HUMAN MEMORY

Neuropsychology & Memory

Neurons and Memory

 Connections between neurons change based on experiences
 Brain is less ‘hard-wired’ than we used to believe
 Lashley provided evidence of plasticity in monkeys in the 1920’s but not widely accepted
until 1960’s
 Neuroplasticity (or brain plasticity)
 Fundamental property of brain (nervous system)
 Capacity of nervous system to modify its organization
 Changes in structure and function as a result of experience
 Changes largely within the synapses

 Synaptic changes that could store memories

 Current dominant theory: Long-term potentiation (LTP)
 Persistent increase in synaptic strength following high-frequency stimulation
 “the molecular and cellular changes mediating the induction of LTP in the hippocampus
are widely considered to provide a basis for memory” (McGaugh, 2000)

 Not all learning-related changes involve changes in synaptic strength (Martin & Morris, 2002)
 Neurogenesis – new evidence suggest that new neurons are formed in some regions of the
brain
 Changes in neuronal excitability – changes in the firing threshold

The Brain: networks of neurons

“There are many steps between synaptic change and behavioral memory.” Squire (pg 8, 1987)
 Lots of interesting questions
 Does “memory” reside in single neurons, or in networks of neurons?

 Are all of the networks the same, or are there differences (i.e., do different regions of the brain deal with different
kinds of things)?

The Brain
Vital Statistics
Number of neurons: 100 Billion
 Adult weight: about 3 pounds
 Adult size: a medium cauliflower Number of synapses (the gap
between neurons): 100 Trillion
 These neurons are connected, organized into networks of neurons
 Networks of neurons hold memories

Frontal Lobe Parietal Lobe

Structure of the brain
 Occipital - vision
 Parietal - sensation
 Temporal – memory, hearing
 Frontal - reasoning, memory
Occipital Lobe
Temporal Lobe

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

So where is memory? It is complicated
Multiple brain regions are involved in encoding (as shown by fMRI)
 For recalling pictures, the right prefrontal cortex and parahippocampal cortex in both hemispheres
are activated.
 For recalling words, the left prefrontal cortex and the left parahippocampal cortex are activated.
 Consolidation of memory involves the hippocampus but the hippocampal system does not store
long-term memory.
 Long Term Memory (LTM) storage occurs in the cortex, near where the memory was first
processed and held in short-term memory.

Seven Sins of Memory

 Hippocampus and nearby structures related to sin of transience
- where new episodic memories are stored Short-term stay
- damaged when one has Anterograde Amnesia Kaya nagkakaroon ng information overloading
 Parts of the frontal lobe related to transience, but even more central to absent-mindedness and
misattribution (and maybe suggestibility)
 Prefrontal lobe is part of the memory and blocking
 Area near front of temporal lobe related to blocking
 Amygdala closely related to persistence
 Not much is known about bias

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
 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
(discussed in detail in your textbook)

Brain and Memory: Amnesia

Amnesia is the general term but there would be specific terms depending on the damage;
1. Diencephalic amnesia - damage to the medial thalamus and mammillary nuclei
2. Medial temporal lobe amnesia - damage to the hippocampal formation, uncus,
amygdala, and surrounding cortical areas
3. Other implicated regions include Anterior Lateral Temporal Lobe and Frontal Lobes

Amnesia
Loss of memory ability - usually due to lesion or surgical removal of various parts of the brain
This mixed way of categorizing amnesia causes
 Relatively spared performance in other domains
some difficulties
 A pure amnesia is relatively rare

3 different kinds of classifications 2 broad categories:

 Source of the disease (e.g., illness, Retrograde: loss of memories for events prior to damage
injury) Anterograde: loss of ability to store new memories of
 Location of the area of damage events after damage
 Functional deficit (i.e., what kind of
memory is impaired)
Injur
y
Time

Causes of Amnesia
 Korsakoff’s syndrome  Migraines
 Hypoglycemia
 Epilepsy
 Electroconvulsive shock
  Traumatic Brain Injury (TBI) (Concussion)
 Alzheimer’s disease
 Other causes include
 Specific brain lesions (i.e. surgical removal)
Psychological
Dissociative Fugue
Psychogenic

