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1 PS3002: Brain & Cognition Cognitive neuroscience and memory John Beech School of Psychology University of Leicester Slide 2 2 Memory and the brain Introduction Memory is extremely varied. What is the substrate of memory in the brain? Is it different for different types of memory? how to ride a bike the relation between the sides of a triangle an episode in ones life Can use: animal models from simple invertebrates to mammals the study of what happens to memory in amnesia following brain damage brain imaging in volunteers to investigate normal encoding, storage, and retrieval recall or recognition. Slide 3 3 Structure of memory Learning vs memory Squire (1987) distinguishes: Learning - process of acquiring new information Memory - persistence of learning in a state that can be revealed at a later time. Learning has an outcome - memory - which itself has a further outcome - a change in future behaviour. Learning need not imply any conscious attempt to learn. Simple repeated exposure can, and indeed usually does, lead to learning, and this is evinced by memory. Slide 4 4 Structure of memory: encoding Encoding is divided into acquisition (registration) and consolidation Storage creates and maintains a permanent record Retrieval uses stored information to create a conscious representation, or to execute a learned behaviour. If there is a deficit in memory, we dont know at which stage this has occurred. [flashbulb memories at times of traumatic or shocking events tend to be very vivid and detailed and readily recalled, but some studies have shown that it is not so much their accuracy which is improved, as the increase in subjective confidence]. Slide 5 5 Time base of memory Memory model of Atkinson & Shiffrin (1986) above. Sensory memory is sub- second to seconds, as when we can recover what was said when we werent paying attention. Short term is seconds to minutes, as with retaining a phone number. Long-term is longerdays, weeks, going up to years, or even a lifetime. Slide 6 6 Short-term memory Peterson & Peterson (1959): Consonant trigrams (e.g.TDK) followed by a no. (e.g. 765). Counts back in 3s (765, 762, 759) and recalled trigram on signal Rapid decline to 32 Alcoholic Korsakoffs Syndrome Sergei Korsakoff at the end of the 19 th century reported anterograde and retrograde amnesia associated with alcoholism. Imbibing a lot of alcohol in the long term produces vitamin deficiencies leading to brain damage (thiamine deficiency (vitamin B 1 ) => periventricular damage). This is more specifically in the diencephalon* (thalamus and mammilliary bodies). The same kind of damage can be produced by strokes or tumours. Recent work by Sullivan & Marsh (2003) has also found deficits in the hippocampus and not just the diencephalon. (*Note that the diencephalon is a subcortical [portion of the brain just below the cerebral cortex] structure made up of the thalamus and the hypothalamus.) Slide 33 33 Alcoholic Korsakoffs Syndrome The similarities in Korsakoffs (implicit memory OK but lose explicit memories) has led people to suggest that the medial temporal lobe is not the only part of the brain for forming explicit memories of facts and events. However, the recent work of Sullivan and Marsh casts some doubt. Korsakoffs patients also confabulate caused by frontal lobe damage. This is not deliberate deception as they appear to believe themselves. This could be due to damage to frontal lobes which have a control function in memory retrieval. Slide 34 34 Korsakoffs syndrome Cermak, Naus & Reale (1976) demonstrated the memory impairment (in LTM) in this condition. Note the strong recency effect showing an intact STM. Slide 35 35 Retrograde Amnesia temporal gradients As previously mentioned, damage to the front part (anterior) of the temporal lobe produces dense retrograde amnesia (forgetting of events before the brain damage). In the case of Alzheimers disease or herpes simplex encephalitis this can go back for decades before the amnesia. Temporal gradient (Ribots Law, 1882) autobiographical memories that are more recent are much more easily damaged compared to early memories. It was first noted in Korsakoffs syndrome patients. But WHY does it occur? 1.Korsakoffs patients were in a more drunken state when learning! But temporal gradients occur in amnesics who do not abuse alcohol. Parts of the diencephalon, the thalamus (blue) and the hypothalamus (red). Slide 36 36 Retrograde Amnesia temporal gradients Temporal gradient (Ribots Law, 1882) 1.Korsakoffs patients were in a more drunken state when learning! But temporal gradients occur in amnesics who do not abuse alcohol. 