Download Memory | Normal brain systems and disorders of memory and more Lecture notes Psychology in PDF only on Docsity!
Memory | Normal brain systems and disorders of memory
Masud Husain Professor of Neurology, Nuffield Dept Clinical Neurosciences, University of Oxford Normal brain memory systems 1 ► (^) Memory has traditionally been fractionated into several different domains. The first dissociation is between short-term memory (STM) and long-term memory (LTM) ► (^) Within STM, working memory refers to brain systems and processes required for the active manipulation or protection of STM contents ► (^) LTM is divided into explicit (declarative) memory versus implicit (non-declarative) memory systems ► (^) Explicit memory is itself further fractionated into episodic memory and semantic memory Memory is fractionated into different systems The traditional view is that these different types of memory are dissociable and served by different brain regions. Short-term & working memory
Memory
Short-term memory (STM) and working memory 2 ► (^) STM is often used to refer to passive storage over seconds ► (^) Working memory refers to executive control over material stored in STM ► (^) STM stores are ‘modality specific’, e.g. visuospatial material may be held in a separate store (visuospatial sketchpad) to verbal material (phonological loop) ► (^) Early focal lesion and functional imaging studies suggested that STM stores reside in posterior parietal cortex (visuospatial material in the right parietal cortex and verbal material in the left) whereas executive control systems reside in dorsolateral prefrontal cortex. This division may be an over-simplification but can be helpful. Working memory refers to STM plus Executive control over the contents of STM Executive control has been attributed to prefrontal brain regions whereas passive stores are considered to reside in posterior parietal cortex. STM stores may interact with LTM systems.^2 ► (^) Verbal STM storage capacity is measured at the bedside using digit span (how many numbers in a sequence can be recalled) ► (^) Visuospatial STM storage capacity is measured using the Corsi blocks (how many spatial locations in a sequence can be recalled) ► (^) Verbal working memory (storage plus executive control) is measured by using reverse digit span (how many numbers in a sequence can be recalled in reverse order) ► (^) Visuospatial working memory is measured by using reverse Corsi blocks (how many location in a sequence can be recalled in reverse order)
‘Slave’storage systems
Crystallized LTM (long term memory) systems
Executive control
mechanisms manipulate contents of STM, e.g., reverse or backward digit span test where people are required to recall a sequence of numbers in reverse
Free recall is harder than recognition tests of memory where people have to choose between alternative possible answers. Some patients might not freely recall a name and address they had been asked to learn minutes before, but if they are given choices of which elements were in the name and address, they can perform better than chance. Episodic memory deficits can arise in progressive neurodegenerative conditions such as Alzheimer’s disease or its prodromal condition, mild cognitive impairment (MCI) ; occur transiently, in conditions such as transient global amnesia (TGA) or transient epileptic amnesia (TEA)^6 ; or can be of sudden-onset and leave a permanent deficit as in limbic encephalitis^7 or herpes simplex encephalitis. TGA versus TEA^13 from Butler & Zeman Nat. Clin. Pract. Neurol. 4, 516 – 521 (2008) Episodic memory deficits associated with confabulation 8 have been associated particularly with Korsakoff’s syndrome^9 or damage to orbitofrontal cortex^8. Remember also that depression, anxiety, stress and poor sleep can also lead to deficits on episodic memory tests. Subjective cognitive impairment or subjective cognitive decline can be related to these symptoms^10. w.nature.com/clinicalpractice/neuro between individuals. Olfactory hallucinations are experienced by about 40% of patients. There is evidence that amnesia in TEA can be either ictal or postictal.^1 The interictal EEG is often normal, but epileptiform features are seen in approxi- mately a third of cases, especially in patients who have experienced sleep deprivation. The EEG should be interpreted with care in elderly patients, as unusual features are not necessarily pathological in such individuals. Persistent memory impairment is reported by about 75% of patients with TEA, with three distinct types of memory difficulty being identi- fied: accelerated forgetting, over days to weeks, of newly acquired information; dense but patchy loss of memories for salient autobiographical events often extending back over several decades; and topographical amnesia. These impairments cause appreciable problems in day-to-day life, but remain illustrated by the present case. The distinctive features of these conditions are illustrated in Table 1. Other reported causes of transient amnesia include transient ischemia, closed head injury, migraine, and medications including anticholinergic drugs and benzodiazepines.