BIOLOGICAL BASES OF BEHAVIOR

Ch. 8
Memory and Amnesia
Contents
Topic 1. Involvement of brain in memory
Topic 2. Memory Disorder (Korsakov, Alzheimer, Parkinson diseases
etc.)
Presented by
Imtiaz Hussain (Lecturer)
Department of Applied Psychology Government P/G College Jhang
9/21/2018 1
 Memory
• Cortex - four lobes
• Occipital - vision Parietal
Frontal Lobe Lobe
• Parietal - sensation
• Temporal – memory,
hearing
• Frontal - reasoning,
memory

Occipital
Lobe
Temporal
Lobe
Brain and Memory
Other Crucial Parts
• Limbic system: controls emotions and
instinctive behavior (includes the hippocampus
and parts of the cortex)
• Thalamus: receives sensory and limbic
information and sends to cerebral cortex
• Hypothalamus: monitors certain activities and
controls body’s internal clock
• Hippocampus: where short-term memories are
converted to long-term memories
 Brain and Memory
• Hippocampus
• Important for formation of new episodic memories
• Important for encoding perceptual aspects of memories
• Novel events, places, and stimuli
• Important for declarative memory
• Especially as part of medial temporal lobe
 Brain and Memory
• Hippocampus
• Recollection vs. Knowing
(familiarity)

• Eldridge et al have shown the

hippocampus is selectively
involved in R, not with K.

• Verfaelle & Treadwell (1993),

using process dissociation
procedure showed similar
pattern.

(Eldridge et al., Nature Neuroscience 2000)

 Amnesia
• Loss of memory ability - usually due to lesion or
surgical removal of various parts of the brain
• Relatively spared performance in other domains
• A pure amnesia is relatively rare
 Amnesia
• Loss of memory ability - usually due to lesion or
surgical removal of various parts of the brain

• Three different kinds of classifications

• Source of the disease (e.g., illness, injury)
• Location of the area of damage
• Functional deficit (i.e., what kind of memory is impaired)

• This mixed way of categorizing amnesia causes some

difficulties
 Amnesia
• Loss of memory ability - usually due to lesion or
surgical removal of various parts of the brain

• Two broad categories:

• Retrograde: loss of memories for events prior to damage
• Anterograde: loss of ability to store new memories of events
after damage
Injury

Time
 Causes of Amnesia
• Korsakoff ’s syndrome
• Traumatic Brain Injury (TBI) (Concussion)
• Alzheimer’s disease
• Other causes include
• Specific brain lesions (i.e. • Epilepsy
surgical removal) • Electroconvulsive shock
• Psychological therapy
• Dissociative Fugue • Drugs (esp. anesthetics)
• Psychogenic • Infection
• Migraines • Nutritional deficiency
• Hypoglycemia
 Amnesia
• Korsakoff ’s syndrome:
• Results from chronic alcoholism and consequent
thiamine deficiency
• Lesions to Medial Thalamus
• Neuropathology: most sources attribute the amnesia to
combined lesions in two diencephalic structures: the
dorsomedial nucleus of the thalamus and the mammillary bodies
of the hypothalamus
 Amnesia
• Korsakoff ’s syndrome
• Generally preserved IQ, including a normal digit span.
• Personality changes, the most common of which is apathy,
passivity and indifference
• inability to formulate and follow through a series of plans
• Lack of insight into their condition.
• How can someone with a shattered memory remember that he
has become unable to remember?
 Amnesia
• Korsakoff ’s syndrome
• Retrograde amnesia with a temporal gradient
• Anterograde amnesia
• Confabulation, which is a tendency to "fill in the gaps" of
one's memories with plausible made-up stories.
• confabulations are rare among chronic Korsakoff patients
who've had the disease for more than 5 years. Patients in the
chronic stage are more likely to say "I don't know" or remain
silent when faced with memory failures rather than to invent
stories.
 Amnesia
• Korsakoff ’s syndrome
• Worst impairments are on episodic memory tests,
including list learning of words, figures, or faces,
paragraph recall.
• Relatively preserved semantic memory, including normal
verbal fluency, vocabulary, rules of syntax, and basic
arithmetic operations
• Intact sensori-motor memory (mirror tracing, mirror
reading, pursuit rotor)
• Intact performance on perceptual tasks (e.g., perceptual
identification, generating category exemplars)
 Amnesia
• Post-traumatic amnesia
• Damage due to lesions as well as twisting and tearing
of microstructure of brain
• Symptomology
• After severe TBI, individuals typically lose consciousness
• After they begin to regain consciousness, there is often a
gradual recovery during which patients have difficulty
keeping tracking of and remembering on-going events,
though there may be islands of lucidity and memory
 Amnesia
Injury