2.Squire (1992): 2 major areas involved in initial and long term storage in memory: (1) The hippocampal formation is responsible for initial processing and then after rehearsal (2) the medial temporal lobes consolidate these memories. This predicts that those with lesions to the hippocampus (e.g. HM), but who have intact anterior temporal lobe structures (as in early onset Alzheimers disease) will have severe anterograde amnesia (no new memories). Slide 37 37 Retrograde Amnesia temporal gradients Temporal gradient (Ribots Law, 1882) Squire (continued): But those with semantic dementia (e.g. Snowden et al. 1989) have the reverse damage no anterograde amnesia, but severe retrograde amnesia (able to have new memories, but recent autobiographical memory impaired). To digress about semantic dementia this is also called fluent progressive aphasia meaning that their actual speech is fluent; however their understanding and recognising of words and putting names to faces and familiar objects gradually worsens (i.e. semantic knowledge deteriorates). There is evidence that the temporal lobes are mainly implicated with memory for words in the left temporal lobe and for faces in the right (Snowden et al. 2004). Slide 38 38 Retrograde Amnesia temporal gradients Temporal gradient (Ribots Law, 1882) Patients with damage to the anterior temporal lobes have resulting dense retrograde amnesia (forgetting lots of events/autobiography before damage) but some patients may still form new long term memories. So the anterior temporal lobes are useful for information storage, but other areas also seem to be capable of acquiring new information. As mentioned before such patients have poorer recall of episodes close to the beginning of the disease (or onset of injury) with gradually better recall further back (i.e. temporal gradient). Slide 39 39 Dissociation of episodic memory within explicit memory Tulving et al. (1991) studied a patient KC who had had subdural hematoma (pool of blood under the sheath covering the brain). Hed had a motorcycle crash at 30 yrs of age. Damage included bilateral damage to the medial temporal lobe especially on left, but also other cortices frontal, parietal and occipital. More damage to left hem. (See next figure). IQ of 94. Could not remember any events from his life, although he knew things that pertained to his life. Thus severe retrograde amnesia - he could recall very few autobiographical episodes from his life before the injury. (This is as if his episodic memory had been wiped clean.) ALSO severe anterograde amnesia. But intact semantic memory, and procedural memory. Thus this patient had a specific loss of episodic memory. Slide 40 40 Tulving et al. 1991 KCs lesions are shown on outline drawings of horizontal sections of his brain, starting from the top moving down going from left to right in the drawings, using computed tomography (CT). The red parts are the lesions due to trauma. Slide 41 41 Tulving et al. (1991) Implicit memory tested by giving three- word sentences together with a related picture. In each the final word critical. Later KC presented with a fragment or conceptual cue consisting of the other two words. KC showed priming effect with the word fragments and they lasted 12 months. Priming in this context means that he was better at generating words from the fragments compared to words previously unseen. Surprisingly he could learn new semantic information it took him longer to learn information than controls, but he forgot it at the same rate. Results like these suggest a separation of the underlying structures subserving semantic and episodic memories. Slide 42 42 Dissociation of episodic memory within explicit memory It might be noted that there is currently a controversy and Bayley and Squire (2002) have suggested that KCs problems in retrieval of autobiographical information may be unrelated to his medial temporal lobe damage because of a more recent report of a patient (EP) who has more extensive medial temporal lobe damage, but who has better recall of autobiographical episodes. So we may still be a little way away from distinguishing the functions of the hippocampus and other medial temporal lobe structures. Slide 43 43 Procedural learning in amnesia The test above examines serial reaction time: Ss have to push buttons according to flashes of lights in a complex sequence. Their index finger corresponds to the first light, the second finger to the second light and so on. The sequence can be random or else they can appear to be random, but in practice there is a complex repetitive sequence. In the repeated sequence situation RT reduces over time as shown on the right hand side. Afterwards it is clear that Ss are unaware when there are these complex repetitions. This is a good paradigm to test procedural learning (or implicit memory) Amnesics (and Korsakoffs patients) also improve their performance. Thus they have reasonable implicit memory, while great difficulties with episodic memory. Slide 44 44 Double dissociation We need to look for a double dissociation; a loss of implicit