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RETROGRADE AND ANTEROGRADE AMNESIA

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Slide 1 - “THE ADVANTAGE OF HAVING BAD MEMORY IS THAT YOU CAN ENJOY GOOD THINGS FOR THE FIRST TIME SEVERAL TIMES.”-FRIEDRICH NIETZSCHE
Slide 2 - RETROGRADE AND ANTEROGRADE AMNESIA Ellie Moradi Colin Schwartz Chris Yco Melissa Bergh
Slide 3 - RETROGRADE AMNESIA:THE UNDERLYING CAUSE & PHYSIOLOGY Inability to access memories prior to damage Often associated with neurodegenerative diseases such as Alzheimer’s Disease Other causes include trauma, tumors, cerebrovascular accident (aneurysm), encephalitis, chronic alcohol use, and hypoxia (lack of oxygen)
Slide 4 - HIPPOCAMPUS
Slide 5 - MEDIAL TEMPORAL LOBE
Slide 6 - Physiology & Causes Cont’d. Hippocampal damage Hippocampus important for episodic and declarative memory Damage makes it difficult to recall memories prior to damage Retrograde amnesia is both extensive and ungraded when damage is limited to hippocampus Damage does not interfere with learning new skills however
Slide 7 - Physiology & Causes Cont’d. Medial Temporal Lobe damage The sparing of remote memory after damage shows that the importance of the medial temporal lobe structures for memory gradually diminish. Often damage is done to the knowledge stores in the MTL affecting the ability to recollect memories or information regardless of when it occurred or was learned
Slide 8 - RELATION TO ALTERED STATES OF CONSCIOUSNESS Memories and past events are contributing factors to being an individual No studies have shown a complete loss of self The individual adapts to the loss of memories
Slide 9 - Characteristics of RA Ribot gradient The tendency to lose new memories more so than old memories Span of loss unique, difficult to pinpoint it Memory loss Retain autobiographical, semantic, procedural, general knowledge Lose episodic (Brandt & Benedict 1993) Trevor Rees-Jones (August 1997)
Slide 10 - What can RA tell us about memory? Memory-Consolidation Theory (McGaugh 1966) New memory has to be consolidated and if interrupted leads to RA Classical evidence: amnesia inversely related to the age of the memory (Duncan 1949) Problems: RA recovery, delayed-onset RA and RA for long-term memory (Krickett Carpenter)
Slide 11 - What can RA tell us about memory? Multi-trace theory (Nadel et al 2000) Hippocampus responsible for encoding and retrieving all episodic memory independent of its age and thus damage randomly causes deficits. Old memories well encoded but can have retrieval problems. Evidence? Ribot gradients only found in partial lesions of hippocampus in rats. No real evidence. If you can figure out a way to test this, let me know.
Slide 12 - What can RA tell us about memory? Semanticization (Cermak 1984) All memories start out as episodic and through over-learning becomes semantic which is independent of hippocampus.
Slide 13 - In concluding RA Should old memory amnesia be considered with RA? No studies to my knowledge comparing brain areas involved in new and old memory RA No consensus about RA cause
Slide 14 - RA and ASC Sense of self endures in RA Theoretically if Ribot gradient went ad infinitum would forget about self? In Semantization, if all memory starts out episodic then awareness externally is episodic and semantic internally
Slide 15 - ANTEROGRADE AMNESIA Anterograde amnesia is a selective memory deficit, resulting from brain injury.
Slide 16 - CAUSES OF INJURY Stroke ischemic stroke, in which a small blood clot becomes wedged in one of the tiny blood vessels supplying the brain, blocking the flow of blood. This blood clot may have formed in the brain, or it may have formed elsewhere, broken free, and traveled through the blood stream to reach the brain Aneurysm An aneurysm is a small local bulge in the wall of a blood vessel, usually an artery. Normally, blood vessels operate like pipes, carrying blood throughout the body to cells which depend on this supply for oxygen and nutrients.
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Slide 18 - AREAS OF INJURY The first, and most well-studied, is the hippocampus. Hippocampus is seen as the gateway through which new information must pass before being stored into long term memory. Once this is damaged, it is almost impossible to create new memories.
Slide 19 - INJURY CONT’D. Long-Term Potentiation (LTP) This occurs when the cAMP-activated protein kinase enters the nucleus of the sensory cell, and activates CREB (cAMP Response Element Binding protein) to trigger protein synthesis. This leads to formation of a variant of the same kinase (cAMP-PK), which is constitutively active, without the need for cAMP. The K+ channel will then be constantly inhibited. At the same time, genes for the synthesis of active-zone protein are promoted, causing increase of the effective synaptic area. This then is a form of long term memory, and illustrates how a short term effect can be converted eventually into a long-term change, in which protein synthesis is required for the transition.
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Slide 21 - Anterograde Amnesia Inability to form new memories. Selective memory deficit resulting predominantly from brain damage. Memories prior to the incident are largely spared. Memory for skills or habits are often spared as well.
Slide 22 - Characteristics of AA Memory lapses may be triggered by nervous or upsetting environments Stuck in a previous time period in own life Most carry on lives normally and happily, until reminded of their deficit by others or out of place objects or activities.
Slide 23 - Hollywood Anterograde Amnesics Finding Nemo (2003) Memento (2001) 50 First Dates (2004)
Slide 24 - Clinical AA The infamous Patient H.M. (Bilateral Temporal Lobectomy) Oliver Sack’s Lost Mariner: Jimmie G. (Korsakoff’s Type) Oliver Sack’s William Thompson (Korsakoff’s Type with much confabulation) Oliver Sack’s Stephen R. (Korsakoff’s Type)
Slide 25 - AA and Alternate States of Consciousness He screams with terror and confusion, and Sacks admits there is nothing that can be done to help him, for like all other anterograde amnesics, he screams "for a past which no longer exists" (The Man Who Mistook His Wife For a Hat: p.42). Living an existence that is not real Never having any ties to reality, which consists of time
Slide 26 - Memory is Consciousness You have to begin to lose your memory, if only in bits and pieces, to realize that memory is what makes our lives. Life without memory is no life at all…Our memory is our coherence, our reason, our feeling, even our action. Without it, we are nothing…(I can only wait for the final amnesia, the one that can erase an entire life, as it did my mother’s…) -Luis Bunuel
Slide 27 - SUMMARY Current autobiographical memories form sense of enduring self? As Siegel concluded, neurotransmitters control consciousness……the fact that serotonin and ACh are altered suggests that memory alteration correlates with an altered state of consciousness.
Slide 28 - REFERENCES Brandt, Ralph & Benedict, Ralph H. B., (1993) Assessment of Retrograde Amnesia: Findings With a New Public Events Procedure. Neuropyschology, 7:217-227 McNaugh, J. L. (1966). Time-dependent processes in memory storage. Science 153, 1351-1358 Duncan, C.P. (1949). The retroactive effect of electroshock on learning. Journal of Comparative and Physiological Psychology, 42, 3244. Meeter, Martijn & Murre, Jaap M. J., (2004) Consolidation of Long-Term Memory: Evidence and Alternatives, Psychology Bulletin, 130:843-857 Clark, Broadbent, Zola, & Squire (2002). Anterograde amnesia and temporally graded retrograde amnesia for a nonspatial memory task after lesions of the hippocampus and subiculum, 4663-4669.