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learning,memory and amnesia

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Learning and Memory
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Page 1: learning,memory and amnesia

Learning and Memory

Page 2: learning,memory and amnesia

The brain changes its functioning in response to experience Learning relatively permanent change in behavior

as a function of training, practice or experience

how experience changes the brain The process by which we acquire knowledge

about the world “more or less a permanent change in

behavior which occurs as a result of practice

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The Stages of Learning

Acquiring wherein one masters a new activity…

Retaining the new acquisition for a period of time

Remembering which enables one to reproduce the learned act or memorized material.

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MEMORY IS A PHASE

OF LEARNING

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Memory How changes are stored and

subsequently reactive The process by which that knowledge of the world is encoded, stored, and later retrieved

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Three Major Categories of Memory Awareness of briefly presented

information and perception of its aftereffects refers to sensory memory

Two forms: Echoic Memory auditory stimuli stored for a few seconds that is necessary for comprehending sounds.Iconic Memory the visual representation of information in the environment

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Short term Memory retains small amounts of information for a few seconds or less than 30 seconds.

Long Term Memory is a mental storage where we keep our knowledge and experiences for a relatively permanent period of time.

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Categories of LTM

Declarative Memory Holds information that are easily verbalized

and described such names of people, concepts, events and experiences.

Sub types:Semantic memoryEpisodic Memory

Procedural Memory holds relatively permanent information that

are not easily verbalized.

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Explicit Memory knowledge of facts- people, places and

the things-meaning of these facts. Conscious memory

Implicit Memory Involves information on how to perform

something; it is recalled unconsciously Used in trained, reflexive motor or

perceptual skills.

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Where are Memories Stored? Memory Storage

Stored diffusely throughout the structures of the brain.

Five areas of the brain have been implicated in the storage of man’s memory.

They are Inferotemporal Cortex, Amygdala, Prefrontal Cortex, Cerebellum and Striatum

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INFEROTEMPORAL CORTEX

Is the cortex of the inferior temporal lobe. It is involved in the visual perception of objects. It is thought to participate in storing memories of visual patterns.

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Amygdala

An almond shaped nucleus in the anterior temporal lobe. It play a role in memory for emotional significance of experiences.

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Prefrontal Cortex

It is composed of numerous anatomically distinct areas that have different connections and functions. There are regions of prefrontal cortex that perform fundamental cognitive processes during all working memory tasks. Involved in the memory for the temporal order of events.

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Cerebellum

Is thought to store memories of learned sensorimotor skills.

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Striatum

it stores memories for consistent relationships between stimuli and responses-the type of memories that develop incrementally over man trials.

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The Hippocampus and Memory for Spatial Location

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The Hippocampus

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It forms part of the limbic system which is composed of brain structures that play a role in memory, emotion and motivation.

The hippocampus and surrounding structures are thought to play crucial roles in the encoding and retrieval of memories

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Spatial Orientation Three types of Spatial Ability

Ability to visualize rotation and flipping over of shapes and diagrams

Ability to reorient objects from different angles

Finding relations between different spatial objects.

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The Hippocampus and Spatial Orientation

The hippocampus helps construct a 3D “mental map” of our surroundings, and is crucial for our ability to move around in the real world.

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What is:

Lobectomy – removal of a lobe or major part of one from the brain.

Lobotomy – Separation of a lobe or a major part of one from the rest of the brain by a large cut but is not removed

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Bilateral Medial Temporal Lobectomy

the removal of the medial portions of both temporal lobes, including most of the hippocampus, amygdala and adjacent cortex.

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Amnesic Effects of Bilateral Medial Temporal Lobectomy

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AMNESIAis a deficit in memory

caused by brain damage, disease, or

psychological trauma.

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There are two main types of amnesia:

retrograde amnesia and anterograde amnesia.

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Retrograde amnesia is the inability to retrieve information that was acquired before a particular date, usually the date of an accident or operation.

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Anterograde amnesia is the inability to transfer new information from the short-term store into the long-term store.

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The Brain’s ability to change its functioning in response to experience.

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Learning deals with how experience changes the brain.

Memory deals with how these changes are stored and subsequently reactivated.

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What is: Lobectomy:is an operation in

which a lobe, or a major part of one, is removed from the brain.

Lobotomy: Separation of a lobe or a major part of one from the rest of the brain by large cut but is not removed.

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What is: Bilateral Medial Temporal

Lobectomy The removal of the medial portions of both temporal lobes, including most of the hippocampus, and amygdala.

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Effects of Bilateral Medial Temporal Lobectomy

The Case of H. M., The Man Who Changed the Study of Memory

Henry Molaison also known as H.M. – an epileptic who had his temporal lobes removed in 1953.

