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Physiological Psychology II
Unit 1. Biological basis of
emotion, stress, and aggression

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1. Biopsychology of emotion: introduction.
Ekman’s primary emotions: anger, disgust (connected to the insula), fear, happiness, sadness,
surprise. Further concluded that all other facial expressions of genuine emotion are composed of
mixtures of these six primaries.

No specific place to determine which emotion we are feeling when looking at brain imaging, except
for disgust.
Ekman and his colleagues have been preeminent in the study of facial expression. They began by
analysing hundreds of films and photographs of people experiencing various real emotions. From
these, they compiled an atlas of the facial expressions that are normally associated with different
emotions.

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UNIVERSALITY OF FACIAL EXPRESSION.

Several studies have found that people of different cultures make similar facial expressions in similar
situations and that they can correctly identify the emotional significance of facial expressions
displayed by people from cultures other than their own.
FACIAL FEEDBACK HYPOTHESIS: The hypothesis that our facial expressions influence our emotional
experience. In a test of the facial feedback hypothesis instructed volunteers to
assume one of two patterns of facial contractions while they viewed a series of
slides; the patterns corresponded to happy or angry faces, although the volunteers
were unaware of that. They reported that the slides made them feel more happy
and less angry when they were making happy faces and less happy and more angry
when they were making angry faces.
Phineas Gage case: he was working in construction, something exploded, and a thick metallic stick
went through his skull and damaging both medial prefrontal lobes (site of planning and emotion).
Due to this Phineas changed drastically his personality.

Amygdala and prefrontal cortex: areas involved on our emotions.

2. Darwin´s theory of the evolution of emotional expression.

Expressions of emotion evolve from behaviours that indicate that what an animal is likely to do next.
If emotional signals are beneficial, they will evolve to more effectively communicate and may lose
their original meaning.

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We all come from ancestors that could express their emotions properly because it means they
survived.
Darwin believed that expressions of emotion, like other behaviours, are products of evolution. He
developed a theory of the evolution of emotional expression that was composed of three main ideas:

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Expressions of emotion evolve from behaviours that indicate what an animal is likely to do
next.
• If the signals provided by such behaviours benefit the animal that displays them, they will
evolve in ways that enhance their communicative function, and their
original function may be lost.
• Opposite messages are often signalled by opposite movements and
postures, an idea called the “principle of antithesis”.
Threat displays, for example, are beneficial – intimidate victims without the costs and risks of fighting.
It saves lives.
DAMASIO’S BOOK: the last phase of dualism (there are two types of matter, and they follow different
rules) is separating reason and emotion.
When you lose mentions, you lose the ability to make rational decisions.
.

THEORIES OF EMOTION (THAT ARE WRONG).

James-Lange:
• Stimulus triggers autonomic/skeletal response which triggers emotion.
• Autonomic/skeletal response necessary for emotion.
Cannon-Bard:
• Stimulus triggers autonomic/skeletal response and emotion.
• Autonomic/skeletal response independent of emotion.
Do we run away because we feel fear? Or do we feel fear because we run away?

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.

Every stress situation will be sorted out by means of spending energy. Spend energy (sympathetic
pathway), save energy (parasympathetic pathway).
Objective: provide energy to our brain.
Physiological reactions have been triggered and they are not away, although fear is because it was a
spontaneous emotion.
Phobia (= excessive fear) is a good example that false negatives are better than positive because you
are more prepared for survival.

3. Emotion and the autonomic nervous system (ANS).

Two important questions:

• Which patterns of ANS activity are associated with specific emotions? Three brain structures
appear most closely linked with emotions: the amygdala, the insula or insular cortex, and a
structure in the midbrain called the periaqueductal gray.
• Are ANS measures effective on polygraphs (“lie detector”)? There is not a separate ANS
profile for each emotion.
There is not a separate ANS profile for each emotion.

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POLYGRAPHY:
Polygraphy is a method of interrogation that employs ANS indexes of emotion to infer the truthfulness
of a person’s responses. Polygraph tests administered by skilled examiners can be useful additions to
normal interrogation procedures, but they are far from infallible.

• Lie detection is really emotion detection.

• Control question technique:
- Use of mock-crime procedure (volunteers participate in it by an examiner, he will
determine hie/her guilt or innocence).
- Physiological response to a target question compared with response to control question.
- Success rate in studies is about 80%, because lying results on sympathetic activation.
• Guilty knowledge technique.
- Concealed information test.
- Merely ask a question that only the culprit would know the answer to.
- Success rate in distinguish guilty vs. innocence is 88% in one study. What is more
important, no innocent volunteers were judged as guilty.

EMOTIONS AND FACIAL EXPRESSIONS.

.

• The meanings of facial expressions appear to be universal (all of us tend to make the same
expressions when going through same situations).
• Six primary emotions: surprise, anger, sadness, disgust, fear, and happiness (naturally
occurring expressions are usually variations of combinations of the basic ones).

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• Facial feedback hypothesis (smiling makes you happier, facial muscles influence emotional
experience).
• Micro expressions (brief facial expressions reveal true feelings, may break through false
ones). Facial expressions that occur within a fraction of a second. This involuntary emotional
leakage exposes a person's true emotions. They help us to differentiate between genuine and

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false facial expressions. A genuine smile is called Duchenne smile.
Different muscles involved in fake and real smiles.
• Current perspectives: Four qualifications for Ekman’s original theory.
- Primary facial expressions are showed purely.
- Existence of other primary emotions.
- Body cues play a key role on emotion expression.
- Ekman’s primary emotions not as universal as thought.
Current perspective: body cues also play a major role in expression of emotion.

Feedback of simulated emotions

• Artificial facial expressions also alter ANS activity.
• Reflecting associations to mirror neurons?
• Tendency to imitate innate and inter-species.

3.1. Emotion primitives (Anderson, 2023).

• Persistence: keep the emotion even if the motive that produces it disappears.
• Scalability: they can go up ↗.
• Generalization: other S can trigger the same state.

A. Strict behaviourist view:

- Animals: behaviour is just what is observable.
Sensory Ss → Behavioural and bodily responses (No emotion).
- Humans:
Emotional Ss → Behavioural and bodily responses → Subjective feelings (emotion).
.

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B. Modified view:
- Animals:
Emotional Ss → Internal emotion state (Feelings?) (Behaviour).
- Humans:
Emotional Ss → Internal emotion state (Feelings and behaviour).

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4. Neural and biochemical mechanisms of emotions.
SHAM RAGE.

• Decorticated cats exhibit extreme and unfocused aggressive responses to any slight Ss.
•.
Hypothalamus must be intact.
What conclusion would you derive from these facts? Either hypothalamus is needed for aggression,
or cortex acting as an aggression inhibitor. Then:

• Is hypothalamus needed for expression of aggression? Yes.

• Cortex serves to inhibit and direct responses?

KLUVER-BUCY SYNDROME.
Rare cerebral neurological disorder.
Major symptoms: urge to put objects into mouth, memory loss, extreme sexual behaviour, placidity,
visual distractibility.
Results from bilateral damage to anterior temporal lobes.
First seen in monkeys, then other species (including humans).
In primates, most of the symptoms of the Kluver-Bucy syndrome appear to result from damage to
the amygdala
PAPEZ CIRCUIT.

• Papez (1937) proposed an emotional circuit.

• Including hypothalamus.
• Involved in emotion and motivation strongly associated to survival and reproduction.
• Also pleasure feelings related to survival, such as eating and sexual behaviour.

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THE FOUR Fs.

Surviving: Fighting, fleeing.
Pleasure related to surviving and reproducing: Feeding, mating.

4.1. Limbic system.

• Including hypothalamus, hippocampus, amygdala, and other nearby areas.
• Primarily responsible for our emotional life.
• Involved in memories’ formation.
Emotional memory: remember what hurts you or produces you damage even if your brain is
completely damaged and you cannot remember anything you know, because its purpose is to avoid
pain.
Amygdala’s main efferences

PAG in the brainstem, goes to PNS.

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4.2. Fear conditioning.

NEURAL MECHANISMS OF FEAR CONDITIONING.
Fear conditioning:

• Pair a neutral Ss (e.g., a tone) with an aversive Ss (e.g., a shock).

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• Present the tone later and the animal will show a conditioned fear response (usually a
defensive behaviour).
AMYGDALA AND FEAR CONDITIONING.

• Lesions of amygdala block fear conditioning.

• The amygdala receives input from all sensory systems.
- Appears to be responsible for adding emotional significance to another Ss.
- Amygdala projects to brainstem regions that control emotional behaviour output.
The pathway from the medial geniculate nucleus to a structure other than the auditory cortex plays
a key role in fear conditioning. This pathway proved to be the pathway from the medial geniculate
nucleus to the amygdala. Lesions of the amygdala, like lesions of the medial geniculate nucleus,
blocked auditory fear conditioning. The amygdala receives input from all sensory systems, and it is
believed to be the structure in which the emotional significance of sensory signals is learned and
retained.
There are two pathways from the medial geniculate nucleus to the amygdala: the direct one, which
you have already learned about, and an indirect one that projects via the auditory cortex. Both routes
are capable of mediating fear conditioning to simple sounds; if only one is destroyed, conditioning
progresses normally. However, only the cortical route is capable of mediating fear conditioning to
complex sounds.
CONTEXTUAL FEAR CONDITIONING AND THE HIPPOCAMPUS.
It has been produced by the conventional fear-conditioning procedure. For example, if a rat
repeatedly receives an electric shock following a conditional stimulus, such as a tone, the rat will
become fearful of the conditional context (the test chamber) as well as the tone. Second, contextual
fear conditioning has been produced by delivering aversive stimuli in a particular context in the
absence of any other conditional stimulus. For example, if a rat receives shocks in a distinctive test
chamber, the rat will become fearful of that chamber.
.

Pair an aversive Ss with the context instead of with a discrete Ss:

• Hippocampus is linked to spatial memory.

• Effect of bilateral hippocampal lesions on contextual fear conditioning.
- Before training – prevents conditioning.
- Shortly after training – blocks retention of conditioning.

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AMYGDALA COMPLEX AND FEAR CONDITIONING.

1. Current synthesis of findings indicates that the lateral amygdala is most critical in conditioned
fear (acquiring, storing, and expressing it).
2. In addition, conditioned fear is supressed by the prefrontal cortex inhibiting the lateral
amygdala.

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3. The hippocampus mediates conditioned fear learning by informing the lateral amygdala about
the context of the fear-related event.
4. The amygdala is thought to control defensive behaviour via outputs from the central nucleus
of the amygdala.

4.3. Fear, defence, and aggression.

Fear: emotional reaction to threat (useful to get away of danger without fight).
Aggressive behaviours: designed to threat or harm. NOT always what looks aggressive is aggressive
(e.g., a lion killing a zebra is not aggressive because it is not for pleasure and without motive, it is for
survival and eating).
Defensive behaviours: designed to protect from threat or harm (motivated by fear).
Social aggression: unprovoked attack on members of one’s own species to establish dominance.
Dominance will reflect on biological fitness (offspring).
Defensive attack: aggressive behaviour, as we cornered. Used to overcome the offensive attack itself.
EMOTIONS AS RESPONSE PATTERNS: FEAR.
Amygdala:

• Lateral Nucleus:
- Sensorial input/Afferences from neocortex, thalamus, and hippocampus. Olfaction is the
only one that does not go through the thalamus.
- Outputs (efferent neurons) to basal, basal-accessory, and central nuclei (AMG).
•
.