^6 The nature of the amnesia during attacks, the frequent occurrence of olfactory hallucinosis, and the location of interictal epileptiform discharges on EEG suggest that in TEA the seizure focus lies in the medial temporal lobes—brain regions inti- mately involved with declarative memory.^7 The present case, in which the peri-ictal PET scan showed focal hypermetabolism in the left hippo- campus with associated high signal on structural MRI, supports this hypothesis.^8 As with the majority of TEA cases,^1 the present patient’s previous structural MRI scans were normal. Over time, however, and possibly Table 1 Distinguishing clinical features of the transient amnesic syndromes. Feature Transient epileptic amnesia Transient global amnesia Psychogenic amnesia Typical age of onset 50–70 years 50–70 years Any age Past medical history None Migraine ‘Organic’ transient amnesia; substance abuse; psychiatric illness Precipitants Waking Cold water; physical exertion; psychological stress Minor head injury; stress; depression Ictal memory profile Anterograde and retrograde amnesia showing within- patient variation; patient might later partially recall attack); retrograde procedural memory intact Profound anterograde amnesia including repetitive questioning; variable retrograde amnesia; intact nondeclarative memory Highly variable: often profound retrograde amnesia with loss of personal identity; relatively preserved anterograde memory; variable procedural memory Duration of amnestic episode Usually <1 h but can last much longer (days) Typically 4–10 h Days or months Recurrence Mean frequency 13 attacks per year Rare Rare Postictal and interictal memory Accelerated forgetting; remote autobiographical memory loss; topographical amnesia Grossly intact, but subtle deficits might persist for several months Variable: patient might be able to ‘relearn’ the past Other features Olfactory hallucinations; oroalimentary automatisms; brief loss of responsiveness Headache and/or nausea Focal ‘neurological’ symptoms or signs, such as hemiparesis
ASE S TU DY
Semantic memory^11 ► (^) Semantic memory refers to recollection of facts, concepts and general knowledge about the world ► (^) The left temporal pole is considered to be a critical brain region for semantic memory Left temporal lobe is crucial for semantic memory This can be tested in patients by assessing semantic knowledge, for example with the Pyramid and Palm Trees test. ► (^) At the bedside semantic memory can be assessed by asking the patient to name objects or line drawings of objects, and then asking them to explain what they are or what they are used for. For example, you might point to a telephone or a watch, or a stethoscope ► (^) Alternatively, give the name of an object and ask them to explain its use. ► (^) Neuropsychologists test semantic memory more formally using tasks that probe semantic knowledge ► (^) For example, in the Pyramid and Palm Trees Test patients have to say which of the two choices are closer semantically to the target object Nature Reviews | Neuroscience Distributed-only view Distributed-plus-hub view Convergent architecture Name Action Colours Motion Name Action Colours Motion Gating architecture Shape Shape Task Task Task- dependent representation Task- independent representation Action Words Sound Shape Colour Motion a b Task- dependent representation (FIG.1b). The principal reason for this claim is that a central function of semantic memory is to generalize across concepts that have similar semantic signifi- cance but not necessarily similar specific attributes. Scallops and prawns have different shapes, colours, shell structures, forms of movement, tastes, names, verbal descriptions and so on, but semantically speak- ing, to seafood-eating humans they enter into similar scenarios and have substantial conceptual overlap. If semantic memory consisted only of the modality- specific content of objects (and the links between them), it is doubtful that we could ever achieve the The distributed-plus-hu first to argue for unified co that abstract away from mod Most earlier proposals of t mute regarding the neuro central aspect of semantic specifically neuroanatomi colleagues9–13^ proposed the zones’ that associate differe and along with other resea articulated the importance o processing. The convergence differs in at least two respects hub view illustrated in FIG. existence of multiple specia for example, one that enco visual representations of s actions, another that enco shape and object name, and that these