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His seizures were dramatically reduces- but so was his memory

Mild retrograde amnesia and severe anterograde amnesia

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Formal Assessment of H.M. Digit Span – H.M. can

repeat digits provided the time between learning and recall is within the duration of STM.

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Formal Assessment of H.M. Block-tapping memory –

span test – this test demonstrated that H.M. has global amnesia– amnesia for information presented in all sensory modality

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Formal Assessment of H.M. H.M. readily “learns” responses

through classical conditioning, but has no memory of conditioning trials

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Scientific Contributions of H.M.’s Case Medial temporal lobes are involved in memory

STM and LTM are distinctly separate – H.M. is unable to move memories from STM to LTM, a problem with memory consolidation

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Medial Temporal Lobe Amnesia

Semantic Memory (General information) may function normally while episodic memory (events that one has experienced) does not- they are able to learn facts, but do not remember doing so.

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Medial Temporal Lobe AmnesiaNot all with this form of amnesia are unable to form new explicit long-term memories

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Amnesia after Concussion :Amnesia after Concussion :Evidence for ConsolidationEvidence for Consolidation

Amnesia of Korsakoff’s Amnesia of Korsakoff’s SyndromeSyndrome

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What is:Concussion

- a temporary disturbance of consciousness produced by a nonpenetrating head injury

Posttraumatic Amnesia-an amnesia following a nonpenetrating blow in the head

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Amnesia after Concussion: Evidence for Consolidation Concussions may cause retrograde

amnesia for the period before the blow and some anterograde amnesia after

The same is seen with comas, with the severity of the amnesia correlated with the duration of the coma

Period of anterograde amnesia suggests a temporary failure of memory consolidation

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Gradients of Retrograde Amnesia and Memory Consolidation

Concussions disrupt consolidation (storage) of recent memories

Hebb’s theory – memories are stored in the short term by neural activity

Interference with this activity prevents memory consolidation. Examples: Blows to the head (i.e., concussion) ECS (electronconvulsive shock)

Long gradients of retrograde amnesia are inconsistent with consolidation theory

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Reconsolidation Each time a memory is

retrieved from LTM, it is temporarily held in STM

Memory in STM is susceptible to post-traumatic amnesia until it is reconsolidated

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The Hippocampus and Consolidation

H.M. has some retrograde amnesia Perhaps the hippocampus stores memories

temporarily (standard consolidation theory) Consistent with the temporally graded

retrograde amnesia seen in experimental animals with temporal lobe lesions

Or, perhaps the hippocampus stores memories permanently, but they become “stronger” over time

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What is:Korsakoff’s (Korsakov’s) Syndrome

- a brain disorder caused by the lack of thiamine (vit.B1 ) in the brain- it was named after the neuropsychiatrist Sergei Korsakoff who popularized the theory

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Six Major Symptoms:1. Anterograde Amnesia2. Retrograde Amnesia3. Confabulation- invented

memories which are taken as true due to gaps in memory

4. Meager content in conversation5. Lack of insight6. Apathy

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Amnesia of Korsakoff’s Syndrome

Most commonly seen in alcoholics (or others with a thiamine deficiency)

Amnesia, confusion, personality changes, and physical problems

Typically damage in the pre frontal cortex – medial thalamus + medial hypothalamus

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Amnesia of Korsakoff’s Syndrome (continued)

Amnesia comparable to medial temporal lobe amnesia in the early stages Anterograde amnesia for episodic memories

Differs in later stages Severe retrograde amnesia develops

Differs in that it is progressive, complicating its study

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•Alzheimer’s disease is associated with a gradually progressive loss of memory often occurring in old age.

•Affects 50% of people over 85.•Early onset seems to be influenced by genes, but 99% of cases are late onset.

•About half of all patients with late onset have no known relative with the disease.

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•Alzheimer’s disease is associated with an accumulation and clumping of the following brain proteins:Amyloid beta protein 42 which produces widespread atrophy of the cerebral cortex, hippocampus and other areas.

An abnormal form of the tau protein, part of the intracellular support system of neurons.

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Accumulation of the tau protein results in: Plaques – structures formed from degenerating neurons.

Tangles – structures formed from degenerating structures within a neuronal body.

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A major area of damage is the basal forebrain and treatment includes enhancing acetylcholine activity.

One experimental treatment includes the stimulation of cannabinoid receptors that limits overstimulation by glutamate.

Research with mice suggests the possibility of immunizing against Alzheimer’s by stimulating the production of antibodies against amyloid beta protein.


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