Central nucleus:
- Inputs (afferent neurons) from basal, basal-accessory, and lateral nuclei.
- Outputs to main cerebral regions involved in emotion processing.
FEAR CONDITIONING.
Individuals born with an innate fear survived better than the ones who do not.
Fear conditioning has no relation with real risk or danger (e.g., we are scared of spiders and
snakes, but they produce very low rates of deaths; instead, we are not afraid of
cars or guns even if they produce a very high rate of deaths).
Amygdala is the one responsible for fear.

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1. Sensory data reaches the thalamus through senses.

2. Data sent to amygdala.
3. Data also sent to cortex.
4. Amygdala does quick threat assessment. Amygdala basically says “goodbye” even without
knowing if the S is good or bad.
5. Amygdala blocs “slow” thinking.
6. “Unthinking” response: Stop the complex brain operations that were activated to react to the
Ss.
First two points are faster (just milliseconds but is crucial).
Brain has to separate systems circuits to decide if we have to react fast or slowly.

4.3.1. Types of aggressive and defensive behaviours.

Threat, defensive behaviour, submissiveness, fighting, predator behaviour, dominance, attack,
observation...

• Colony-intruder model of aggression and defence in rats: study interaction between alpha
male of an established colony with a small male intrude (more likely to attack if you think you
will win). The intruder eventually stops running and turns to face the alpha male.
If the defending intruder stands firm against this “lateral attack,” the alpha often reacts by
making a quick lunge around the defender’s body in an attempt to bite its back.
• Observation of cats and mice: cat “plays” with prey is actually a combination of attack and
defence behaviour. Different cats reacted to mice in different ways: Some were efÏcient
mouse killers, some reacted defensively, and some seemed to play with the mice.
The cats that appeared to be playing with the mice were simply vacillating between attack
and defense. The second conclusion was that one can best understand each cat’s interactions
with mice by locating the interactions on a linear scale, with total aggressiveness at one end,
total defensiveness at the other, and various proportions of the two in between.
• Target-site concept: aggressive behaviours designed to attack specific sites on body,
defensive to protect specific sites.

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If you are always submissive, not only they will see you weak, but also you will not be able to continue
with your lineage. This is because you need dominance for mating, and then to have offspring.
AGGRESSION AND TESTOSTERONE.
Non-primates: T release around the birth of male rats prepares them for T-activated social aggression

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at maturity. Threats of high rank individuals will always be more effective than others, in order to
avoid fight.
Mating and fighting in animals are so difÏcult to distinguish because in nature aggression and sexual
behaviour are really connected.
T increases or has no effect on social aggression, depending on species; castration
decreases or has no effect on social aggression in same species. But if they have
previous experience, they will keep the dominance behaviour for some more time
until it disappears. Going up in the rank of dominance increases T, but not the
other way round, in this case it has no effect.
In humans, social aggression does not increase along with higher T levels at puberty. Also, most
aggressive outbursts are defensive attack (not T related), not social aggression.
Social aggression in humans: .

• Does not decrease with castration or increase with T injections.

• Violent criminals and aggressive male athletes may have high T levels, but this may be the
result (not cause) of aggressive behaviour).
Possible sources of discrepancies in human studies:

• Measured blood T level; should measure brain T levels.

• Failure of researchers to distinguish between social aggression (T-related, for establishing
dominance) and defensive aggression (e.g., when cornered).
TRIPLE IMBALANCE HYPOTHESIS.
Aggressive behaviour depends on other chemicals besides T, notably cortisol and serotonin.

• Aggression levels are highest when cortisol levels are low and T levels are high. If cortisol
occupies the T receptors first than T itself, cortisol acts as T.
• Serotonin tends to inhibit violent impulses.
• Increased T levels in women → increased importance given to social status, and decreased
ability to recognize angry faces. Women are better at recognising emotions on someone’s
face, but if they are injected with T, they become worse at identifying facial expression of
emotions.
What does T do?

• Testosterone alters the way people respond to stimuli.

• May increase the response of the amygdala to angry expressions.
• Decreases ability of the cerebral cortex to identify and regulate emotion.

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SEROTONIN (5HT).

• Studies also suggest a connection between aggressive behaviour and low serotonin release.
• Turnover is the amount of a neurotransmitter that is released and resynthesized by neurons.
• Valzelli’s (1973) study with male juvenile mice found that social isolation decreased serotonin
.

turnover and increased aggressive behaviour.

5HT and aggression:

ATTACK BEHAVIOURS.
5-hydroxyindoleacetic acid (5-HIAA).

• Serotonin metabolite.
• In cerebrospinal fluid, blood, and urine.
• Allows researchers to infer turnover rate.
High levels of 5-HIAA imply much serotonin release and turnover.
Research with monkeys has demonstrated that low levels of 5-HIAA increases the probability of
attack on a larger monkey (few survived past age six).

Why did evolution select for a low 5HT turnover if individuals tend to die younger?
Survival + Reproduction!!

• Monkeys with high levels of 5-HIAA were more likely to survive

• Evolution seems to select for an intermediate amount of anxiety and aggression.
• Evolution might also select for high aggressive behaviours.
- May die young but are more likely to achieve a dominant position within the troop.

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4.4. Brain mechanisms of human emotion: cognitive neuroscience.

Three main points have advanced the understanding of brain mechanisms of emotion:

• Brain activity associated with each human emotion is diffuse.

.

• There is usually motor and sensory regional activity along with an emotional response.
• Brain activity for experienced, imagined, or observed emotion is similar.
AMYGDALA AND HUMAN EMOTION.
Amygdala provides a fast evaluation, useful for needed fast responses.
Amygdala in humans appear to have a more general role in emotions, not just in fear. Also appears
to play a role in evaluating the emotional significance of situations.
Increased activity in the primary frontal cortex:

ORBITOFRONTAL CORTEX (OFC).

Afferences from:

• Dorsomedial thalamus.
• Temporal cortex.
• Ventral tegmental area (VTA).
• Olfactory system.
• Amygdala.
• Frontal lobes (decision making, evaluating).
What is going on in the environment? Planning (not just thinking about the first step): frontal lobes.
Efferences to (send information to):

• Cingulate cortex.
• Hippocampus formation (to form memories, but it is not a memory storage).
• Temporal cortex.
• Lateral HPT (basic survival functions).
• Amygdala.

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Influencing behaviour as well as physiological and emotional responses.

OFC: intermediary of brin mechanisms in emotional responses and automatic control mechanisms of
complex behaviours.

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MEDIAL PREFRONTAL LOBES AND HUMAN EMOTION.
Emotion and cognition are better studied as components of the same system.
Medial portions of the prefrontal lobes are sites of emotion – cognition interaction.
Medial prefrontal lobes are active during either emotional suppression or reappraisal paradigms (re-
evaluate circumstances because things change). In the brain, areas and circuits that deal with
emotions also deal with cognition.
Many other roles for this area in emotion have been suggested; likely it performs many functions.
LATERALIZATION OF EMOTION.
There is asymmetry and our emotions are also like that.
Early theories of lateralization may have been too general.
Asymmetry of facial expression studies indicate that a majority of people have right-hemisphere
dominance for facial expressions (similar in monkeys).
Both hemispheres innervate the Frontalis muscle. Only contralateral cortex innervates the rest of the
facial expression muscles. It opens the possibility of asymmetry based on asymmetric brain activity,
so we can show asymmetric expressions on our faces.

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4.4.1. Current perspectives.
Emotional situations produce widespread activation in the brain, not just in the amygdala.
Brain areas activated by emotion are also activated by other psychological processes.
The same emotional S often activate different areas in different people.

5. Last thing about human aggression: homicide.

“Humans are the only individuals that kill themselves” is a wrong afÏrmation because all living things
do it.

• Kill: is necessary across history.

• Murder: kill someone for a reason (not for survival).
SOME QUESTIONS.

• Main victims of homicide? Male, people with less power...

• Perpetrators? Mainly male, aggressive/young male.
• Motives? Trauma, revenge, fear, anger, desperation, jealousy, pleasure, power...
Global study in homicide, 2013. UNODC (United Nations OfÏce on Drugs and Crime):
Main victims of homicide: Mostly males died from homicide.

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Perpetrators: Before sexual maturity, the rate is not so different among men and women, but when
we arrive to 15-44 years old, many more men executed homicide than women. Males are biologically
most prone to be a perpetrator of a homicide.
More terms: Infanticide (infant homicide) – neonaticide (newborn homicide).
Motives: power, jealousy...

5.1. Evolutionary function of homicide?

If a behaviour happens in each generation and persists happening is because it plays
a role in nature. Which is the purpose of homicide? Survival, dominance, kill or be
killed, reproduction...
But mainly; intra-male sexual competition strategy to get rid of rivals, in order to
pass their genes to future generations. It will reinforce and improve the offspring, as the male that
survives is supposed to be stronger and to have better traits.

6. Stress and health.

• Stress: reaction to harm or threat.
• Stressors: S that cause stress.
Stress per se is not a bad thing, the bad thing is chronic stress. E.g., standing up is a very stressful
situation as the levels of adrenaline increase exponentially; this stress is necessary to cope with basic
situations of life. Stress is a reaction that prepare us to deal with this kind of thing.

• Chronic psychological stress: most clearly linked to ill health. Stressing your body and keeping
it stressed, without recovering, where your resources/energy will be exhausted. It is a process
of catabolism (breaking down molecules).
In the short-term, stress is adaptative; in the long-term, it is maladaptive.
Origin of “stress” word: Kind of tension that iron structures suffer when they are subjected to
something that leaves them hanging.
Exercising our body increases our stress so much, and as we know exercise is healthy. But the problem
comes when we sustain this stress for a prolonged period of time.
When we pass through stressful situations, the objects that surround us during this period will remind
us about the stressful situation in the future (e.g., if I am holding a pen during stressful moments,
that pen will remind me about that moment).
.

Should distinguish and separate stress and stresses.

*Acute: has a beginning and end.

*Chronic: never ends.

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CONCEPTS OF STRESS.
Hans Selye (1979) defined stress as the non-specific response of the body to any demand made upon
it.
Threats on the body activate a general response to stress called the General

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Adaptation Syndrome (GAS).
There is something common to being ill.
Placebo effect: One rats injected with poison and the ones who were not injected
with poison but with an innocuous substance showed the same reaction. The rats were reacting to
the fact of being manipulated, injected with things... More than to the “injections” themselves.
The general adaptation syndrome:

• Alarm stage: increased sympathetic nervous system activity.

• Resistance stage: sympathetic response declines; adrenal cortex releases cortisol and other
hormones; prolonged alertness.
• Exhaustion stage: occurs after prolonged stress; inactivity, vulnerability, and decreased
energy; heightened responses.
Sapolsky (1998) argues that the nature of today’s crises are more prolonged. Accounts for widespread
stress-related illnesses and psychiatric problems in industrial societies.
Long-term, inescapable issues activate the GAS which is harmful to our health over time.
A reaction to stress: hair/weight loss, insomnia, dermatitis, headache/migraines, dizziness...
We have a problem with chronifying the stress: it means that there are some situations that must not
last more than some minutes/hours/days (acute), and we make it chronic.
Stress is oriented to increase the probability of survival.

*Mirror neurons: types of neurons we have in our brain.

THE STRESS RESPONSE. What they do is to react at a similar degree when we see an
.
action (e.g., someone raising his hand) and when we
Stress triggers stress hormones: perform it (e.g., me raising the hand).

• HPA: hypothalamus-anterior-pituitary adrenal-cortex system (glucocorticoids).

• SNS: epinephrine, and norepinephrine and cytokines (causing inflammation and fever).
Selye neglected sympathetic nervous system.
Individual differences, such as atÝtude, affect the magnitude of the stress response.
Example: women awaiting surgery who were “certain” they did not have breast cancer had milder
stress than others.

