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Amnesia Danielle Noftle Neuropsychology of Abnormal Amnesia Danielle Noftle Neuropsychology of Abnormal

Amnesia Danielle Noftle Neuropsychology of Abnormal - PowerPoint Presentation

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Amnesia Danielle Noftle Neuropsychology of Abnormal - PPT Presentation

Behaviour November 19th2015 Presentation Outline Introduction History Patient HM Categories of Amnesia Memory Consolidation Neurotransmission Squires Taxonomy of memory Neuroanatomy Neuroendocrinology ID: 1034810

amnesia memory amp consolidation memory amnesia consolidation amp hippocampus brain information events california damage squire long neuron temporal stress

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1. AmnesiaDanielle NoftleNeuropsychology of Abnormal BehaviourNovember 19th/2015

2. Presentation OutlineIntroductionHistory: Patient H.M.Categories of AmnesiaMemory ConsolidationNeurotransmissionSquire's Taxonomy of memoryNeuroanatomyNeuroendocrinologyAnimal Models/Assessment

3. IntroductionAmnesia: a condition in which memory (either stored memories or the process of committing something to memory) is disturbed or lost Different from everyday forgetting or absent-mindednessOrganic or neurological causes (i.e. damage from physical injury)Functional or psychogenic causes (i.e. PTSD)

4. Atkinson-Shiffrin Model of Memory

5. History: Patient H.M. (1953)Most widely studied clinical case of amnesia to date Doctor's bilaterally resected his medial temporal lobes Removals extended posteriorially for approx. 8cm - included uncus, amygdala, hippocampal gyrus and anterior 2/3's of hippocampus

6. Patient H.MSurgery treated his epilepsy BUT destroyed his ability to form new LTMs Severely impaired his episodic memoryBUT H.M. had above average intelligence Performed normally on standard tests of perception, short term memory and language comprehension

7. Patient H.M. https://www.youtube.com/watch?v=KkaXNvzE4pk

8. Types of Amnesia1) Infantile Amnesia: common inability of adults to remember the earliest years of their childhood, typically from birth until around four years old

9. Types of Amnesia2) Global Amnesia: Patients can appear normal to casual observationNormal intellectual capacity, digit span and intact social skillsDefect lies in retaining new memories and in recalling memories acquired just before amnesia

10. Examples of Global Amnesia:A. Wernicke-Korsakoff Syndrome (WKS) Caused by thiamine deficiency due to chronic alcohol abuse - thiamine helps produce energy needed for proper neuronal function After passing of acute stage - patient is alert and responsive, and has normal intellectual capacity

11. Korsakoff Brain

12. B. Bilateral Electroconvulsive TherapyPrescribed for treatment of severe depressionAmnesia is common side effect but often temporary

13. Categories3) Psychogenic amnesia: A.k.a. functional amnesia or dissociative amnesiacharacterized by abnormal memory functioning in the absence of structural brain damage or a known neurobiological cause

14. DSM-V: Dissociative Amnesia CriteriaUnable to recall autobiographical memory associated with a traumatic eventThe recall of traumatic events is usually unconsciousThe inability to recall traumatic events creates distressThe memory dysfunction does not have a physiological causeThe memory dysfunction is not dissociative identity disorderThe memory loss is not a result of substance abuse or other substance

15. Categories4) Amnesia from DIFFUSE brain damage damage to several areas of the brainoften caused by closed brain injuries, Korsakoff syndrome etc5) Amnesia from FOCAL brain damageconfined to one area of the brain brain tissue is damaged at the site where the injury occurred (ex. surgery)

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18. Anterograde AmnesiaInability to remember events and facts encountered after the onset of illnessCaused by damage to hippocampus, fornix, or mammillary bodiesMore common in amnesic patients than retrograde amnesiaIntact intelligence, personality and judgment but day-to-day functioning is poorRecent events aren't transferred to long term memory (encoding)

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20. Retrograde AmnesiaInability to remember events that occurred prior to injury (retrieval)Caused by damage to medial temporal lobe, diencephalon, and basal forebrain Ribot's Law: retrograde amnesia is characterized by a time gradient (a.k.a. temporally graded amnesia) occurs because memory for recent events is more fragile than memory for remote events Lead to discovery of memory consolidation

21. Memory ConsolidationProcess of stabilizing a memory trace after the initial acquisitionBegins at synaptic level - brain forms new pathways to the information it encountersInvolves reorganization in nervous system: Level 1: synaptic consolidation - occurs rapidly at the site of synapses Level 2: systems consolidation - gradual reorganization of circuits within brain regions

22. Memory Consolidation: Stages 1) information is bound to a memory trace by the hippocampus 2) initial binding involves a short-term consolidation process - a.k.a cohesion (completed within seconds to minutes) 3) long-term consolidation begins: hippocampus is needed for initial storage and recovery 4) neocortex then sustains permanent memory trace and mediates its retrieval

