Week 4: Memory Disorders Flashcards
(36 cards)
Retrograde amnesia
Poor recall for memories BEFORE onset of amnesia
Anterograde amnesia
Loss of ability to form new memories AFTER onset of amnesia
Global amnesia
Severe anterograde amnesia, moderate retrograde amnesia
Temporal gradient
Older memories are less impaired than newer memories
Korsakoff’s syndrome (aka deincephalic amnesia)
Caused by vitamin B1 deficiency from chronic alcoholism. Experience poor ability to remember events before and after onset of amnesia
Semantic dementia
Severe problems with SEMANTIC memory (e.g. information about
meanings of words and concepts) but intact episodic memory. Always involves
degeneration of the ANTERIOR TEMPORAL LOBE.
Dissociation
Identification of a SINGLE brain region responsible for a cognitive process
Single dissociation
Identify that brain damage to one structure disrupts one cognitive
process but not another.
Double dissociation
Identify that brain damage to one structure disrupts one cognitive
process (‘X’) but not another (‘Y’). Also, identify that brain damage to different structure
disrupts cognitive process ‘Y’ but not ‘X’.
Misinformation effect
Refers to the finding that memories are easily distorted by misleading info presented after
Confirmation bias
Tendency to recall information in a way that confirms pre-existing beliefs.
Brain structures and episodic and semantic memory (recap)
Damage hippocampus = episodic affected
Damage para-hippocampal cortex = semantic affected
Damage to both brain regions = both memory poor
Potential causes of amnesia:
- surgery (e.g. patient HM)
- chronic alcohol abuse
- brain tumours
- bilateral stroke
- encephalitis (brain swelling, typically due to infection)
- Dementia (Alzheimer’s disease)
- Closed head injury
Retrograde amnesia
Poor recall of memories formed BEFORE onset of amnesia.
(Greater impact on episodic (personal) than semantic memories (general knowledge)).
TEMPORAL GRADIENT - older memories less impaired than newer ones
Explanations for temporal gradient:
CONSOLIDATION THEORY:
- Physiological process in the hippocampus leads to formation of long-lasting memories
- consolidated memories stored elsewhere, protecting them from effects of hippocampal damage (= memories in there a longer time = less likely to lose)
SEMANTICISATION:
- Episodic memories become more like semantic ones over time (less personal, more vague) = older memories protected from effects of brain damage…
REDUCED LEARNING OPPORTUNITY:
- episodic memories depend on a single learning experience = reduced learning opportunity explains emnesia
- semantic memories depend on several learning experiences (e.g. taught some facts more than once)
Anterograde amnesia
Loss of ability to form new memories AFTER onset of amnesia
* Results from damage to the areas of the brain that are involved in forming new memories * Damage to the hippocampus the main cause in most instances * Mammillary bodies and fornix also commonly involved
Global amnesia
- Moderate retrograde amnesia and severe anterograde amnesia
- Results from lesions of structures in the medial temporal lobe, specifically the hippocampus
- Patient HM
Patient H.M.
- most studied amnesiac patient
- suffered from severe epilepsy from age 10
- at 27yrs, had surgery to remove the entire medial temporal lobe (including hippocampus)
- moderate retrograde and severe anterograde amnesia (global amnesia)
Korsakoff’s syndrome
AKA diencephalic amnesia
- vitamin B1 deficiency from chronic alcoholism
- ## damage to mammilary bodies in hypothalamus
– Poor ability to remember events before and after onset of amnesia (retrograde & anterograde) – Some new learning ability (e.g. motor skills) – Slight impairment of STM (e.g. digit span)
Symptomology of Korsakoff’s syndrome & issues
- Typically had gradual onset – Events happened before or after amnesia onset?
- Brain damage widespread (hippocampus and frontal) – damage to frontal lobes = other cognitive deficits
- Precise pattern of damage varies across patients – difficult to generalise across patients
- Brain plasticity and learning of compensatory strategies – does not provide a direct assessment of the impact of brain damage of the LTM
Semantic dementia
Severe problems with semantic memory, but intact episodic memory
- loss of info on meaning of words/concepts
- difficulty naming pictures/objects, single word comprehension, categorising, and knowing the uses of objects
Episodic memory and most executive functions (e.g. attention) reasonably intact in the early stages
* Always involves degeneration of the anterior temporal lobe – Where semantic memories are stored – Perirhinal and entorhinal cortices where semantic memories formed
Double dissociation
Amnesia and semantic dementia point to a double dissociation in LTM
Amnesia = hippocampus
– Poor episodic memory (‘X’)
– Intact semantic memory (‘Y’)
Semantic dementia = anterior temporal lobe
– Poor semantic memory (‘Y’)
– Intact episodic memory (‘X’)
Eyewitness testimony
The Innocence Project (2008) “Eyewitness misidentification is the single greatest cause of wrongful convictions nationwide, playing a role in more than 75% of convictions overturned through DNA testing.” Still, the criminal justice system profoundly relies on eyewitness identification and testimony for investigating and prosecuting crimes.
(Wells & Olson, 2003)
Memory errors (3)
- forgetting
- intrusions
- bias