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Selye attributed the stress response to the activation of the anterior-pituitary adrenal-cortex system.
He concluded that stressors acting on neural circuits stimulate the release of adrenocorticotropic
hormone (ACTH) from the anterior pituitary, that ACTH in turn triggers the release of glucocorticoids
from the adrenal cortex, and that the glucocorticoids produce many of the components of the stress
response.

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Stressors activate the sympathetic nervous system, thereby increasing the amounts of epinephrine
and norepinephrine released from the adrenal medulla.
When a stressor appears, the brain:

• Stimulates the anterior pituitary, which secretes something into the bloodstream that also
stimulates the adrenal cortex and produces glucocorticoids. (Takes more time for it to act as,
through the bloodstream, information is slower sent (minutes)).
• Stimulates the sympathetic nervous system, which sends electric signals, stimulates the
adrenal medulla, and produces norepinephrine and epinephrine. (Takes less time (fractions of
a second) to reach its objective and react, as information is sent through nerves).

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STRESS PATHWAYS OF THE BODY.

STRESS AND THE HPA-AXIS.

• HPA axis becomes dominant response to prolonged stressors.

• Activation of the HPT induces pituitary gland to secrete adrenocorticotropic hormone (ACTH).
• ACTH stimulates adrenal cortex to secrete cortisol.
• Cortisol helps to mobilize energies to fight a difÏcult situation.
Psychoneuroimmunology: The study of the interaction of psychological factors, the nervous system,
and the immune system.
PSYCHOSOMATIC DISORDERS: THE CASE OF GASTRIC ULCERS.

• Gastric ulcers – lesions of stomach lining and duodenum. In extreme cases: life-threatening.
• More common in those who are stressed; readily created in the animal lab.
• Ulcers are caused by a bacterium – stress appears to make the body vulnerable to these
bacteria (increases the susceptibility of the stomach wall to damage).
• 75% of healthy subjects have the bacteria.

6.1. Stress and the immune system.

Immune system: cells that protect the body against viruses and bacteria by producing leukocytes
(white blood cells).

• B-cells: leukocytes that mature in the bone marrow and secrete antibodies.
• Antibodies: Y-shaped proteins that attach to particular kinds of antigens.
• Antigens: any substance which provokes an adaptive immune response.

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Divisions of the mammalian immune system

Innate immune system:
• First line of defense.
• Triggered when receptors called toll-like receptors bind to molecules on the surface of the
.

pathogens or when injured cells send out alarm signals.

• Attacks generic classes of pathogens. Reacts with: inflammation and phagocytosis.

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Adaptive immune system (more recently evolved):
• Targets specific pathogens identified by their antigens.
• It is slower, specific, and has memory (the basis of effectiveness of vaccination → leads to
immunization).
• Cytokines activate lymphocytes (white blood cells).
• Cell-mediated immunity by T-cells; antibody-mediated immunity by B-cells.
• T-cells: attack intruders directly and help other T-cells or B-cells to multiply.
• Natural killer cells: leukocytes that attack tumour cells and cells that are infected with viruses.
Disgust: survival related emotion.
Two adaptive barriers against infection:

6.1.1. How does stress influence immune function?

Immune system is the fastest adaptive system.
Stress does not mean a bad thing.
Effects of stress on immune function depends on the kind of stress:

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• Acute stress: improve immune function (that is why active people is healthier than sedentary
people).
• Chronic stressors: impair immune function. It is not a natural response to keep stress on a
high level. It is a side effect of the symbolic capacity of the human brain.
Many ways that stress can impact immune function: Effects of stress can be good (adaptive and

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healthful), bad, or mixed.

During an infection, leukocytes and other cells produce small proteins called cytokines.

• Combat infection and communicate with the brain to inform of illness.

Cytokines in the brain produce symptoms of illness.

• Fever, sleepiness, lack of energy, etc.

• Sleep and inactivity are the bodies way of conserving energy to fight illness.

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Psychoneuroimmunology deals with the way in which experiences alter the immune system. Also
deals with how the immune system influences the central nervous system.
In response to a stressful experience, the nervous system activates the immune system. Immune
system increases production of natural killer cells, leukocytes, and cytokines. The cytokines can trigger
symptoms of illness as a reaction to the stress itself.

• Prolonged stress response is damaging to the body.

• Prolonged high [Cortisol] detracts from the synthesis of proteins of the immune system
(impeding anabolism).
• Prolonged stress of longer than a month significantly increases the likelihood of illness.
Because of high cortisol levels going out.
Working out so much or nothing decreases immune system function, but a moderate workout is good
for our immunity (inverse U shape graph).

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6.2. Stress and the hippocampus.

Hippocampus has many glucocorticoid receptors.
Following stress:

• Dendrites of pyramidal cells are shorter and less branched. Less info. being able to reach the

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neurons. Info. is getÝng in, but some is lost.
• Adult neurogenesis of granule cells reduced. .

Effects blocked with adrenalectomy; produced with corticosteroids. Cannot produce cortisol.

• Prolonged stress can also be harmful to the hippocampus and can affect memory.
• Cortisol enhances metabolic activity in the body.
• Neuron has many receptors for cortisol, but there is under the attack of many cortisol
molecules (cortisol breaks everything) so, the neuron deletes receptors to prevent cortisol
getÝng in (down-regulation: decrease in total receptor number in the cell due to endocytosis
and subsequent degradation of the receptors caused by long-term exposure to agonists).
For this reason, cortisol keeps high; because neurons stop knowing how much cortisol
molecules there are outside (cannot see the enemy), and the neuron cannot manage and
reduce the amount of molecules because it does not know how much there is!
• When metabolic activity is high in the hippocampus, the neurons are more sensitive to
damage by toxins or over-stimulation.
• Stress also impairs the production of new hippocampal neurons.
WHY DOWN-REGULATION?

Glucocorticoid receptors (GR) (GR active during high levels of cortisol) and mineralocorticoid
receptors (MR) (MR sensitive to low levels of cortisol, regulates cortisol when levels are low).

• Defense mechanism against de-catabolic effects produced by high C levels.

• Affecting memory.
• Impairing HPA regulation (negative feedback).
• Common feature in clinical depression.

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Lower back pain, as depression: cannot be proven that you have it because a doctor cannot know
that you are suffering pain. We are talking about idiopathic pain (not known cause of pain).
Ways to reduce stress or control our response to it:

• Breathing routines, exercise, meditation, distraction, and addressing issues.

•

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Social support from a loved one helps to reduce stress.
- Reduces response in several brain areas, including the prefrontal cortex.

6.2.1. Animal models of stress.

• Some early models used levels of stress that might not have a human equivalent.
• There are two problems with this research: ethics and use of extreme/unnatural forms of
stress).
• Some more recent models use social stresses (e.g., subordination stress → used
in dominance hierarchies). A chronic social threat that induces this type of stress
is the so-called bullying.

6.3. Early experience of stress.

.

Stress of mistreatment early in life may cause brain and endocrine abnormalities later in life. Early
stress can lead to an increase the intensity of future stress responses.

• Key piece: rat pups handled (having contact with) by researchers had more adaptive stress
response in adulthood (fewer circulating glucocorticoids following stress), probably due to less
negative feedback from hippocampal glucocorticoid receptors.
• A good example of epigenetic (“not of the genes”) transmission: fearful, poor-grooming
mothers raise daughters who become fearful, poor grooming mothers.
Importance of early experiences is very high. We should receive coping strategies and also adequate
levels of stress. Important to know how to face stress and cope with it.

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Basic components of emotions.

Types of internal states and levels of emotion primitives during evolution (from fewer to more):
.

Reflex behaviours (first level) (simplest one)

↓
Arousal (can be operationalised. A general state that can trigger different things)
↓
Drive (it is general arousal oriented to a specific set of S or behaviour)
↓
Motivation (something that stimulates a person to act and behave to achieve a desired goal) (has
rewarding value, e.g., aggression is reinforcing itself)
↓
Emotion states (internal states that would affect the probability to perform different types of
behaviour)
↓
Subjective feelings (appear later in evolution).
OCCAM’S RAZOR (PARSIMONY PRINCIPLE).
Theory parsimony, also known as theory simplicity or Occam's Razor, is a principle in science and
philosophy that suggests that the simplest explanation or theory is often the best one.

E.g., thist.

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Physiological Psychology II
Unit 2. Biological basis of
learning and memory

Experiences change us; encounters with our environment alter our behaviour by modifying our
nervous system.
As many investigators have said, an understanding of the physiology of learning and memory is the
ultimate challenge to neuroscience research.
The brain is complex, and so are learning and remembering. However, despite the difÏculties, the
long years of research finally seem to be paying off.
.

1. Definition of learning and memory.

*Psychosomatic: Psyche (was the soul, now
the brain) + somatic (body).
Learning is a product of human nature and human condition.
When does learning begin? After the moment that the NS develops in the womb. It has been proven
that babies inside the womb can learn to identify his dad’s voice or even the language their culture
uses.
Learning consists of building new branches, connections (neuroplasticity derived from experience) ...
Or/and reinforcing these new connections. It has to do with experience. The stronger the
branches/connections, the higher the probability to behave that way; then, the behaviour will be
automatized. Learning is the process by which experience modifies our NS, and hence our behaviour.
The experiences are not stored, they change the way we perceive, act, think, and plan. They modify
the structure of the NS.
Homunculus: writes the same story in the same way, it is influenced by the experience. It affects the
interpretation.
Not everyone remember the same things in the same way, so when the moment of retrieving it the
memory of a situation, maybe two people have different views from that moment and one can forget
of some details that the other one remembers.
Steps of learning and memory:

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TYPES OF LEARNING AND MEMORY.

Learning:

• Non-associative.
- Sensitization.

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- Habituation.
• Associative:
- Classical conditioning.
- Operant conditioning.
- Appetitive conditioning (rewarded by attainment of positive reinforcement).
- Avoidance (aversive) conditioning: rewarded by ending negative reinforcer.
o Active avoidance: response required.
o Passive avoidance: suppression of tendency required.
Memory:

• Short-term memory: working memory, spatial and nonspatial.

• Long-term memory: reference memory, spatial and nonspatial.
- Procedural (implicit): skill learning, priming, conditioning.
- Declarative (explicit): semantic (facts), and episodic (events).

1.1. The nature of learning.

PERCEPTUAL LEARNING.

• Learning to recognize a particular stimulus. Primary function of this type of learning → the
ability to identify and categorize objects and situations.
• Process by which the ability of sensory systems to respond to stimuli is improved through
experience.
• It occurs through sensory interaction with the environment as well as through practice in
performing specific sensory tasks.
S-R LEARNING.

• Learning to automatically make a particular response in the presence of a particular stimulus

(includes classical and instrumental conditioning).
CLASSICAL CONDITIONING – LEARNING PROCEDURE.

• Unconditioned Response or UR: response to the US.

• Conditioned stimulus or CS: Ss, which when paired with the US during training, comes to elicit
a learned response.
• Conditioned response or CR: response to the presentation of the CS.
.

Psychological disorders come from evolution, so it can have an adaptive function if it has been
preserved. These disorders are extremes of a quality that has some adaptive segment. Need to know
the origin of trauma to treat it.

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INSTRUMENTAL (OPERANT) CONDITIONING.

The effects of a particular behaviour in a particular situation increase (reinforce) or decrease (punish)
the future probability of the behaviour. Punishment is needed and it is absolutely effective.

• Reinforcing Ss: appetitive Ss that makes the behaviour become more frequent.
•

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Punishing Ss: aversive Ss that makes the behaviour become less frequent.
A simple neural model of instrumental or operant conditioning:

OVERVIEW: PERCEPTUAL, S-R, AND MOTOR LEARNING.