zones become di representing different seman because humans frequently in man-made objects, the zon and action might be more im man-made artefacts than for Similarly, because animals m the zone that links shape to special salience for knowled aspects of the convergence- variant of the distributed-on represented in FIG. 1a. By con hub view proposes that, in anatomical pathways betwee and linguistic regions, the ne memory requires a single con supports the interactive activ all modalities, for all semant Do the distributed-only positions result in different tributed-plus-hub perspective produce a semantic impairme modality of input (objects, pic and so on) and of the modal naming an object, drawing i contrast, from the distributed of focal brain damage would such a generalized impairme two important empirical ques eralized impairments of sem if so, are they caused by rela The evidence pertinent to th studies that have both invest semantically impaired patien mine the specific locus of the an overview of this evidence resulting conclusions are con by, evidence from functiona healthy adults performing s consider evidence from com Figure 1 | Two theoretical positions regarding the neuroanatomical distribution of the cortical semantic network and schematic models based on these views. Both positions hold, in agreement with most investigators, that the network is widely distributed and partly organized to conform to the neuroanatomy of sensory, motor and linguistic systems. a | The distributed-only view suggests that these widely distributed regions, along with the diverse connections between them (shown as green lines), constitute the whole semantic network. The flow of activation through this network can be ‘gated’ by a representation of the current task (right-hand panel): for instance, if the task is to name a line drawing of a familiar object, activation will flow from a representation of object’s shape to a representation of its name. Associations between different pairs of attributes are encoded along different neuroanatomical pathways. b | By contrast, the distributed-plus-hub view posits that, in addition to these modality- specific regions and connections, the various different surface representations (such as shape) connect to (shown as red lines), and communicate through, a shared, amodal ‘hub’ (shown as a red area) in the anterior temporal lobes. At the hub stage, therefore, associations between different pairs of attributes (such as shape and name, shape and action, or shape and colour) are all processed by a common set of neurons and synapses, regardless of the task. The right-hand panel (labelled ‘convergent architecture’) illustrates the model equivalent of the distributed-plus-hub view.
Case 3 13 | Nature Clinical Practice Neurol, now Nat Rev Neurol (2008) 4: 516 A 54 year-old right-handed academic presented the four year history of recurrent episodes of transient amnesia and a progressive decline in memory. His first episode began abruptly as he emerged from the shower one morning. He could not recall events. Alone in the house and curious as to why he should be showering so late in the day he went out of his car and felt that the bonnet was warm, implying that he had already been out. After about an hour the patient’s memories from earlier in the day gradually returned. Over the next three years the patient experienced six further amnestic attacks. They all occurred on waking and were characterized by retrograde amnesia for events of the past few days or weeks. Between attacks, the patient began to notice persistent memory deficits. His recollection of many salient, personal events, such as family holidays and weddings from the past 30 years became sketchy or completely absent. § MMSE: 27/30, consistently failing to recall three words after a brief delay § CT brain: Unremarkable Notes Case 4 6 | Nat Rev Neurol (2013) 9: 86 A 65 - year-old woman experienced an episode of amnesia after working hard in the garden for some hours. She began asking repeatedly “Where am I?”, “What time is it?” and “Why are all these branches lying around?” She appeared perplexed and irritated. She was profoundly amnestic, with a retention span of three minutes and retrograde amnesia extending 20–30 years in the past. The amnesia resolved over about seven hours, although the patient continued to feel irritable and anxious for some days. § MRI brain: Focal diffusion weighted signal changes in the hippocampus Notes