Time

• Retrograde amnesia
• Refers to difficulty remembering events that occurred
prior to injury
• The duration of amnesia varies but can extend back for
several years
• Rare, short-lived
• Typically due to brain trauma
 Amnesia
Injury

Time

• Retrograde amnesia
• Duration of retrograde amnesia typically shrinks as time passes
• e.g., Russell (1959) described case of TBI as a result of a motorcycle
accident
• 1 week post accident patient had lost 11 years of memory extending back
from injury
• 2 weeks post accident patient had last 2 years of memory
• about 10 weeks post injury memories of the last two years gradually
returned
• This pattern of results suggests that retrograde amnesia is a
retrieval problem
• The pattern of damage/recovery -- from most distant to most
recent -- has been argued by some to reflect a failure of
consolidation (Ribot’s Law)
 Amnesia
Injury

Time

• Retrograde amnesia
• Butters & Cermak (1986) reported a case study of an
eminent scientist (born 1914) who had written his
autobiography only two years prior to becoming
amnesic
• Tested him by asking him questions all drawn from his
autobiography Recall of information from PZ autobiography

80
70
Percent recall

60
50
40 Recall
30
20
10
0
1916- 1930- 1940- 1950- 1960- 1970-
1930 1940 1950 1960 1970 1980
 Amnesia
Injury

Time

• Anterograde amnesia
• Refers to problems of learning new facts
• Specific to episodic memories
• Procedural memories intact
• Implicit memory performance normal
 Amnesia
• Anatomy of anterograde amnesia
• Damage to the hippocampus or to regions that supply its
inputs and receive its outputs causes anterograde amnesia
• How does the hippocampus form new declarative
memories?
• Hippocampus receives info about what is going on from
sensory and motor assc. cortex and from some subcortical
regions
• It processes this info and then modifies the memories being
consolidated by efferent connections back to these regions
• Experiences that lead to declarative memories activate the
hippocampal formation
• The hippocampal formation enables us to learn the relationship
between the stimuli that were present at the time of an event (i.e.
context) and then events themselves
 Amnesia
• Anatomy of anterograde amnesia
• Damage to other subcortical regions that connect with
the hippocampus can cause memory impairments
• Limbic cortex of the medial temporal lobe
• Semantic memories – a memory of facts and general info;
different from episodic memory
• Destruction of hippocampus alone disrupts episodic memory
only; must have damage to limbic cortex of medial temporal lobe
to also impair semantic memory (and thus all declarative memory)
• Fornix and mammillary bodies
• Patients with Korsakoff’s syndrome suffer degeneration of the
mammillary bodies where the efferent axons of the fornix
terminate in the mammillary bodies
• Damage to any part of the neural circuit that includes
the hippocampus, fornix, mammillary bodies and
anterior thalamus cause memory impairments
 Amnesia

• Theoretical implications of amnesia

• Provides evidence for STM versus LTM distinction
• Supports the notion that there are different systems
mediating explicit (episodic) and implicit (procedural
memory)
• May indicate that semantic and episodic memory can
be fractionated
• May provide insight into nature of consciousness
 Alzheimer’s Disease
• Alzheimer’s disease
• cortical, progressive dementia
• disease is associated with the development of neuro-
fibrillary tangles and plaques
• The brain has billions of neurons, each with
an axon and many dendrites.
• To stay healthy, neurons must communicate
with each other, carry out metabolism, and
repair themselves.
• AD disrupts all three of these essential jobs.
 Alzheimer’s Disease

• Alzheimer’s disease Preclinical AD

• Signs of AD are first noticed in
the entorhinal cortex, then
proceed to the hippocampus.
• Affected regions begin to
shrink as nerve cells die.
• Changes can begin 10-20 years
before symptoms appear.
• Memory loss is the first sign of
AD.
 Alzheimer’s Disease
Mild to Moderate AD • AD spreads through the brain. The
• Alzheimer’s disease cerebral cortex begins to shrink as
more and more neurons stop working
and die.
• Mild AD signs can include memory
loss, confusion, trouble handling
money, poor judgment, mood changes,
and increased anxiety.
• Moderate AD signs can include
increased memory loss and confusion,
problems recognizing people, difficulty
with language and thoughts,
restlessness, agitation, wandering, and
repetitive statements.
 Alzheimer’s Disease
Severe ADs
• In severe AD, extreme shrinkage
• Alzheimer’s disease occurs in the brain. Patients are
completely dependent on others for
care.
• Symptoms can include weight loss,
seizures, skin infections, groaning,
moaning, or grunting, increased
sleeping, loss of bladder and bowel
control.
• Death usually occurs from aspiration
pneumonia or other infections.
Caregivers can turn to a hospice for
help and palliative care.
Alzheimer’s Disease
Alzheimer’s Disease