Motor Learning – learning to make a new response.

Question: Is that how we learn to smile?
Accidental response (baby smiles) → Reinforcement (father picks up the baby) → Deliberate Response
(baby keeps smiling).

1.2. Circularity.
Using a premise to prove a conclusion that in turn is used to prove the premise: a circular argument.
Circular definition (using an example): “Oak” is a tree which has catkins and grows from an acorn.
"Acorn" is the nut produced by an oak tree.

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Could you produce a non-circular scientific definition of reinforcement?

• Aiming at Midbrain Reticular System.

• Reaching Medial Forebrain Bundle. .

• Finding the brain substrate of reinforcement.

2. Types of memory.
Hebb (1949) differentiated between two types of memory:

• Short-term memory: memory of events that have just occurred.

• Long-term memory: memory of events from times further back.
Differences:

STM LTM
Has a limited capacity.
Capacity is not limited.
Fades quickly without rehearsal.
Persists.
Retrieval of memories lost from STM do not
Memories can be stimulated with a cue or hint.
benefit from the presence of a cue.

↓ The taxonomy of memory ↓

Researchers proposed that all information enters STM where the brain consolidates it into LTM.
Later research has weakened the distinction between STM and LTM:

• Not all rehearsed short-term memories become long-term memories.

• Time needed for consolidation varies.
• Epinephrine and cortisol enhance consolidation of recent experiences → Stress!
• Reconsolidated memory is strengthened again by a process that requires protein synthesis.

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Working memory:

• Proposed as an alternative to short-term

memory.
• Emphasis on temporary storage of
information to actively attend to it and work

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on it for a period of time.
Common test of working memory is the
delayed response task: Requires responding
to something you heard or saw a short while
ago.

• Research points to the prefrontal cortex

for the storage of this information.
• Brain may use elevated levels of calcium to potentiate later responses.
• Older people often have impairments in working memory.
• Changes in the prefrontal cortex (PFC) are assumed to be the cause.
• Declining activity of the PFC in the elderly is associated with decreasing memory.
• Increased activity in this area indicates compensation for other regions in the brain.

2.1. The hippocampus and Amnesia.

Amnesia is the loss of memory.

• Studies on amnesia help to clarify the distinctions between and among different kinds of
memories and their mechanisms.
• Different areas of the hippocampus are active during memory formation and retrieval.
• Damage of the HPC results in amnesia.
↓ The major components of the limbic system and their relationship with the hippocampus ↓

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• H.M. is a famous case study in psychology who had his hippocampus removed to prevent
epileptic seizures. Afterwards, H.M. had great difÏculty forming new long-term memories.
• STM or working memory remained intact. It suggested that the hippocampus is vital for the
formation of new long-term memories. .

• H.M. showed massive anterograde amnesia after the surgery.

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Retrograde and Anterograde amnesia:

• Retrograde amnesia: cannot remember events prior to the brain damage. The fact that
retrograde amnesia extends back for a limited period of time suggests that a gradual process
controlled by the hippocampal formation transforms memories into permanent storage.
• Anterograde amnesia: cannot later remember events that occur after the brain damage. The
investigators discovered that a region of the hippocampal formation called field CA1 was
primarily affected, and the neurons had completely degenerated.
*Case of Cliver Wearing: the man with no STM*

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IMPLICIT MEMORY.

• Emotional conditioning.
• Procedural (automatic) skills (learn something and automatize it) → E.g., for me: Driving a car,
riding a bike, playing the piano...

The basal ganglia.

• HPC not responsible for all memory, as gradual learning still takes place.
• Implicit learning or habit learning depends on the basal ganglia.
People with Parkinson’s disease have impairments of the basal ganglia and cannot develop implicit
memory.
H.M. had difÏculty with episodic and declarative memory:

• Episodic: ability to recall single personal events.

• Declarative: ability to state a memory into words.
H.M.’s procedural memory remained intact:

• Procedural memory: ability to develop motor skills (remembering or learning how to do

things).
Amnesiac patients remember better self-produced descriptions:

Patient H.M. also displayed greater “implicit” than “explicit” memory, as most patients with amnesia
do:

• Explicit memory (declarative): deliberate recall of information that one recognizes as a

memory.
• Implicit memory: the influence of recent experience on behaviour without realising one is
using memory.
People with amnesia generally show this pattern:

• Normal working memory.

• DifÏculty forming new declarative memories (anterograde amnesia).
• Some degree of retrograde amnesia (episodic memories!).
• Better implicit than explicit memory.
• Nearly intact procedural memory.

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2.1.1. Role of the hippocampus.

Research of the function of the hippocampus suggests that it is especially important for:

• Hypothesis #1: declarative memory functioning (especially episodic).

• Hypothesis #2: spatial memory.

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• Hypothesis #3: contextual learning and binding.
HPC AND DECLARATIVE MEMORY.
Research shows that HPC damage impairs abilities on two types of tasks:

• Delayed matching-to-sample tasks: subject sees an object and must later choose the object
that matches.
• Delayed non-matching-to-sample tasks: subject sees an object and must later choose the
object that is different than the sample.
THE HPC AND SPATIAL MEMORY.

• fMRI: Spatial tasks enhance hippocampal activity.

• PET: Taxi drivers.
- Show more hippocampal activity when answering spatial (giving directions) than
nonspatial questions.
• MRI: Taxi drivers have larger posterior HPC.
Applied in rodents:
Damage to the hippocampus also impairs abilities on spatial tasks such as:

• Radial mazes: a subject must navigate a maze that has eight or more arms with a reinforcer
.

at the end.

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• Morris water maze task: a rat must swim through murky water to find a rest platform just
underneath the surface.

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(a) Environmental cues present in the room provide information that permits the animals to
orient themselves in space.
(b) According to the task, start positions are variable or fixed. Normally, rats are released from
a different position on each trial. If they are released from the same position every time, the
rats can learn to find the hidden platform through stimulus-response learning.
.

(c) The graphs show the performance of normal rats and rats with hippocampal lesions using
variable or fixed start positions. Hippocampal lesions impair acquisition of the relational task.
(d) Representative samples show the paths followed by normal rats and rats with hippocampal
lesions on the relational task (variable start positions). (Adapted from Eichenbaum, H., A
cortical – hippocampal system for declarative memory, Nature Reviews: Neuroscience, 2000,
1, 41–50. Data from Eichenbaum et al., 1990.)

The figure shows the relation between volume of gray matter of the hippocampus (right) and
caudate nucleus (left), and errors made on test trials in a virtual maze that could only be
performed by using a response strategy.

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Increased density of the caudate nucleus was associated with better performance, and
increased density of the hippocampus was associated with poorer performance.
Applied in birds:

Place cells in the Hippocampal formation:

Place Cell: Neuron that becomes active when animal is in particular location in environment; most
typically found in hippocampal formation.

Hippocampal formation and memory consolidation:

HPPC:

• Takes part in memory consolidation for a limited time.

• Rol = helping to establish memories in Cortex.

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Spatial Learning (Bontempi et al, 1999):

• + 5 days: HPPC activity &+ performance.

• + 25 days: correlation does not show.
HPPC needed for new spatial learning; not for information learned one month before.

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Cortex takes over the role of retaining the information.
Mice trained at Morris Maze (Maviel et al., 2004): Deactivated HPPC (lidocaine):

• 1 day after: they do not remember the task.

• 30 days after: normal performance.

HIPPOCAMPUS AND RELATIONAL LEARNING.

.

Hippocampal lesions in rats. Morris Maze.

• Released from same place: no effect.

• Released from different locations: no learning.

CONTEXTUAL LEARNING.

• Hippocampus may also be important for contextual learning.

• Remembering the detail and context of an event.
• Damage to the hippocampus impairs recent learning more than older learning.
- The more consolidated a memory becomes, the less it depends on the hippocampus.
Past experiences more related to context because you forget details.

• Short delay: best if re-tested in the same place. Memory depends on the context.
• Long delay: places does not matter. Memory less context dependent.
No differences for rats with damaged HPC.

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Remembering about memory (summary):

• Learning depends on connections between two brain areas (Ivan Pavlov).

• Learning does not depend on new cortical connections (Karl Lashley).
• Damaged hippocampus impairs formation of long-term declarative memories (episodic!).
• Implicit and short-term memories hold. New procedural memories can be formed.

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• Hippocampus: theories focus on its role in declarative and spatial memories, and memory for
context and details.

3. Synaptic mechanisms of learning and memory.

Effects of experience on the structure of the NS. Definition of synaptic plasticity. Learning
(strengthening or creating connections) in a simple NS. Promoting long-term. Depression and long-
term memory. Neurochemistry of memory.
SYNAPTIC PLASTICITY: LTP (Long Term Potentiation) AND LTD.
Intense electrical stimulation (120 pulses at 12 pulses/second) of axons leading from the entorhinal
cortex to the dentate gyrus caused a persistent increase in the synapses’ strength. (L∅mo, 1966)
L∅mo and Bliss (1968): Long Lasting Potentiation (LLP).

3.1. Learning and the Hebbian synapse.

A Hebbian synapse occurs when the successful stimulation of a cell by an axon leads to the enhanced
ability to stimulate that cell in the future

• Increases in effectiveness occur because of simultaneous activity in the presynaptic and

postsynaptic neurons.
• Such synapses may be critical for many kinds of associative learning.

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1st synapse is innate, 2nd learned. So, for the second one the probability is lower.
A SIMPLE MODEL OF LEARNING PROCESS.

3.2. Consolidation.
Consolidation:

• Process by which short-term memories are converted to long-term memories.

• Korsakoff’s Syndrome – permanent anterograde amnesia caused by brain damage from
chronic alcoholism or malnutrition.

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.

Brief summary of LTP (six steps):

1. Repeated glutamate excitation of AMPA receptors depolarizes the membrane.
2. The depolarization removes magnesium ions that had been blocking NMDA receptors.
3. Glutamate is then able to excite the NMDA receptors, opening a channel for calcium ions to
enter the neuron.
4. Entry of calcium through the NMDA channel triggers further changes.
5. Activation of a protein sets a series of events in motion.
6. More AMPA receptors are built, and dendritic branching is increased.

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Physiological Psychology II
Unit 3. Biological basis of higher
cognitive processes

1. Brain lateralisation: introduction.

The left and right hemisphere exchange information primarily through a set of axons called the corpus
callosum.
Other areas that exchange information include :

• The anterior commissure.

• The hippocampal commissure.
• A few other small commissures.
Information crosses to the other hemisphere with only a brief delay.
The two hemispheres are not mirror images of each other.
Division of labour between the two hemispheres is known as lateralisation/asymmetry.
In most humans, left side specialized for language.
The corpus callosum allows each hemisphere of the brain access to information from both sides.
Commissures are bands of myelinated fibers that facilitate communication between the left and right
hemispheres of the brain.
.

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Lateralisation of function: each hemisphere

specialised for different functions.
Each hemisphere connected to the contralateral
(opposite) side of the body.
.

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Example: Skin receptors and muscles on the right
side of the body are mainly connected to the left
hemisphere.

Visual connections to hemispheres:

Each hemisphere gets input from the opposite half of the visual world.

• Left hemisphere connects to the left half of each retina and thus gets visual
input from the right half of the world (right visual field).
• Right hemisphere connects to the right half of each retina and thus gets visual
input from the left half of the world left visual field.
Half of the axons from each eye cross to the opposite side of the brain at the optic
chiasm.
Auditory system:

• Differently arranged.
• Each ear sends the information to both sides
of the brain.
• The contralateral connections are stronger.

2. Tests of brain lateralisation.

SODIUM AMYTAL TEST (WADA TEST):

• Selective hemispheric anaesthesia technique.