Case 5 1 | Ch 11 Husain M & Schott J Oxford Textbook of Cognitive Neurology & Dementia NA was a 71-year-old right-handed professional woman who presented with a four year history of progressive difficulty thinking of words, especially nouns. She reported difficulty reading or following what she was watching on the television. She had forgotten how to cook. § Spontaneous speech was characterized by word finding difficulty and insertion of general substitutions (e.g. ‘thingy’) or replacement of words with related ones (e.g. ‘knife’ for ‘scissors’) § Object naming profoundly impaired § MRI brain: Severe left temporal lobe atrophy Notes Case 6^14 | JAMA Neurol (201 6 ) 73 : 1248 A man in his 70s with a history of chronic cognitive decline attributed to hepatic encephalopathy presented with one week of confusion, worse than his baseline state. He had a history of alcoholic cirrhosis. Examination revealed anterograde worse than retrograde memory deficits. There was no evidence of asterixis, nystagmus, ophthalmoplegia ataxia. § MRI brain: Hyperintensity in the periaqueductal grey matter, mamillary bodies and medial thalamic nuclei, together with volume loss in the corpus callosum and generalised cortical atrophy. Notes
Subsequently, he was unable to continue working, encountering difficulty remembering names of clients and getting lost driving in familiar locations. On the Addenbrooke’s Cognitive Examination-III (ACE-III) screening test he scored 85/100 with the most notable deficiencies in memory (18/26) and verbal fluency (10/14). Detailed neuropsychological assessment now revealed a global decline in performance from two years earlier, including in memory (both immediate and delayed verbal and visual recall) but also in attention, executive function and processing speed. Thus cognitive impairment affected several domains and extended beyond deficits in episodic memory. Ambulatory EEG demonstrated abnormal focal sharp and slow wave discharges involving both right and left temporal lobes. § MRI brain: Slight atrophy of the body and tail of the hippocampus on the right He continued to experience partial sensory seizures as well as brief periods of disorientation which were considered to be complex partial seizures. His cognitive impairment continued to have a major impact on everyday life. A further clinical diagnosis was made. He was started on a new treatment and the dose of lamotrigine was increased further to 200 twice daily. Despite this, both types of seizure continued. Therefore levetiracetam was added. With levetiracetam 250 mg twice daily there were no further overt seizures. On the ACE
- III his performance initially improved to 96/100, which was attributed to better control of seizures. Repeat EEG performed two years later showed no evidence of epileptiform activity but the ACE-III score declined to 87/100. § Repeat MRI brain: MRI showed further slight atrophy of the medial temporal lobe, most prominently on the right. Notes
Recommended general reading
- Hodges J (20 1 7) Cognitive Assessment for Clinicians 3 nd^ ed
- Husain M & Schott J (2016) Oxford Textbook of Cognitive Neurology & Dementia
References
- Oxford Textbook of Cognitive Neurology and Dementia. (Oxford University Press, 2016).
- Baddeley, A. Working memory: looking back and looking forward. Nat. Rev. Neurosci. 4, 829 – 839 (2003).
- Harris, L., Humphreys, K., Migo, E. & Kopelman, M. in Oxford Textbook of Cognitive Neurology and Dementia (eds. Husain, M. & Schott, J. M.) (2016).
- Moscovitch, M., Cabeza, R., Winocur, G. & Nadel, L. Episodic Memory and Beyond: The Hippocampus and Neocortex in Transformation. Annu. Rev. Psychol. 67, 105 – 34 (2016).
- Squire, L. R. & Wixted, J. T. The Cognitive Neuroscience of Human Memory Since H.M. Annu. Rev. Neurosci. 34, 259 – 288 (2011).
- Bartsch, T. & Butler, C. Transient amnesic syndromes. Nat. Rev. Neurol. 9, 86 – 97 (2013).
- Dalmau, J. & Graus, F. Antibody-Mediated Encephalitis. N. Engl. J. Med. 378, 840 – 851 (2018).
- Schnider, A. Spontaneous confabulation and the adaptation of thought to ongoing reality. Nat. Rev. Neurosci. 4, 662 – 671 (2003).
- Arts, N., Walvoort, S. & Kessels, R. Korsakoff’s syndrome: a critical review. Neuropsychiatr. Dis. Treat. Volume 13, 2875 – 2890 (2017).
- Mendonça, M. D., Alves, L. & Bugalho, P. From Subjective Cognitive Complaints to Dementia: Who is at Risk?: A Systematic Review. Am. J. Alzheimers. Dis. Other Demen. 31, 105 – 14 (2016).
- Patterson, K., Nestor, P. J. & Rogers, T. T. Where do you know what you know? The representation of semantic knowledge in the human brain. Nat. Rev. Neurosci. 8, 976 – 987 (2007).
- Petersen, R. C. Clinical practice. Mild cognitive impairment. N. Engl. J. Med. 364, 2227 – 34 (2011).
- Butler, C. R. & Zeman, A. A case of transient epileptic amnesia with radiological localization. Nat. Clin. Pract. Neurol. 4, 516 – 521 (2008).
- Segal, J. B., Bouffard, M. A. & Schlaug, G. Characteristic Neuroimaging Abnormalities of Korsakoff Syndrome. JAMA Neurol. 73, 1248 – 1249 (2016).
- Cash, S. S., Larvie, M. & Dalmau, J. Case records of the Massachusetts General Hospital. Case 34-2011: A 75-year-old man with memory loss and partial seizures. N. Engl. J. Med. 365, 1825 – 33 (2011).
