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PSY361 exam 4; part 1

Terms in this set (19)

Review the types of memory impaired in patient HM and what types of memory are ‎intact
Patient HM lost his ability to form Long Term memories. He could only remember memories from before his surgery. Although he could not form long term memories he was still able to form short term memories.

He was able to perform tasks such as the digit span task, as well as the match to sample task.

Although his short term memory was still intact, distractions were a limiting factor. He could only memorize as long as he had no distractions. Even simple distractions such as a loud noise would disturb patient HM.

While he could not form new memories (both episodic and semantic), he was able to retain some information in short term memory, so long as he was not distracted. This information would never be consolidated into long term memory.
‎What types of memory task could HM learn?‎
Although Patient H.M. had an extreme inability to form new declarative memories, he had NOT entirely lost long term memory, because his procedural, nondeclarative, memory was intact. He could learn new skills, evidenced by his performance on perceptual motor tasks, such as the pursuit rotor and the reverse mirror reading task. His skill level increased and his number of errors decreased every day he practiced, but he had no memory of having practiced it before.

HM had his long term memory impaired and suffered from retrograde and anterograde amnesia. His short term memory was intact as well as his procedural memory. He could learn the Match to sample task, the Mirror-Drawing task and the Incomplete-drawing test.
Review the basic memory problems associated with Korsakoff's disease and the part of ‎the brain affected by the disease.‎
Patients with this disease show anterograde and retrograde amnesia. Part of the brain affected with Korsakoff is the diencephalon. This disease occurs in chronic alcoholics due to vitamin deficiency (thiamine). Korsakoff's patients often exhibit
What is a confabulation?‎
false memories (not lies or delusions) invented to fill in the gaps in memory.
When a patient has a head injury and begins to recover, what changes do you see in their ‎retrograde memory impairment?‎
Patients with head injuries often exhibit post-traumatic amnesia, severity of which is a good indicator of how one will recover. Over time, retrograde amnesia tends to improve. However, memory from the time of coma, the time of injury, will never come back. There is also improvement in anterograde amnesia as the patient recovers.

Patients always have some degree of lasting retrograde amnesia though.
What is the serial position curve? ‎
The serial position curve is a distribution graph that shows the accuracy of recall. This curve shows that when people try to remember a list of numbers or words, we typically tend to remember words at the beginning and/or at the end of a list, but we do not usually remember middle numbers/words as well (the serial positioning effect).
What are the primacy and recency effects?‎
Primacy effect: Remembering words at the beginning of a list

Recency effect: Remembering words at the end of a list
What is the difference between declarative and procedural memory? ‎
Declarative memory: explicit and accessible to conscious awareness. Things you know that you can tell others Semantic, and episodic

Procedural: Things you know that you can show by doing, memory of how to do things
Which region of the brain is important for declarative memory?‎
The hippocampus and surrounding temporal lobe areas are important for forming declarative memories.
Which region of the brain is important for short-term memory?‎
The frontal lobe is important for Short term memory
What is the difference between semantic and episodic memory?‎
Semantic: general knowledge, stored and undated; memory for info and facts (example: The capital of France)

Episodic: refers to individual episodes, dated recollections of personal experiences. remembering specific things of life (example: your first day of school.)
Review the parts of the brain affected by Alzheimer's disease (AD). ‎
Parts of the brain affected by AD (also order of cell loss)
a.Entorhinal cortex
b.Hippocampus
c.Amygdala
d.Prefrontal cortex
e.Inferior temporal cortex
f.Posterior parietal cortex
Where do the plaques and tangle first appear? ‎
Plaques tend to build up BETWEEN nerve cells while Tangles form INSIDE cells
Which lobe of the brain is not as affected by AD?‎
The occipital lobe is not affected by AD
Which proteins are found in plaques and tangles?‎
Tangles are formed when protein Tau
Review the basics symptoms of AD (e.g. memory, agnosia, aphasia, apraxia, ‎executive dysfunction) .‎
a.Memory loss: amnesia, learning and recall problems
b.Disorientation of time and space
c.Personality changes: childlike and aggressive
d.Language problems: aphasia
e.Inability to carry out motor activities despite intact motor function (apraxia) able to do things, but not if asked to do it.
f.Inability to recognize objects and faces (agnosia)
g.Impaired executive functioning: problem solving, planning and strategy problems
h.Mood disturbances: depression and anxiety

Symptoms must cause social/occupational dysfunction
Course characterized by gradual onset and continual cognitive decline
Rule out other causes of impairment
Review what is known about the genetics of AD.

Which genes are related to sporadic ‎AD and which are related to familial AD?

What do we know about the ApoE E4 ‎allele as a risk factor for AD?‎
Early onset of around 55 yrs. Of age. Rapid degeneration (familial AD) not typical AD
If parent has it there is 50% risk for children
Gene related to familial AD is chromosome 21, 14 and 1

Late onset starting at 65 yrs. Of age. gradual and slow degeneration (sporadic AD) slower disease progression: gene related to this type of AD is chromosome 19

What we know about the ApoE E4 allele: 15% risk of AD for E4
E4 is more common in AD patients, related to age of onset and rate of decline. Some E4 people don't develop AD and some who lack E4 do develop AD.

Basically, if you have E4 you are more likely to have a bad outcome if something happens to your brain.
What changes in the brains of AD patients can you see on a MRI? ‎Which changes cannot be seen on a MRI?‎
Evidence from neuroimaging- cannot see plaques and tangles in MRI, only by autopsy

Clues: massive cell loss and enlarged ventricles, occipital lobe is not as affected.
Which neurotransmitter has been shown to be particularly decreased in patients with ‎AD?‎
Acetylcholine

Levels of Acetylcholine also decrease in normal aging, but AD patients have severely lowered levels, by as much as 60 - 90%.
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