• Objective: Temporary inactivation of one cerebral
hemisphere by conducting a catheter through the femoral
artery to the internal carotid artery, where the anaesthetic
(sodium amytal) is released.
It is a reliable test, but it is also really invasive.

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• Procedure:
- The injection anesthetizes one hemisphere for a few minutes, thus allowing the capacities
of the other hemisphere to be assessed.
- Patient is asked to recite well-known series (e.g., letters of the alphabet, numbers in
ascending order...) and to name and remember pictures/words of common objects.

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- The procedure is repeated with the other hemisphere.
• Applications (candidates for epilepsy surgery, which consists of the...):
- To assess hemispheric representation of language.
- To assess the risk of post-surgical memory impairment.
• Assessment of hemispheric representation of language:
- Set of brain areas that play a key role in the cognitive function (eloquent areas).
- Eloquent areas for language are predominantly located in the left hemisphere (in most
cases) on the right hemisphere:
o Typical representation: left hemispheric dominance for language.
o Atypical representation: right hemispheric or bilateral hemispheric dominance for
language.
- Epilepsy: possible brain reorganisation of language in brain damage → + propensity to
atypical representation.
Atypical representation most likely when:
o Left manual dominance.
o Brain damage occurs at younger ages (< 5-6 years).
o Brain damage affects the left hemisphere.
o Brain damage affects extratemporal regions (regions outside the temporal lobe).
- Left hemisphere injection → left hemisphere inactivation → language assessment (brief)
→ recovery period (around 30 minutes). Then repeated with the right hemisphere.
- Right hemisphere injection → right hemisphere inactivation → language assessment.
Interpretation: Language is predominantly supported by the hemisphere whose
anaesthesia results in language deficits.
.

• Assessment of risk of post-surgical memory impairment:

- To know it, together with the rest of the tests, makes it possible:
o Choosing one type of surgery over another.
o Decision making on extent of surgical resection.
o Decision making on the need for other techniques during assessment (intracranial
electrode stimulation).
To avoid: Resection of eloquent language areas, and post-surgical aphasia.
- Memory decline, mainly specific to verbal material, after temporal lobe resection in 30-
60% of patients with epilepsy.

TWO MODELS:
- Functional reserve model (Chelune, 1995):
o Functional integrity of the hemisphere contralateral to the epileptogenic focus
predicts the evolution in memory functioning after temporal lobe resection.
o Better functional integrity of the contralateral hemisphere → better prognosis.

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Case report 1:
- Right temporal lobe epilepsy → surgery?
- Left hemisphere dominance for verbal memory.
- Neuropsychological evaluation:
▪ Preserved verbal memory.
▪ Impaired visual memory.
Functional integrity of the hemisphere contralateral to the epileptogenic focus?
Prognosis after surgery?
- Functional adequacy model (Kneebone et al., 1995):
o Functional adequacy of the ipsilateral temporal lobe to the epileptogenic focus
predicts the evolution in memory functioning after temporal lobectomy.
o The more functional the ipsilateral temporal lobe → the greater the risk of memory
decline.

Case report 1:
- Right temporal lobe epilepsy. → surgery?
- Left hemisphere dominance for verbal memory.
- Neurophysiological evaluation:
▪ Preserved verbal memory.
▪ Impaired visual memory.
Case report 2:
- Right manual dominance.
- No brain lesion.
- Left temporal lobe epilepsy → surgery?
- Neuropsychological evaluation:
▪ Preserved verbal memory performance.
Functional adequacy of the ipsilateral hemisphere to the epileptogenic focus? Prognosis
after surgery?
- Left hemisphere injection (left hemisphere inactivation) → memory assessment.
- Right hemisphere injection (right hemisphere inactivation) → memory assessment.
Interpretation of both:
Memory is predominantly supported by the hemisphere whose anaesthesia results in
memory deficits.

Result indicating good prognosis Result indicating poor prognosis

Lack of memory impairment after
Transient memory impairment after inactivation of the hemisphere
inactivation of the hemisphere contralateral contralateral to the area to be resected by
to the area to be resected by surgery. surgery.
No memory impairment after inactivation of Transient memory impairment after
the hemisphere to be resected. inactivation of the hemisphere to be
resected.
Contralateral hemisphere supports memory Ipsilateral hemisphere supports memory
functions. functions.
No postsurgical memory decline. Postsurgical memory decline.

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To know it, together with the rest of the tests, makes it possible:
- Decision making on whether or not to perform surgery.
- Choosing one type of surgery over another.
- Decision making on extent of surgical resection.

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To avoid post-surgical memory decline.
DICHOTIC LISTENING TEST.

• Non-invasive test and can be administered to healthy people.

• Spoken digit sequences are presented through earphones the digits of each sequence are
presented simultaneously, one to each ear.
• The person is then asked to report the digits.

Kimura: most people report slightly more of the digits presented to the right ear than the left → Right
ear advantage for language processing
Interpretation: although the sounds from each ear are projected to both hemispheres, the
contralateral connections are stronger → superiority of the left hemisphere for language processing.

FUNCTIONAL BRAIN IMAGING.

• Mapping of brain activity while the patient performs some cognitive activity (verbal
comprehension, reading, verbal recall.
• Functional magnetic resonance imaging (fMRI).
Brain activation in patients with epilepsy during the verbal comprehension paradigm.
Cano-López et al. Neuroimage: Clinical 20 (2018) 742-752.

• Epilepsy a condition characterized by repeated episodes of excessive synchronized neural

activity (seizures).
• Participants were instructed to listen and understand a short story.

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Patient A had a right hemisphere

epileptic focus and presented left

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hemisphere specialisation for
language.
Patient B had a left hemisphere
epileptic focus and presented right
hemisphere specialisation for
language.
How is this possible?
.

3. The split brain.

CutÝng the corpus callosum: Damage to the corpus callosum prevents the two hemispheres from
exchanging information.
GROUNDBREAKING EXPERIMENT OF MYERS AND SPERRY.

• Cats were trained to perform a simple visual discrimination task.

• Each trial each cat was confronted by two panels one with a
circle on it and one with a square on it.
• The relative positions of the circle and square (right or left) were
varied randomly so the cats had to learn which symbol to press in
order to get a food reward.

To restrict visual information to one hemisphere they:

• Cut the corpus callosum.

Visual information could not cross the contralateral hemisphere.
• Cut the optic chiasm.
• Blindfolded one eye → restricted the visual information to the hemisphere ipsilateral to the
uncovered eye.

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Split brain cats with one eye patched:

Learn the task as well as controls → Each hemisphere can learn independently.
When the patch was transferred to the other eye, they demonstrated no memory → then the cats
relearned the task as if they had never seen it before.
Intact cats or those with an intact corpus callosum or optic chiasm with one eye patched:

• Learn the task.

• When the patch was transferred to the other eye, they demonstrated memory.
Conclusions: Cat brain has the capacity to act as two separate brains. The function of the corpus
callosum is to transmit information between them. → Similar findings with split brain monkeys.

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COMMISSUROTOMY IN HUMANS WITH EPILEPSY.

This procedure was used as a treatment for epilepsy the corpus callosum was cut to prevent seizures
from spreading from one hemisphere to the other.
The therapeutic benefits of commissurotomy turned out to be even greater than anticipated: Despite

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the fact that commissurotomy is performed in only the most severe cases, many commissurotomized
patients do not experience another major convulsion.
Effectiveness in seizures control, but what about their cognitive and behavioural effects? → studies
with split brain people.

3.1. Studies with split-brain people.

They maintain normal intellect and motivation, but they tend to:

• Use hands independently in a way others cannot.

• Respond differently to stimuli presented to only one side of the body.

Testing procedure:
1. The patient is asked to fixate on the centre of a display screen
2. Visual stimuli is flashed onto the left or right side of the screen for 0.1 second (exposure
time is long enough to perceive the stimuli but short enough to preclude the confounding
effects of eye movement). .

3. Stimuli presented in the left visual field is transmitted to the right visual cortex and vice
versa.

Sperry (1974) showed subtle behavioural differences for spilt brain people:
Because the left side of the brain is dominant for language in most people, most split-brain people
have difÏculty naming objects briefly viewed in the left visual field.

Evidence that the hemispheres of split-brain patients can function independently:

Object presented to the left hemisphere.
• By touching with the right hand or viewing in the right visual field.
• Patient could pick out the correct object with the right hand.
• Could not pick out the correct object with the left hand.
• Could name the correct object.

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Object presented to the right hemisphere.

• By touching with the left hand or viewing in the left visual field.
• Patient could pick out the correct object with the left hand.
• Claimed nothing had been presented.
• Could not pick out the correct object with the right hand.

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Sperry (1974): A small amount of information can still be transferred via several smaller commissures.

Immediately after surgery:

• Each hemisphere can only quickly and accurately respond to information that reaches it
directly .

• Smaller commissures allow a slower response.

Later: the brain learns to use the smaller connections.
Integrating information between both hemispheres remains difÏcult.

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Right hemisphere is better at perceiving emotions (e g identify lies).

• Lesions to parts of the right hemisphere leads to difÏculty perceiving other’s emotions
difÏculty to understand humour and sarcasm and a monotone voice.
Left hemisphere lesion increases ability to accurately judge emotion → Associated with decreased
interference from the left hemisphere.

QUIMERIC FACE STUDIES.

Using an image editor programme, the face is separated into two halves.
With the “mirror” effect a single face is formed with each half.

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In the previous pictures:

• Part “A” represents the right side of the face.

• Part “B” represents the left side of the face.
The left side of the face is usually more expressive than the

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right side (contralateral control of the facial nerve over the
lower half of the face).

• The right hemisphere is also better at processing

spatial relationships.
• The left hemisphere seems to focus more on visual
details and the right hemisphere focuses more on
visual patterns.
The Z lens:

• Limits visual input to one hemisphere.

• Created by Zaidel to study functional asymmetry in split
brain patients.
• Zaidel developed a lens, called the Z lens, that limits
visual input to one hemisphere of split-brain patients while
they scan complex visual material such as the pages of a book.
• It is a contact lens that is opaque on one side (left or
right), so that visual input reaches only one hemisphere.
• It moves with the eye, it permits visual input to enter only
one hemisphere, irrespective of eye movement.
• The usefulness of the Z lens is not restricted to purely
visual tests.

3.2. Cross-cuing in split-brain patients.

Communication across hemispheres via non neural route.
Example: Green/red test.

• A red or a green light is flashed in the left visual field.

• Split brain patient is asked to name the colour red or green.
.

• Most split-brain patients 50 correct answers on this task.

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• One patient developed the ability to perform it almost perfectly. Why?

- On the trials when the patient initially said (the left hemisphere) the incorrect colour, his
head shook, and the patient then changed his guess to the other, correct colour.
- Apparently, the right hemisphere (which knew the correct answer) heard the incorrect
guess of the left hemisphere, and signalled to the left hemisphere that it was wrong by

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shaking the person’s head.

3.3. Doing two things at once.

If the two hemispheres of a split-brain patient are capable of independent

functioning, then they should be able to do two different things at the
same time Can they?

Procedure:

• 2 different stimuli appeared simultaneously on the test screen.

• The split-brain patient is asked to simultaneously reach into two bags (one with each hand)
and grasp in each hand the object that was on the screen.
✓ Patient takes an orange in her/his right hand and a pencil in her/his left hand.
• After grasping the objects, but before withdrawing them, the patient is asked to tell the
researcher what was in the two hands.
X Patient’s response 2 oranges.
HELPING-HAND PHENOMENON.

• 2 different stimuli appeared simultaneously on the test screen.

