Answer the following questions in your journal.
1.
2.
3.
4.
5.
6.
7.
What type of memory is lost in patients who suffer
from episodic amnesia?
Which part of the brain is typically damaged in
people who suffer from episodic amnesia?
What is psychogenic amnesia?
What was Karl Lashley’s hypothesis?
What region of the brain is responsible for explicit
memory? How do we know?
Why was Karl Lashley unable to find evidence to
support his hypothesis?
What region of the brain is responsible for implicit
memory? How do we know?
Episodic Memory
Episodic memory = autobiographical memory
 Personal memory of our presence and role in
specific events.
 It’s what allows us to create a sense of time and a
personal role in the changing world
What would life be like without personal
memories?
Episodic Amnesia
 A form of amnesia associated with a loss of
personal memories only
 Memory for events are intact, but patients
don’t recall their personal role in these
events.
Case study: patient K. C.
 Short term memory intact
 Cognitive abilities intact (can still play chess)
 He knows facts about himself but has no
memory for events that included him personally
 Ex: he is unable to describe an event that took
place in school that specifically included him
but could recall going to school and the
knowledge he gained there
Episodic amnesia
 Associated with frontal lobe injuries
 May be unique to humans, due to their highly
developed frontal lobes.
 Not only associated with brain injury, also occurs
in patients with psychiatric disorders  called
 These patients have reduced activity in the
frontal lobe of their brain, which blocks the
retrieval of autobiographical memories.
Episodic Amnesia is associated with brain
damage in the frontal regions
Amnesic patient with a
brain infection
Patient with psychogenic
amnesia
Figure 14-6:
Early studies of Memory
 Karl Lashley’s hypothesis:
 Memories are represented in the circuitry of the
brain used to learn solutions to problems
 If this circuitry is removed or damaged, amnesia
should result.

Wasn’t able to find evidence to support his theory
Case Study: Patient Henry Molaison (H. M)
 In 1953, William Scoville
performed a bilateral
medial-temporal lobe
resection on patient H.M.
for relief of severe epilepsy.
Patient H. M.
Brain regions removed
in H. M.’s surgery:
• Hippocampus
• Amygdala
Post surgery- Patient H. M.
 Following the surgery, H.M. suffered from a severe
amnesia
 He could not recall any specific events that
happened after the surgery (no explicit memory)
 Despite this deficit, H.M. had an above average IQ,
he performed well on perceptual tests, and he could
still recall events from his childhood and faces
 H.M.’s performance on implicit memory tests was
intact
What did Karl Lashley do wrong?
 Most of his tests were measures of implicit
memory, not explicit memory.
 Had he used a test of explicit memory, he
would have found a memory deficit in his
rats similar to H.M.s
Case Study- patient J.K.
 Developed Parkinson’s disease in his mid 70s
 causes damage to dopaminergic cells in the basal ganglia
 Impaired ability to perform tasks that he had
done all his life

Example: turning off the radio
 Could still recall explicit events
 Thus selective damage to the basal ganglia causes
impaired implicit memory but leaves explicit memory
intact.
Read the article and answer the following in
your journal
1. Who?
2. What’s the problem?
3. Signs and symptoms.
4. Cause.
5. Cure?
Important points
1. Who? : Joe R, 62 year old man, average intelligence, no
obvious sensory or motor difficulties
2. What’s the problem?: Korsakoff’s syndrome
3. Signs and symptoms:
 Severe loss of memory, both anterograde and retrograde
amnesia
 Make up plausible stories of past events rather than
admit they don’t remember
 Indifferent to suggestions that they have a memory
problem
 Apathetic to things going on around them
Anterograde vs. Retrograde Amnesia
Korsakoff’s Syndrome
Normal
patient
Korsakoff
patient
4. Cause:
 Thiamine (Vitamin B1) deficiency from prolonged intake
of large quantities of alcohol
 Death of brain cells in the thalamus, mammillary bodies
and hypothalamus
 Cortical atrohpy (shriveling) in the frontal lobe
5. Cure?
 Only 20% of patients show recovery after a year on a
vitamin B1 –enriched diet
Alzheimer’s Disease
1) Define the following words:
- brain atrophy:
partial or complete wasting away (shrinking) brain tissue
- neuropathology:
A disease of neural (brain) tissue
- Afflicted:
To be affected by
- Postmortem:
After death
dementia (or demented):
The loss of brain function that occurs with certain diseases. It
affects memory, thinking, language, judgment, and behavior.
http://www.hbo.com/alzheimers/the-films.html
2) What is the only reliable diagnostic test for
Alzheimer’s disease?
Postmortem examination of cerebral tissue revealing
the presence of neuritic plauqes (amyloid protein) and
neurofibrillary tangles
3) What 2 principal neuronal changes take place in
Alzheimer’s disease?
- Loss of cholinergic cells in the basal forebrain
- Development of neuritic plauqes in the cerebral
cortex
4) What is a treatment for Alzheimer’s disease?
Cognex - cholinergic agonist: it increases levels of the
neurotransmitter acetylcholine
5) What is a neuritic plaque?
A bundle of cells often found in the cerebral cortex of
Alzheimer’s patients. It consists of a protein (amyloid)
core surrounded by bits and pieces of degenerated
cells.
6) Where in the brain of Alzheimer’s patients are
neuritic plaques more commonly found?
In the temporal lobe areas related to memory.
7) Where in the brain of Alzheimer’s patients are
neurofibrillary tangles most commonly found?
In the cerebral cortex and hippocampus
http://www.hbo.com/alzheimers/supplementary-understanding-and-attackingalzheimers.html
Thursday, May 3rd:
Test on Learning and Memory Unit
Learning vs. memory
Studying Learning and Memory in the Laboratory
Different kinds of learning
Reinforcement
What Makes Explicit and Implicit Memory
Different?
6. What Is Special about Personal Memories?
7. Amnesia case studies
1.
2.
3.
4.
5.
1.
K. C., H. M., J. K. Joe R.
8. Alzheimer’s Disease