Pet Scan of Pet Scan of Alzheimer’s

Normal Brain Disease Brain
 Alzheimer’s Disease

• Criteria
• deficit in two or more areas of cognition, at least one of
which is memory
• interferes with social or occupational functioning
• decline from premorbid level
• gradually progressive course
• rule out other causes
 Alzheimer’s Disease

• The Hallmarks of AD
• The brains of people with AD have an abundance of
two abnormal structures:
• Beta-amyloid plaques
• Dense deposits of protein and
cellular material that accumulate
outside and around nerve cells
An actual AD plaque
• Neurofibrillary tangles
• Twisted fibers that build up inside
the nerve cell
An actual AD tangle
 Alzheimer’s Disease

Beta-amyloid Plaques
Amyloid precursor protein (APP) is the precursor
to amyloid plaque.
1. APP sticks through the neuron membrane.
2. Enzymes cut the APP into fragments of
protein, including beta-amyloid.
3. Beta-amyloid fragments come together in
clumps to form plaques.

In AD, many of these clumps form, disrupting

the work of neurons. This affects the
hippocampus and other areas of the cerebral
cortex.
 Alzheimer’s Disease

• Alzheimer’s disease
• three types of memory problems
• episodic memory impaired (e.g., free recall)
• executive function (Baddeley appears to be affected)
• semantic memory is also impaired
• note: pure amnesics do not have the latter two
impairments
 Neuropsychology of
Memory
• Consciousness
• Tulving has proposed that different memory systems
have associated with them different levels of
consciousness
• noetic -- awareness
• episodic memory -- autonoetic, self awareness
• semantic memory -- noetic, aware of the information, but
not aware of event
• procedural memory -- anoetic no conscious awareness
 Parkinson's disease

Parkinson's disease affects the nerve cells in the brain

that produce dopamine. Parkinson's
disease symptoms include muscle rigidity, tremors, and
changes in speech and gait. After diagnosis, treatments
can help relieve symptoms, but there is no cure.

Parkinson's disease dementia is a decline in thinking

and reasoning thatdevelops in someone diagnosed
with Parkinson's disease at least a year earlier.
Common symptoms include: Changes in memory,
concentration and judgment.
 Main Symptoms of
Parkinson's
The main symptoms of Parkinson's include:

• uncontrollable shaking and tremors.

• slowed movement (bradykinesia)

• balance difficulties and eventual problems standing

up.

• stiffness in limbs.
 Parkinson's disease can't
be cured
Parkinson's disease is a chronic, degenerative neurological disorder that
affects one in 100 people over age 60. While the average age at onset
is 60, some people are diagnosed at 40 or younger.

Parkinson's disease can't be cured, but medications can help control

your symptoms, often dramatically. In some later cases, surgery may be
advised. Your doctor may also recommend lifestyle changes, especially
ongoing aerobic exercise.

Patients with stage four Parkinson's disease have

visible bradykinesia and rigidity. In most cases, stage four patients need
assistance to walk, stand, and move. When patients reach stage five –
the final stage of Parkinson's disease – they will have severe posture
issues in their back, neck, and hips.
 Neuropsychiatric Disturbances

Parkinson's disease can cause neuropsychiatric disturbances, which can range from
mild to severe. This includes disorders of cognition, mood, behavior, and thought.

Cognitive disturbances can occur in the early stages of the disease and sometimes
prior to diagnosis, and increase in prevalence with duration of the disease.

The most common cognitive deficit in PD is executive dysfunction, which can

include problems with planning, cognitive flexibility, abstract thinking, rule
acquisition, inhibiting inappropriate actions, initiating appropriate actions, working
memory, and control of attention.

Other cognitive difficulties include slowed cognitive processing speed,

impaired recall and impaired perception and estimation of time. Nevertheless,
improvement appears when recall is aided by cues. Visuospatial difficulties are also
part of the disease, seen for example when the individual is asked to perform tests
of facial recognition and perception of the orientation of drawn lines
Brain areas in PD
Stages of PD