• The split-brain patient is asked to pick up the presented object from a group of objects on a
table (in full view).
- The right hand reaches out to pick up the orange under the direction of the left
hemisphere.
- The right hemisphere (that saw a pencil) sees what is happening and considers that an
.

error is being made.

- The right hemisphere deals with this problem the left hand pushes the right hand away
from the orange and redirected it to the pencil.
The special ability of split brains to do two things at once has also been demonstrated on tests of
attention. Each hemisphere of split-brain patients appears to be able to maintain an independent
focus of attention. This leads to an ironic pattern of results:
Split-brain patients can search for, and identify, a visual target item in an array of similar items more
quickly than healthy controls can — presumably because the two split hemispheres are conducting
two independent searches.

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VISUAL COMPLETION PHENOMENON: Chimeric figures test.

• Pictures composed of fused together half faces of two

different people.
• Split brain patients were asked to describe what they
saw.
• They reported seeing a complete, bilaterally symmetrical
face.
• When the patients were asked to describe what they saw,
they usually described a completed version of the half that had
been presented to the right visual field (i.e., the left hemisphere).

3.4. Dual mental functioning and conflict in split-brain patients.

In most split-brain patients the left hemisphere seems to control most everyday activities.
In a few split-brain patients the right hemisphere takes a more active role in controlling behaviour →
conflicts between the left and right hemispheres.
The case of Peter:

• Commissurotomy at 20 years (to control seizures)

• Wada-test: left hemisphere dominant for language.
• He could not respond with the left side of his body to verbal input → his left hemisphere could
not control the left side of his body via ipsilateral fibers.
• Left hemisphere tries to force the left hand with his right hand to do what was needed.

3.5. Independence of split-brain hemispheres: current view. .

In most split-brain patients some communication of information between hemispheres.

• The emotional content of images presented to the right hemisphere is reflected in patients’
speech, as well as in their nonverbal behaviour → Emotions pass across hemispheres.
• The relevance of the difÏculty of the task.
- Simple tasks are best processed in one hemisphere the hemisphere specialised for the
specific activity.
- Complex tasks require both hemispheres.

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One factor that has been shown to contribute substantially to the hemispheric independence of split-
brain patients is task difÏculty. As tasks become more difÏcult, they are more likely to involve both
hemispheres of split-brain patients.
It appears that simple tasks are best processed in one hemisphere, the hemisphere specialized for
the specific activity, but complex tasks require the cognitive power of both hemispheres.

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4. Differences between left and right hemispheres.
Anatomical asymmetries of the brain:

• Planum temporale: an area of the temporal cortex that is larger in the left hemisphere in 65
of people.

Before we introduce you to some of the differences between the left and right hemispheres, we need
to clear up a common misconception: For many functions, there are no substantial differences
between the hemispheres; and when functional differences do exist, these tend to be slight biases
in favour of one hemisphere or the other — not absolute differences.

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SUPERIORITY OF THE LEFT HEMISPHERE IN CONTROLLING IPSILATERAL MOVEMENT.

fMRI studies ipsilateral movement: .

Complex, cognitively driven movements made by one hand.

↓

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Most of the activation the contralateral hemisphere.
Some activation ipsilateral hemisphere → substantially greater in the left hemisphere (than in the
right).
Left hemisphere lesions: more likely to produce ipsilateral motor problems (e.g., accuracy of left-
hand movements).
SUPERIORITY OF THE RIGHT HEMISPHERE IN SPATIAL ABILITY: EVIDENCE.

• Levy (1969):
o A three-dimensional block of a particular shape was placed in the right hand or the left
hand of split-brain patients.
o The patients palpated the block.
o The patients were asked to point to the two-dimensional test stimulus that best
represented what the three-dimensional block would look like.
o Results:
- Right hemisphere (left hand) fast and silent performance.
- Left hemisphere (right hand) hesitant and accompanied by a
running verbal commentary.
• Neglect is more likely after right hemisphere lesions.

SUPERIORITY OF THE RIGHT HEMISPHERE IN EMOTION.

• Studies of unilateral brain lesions general right hemisphere dominance for emotional
processing.
• fMRI studies inconsistent results. Although the study of unilateral brain lesions suggests a
general right-hemisphere dominance for some aspects of emotional processing, functional
brain imaging studies have not provided unambiguous support for this view.

What is the person in the picture thinking or feeling?

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SUPERIORITY OF THE RIGHT HEMISPHERE IN MUSICAL ABILITY.

Other evidence right temporal lobe lesions are more likely to disrupt music discrimination.
Kimura (1964) compared the performance of 20 right-handers on the standard digit version of the
dichotic listening test with their performance on a version of the test involving the dichotic
presentation of melodies. Kimura simultaneously played two different melodies— one to each ear —
and then asked the participants to identify the two they had just heard from four that were
subsequently played to them through both ears. The right ear was superior in the perception of digits,
whereas the left ear was superior in the perception of melodies. This is consistent with the
observation that right temporal lobe lesions are more likely to disrupt music discriminations than are
left temporal lobe lesions.
HEMISPHERIC DIFFERENCES IN MEMORY.

• Relationship between memory processes with each hemisphere.

o Left hemisphere: specialised for encoding episodic memory.
• Relationship between specific materials with each hemisphere.
o Left hemisphere: verbal material.
o Right hemisphere: nonverbal material → more inconsistent relationship.
What could this be due to?
CURRENT VIEW.

• Be careful not to oversimplify.

• There are doubts that any one person habitually relies only on one hemisphere.
• Most tasks require cooperation from both hemispheres.
• Clusters of abilities (e.g., language) are composed of different individual cognitive processes.
• It is important to understand lateralisation in terms of individual cognitive processes (e.g., for
language speech perception, verbal comprehension, naming...).

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The human connectome project:

• Brain networks or ‘connectomes’:

o Hub nodes: functionally valuable → integrative processing and adaptive behaviours.
o Hubs have higher metabolic demands and longer-distance connections than other
brain regions.

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5. Development of lateralisation and handedness.
.

THEORIES OF THE EVOLUTION OF BRAIN LATERALISATION.

General premises:

• It is advantageous for areas of the brain that perform similar functions to be located in the
same hemisphere.
• It is advantageous to place some functions on one side of the brain and others on the other
side to minimize redundancy of function between hemispheres.
Analytic-synthetic theory
Motor theory
Linguistic theory
Analytical-synthetic theory:

• Left hemisphere: operates in a logical, analytical, computerlike fashion,

analysing and abstracting stimulus input sequentially and attaching verbal labels.
• Right hemisphere: is a synthesizer, which organises and processes information
in terms of gestalts (wholes).
• Limitation: it is not possible to specify the degree to which any task requires
either analytic or synthetic processing → empirical tests?

Motor theory:

• Left hemisphere: specialised for the control of fine movements →

speech requires fine movements.
• Evidence: lesions that produce aphasia often produce other
motor deficits.
But why motor function became lateralised in the first place?

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Linguistic theory:

• Primary role of the left hemisphere is language.

• Evidence: left hemisphere lesion can disrupt the use of sign language but not pantomime
gestures.

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The case of W.L., the man who experienced aphasia for sign language:
W.L. is a congenitally deaf, right-handed male who grew up using American Sign Language. Seven
months prior to testing, W.L. was admitted to hospital complaining of right-side weakness and
motor problems. A CT scan revealed a large left fronto-temporo-parietal stroke. At that time,
W.L.’s wife noticed he was making many uncharacteristic errors in signing and was having
difÏculty understanding the signs of others.
W.L.’s neuropsychologists managed to obtain a 2-hour videotape of an interview with him
recorded 10 months before his stroke, which served as a valuable source of pre-stroke
performance measures. Formal poststroke neuropsychological testing confirmed that W.L. had
suffered a specific loss in his ability to use and understand sign language. The fact that he could
produce and understand complex pantomime gestures suggested that his sign-language aphasia
was specific to language.

DEVELOPMENT OF LATERALISATION.
Corpus callosum:

• Matures and gradually grows and thickens as myelin increases around certain axons from
childhood through adolescence.
• Young children have difÏculty comparing information from the left and right hand.
• Research suggests that children younger than 6 do not have a mature corpus callosum.
• Being born with a condition where the corpus callosum does not completely develop.
o Results in extra development of:
- Anterior commissure: connects the anterior parts of the cerebral cortex.
.

- Hippocampal commissure: connects the left and right hippocampus.

o It allows better performance on some tasks compared with split brain people.
Handedness: relationship between manual dominance and hemispheric dominance for language.

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Physiological Psychology II
Unit 4. Biopsychology of
language

1. Language: introduction.
Language ability to encode ideas into signals.
Characteristics:

• It has a universal design 2 components:

Grammar:
Words: Morphology.
Association between sound and meaning. Syntax.
Phonology.
• Complex language develops spontaneously in children.
• The ability to learn a language is innate.
Why is language different from other forms of communication?

• Creativity: we use words and grammatical rules to create something new.

• Form: it has unlimited use with a limited number of meanings.
• Content: it is not just an exchange of facts it can communicate abstractions.
• Use: means of social communication and organises our memories.

2. Neural models of language.

Phrenology (18th-19th century), with Gall and Spurzheim localises language in the left eye.
1960s neural models of language based on clinical
case studies (aphasias):

• Relationship between linguistic behaviour

and brain autopsy.
P. Broca (1861):

• Motor area of language: inferior portion of

the left prefrontal cortex.
• Famous patient: Leborgne ("tan” patient).

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K. Wernicke (1874):

• “Centre for auditory word pictures” left temporal gyrus.

• Formulated a connectionist neural model set of fibers from Wernicke's area to Broca's area
whose lesion would cause repetition deficits → Conduction aphasia.

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The Wernicke Licht Heim model:

• Inclusion of an "object concept centre" (Wernicke Licht Heim house).

• First to describe transcortical motor aphasia and transcortical sensory aphasia.

Holistic model of language: Dejerine (1892):

Left angular gyrus lesion:

• Alexia.
• Agraphia.

Holistic models of language: Pierre Marie (1906):

Unique type of aphasia due to a lesion in a perisylvian quadrilateral.

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The Wernicke-Geschwind (1970):

• Seven components.
• All in the left hemisphere.
• Interaction of these components:
- Conversation.

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- Reading aloud.
.

Evidence from studies of the effects of cortical lesions:

Lack of permanent disruption of language related abilities after surgical excision (indicated in orange)
of the classic Wernicke Geschwind language areas (outlined with the dotted lines).

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• Lesions destroying Broca’s area → no permanent effect.

• Lesions of arcuate fasciculus and angular gyrus → no permanent effect.
• Large portions of Wernicke’s area removed → no permanent effect.
Evidence from structural neuroimaging studies with patients with aphasia:

• Damage not restricted to Broca’s area or

Wernicke’s area.
• Significant damage to subcortical white
matter.
• Large anterior lesions → expressive
symptoms.
• Large posterior lesions → receptive
.

symptoms.
• Brain damage sometimes does not affect
the Wernicke Geschwind areas → medial frontal
lobe, subcortical white matter, basal ganglia, or
thalamus.
Evidence from studies of electrical stimulation of the cortex:
Penfield and Roberts 1959 effects of cortical stimulation on speech.

Right hemisphere stimulation almost never disrupted speech.

• Ojemann et al (1983) language tasks during cortical stimulation.

- F3 stimulation speech arrest.
- Temporal lobe stimulation naming errors.
- Areas that disrupted language beyond Wernicke Geschwind model.
- Differences among the patients in the organization of their language abilities.
Language cortex is organised like a mosaic with the discrete columns of tissue that perform a
particular function widely distributed throughout the language areas of cortex.

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Studies with bilingual patients:

• High variability of representation of the languages they are fluent in.