memory, without loss of explicit memory (having shown a loss of explicit memory and no loss in implicit memory in amnesics.) Gabrielli et al. 1995 tested a patient MS who had a right occipital lobe lesion. Areas 18,19, leaving a LVF hemianopia When shown words for later recall, he had explicit memory for them, but failed to show implicit perceptual priming (decreased exposure time needed to identify a familiar word compared to time for an unfamiliar one). In detail: before both tasks a list of words were presented briefly and then read aloud. (Note that this meant they saw them perceptually, but briefly and also then heard the words). In the implicit memory task the words were presented visually and then masked (XXXX). Durations of presentation increased from 16ms until the word could be read. If they had implicit memory, they should be faster with the words they had previously seen, compared with new words. Slide 45 45 In search of double dissociation between implicit and explicit memory In the explicit memory task again a list of words was shown and then in the recognition task old and new words were presented and they had to identify the old words. The patient was good at this task, but failed to show implicit perceptual priming. Hence this lesion impaired implicit but not explicit memory. Slide 46 46 Gabrielli et al. 1995 Summary: Occipital lobe lesion patient Results patient good at recognition task, but poor at implicit memory in other words, has a poor implicit memory List of words briefly shown List of words only heard Implicit memory Word XXXX old + new RT task Explicit memory old + new Recognition task Slide 47 47 Evidence against the Atkinson & Shiffrin model Atkinson & Shiffrin proposed in their model above attended items go from sensory memory into STM and if rehearsed move into LTM. Along the way processes of decay and interference (either or both) results in information loss. An important aspect was its serial nature information moves from one stage to the next. But the evidence doesnt support this. Shallice and Warrington (1969), patient with left perisylvian* damage who had reduced digit span (2 instead of the normal 5-9 items), but amazingly he had an intact ability to form long-term memories (e.g. could talk about the latest news). Hence it cannot be the case that information going into short term memory is a necessary precursor to it going into long term memory. It means that information can go straight from sensory memory into LTM. (*the perisylvian area is in the upper part of the temporal lobes in both hemispheres, and is implicated in language functioning in the left hemisphere. It is typically larger in the left hemisphere than in the right.) Slide 48 48 Another double dissociation: this time between STM and LTM This points to a double dissociation between STM and LTM: The Shallice & Warrington patient shows a patient with a very impaired STM, but with an intact LTM. We have also seen how it is possible for LTM structures to be destroyed in the anterior medial temporal lobes but the STM left intact in semantic dementia. The patient HM is an illustration that the hippocampus structures are important for the transfer/consolidation of episodic information into LTM, even though HMs STM was intact and a proportion of the structures in LTM were intact. Given the shortcomings of the serial model of memory, there was a need for a different perspective, which was the motivation for the working memory model developed by Alan Baddeley. Below in order: Tim Shallice, Elizabeth Warrington and Alan Baddeley Slide 49 49 Brain structures & STM Going back to the Baddeley model, there is some neurological evidence for the brain structures involved in this, in that function of the phonological loop is impaired by lesions of the supra- marginal gyrus (Brodmann area 40) and/or left pre-motor region (area 44). [In the absence of deficits in speech comprehension and production]. Baddeleys visuo-spatial scratchpad is impaired by lesions in parieto-occipital regions. Right sided lesions have more effect. Difficulty with spatial tasks such as repeating a sequence of objects touched. Left sided lesions => problems with STM of visually presented material. Slide 50 50 Slide 51 51 Brodmann Slide 52 52 Summary of memory Slide 53 53 Levels of processing models Another model to challenge the Atkinson and Shiffrin was one proposed by Fergus Craik and Robert Lockhart (1972). They proposed the levels of processing model in which items that were processed deeper were consolidated into LTM. Written words were presented in 3 conditions: 1.Ss had to identify if they were in upper or lower case letters this was a superficial level. 2.Ss judged if words rhymed with each other an intermediate level as processing for meaning still not involved. 