23. Memory Consolidation Reactivation: Major mechanism of consolidationOccurs during sleep or periods of relaxed wakefulnessHippocampus replays neural activity associated with memoryActivity occurs in network connecting hippocampus and cortexResults in formation of connections between cortical areas

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25. Neurotransmission: Long-Term PotentiationImportant process of memory consolidationLTP refers to enhanced firing of neurons after repeated stimulation First time neuron 'A' is stimulated, neuron 'B' fires slowlyBUT after repeated stimulation, neuron 'B' fires much more rapidly to same stimulus

26. Glutamate and LTPGlutamate binds to the receptors for AMPA and NMDA - both are extremely important for LTPWhen binded with AMPA: sodium ions enter the post-synaptic neuron. Increase in sodium causes depolarization When depolarization triggers an action potential - nerve impulse is transmitted to the next neuron

27. Glutamate and LTPWhen binded with NMDA:admits calcium ions into the post-synaptic cell BUT at resting potential - the calcium channel is blocked by magnesium ions so even if glutamate binds to the receptor, calcium cannot enter the neuron For magnesium ions to leave the channel, the dendrite’s membrane potential must be depolarized

28. Glutamate and LTPafter sustained activation AMPA - postsynaptic neuron becomes depolarized magnesium then withdraws from the NMDA receptors and allows large numbers of calcium ions to enter the cell increased concentration of calcium makes this synapse more efficient for an extended period

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30. Demonstration: Long Term Memory - Encoding and RetrievalRead the following words:Apple, desk, shoe, sofa, plum, chair, cherry, coat, lamp, pants, grape, hat, melon, table, glovesNow write down as many as you can

31. DemonstrationLook at the list you created and notice whether similar items (ex. apple, plum) are grouped together - if so, supports idea of a retrieval cue: a word or other stimulus that helps a person remember information stored in memory for other words in that category

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33. Squire's Taxonomy of Memory2 separate memory systems:1) Explicit or Declarative Memory Info is available later as a conscious recollectionIncludes semantic (facts) and episodic (events) memoryEpisodic memory is lost in amnesia - Patient H.M. Capacity for declarative memory depends on damage to hippocampus and surrounding structures

34. Squire's Taxonomy of Memory2) Implicit or Nondeclarative MemorySpared (nondeclarative) memory abilities do not depend on hippocampal structuresIncludes procedural memory, priming and perceptual learning, classical conditioning and nonassociative learning They all reflect ways in which performance can change as the result of experience, but without a conscious recollection of any previous event or fact

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36. Neuroanatomy:Medial Temporal LobeIncludes:Perirhinal CortexParahippocampal Cortex Entorhinal CortexHippocampus

37. Medial Temporal Lobe Structures of MTL have reciprocal connections with neocortex MTL binds distributed storage sites together in neocortex that represent a whole memory

38. Medial Temporal LobeSupports capacity for conscious recollections of facts and events (explicit memory) Role of the MTL is only temporary damage to the MTL produces temporally graded retrograde amnesia

39. Fields of the Hippocampus1) Dentate Gyrus (DG) - tightly packed layer of small granule cells 2) Cornu Ammonis (CA) areas: CA4, CA3, CA2 & CA1 - filled with densely packed pyramidal cells (like those found in neocortex) 3) Subiculum 4) Presubiculum and parasubiculum 5) Then a transition to entorhinal area of the cortex

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41. Hippocampus Fields and MemoryLesion to CA1 area of hippocampus breaks the chain of information-processing Has huge influence on the functioning of the hippocampal formation Subicular complex and entorhinal cortex are main sources of output from the hippocampus to subcortical structures

42. Amygdala Encodes emotional aspects of memoryThe basolateral complex of the amygdala (BLA) - moderate concentration of glucocorticoid receptors (GRs) BLA is involved in mediating glucocorticoid effects on memory consolidation

43. AmygdalaA GR agonist infused into the BLA after training enhances memory consolidationVs. lesions or inactivation of the BLA which blocks memory-enhancing effects of glucocorticoidsModulation hypothesis: after an emotionally arousing experience amygdala engages stress-related hormones and neurotransmitters to enhance memory consolidation

44. Neuroendocrinology: Stress and AmnesiaStress activates the hypothalamus–pituitary–adrenal (HPA) axisresults in the release of glucocorticoid hormones from the adrenal cortexAcute elevations in glucocorticoids enhance the consolidation of new information BUT impairs the retrieval of already stored information Chronically elevated glucocorticoid levels results in a cumulative strain on hippocampal function

45. HPA Axis

46. Stress and Amnesiaadrenal cortex synthesizes GCs from available cholesterol and secretes cortisol into the bloodstreamapproximately 95% of secreted cortisol becomes bound to proteins (such as globulin and albumin) remaining cortisol is free to bind to receptors in cortical and subcortical structures (including the hippocampus, amygdala, hypothalamus and pituitary)