• Bilingual from birth: they create new neural circuits for the different languages grey matter.

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.

COGNITIVE NEUROSCIENCE APPROACH TO LANGUAGE.

Premises:
Language combination of several cognitive processes which may be organised separately in different
parts of the brain.

• Phonological analysis: analysis of the sound of language.

• Grammatical analysis: analysis of the structure of language.
• Semantic analysis: analysis of the meaning of language.

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• Brain areas involved in language are not dedicated exclusively to that purpose.
• Brain areas involved in language are likely to be small, widely distributed, and specialised.
Functional neuroimaging studies:

• Positron emission tomography (PET) in patients with aphasia: cortico-subcortical alterations

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in structurally intact regions.
• Left prefrontal region phonological coding.
• Left temporo-parietal region semantic processing.
• High inter-individual variability.

Substantial right hemisphere activity is recorded during various language related cognitive tasks even
though language tends to be lateralised to the left hemisphere. Why do you think this happens?

Cognitive neuroscience
Wernicke-Geschwind model
approach
Functional brain imaging: Brain-damaged patients:
Can’t prove causation! No language impairments
Methods
Right hemisphere activity derived from right hemisphere
during language tasks. lesions.
Small. Large.
Language areas Widely distributed. Circumscribed.
Specialised. Homogeneous.

CONCLUSIONS.

• Initial neural models: very simple (few centres and unidirectional pathways)
• Brain electrical stimulation and functional neuroimaging studies: language is the result of
synchronised activity of several neural centres networks linked by reciprocal cortico-
subcortical connections bidirectionality.
• It is erroneous to locate a linguistic function in one brain area and to attribute the loss of a
complete function to a specific area.
• Language: a system consisting of multiple, relatively independent regions organised with
considerable inter individual variability.
• Clinical case studies: data very useful for the formulation of hypotheses or confirmation of
.

neural models.

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• Alternatives to classical models.

- Different models with one aspect in common classically primordial areas are considered
as nodules (hubs).
- The functional importance of the nodule is relativised, and the network becomes relevant.

3. Evaluation of aphasia.
3.1. Language assessment.
EXPRESSIVE LANGUAGE.
The Boston Diagnostic Aphasia Examination test (Goodglass, 2005): The patient is asked to say what
is happening in the picture → spontaneous language.

Phonemic fluency (Spreen Benton, 1977):

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Semantic fluency (animals) (Rosen, 1980):

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COMPREHENSION:
Token Test (De Renzi & Vignolo, 1962):

• The patient is asked to arrange the cards according to the instructions in hierarchical order
(depending on difÏculty).
• Verbal tenses, passive voices, and temporal expressions.

REPETITION.
The Boston Diagnostic Aphasia Examination test (Goodglass, 2005):

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NAMING.
The Boston Naming Test (Goodglass, 2005):

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• 60 items.

If the answer is
Spontaneous incorrect:
naming phonemic key

If the answer is
incorrect:
semantic key

• Total score = number of spontaneous correct answers + correct answers with semantic keys.
READING COMPREHENSION.
The Boston Diagnostic Aphasia Test (Goodglass, 2005):
Patient has to read the first-column sentences, then select the correct answer regarding the sentences
on the second-column sentences.

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WRITING.
The Boston Diagnostic Aphasia Examination Test (Goodglass, 2005):
1. What is the relationship between the people in the picture?
2. What is happening behind the woman?
3. Why does the girl tell the boy not to make noise?
4. Why do you think the boy might get hurt?
5. What else is happening right in front of the mother?
Scoring:

• Mechanics (motor patterns of writing).

• Access to written vocabulary.
• Syntax.
• Adequacy of content.
Usually in aphasia the writing is very similar to the speech.
EXPLORATION OF OTHER AREAS.

Exploration of the motor status Exploration of the sensory status

Hemiplegia: complete analysis of the
musculature on one side of the body. (Motor Hemisensory deficit: lack of sensation on one
aphasia). It is a complete paralysis. side of the body. Usually contralateral to the
Hemiparesis: reduced motor strength or partial brain lesion.
paralysis on one side of the body. Normal.
Normal: Motor status can be normal too.

Visual fields.
Additionally, it is important to explore emotional fields. Some
patients with aphasia suffer from:

• Hemianopsia: absolute or significant loss of vision in half

of the visual field.
• Quadrantanopsia: absolute or significant loss of vision in
one quadrant of the visual field.
.

Vascular territory.

In the anterior, middle, and posterior part of the brain.

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Lobe.

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See if there is a structural lesion on any lobe.

4. Semiology of aphasia.
Aphasia: total or partial impairment in the neural mechanisms involved in the production,
comprehension, repetition, naming and/or reading and writing in people who have already acquired
language.
Types of aphasia:

• Broca's aphasia.
• Wernicke's aphasia.
• Conduction aphasia.
• Global aphasia.
• Transcortical motor aphasia.
• Transcortical sensory aphasia.
• Transcortical mixed aphasia.
• Anomic aphasia.

4.1. Broca’s aphasia.

Non-fluent aphasia: inability to produce language, but relatively preserved comprehension.
Expressive language:
.

• Slow, laborious, and non-fluent speech.

• Great difÏculty saying function words (grammatical meaning) a, the, some, in, about...
• Correct use of content words ( verbs, adjectives, and adverbs) apple, house, throw...

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Deficit awareness. Major deficits:

Agrammatism:

• DifÏculty using grammatical constructions.

• Patients rarely use function words or grammatical markers such as ed or auxiliaries such as

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have (e.g., I have gone).

Articulation difÏculties: Patients mispronounce words (e.g., lipstick is pronounced “likstip”).

Anomia: Word finding difÏculty → Facial expressions and frequent use of sounds (e.g., “uh”).
Paraphasias: insertion or substitution of erroneous words in conversation.

• Phonemic paraphasias → “dat” instead of “.

• Semantic paraphasias →“ instead of cat”.
Writing: the handwriting reflects their speech deficits.

Use of very few words, but the words do make some sense.

SUMMARY OF BROCA’S APHASIA.

Spontaneous language Non-fluent

Comprehension Relatively preserved
Repetition Deficit
Naming Deficit
Reading comprehension Variable
Writing Deficit
Motor function Hemiplegia
Sensory function Relatively preserved
Visual field Normal
Vascular territory Middle cerebral artery
Frontal (surrounding cortical and subcortical
Lobe regions)
Basal ganglia
.

Axial neuroimaging section

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4.2. Wernicke’s aphasia.

Fluent aphasia: impaired verbal comprehension and easily articulated fluent speech.
Patients seem unaware of their deficits (anosognosia).
Expressive language:

• Use of grammatical words :“the”, “but”...

• Use of complex verb tenses and subordinate clauses.
• Use of few contents words.
Speech at normal or faster than normal rate, although the content makes no sense.

Paragrammatisms: (multi word paraphasias language errors in the structure of sentences that occur
during speech or writing ( verb tense errors, incorrect word order).
DifÏculty finding words → impairment of reading and writing.

• Writing they preserve their natural premorbid handwriting, but the content may be
unintelligible.

There are many, less forced, words, but they don’t make much sense.
The handwriting is better than in the case of Broca’s aphasia.
Repetition:

• Paraphasias and neologisms.

• Broadening: adding a word or phrase or using a more complex form than the one given by the
examiner.

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SUMMARY OF WERNICKE’S APHASIA.

Spontaneous language Fluent

Comprehension Deficit
Repetition Deficit
Naming Deficit

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Reading comprehension Deficit
Writing Deficit
Motor function Normal
Sensory function Relatively preserved
Visual field Hemianopsia
Vascular territory Middle cerebral artery
Posterior portion of the superior temporal
Lobe
gyrus

Axial neuroimaging section

4.3. Conduction aphasia.

Fluent aphasia.
Meaningful fluent speech and relatively good verbal comprehension, but important deficits in
repetition:

• Lower difÏculties in repeating one syllable words, but polysyllabic words become tongue
twisters.
• Better performance in repeating real words than nonsense words.

Deficits in repetition:
When the patient is asked to repeat a word, he/she usually say a word with the same meaning or
one that is related.

Phonemic paraphasias → “dat” instead of “cat”.

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SUMMARY OF CONDUCTION APHASIA.

Spontaneous language Fluent

Comprehension Preserved
Repetition Deficit
Naming Deficit

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Reading comprehension Relatively preserved .

Writing Deficit
Motor function Hemiparesis
Sensory function Hemisensory deficit
Visual field Normal
Vascular territory Middle cerebral artery
Lobe Parietal: arcuate fasciculus

Axial neuroimaging section

4.4. Global aphasia.

Non-fluent aphasia.
All language processes are altered → there is no longer a distinctive pattern of preserved and altered
components.
Better understanding of aspects of the patient's own life compared to performance on formal verbal
comprehension tests.
Some patients: unable to voluntarily produce verbal sounds.

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SUMMARY OF GLOBAL APHASIA.

Spontaneous language Non-fluent

Comprehension Deficit
Repetition Deficit
Naming Deficit
Reading comprehension Deficit
Writing Deficit
Motor function Hemiplegia
Sensory function Hemisensory deficit
Visual field Normal
Vascular territory Middle cerebral artery
Fronto-temporo-parietal (large cortical lesion
Lobe
or subcortical lesion)

Axial neuroimaging section

4.5. Transcortical motor aphasia.

Transcortical: syndromes in which the ability to repeat is much better preserved than the
spontaneous speech.
Non-fluent aphasia.
Impaired speech production (especially initiation), with more preserved repetition than in Broca's
aphasia.

• DifÏculty initiating and organising responses in conversation unless the question is so

structured that it can be answered with a factual one-word response.
SUMMARY OF TRANSCORTICAL MOTOR APHASIA.

Spontaneous language Non-fluent

Comprehension Preserved
Repetition Preserved
Naming Deficit
Reading comprehension Relatively preserved
Writing Deficit
Motor function Hemiplegia
Sensory function Relatively preserved
Visual field Normal
.

Vascular territory Anterior/Middle cerebral artery

Frontal: small subcortical lesion above the
Lobe
Broca’s area.

Axial neuroimaging section

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Evaluator: “What happened to you to bring you to the hospital?”

Patient: “Well I was I can’t”.

4.6. Transcortical sensory aphasia.

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Fluent aphasia.
Impaired verbal comprehension, with more preserved repetition than in Wernicke's aphasia.

SUMMARY OF TRANSCORTICAL SENSORY APHASIA.

Spontaneous language Fluent

Comprehension Deficit
Repetition Preserved
Naming Deficit
Reading comprehension Deficit
Writing Deficit
Motor function Normal
Sensory function Relatively preserved
Visual field Hemianopsia
Vascular territory Posterior/Middle cerebral artery
Lobe Temporo-occipital

Axial neuroimaging section

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4.7. Transcortical mixed aphasia.
• Non-fluent aphasia.
• Inability to understand, naming and writing.
• Visual disorders.
SUMMARY OF TRANSCORTICAL MIXED APHASIA.

Spontaneous language Non-fluent

Comprehension Deficit
Repetition Preserved
Naming Deficit
Reading comprehension Deficit
Writing Deficit
Motor function Hemiplegia
Sensory function Hemisensory deficit
Visual field Hemianopsia
Vascular territory Anterior/Middle/Posterior cerebral artery
Lobe Fronto-temporo-occipital

Axial neuroimaging section

4.8. Anomic aphasia.

• Fluent aphasia.
• Inability to name, but fluent and grammatically well-formed speech-
• Difference from other aphasias: lack of phonemic and semantic paraphasias.
• Circumlocutions: strategy by which people with anomia find alternative ways to say
something when they are unable to say the most appropriate word (description of the object's
function, appearance, location, category...).