Damage can occur due to accident, disease (meningitis, encephalitis)

 AD - growths (protein plaques and tangles within the neurons) in brain disrupt neuron
communication, loss of memory and other cognitive abilities, especially with two or more tasks at
once

Korsakoff’s syndrome
 Results from chronic alcoholism and consequent thiamine deficiency
 Lesions to Medial Thalamus Note: The brain of an alcoholic shrinks
 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
Effects:
1. Generally preserved IQ, including a normal digit span.
2. Personality changes, the most common of which are apathy, passivity and indifference.
Apathy - opposite of empathy, total absence of conscience.
Passivity - opposite of activity, walang gana
Indifference - lack of energy and sympathy

3. Lack of insight into their condition. (Ego-syntonic)

4. Retrograde amnesia with a temporal gradient. This does not mean total forgetfullness
5. Anterograde amnesia
6. Confabulation, a tendency to "fill in the gaps" of one's memories with plausible made-up stories.

Confabulations are rare among chronic Korsakoff Feigned insanity

patients who've had the disease for more than 5 - Nagkukunwaring may psychological disorder para mang
years. deceive at hindi ma-accused na guilty

7. Worst impairements but not everything is deteriorated.

 Episodic memory impairement
 Prosopagnosia- dificulty recognizing faces.
8. Relatively preserved semantic memory, including normal verbal fluency, vocabulary, rules of
syntax, and basic arithmetic operations.
9. Intact sensori-motor memory (mirror tracing, mirror reading, pursuit rotor).
10. Intact performance on perceptual tasks (e.g., perceptual identification, generating category
exemplars).
 Acute Stress Post-Traumatic
Post-traumatic amnesia Disorder Stress Disorder
Symptoms
 Damage due to lesions as well as twisting Onset of symptoms Symptoms present
3 weeks after the slower and last longer. Can
and tearing of microstructure of brain traumatic be up to years if left
experience untreated
Symptomology
 After severe Traumatic Brain Injusry (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

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
 Duration of retrograde amnesia typically shrinks as time passes

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)
 Anterograde amnesia
Refers to problems of learning new facts
 Specific to episodic memories
 Procedural memories intact
 Implicit memory performance normal

Example: Henry Molaison (Patient H. M.) Case

Functional characteristics
 Declarative and nondeclarative memories
- Explicit
- memory that can be verbally expressed,
such as memory for events, facts, or
specific stimuli; this is impaired with
anterograde amnesia
- memory whose formation does not depend on the
hippocampal formation; a collective term for
perceptual, stimulus-response, and motor memory;
not affected by anterograde amnesia; these control
behavior; cannot always be described in words

 Although patients can learn other tasks, they cannot recall ever learning them
 Learning and memory involve different processes
 Episodic memory is impaired
 Both autobiographical and nonautobiographical episodic memory
 Verbal learning is disrupted in anterograde amnesia
 e.g. H.M. did not learn any new words after his surgery
 Perceptual learning
 e.g. recognize broken drawings; also faces and melodies
 Stimulus-response learning
 Working memory is intact
 Semantic memory is spared
 Procedural memory is intact

Anatomy of anterograde amnesia

Damage to the hippocampus or to regions that supply its inputs and receive its outputs causes
anterograde amnesia. - responsible for receiving and encoding
- responsible for formation of new episodic memories

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

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
Damage to other subcortical regions that connect with the hippocampus can cause memory impairments
 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

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
Can be divided into several parts

 May provide insight into nature of consciousness

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 do its jobs;
 communicate with each other
 carry out metabolism
 and repair themselves.
 AD (precinical) disrupts all three of these essential jobs

Preclinical AD
 Signs of AD are first noticed in the entorhinal cortex, then proceed to the hippocampus.
Patients with Severe AD can
 Affected regions begin to shrink as nerve cells die. suffer from Profound
Disability Disorder.
 Changes can begin 10-20 years before symptoms appear.
They need Palliative Care,
 First sign of AD = Memory loss meaning, they have total
dependence on others
 Symptoms persist after several years
 Has no cure PROGRESSION REGRESSION
 Progresses over time.
 Alzheimer’s Disease (AD)
AD spreads through the brain. The cerebral cortex begins to shrink as more and more neurons stop working and die.