47. Stress and AmnesiaGlucocorticoid effects on memory consolidation Glucocorticoid effects on memory consolidation follow an inverted U-shape moderate doses enhance memory vs. higher doses are less effective or may even impair memory consolidation

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49. Animal Studies1) Match-to-sample TasksDeveloped during era of behaviorismAnimal (often pigeon) presented with a colored stimulus sample It would then proceed to peck at sample Bird is then presented with two comparison stimuli - one comparison stimulus matches the sample (same color) and the other doesn't If bird pecks the matching comparison then it is rewarded

50. Animal Studies2) Delayed matched-to-sample very similar to match-to-sample tasks only difference - before choosing the correct response there is a short delay delay can vary in length - determines how long animal can retain information in their working memoryIf animal responds correctly over fifty percent of the time - it shows that it has retained information

51. Chimp Vs. Human! Working Memory Testhttps://www.youtube.com/watch?v=zsXP8qeFF6A

52. Assessment Wechsler Memory Scaleoriginal WMS consisted of seven subtests assessed orientation, span of attention, immediate recall of stories and novel geometric figures, and the ability to learn paired wordsBUT there were many critiques: validity, standardization and psychometric propertiesWMS-Revised was then created 5 standardized scores were computed: general memory, attention-concentration, verbal memory, visual memory, and delayed recall

53. AssessmentVerbal TestsDigit Span examiner presents increasingly long sequences of digits examinee is then asked to repeat each sequence in the same order presented Once a maximum digit span is achieved in the forward direction the examinee is asked to repeat backwardImmediate recall spanRepetition of information immediately after it's presentation

54. ReferencesAmy L. Alderson & Thomas A. Novack (2002) Neurophysiological and Clinical Aspects of Glucocorticoids and Memory: A Review. Journal of Clinical and Experimental Neuropsychology, 24:3, 335-355Bliss, T. V. P., & Collingridge, G. L. (1993) A synaptic model of memory: long term potentiation in the hippocampus. Nature Publishing Group.John P. Aggleton & Richard C. Saunders (1997) The Relationships Between Temporal Lobe and Diencephalic Structures Implicated in Anterograde Amnesia, Memory, 5:1-2, 49-72, DOI: 10.1080/741941143Marie D. Sauro, Randall S. Jorgensen & C. Teal Pedlow (2003) Stress, Glucocorticoids, and Memory: A Meta-analytic Review, Stress, 6:4, 235-245 Kritchevsky, M., Chang, J., & Squire, L. R. (2004). Functional amnesia: Clinical description and neuropsychological profile of 10 cases. Learning & Memory, 11(2), 213-226. doi:http://dx.doi.org/10.1101/lm.71404McCann, D. & Weiten, W. (2013). Psychology Themes and Variations. Nelson Education.

55. ReferencesZola-Morgan, S., Squire, L. R., & Mishkin, M. (1982). The neuroanatomy of amnesia: Amygdala-hippocampus versus temporal stem. Science, 218(4579), 1337-1339. Retrieved from http://ezproxy.library.yorku.ca/login? url=http://search.proquest.com/docview/616757258?accountid=15182de Quervain, D. J. -., Aerni, A., Schelling, G., & Roozendaal, B. ( (2009). Glucocorticoids and the regulation of memory in health and disease. Frontiers in Neuroendocrinology, 30(3), 358-370. doi:http://dx.doi.org/10.1016/j.yfrne.2009.03.002Goldstein, B. E. (2011). Cognitive Psychology: Connecting Mind, Research, and Everyday Experience. Wadsworth, Cengage LearningRoozendaal, B. (2002). Stress and Memory: Opposing Effects of Glucocorticoids on Memory Consolidation and Memory Retrieval. Department of Neurobiology and Behavior, University of California, Irvine, California 92697-380. doi:10.1006/nlme.2002.4080 Squire, L. (2004). Memory systems of the brain: A brief history and current perspective. Departments of Psychiatry, Neurosciences, and Psychology, University of California, San Diego, La Jolla, CA 92093, USA

56. ReferencesAlvarez, P. & Squire, L. (1995) Retrograde amnesia and memory consolidation: a neurobiological perspective. Current Opinion in Neurobiology 1995, 5:169-177 Squire, L. (1982). THE NEUROPSYCHOLOGY OF HUMAN MEMORY. Department of Psychiatry, University of California at San Diego, School of Medicine, La Jolla, California 92093 Moss, M. (2009). Animal Models of Amnesia. Boston University School of Medicine, Boston MASquire, L. & Zola-Morgan, S. (1990). The Neuropsychology of Memory Parallel Findings in Humans and Nonhuman Primates. Veterans Affairs Medical Center Sun Diego, California 92161 and Department of Psychiahy University of California San Diego, La Jollu, California 92093Race, E. & Verfaellie , M. (2012). Amnesia and the Brain. Boston: Elsevier Inc.