3.Ss had to make a judgement about a word (e.g. Lamppost -can it rotate?) this was considered to be deep processing. Slide 54 54 Levels of processing models Written words were presented in 3 conditions: 1.Ss had to identify if they were in upper or lower case letters this was a superficial level. 2.Ss judged if words rhymed with each other an intermediate level as processing for meaning still not involved. 3.Ss had to make a judgement about a word (e.g. Lamppost -can it rotate?) this was considered to be deep processing. Found that memory better if deep processing involving semantic processing was used. This is compared to information coded visually or phonologically. Thus theres an incompatibility with the STM- LTM formulation of Atkinson & Shiffrin because it wasnt about just holding information in STM long enough, it was instead about the type (superficial vs deep) of processing taking place. Slide 55 55 Examples of animal work of memory Studies in monkeys help to clarify role of hippocampus, in conjunction with surrounding structures and adjacent cortex in memory. However functional capabilities of monkeys differ from humans, so need to choose a suitable memory task for animal experiments. Slide 56 56 Animal models of memory Delayed non-matching to sample (or DNMS) task. Animal has to identify which is the new item in a pair. This is a test of declarative memory. In (b) is shown object covering food. Allowed to take food. In (c) hatch closed for a time delay. In (d) shown old object (+) and new object (on its right). Animal has to choose the new object to get reward. In the picture the monkey is making an error and doesnt get reward. Random sides to avoid position bias. Thus has to learn to choose each time a new stimulus so has to remember previous stimuli. This paradigm can test retention in STM. Slide 57 57 Animal models of memory Mishkin (1978) did the classic studies with this lesion to hippocampus and/or amygdala. Found deficits only if lesion include the amygdala as well as hippocampus proper. This was paradoxical with regard to human studies, e.g. RB (mentioned before briefly) who had amnesia from lesion restricted to CA1 cells within each hippocampus, but not including the amygdala. Followed up by Zola et al. (1993). Extended Mishkins work by creating separate lesions of cortex surrounding the hippocampus which had been included in Mishkins lesions of hippocampus and amygdala together. Slide 58 58 Zola et al. found that lesions of this surrounding temporal cortex [para-hippocampal gyrus, peri-rhinal cortex] were sufficient when hippocampus was damaged; lesions of amygdala were not necessary or sufficient. Overall conclusion is that it is the hippocampus together with its input and output connections via surrounding cortex which are important for episodic memory. This is episodic memory, although the time scale seems a bit different. Slide 59 59 Summary Memory from the cognitive perspective Introduction different kinds of memories explicit vs. implicit and episodic vs. semantic. Encoding, storage & retrieval. Learning vs. memory. The Atkinson & Shiffrin model Sensory M, STM & LTM. Baddeley & Hitch model. Implicit vs. explicit and the perceptual representation system within implicit memory. Neurobiology of memory Amnesia and the temporal lobes. The case of HM no HC bilaterally STM normal, implicit M normal. But transfer of episodic memory to LTM blocked. HC important for new explicit episodic memories. The anterior medial temporal cortex damage => dense retrograde amnesia loses decades of info. Slide 60 60 Summary Neurobiology of memory (continued) Squire 1992: if HC damaged then pathway to ATL (ant. temp. lobe) is blocked => severe anterograde amnesia (no new episodic memories as with HM). Implicit OK. If HC OK, but ATL damaged, then severe retrograde amnesia Tulvings KC damaged ATL virtually no episodic, but intact semantic & implicit. Shows separation of episodic and semantic memories. Double dissociation between explicit and implicit: ATL = anterior temporal lobes & LVF hem = LVF hemianopia ExplicitImplicit AmnesicsLost episodic. OK LVF hem Gabrielli-MS OKLost Slide 61 61 Summary Neurobiology of memory (continued) More recent evidence produces problems for the Atkinson & Shiffrin model, esp with regard to serial passage from STM to LTM. Neurobiological evidence for separation between STM & LTM and double dissociation: STMLTMHC?Comment Shallice & W.ImpairedIntactOKOtherwise OK-ish Milner - HMIntactSome damageNo HCSevere anterograde amnesia Semantic dem.IntactimpairedOKSevere retrograde amnesia Slide 62 62 Summary We also covered: Brain structures and STM and in particular working memory. There appear to be credible substrates for the model of Baddeley and Hitch. Levels of processing was covered. Animal work as an example of further approaches to the study of the biology of memory. In conclusion these biological findings lend credence to their corresponding psychological models.