This has lead to the concept of a perceptual representation system (PRS) for this form of priming (Ochsner, Chiu, & Schacter, 1998). Priming shows some perceptual specificity effects – simply changing the case that words are presented in leads to a reduction in priming. This kind of specificity has also been observed in the auditory domain (Church & Schacter, 1994) with changes in fundamental frequency or voice intonation reducing facilitated perception of degraded spoken words. Priming of these sorts is said to be data driven and seems to be strongly intertwined with the perceptual process itself. Perhaps receptors are uncovered or some other shorter term form of LTP occurs a few levels up in the perceptual hierarchy. The nodes for these words may be primed up to be more readily activated on re-presentation of the word. There are also concept15 driven forms of priming – for example, presentation of words with negative connotations has been shown to negatively bias participants ratings of neutrally presented people in a later task (Roediger, 1990). Research on priming has regenerated interest in the possible role of unconscious processes (Jacoby, Lindsay & Toth, 1992; Loftus & Klinger, 1992). Do the dissociations between implicit and explicit memory observed in amnesics and normal participants provide solid justification for such a division, with the explicit memory system dependent on the medial temporal lobes? A case of a patient with preserved recall but poor visual priming provides a double dissociation (Gazzaniga et al., 1998). The damaged area was in the extrastriate cortex (which makes sense in terms of the PRS concept). Arguing against this rigid division, the above completion of the double dissociation is tentative at best. Also, amnesics do not show quite the same perceptual specificity effects in priming tasks as normal participants do (Schacter, 1995). Explicit memory probably relies on some implicit forms of memory, but implicit memory, by definition, does not depend on explicit memory. What is it that makes us conscious that we are remembering something? Is it an overwhelming sense of familiarity or does some sort of affect tag connected to it (from the limbic system) indicate this to us. The flow of information in memory processes is not restricted to the medial temporal lobes: Because we attribute something as a memory indicates some frontal lobe involvement. Indeed, there are direct connections between the diencephalic memory structures and frontal lobes. What about other forms of memory such as working memory and skill learning and the sometimes powerful role of emotions? How might they be manifest in the brain?16 OTHER BRAIN STRUCTURES AND MEMORY SYSTEMS The frontal lobes have intricate connections to posterior regions including sensory and association cortices and the limbic system (Shimamura, 1995). In general, the function of this region has been summarized as effecting inhibitory control of extraneous activity and gating. The frontal lobes have been suggested as important in working memory. Broca’s area has been related to the phonological loop (Gazzaniga et al., 1998): By projecting to posterior regions, the dorsolateral prefrontal cortex might keep sensory regions active so that they can be held in memory. LTM could possibly be reactivated (into working memory) by frontal projections to the lateral anterior temporal lobes. Patients with frontal lobe damage show attention and concentration deficits that can lead to poor working memory (e.g., digit span) yet they show good explicit recognition memory (Shimamura, 1995). (This is the opposite pattern to MTL patients, giving a good dissociation between working memory and LTM.) Frontal patients show poor recall – this has been explained as being due to poor search and retrieval strategies, with the inability to inhibit irrelevant memory associations (Shimamura, 1995). (Maybe this could be related to Baddeley’s working memory model: Recall depends on activating LTM into working memory while in recognition the stimuli enter more directly through attention). Deficits observed in elderly people also show a similar pattern including poor source memory and prospective memory. Both of these forms of memory require good search and retrieval strategies. This pattern has been interpreted in terms of prefrontal cortex decline – it is amongst the earliest brain regions to decline with natural aging (West, 1996).17 Other brain structures appear to enable some forms of memory too – dissociations between non-declarative forms of memory have been observed. Patients with Alzheimer’s disease (diffuse cortical association area damage) show reduced perceptual priming and spared procedural, motor learning tasks while patients with Huntington’s disease (damaged basal ganglia) show the opposite pattern (Schacter, 1995). Squire and Knowlton (1995) linked brain regions and systems to memory kinds that fit the distinctions made in cognitive psychology quite well, but note that we need to make specific identification where synaptic changes actually occur to gain further insights. Emotions are known to sometimes have powerful effects on memory (Matlin, 1996). A traumatic event may elicit strong emotions that enable vivid memories of the event to persist well after the event. Research on flashbulb memories suggest that while the memory may be vivid it might not necessarily be very accurate (Matlin, 1996). There are important brain mechanisms that modulate memory storage in response to emotion – this can occur through stress hormones (Cahill & McGaugh, 1998). Stress hormones increase blood sugar levels and arousal that may aid forming a memory trace (e.g., extra energy available in the brain). The hormones themselves have been shown to have modulatory roles in memory (effects of direct injections in animal learning tasks have shown that small amounts are beneficial while larger, more chronic doses are detrimental). The amygdala is a key brain region in emotional memory encoding (e.g., aversive conditioning has been shown to depend on this region (Davis, Campeau, Kim & Falls, 1995). Activity in the amygdala has also been shown to modulate other memory systems such as the hippocampus (Cahill & McGaugh, 1998). The above mechanisms may help explain why emotionally18 powerful events are sometimes remembered vividly, but our understanding is far form complete. There are a multitude of brain structures and mechanisms that appear to be involved in different forms of and aspects of memory and probably many more that remain to be discovered. The linking of brain structures to memory functions is only a start – the real question lies in how these structures actually work in enabling these functions. DISCUSSION In this essay I have attempted to relate brain mechanisms to psychological processes involved in memory. In order to successfully find such links it becomes obvious that we need to be able to clearly conceptualise and characterise aspects of memory on a psychological basis if we are to identify them in the brain – indeed, this could conceivably be the ultimate goal. Neuroscience based research can help clarify and direct these concepts at the psychological level – for example, the simplistic division of STM and LTM needs to be modified based on cellular data. The argument for separate explicit and implicit memory systems seems to be supported by studies of amnesia. Dissociable memory systems within the implicit domain receive some support too. But what about the explicit domain – what, exactly, are the differences between semantic and episodic memory in terms of brain functions? If explicit memory depends on the medial temporal lobe system as and integral component then do semantic memory deficits show the same pattern as episodic deficits do in amnesic patients? It would be interesting to see if semantic memory follows the same pattern of temporally graded retrograde loss as episodic memory does. (This would not be19 easy to test as it is difficult to know when patients may have learnt semantic knowledge before their brain damage.) Semantic memory is independent of the context it was learnt in, yet there would be an episodic trace of these occasions (somewhere) – what allows this divorce? Is the former cortico-cortical and the latter hippocampocortical? Perhaps there is parallel encoding into both memory systems when learning semantic associations with semantic storage outlasting episodic storage due to deep meaningful encoding. Is meaningful encoding successful because of widespread cortico-cortical connections reflecting related associations (‘integration into semantic networks’ (Matlin, 1996))? Should semantic memory be considered as ‘affectless’ and purely verbal only? The fact that the hippocampus is part of the limbic system and that information from the medial temporal lobe system reaches the orbitofrontal cortex (associated with ‘affect tags’ to stimuli (Gazzaniga et al., 1998)) might suggest that affect should not be ignored in explicit memory. Perhaps explicit memory could be divided into affective and verbal components that reverberate in a feedback loop, with episodic and semantic memory reflecting different manifestations of it. While these ideas are speculative, more clearly defined divisions of memory without the explicit domain may be fruitful. In conclusion, the cognitive neuroscience approach is inspiring a deeper appreciation of what memory really is and how it works.
Posted on: Sun, 30 Jun 2013 21:02:28 +0000

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