Mild AD Moderate AD Severe AD (extreme brain shrinkage)

memory loss increased memory loss weight loss
confusion Increased confusion seizures
poor judgment prosopagnosia skin infections
trouble handling money difficulty with language and thoughts They create unusual sounds (groaning,
moaning, or grunting)
mood changes restlessness increased sleeping
increased anxiety agitation loss of bladder&bowel control
wandering No concept of self-care
repetitive statements pneumonia
Death

Criteria for Alzheimer’s Disease

 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 cause
- not due to lesion or accident but rather due to degeneration

The Hallmarks of AD
The brains of people with AD have an abundance of two abnormal structures:

Beta-amyloid plaques Neurofibrillary tangles

= Dense deposits of protein and cellular = Twisted fibers that build
material that accumulate outside and
around nerve cells up inside the nerve cell

AD
Affected ang semantic memory
 system for storing, organizing, and manipulating information pertaining to the meaning
of words, concepts, and their associations
 conceptualized as a broadly distributed network
 enables judgments about the properties and functions of items

Semantic Memory Performance in AD

 naming and word generation to semantic cues both require semantic memory, both impaired in AD
Recapitulation during retrieval
Introduction
Encoding
 Memory performance depends on the similarity of conditions at
- pagpasok ng info
encoding to those at retrieval. This finding and memory others suggest Retrieval
that encoding and retrieval processes are closely related to each other -paglabas ng info
 It is widely believed that the brain regions activated at encoding will
tend to be activated at retrieval

Hypermnesia
“Photographic” extreme memory ability (a mnemonist)

LATERIZATION OF THE BRAIN

The Left and Right Hemishpere

Left Hemisphere (LH) Right Hemisphere (RH)

 Synthesis or summary
 Serial or sequential events
 Provides summary of events
 Controls sequence of behavior  Gestalt Theory
Controlling your reactions
The whole is equal to some of its parts
 Verbal activities
Yung pagsasalita natin, pati content Example: The Figure Ground Gestalt
ng sinasabi natin. Speech production Principle

 Reading and writing

Learning Disorders
Dyslexia- problem in reading
Dysgraphia- problem in writing
 Responsible for semantic perception. To
Dyscalculia- problem in numbers
perceive objects correctly
 For navigating
 Provides detailed series of events  Construction of 3D objects
Note:
Left-brained people are more likely
to develop OCD

Left Brain (LH) Right Brain (RH)

Information Processing
Linear manner Hollistic manner
Very rigid and critical Thinking as a whole. Logical thinking
Project Management
Critical Clarity
Identifies important and specific details Identifies the whole
 Perception
Analytical Creative
Step by step or systematical Whatever pattern or sequences
Workflow
Sequential manner Randomly
Follows rigid process Having your own process
Problem Solving
Analyzes each step Intuitive
Study every step. Process of elimination Uses intuition to solve the problem

Next Lesson: Vision and Auditory

 Audition and Vision
"If a tree falls in a forest and no one is around to hear it, does it make a sound?" is a philosophical thought experiment that raises
questions regarding observation and perception.

Sound
 As a physical stimulus begins with the movement of an object in space
 Movement sets off waves of vibration in the form of miniature collisions between adjacent
molecules that produce outwardly-moving bands of high and low pressure.
 For humans, the medium that carries sound is usually air, but we can also sense sounds that travel
through liquids and solids.

Sound energy, like electromagnetic energy, can be described in form of waves

High amplitude waves are perceived as loud sounds

Amplitude
 Height of waves (intensity) Low amplitude waves are perceived as soft sounds

 Indicate the amount of vibration produced by

the sound, which in turn perceived as
loudness by the listener.

Frequency 
Low frequency are perceived as low-pitched sounds
 Number of cycles per unit of time
High Frequency are perceived as high-pitched sounds
(wavelength) 
 Indicates pitch 