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SUMMARY OF ANOMIC APHASIA.

Spontaneous language Fluent

Comprehension Preserved
Repetition Preserved
Naming Deficit
Reading comprehension Preserved
Writing Preserved
Motor function Normal
Sensory function Normal
Visual field Normal
Vascular territory Middle cerebral artery
Lobe Temporal
.

Axial neuroimaging section

Aphasia in people who are deaf:

• Sign language: grammar based on visual and spatial nature → right hemisphere?
• Cases of aphasia for signs in people who are deaf: mainly lesions of the left hemisphere.
The same language-related regions of the brain are activated by deaf and hearing people when they
decide whether two written words rhyme → Broca’s area.
(McSweeney et al., 2008b)

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Lesions in the right hemisphere in people who are deaf:

• DifÏculty maintaining a coherent topic.

• DifÏculty with subtle uses of spatial features.
Stuttering:

• A speech disorder characterised by frequent pauses prolongations of sounds or repetitions of

sounds, syllables, or words that disrupt the normal flow of speech.
• It rarely occurs when a person says a single word or is asked to read a list of words.
• Most often at the beginning of a sentence (especially if long or grammatically complex) →
disorder of coordinating the motor sequences needed to produce fluent speech?

Problem: lack of auditory feedback from sounds of the person’s own speech (lack of activity in the
temporal lobe).
Intervention: delayed auditory feedback.

• Procedure in which a person wearing headphones tries to speak normally while hearing
his/her own voice, which has been electronically delayed 50 200 msec).

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5. Neural plasticity and recovery from aphasia.

SPONTANEOUS RECOVERY.
Neural changes and mechanisms of the nervous system to respond to changes following acquired
brain injury.

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Related to:

• Normalisation of hemodynamic in areas of ischemic penumbra.

Ischemic penumbra = area around the structural lesion in which there is hypometabolism of
the cells that have survived the ischemic event.
• Disappearance of cerebral edema and intracranial hypertension.
Cerebral edema = area of inflammation around the structural lesion.
• Reduction of the diaschisis effect.
Diaschisis = reversible functional deactivation that occurs in regions located at a
distance from the lesion, due to fiber disruption.
These regions are shown to be affected, even though there has been no neuronal death in
them.
• Reabsorption of bleeding.
Acute phase: > recovery within 3 months after brain injury.

FACTORS THAT INFLUENCE LANGUAGE RECOVERY.

Smaller lesion size: better prognosis.

Stronger relationship for verbal fluency and Younger age: better prognosis.
smaller for verbal comprehension.

Other personal factors.

Left handedness: more bilateral representation of language → better prognosis after brain damage.
Women vs. men: more bilateral representation of language → better prognosis after brain damage.
Greater cognitive reserve: better prognosis.
Ethology:
Progressive disorders (neurodegenerative diseases): decline in language.
Static disorders (strokes, traumatic brain injury): tendency to language recovery.
Bilateral hemispheric lesions: poor prognosis.
Traumatic brain injury vs stroke and tumours: better prognosis due to:
• They involve preservation of some linguistic areas and are usually associated with anomic
aphasia.
Occur in younger population.

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Aphasic profile:
Critical factor in recovery.
Broca's aphasia and conduction aphasia: progress to anomia.
Wernicke's aphasia:
• Patients with better auditory comprehension: improve phonemic recognition and
repetition → progress towards anomia.
• Patients with poorer auditory comprehension: improve comprehension → progression
towards conduction aphasia.
Patients with impaired speech comprehension vs. patients with impaired fluency: better
prognosis.

6. Semiology of alexia.
Reading (and writing) of people with aphasia: typically resemble their expression and comprehension
abilities.
Reading processes:

• Whole word reading: reading by recognising a word as a whole → “sight reading”

• Phonetic reading: reading by decoding the phonetic significance of letter strings → “sound
reading”.
Relevance of the type of word (glab trisk chint)

Brain circuits:
.

Visual word form area a region of the fusiform gyrus on the

base of the temporal lobe that plays a critical role in whole
word recognition.

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Phonetic reading:
Temporoparietal cortex.
Inferior frontal cortex (including Broca’s area).

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Alexia:

• Reading impairment as a consequence of brain injury in people who already know how to
read.
• ≠ Dyslexia (difÏculties in reading when children are learning to read).
• Common after lesions at the temporo-parieto-occipital junction (TPO) in the angular gyrus.

TYPES OF ALEXIA.
Pure alexia:
.

• “Pure word blindness” or alexia without agraphia.

• Patients can recognise words that are spelled aloud to them.
• Lesions that prevent visual information from reaching the visual association cortex of the left
hemisphere.

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Surface alexia:

• Patients can read words phonetically but have difÏculties reading irregularly spelled words by
the whole word method.
• Need to listen to their own pronunciation to understand what they are reading.

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“Pair” without additional information → pair, pear or pare?

Phonological alexia:

• Patients can read by the whole word method but cannot sound words out.
• They can read familiar words but has difÏculty reading unfamiliar words or pronounceable
nonwords.

Direct alexia:
Patients can read words aloud without understanding them.

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Developmental dyslexia:

• Heterogeneous and complex syndrome.

• Reading difÏculties in a person with normal intelligence and perceptual ability → main deficit:
phonological processing.
• Genetic origin or caused by prenatal or perinatal factors
• Relevance of cultural factors: English speakers 2x more likely than Italian → Complexity may
contribute (irregular words).
• Characteristics:
- Deficient phonological awareness: difÏculty blending or rearranging the sounds of words
that they hear → difÏculty to read phonetically.
o DifÏculty recognizing that if we remove the first sound from “cat” we are left with
the word “at”.
- DifÏculty in writing: spelling errors, poor spatial arrangements of letters, omission of
letters, and weak grammatical development.
- Subtle sensory and motor deficits.
- Reduced activation in left parietal and left occipitotemporal cortices (fMRI).

7. Semiology of agraphia.
Agraphia: Impairment of the ability to produce written language as a result of brain injury in people
who had already acquired writing.
Types of agraphia: .

• Phonological agraphia:
- Patients are unable to sound out words and write them phonetically.
- They cannot write unfamiliar words or pronounceable nonwords.
- They can visually imagine familiar words and then write them.
- Lesion regions involved in phonological processing and articulation.
o Broca’s area.
o Ventral precentral gyrus.
o Insula.
Whole-word writing: good.
Phonetic writing: poor.

• Orthographic agraphia:
- Disorder of visually based writing.
- Patients can only sound words out.
- They can spell regular words (e g care or tree).
- They can write pronounceable nonsense words.

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- DifÏculty writing irregular words:

o “Half” is writing as “haff”.
o “Busy” is writing as “bizzy”.
- Lesion: posterior inferior temporal cortex.
Whole-word writing: poor.

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Phonetic writing: good.

• Direct agraphia/semantic agraphia:

- Patients can write words that are dictated to them but cannot understand these words.
- They cannot translate their thought into words (cannot communicate by means of
writing).
- Ability to spell phonetically is intact → they can spell pronounceable nonwords.

8. Semiology of acalculia.
Acalculia:
Impaired ability to perform calculations as a result of a brain injury (usually left parietal, right parietal
or bilateral) in patients that have already acquired this ability.
Types (Hécaen, 1962):

• Acalculia with alexia and agraphia for numbers/aphasic acalculia: difÏculty in reading and
writing numbers. Often associated with aphasia.
• Spatial acalculia: associated with alterations in spatial processing → the order
and position of digits in space is not maintained.
• Anarithmetic acalculia/primary acalculia: impairment in the performance of
mathematical operations not associated with other cognitive deficits.

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Physiological Psychology II
Unit 5. Biopsychology of
psychiatric disorders

1. Psychiatric disorders.
Disorders of psychological function that require treatment. Diagnosis is guided by the DSM of the
American Psychiatric Association (currently the DSM V).
Schizophrenia:
1. What is schizophrenia?
- Schizophrenia: It is characterized by a loss of contact with reality.
- Positive symptoms.
- Negative symptoms.
- Diagnosis.
2. Clinical characteristics.

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3. Causal factors.
- Genetics.
- Adoption.
- Maternal stress.
- Prenatal infections.

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- Socioeconomic factors.
- Urban birth/life.
- Childhood adversity.
.

4. Neural basis.

DOPAMINE THEORY OF SCHIZOPHRENIA.

Theory supported by:
• Reserpine is a dopamine antagonist (same afÏnity as dopamine but there will be no
effect (blocks the receptor, impedes positive symptoms)). Not at the same time
hallucinations and negative symptoms.
• Stimulants (dopamine agonists) trigger schizophrenic episodes in healthy people.
1963 Carlsson and Lindqvist: Found chlorpromazine (an antagonist of dopamine) increased
dopamine metabolites (NOT MOLECULES).
1970 Snyder and colleagues: Binding afÏnity of dopamine antagonists (↓ positive symptoms).

• Discovery of receptor subtypes of dopamine.

• D2 receptors. If you block D2 receptors = ↓ positive symptoms. If D2 bind more (↑),
positive symptoms ↑.
• Key findings that still do not fit.

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5. Treatment.
Chlorpromazine:

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Binding D2 receptors:

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6. Brain scans.
SCHIZOPHRENIA AS A NEUROLOGICAL DISTURB.
Neuro-evolutive theory: Positive symptoms of schizophrenia are due to a fail in migration of
neurons.

• It supports the idea of dopamine, but that one was simpler.

• If stress or something is happening during the migration period, this fail could happen.
The migration is like a re-structuration of the brain.
Schizophrenia and brain damage:
Neurological symptoms suggestive of brain damage:

• Catatonia and facial dyskinesias.

• Rapid or slow blinking rates.
• Fixed gaze or avoidance of eye contact.
• Absence of blinking reflex to a clap.
• Episodes of eye deviation with speech interruption.
• Spasmodic eye movements.
• Poor visual tracking of an object.
• Inability to move eyes without the head.
• Weak pupillary reaction to light.
• Continuous elevations of the eyebrows.
SCANS OF SCHIZOPHRENIA:

Patient with schizophrenia and healthy monozygotic twin.

In the brain of people with schizophrenia, these things fail:

• Enlargement of the ventricles (loss of brain tissue).

• Degeneration or abnormalities in development (medial temporal lobe, frontal lobes,
medial part of diencephalon).
.

• Reduce volume of the hippocampal formation.

• The degree of brain abnormalities is related to the severity of negative symptoms. If
there are a lot of negative symptoms = more brain damage.

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MRI OF CORTICAL LOSS IN ADOLESCENT WITH SCTIZOPHRENIA:

Structural MRIs reveal cortical loss in adolescent patients with schizophrenia. Here red
.

indicates area of greatest tissue loss. (From Thompson et al., 2001).

Cortical loss is present in adolescents. They have studied this loss in adolescents because from
childhood to adolescence you can see a drastically change (as adolescents brain is constantly
changing). In adulthood this loss will be present but not as drastically developed as in
adolescence).

2. Introduction to major affective disorders.

Affective disorders:

• Psychiatric disorders characterized by disturbances of mood or emotion.

• Also known as mood disorders.
• Includes depression and mania.
Types of depression:

• Unipolar or Bipolar.
• Reactive vs. Endogenous.

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2.1. Affective disorders: depression and mania.

• Depression: normal reaction to loss, abnormal when it persists or has not cause.
• Mania: overconfidence, impulsivity, distractibility, and higher energy.
Bipolar disorders:

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1. Defining bipolar disorders.
• Hypomania – Not as severe as Mania.
o Reduced need for sleep.
o High energy.
o Positive affect.
• Mania – Elevated mood. Terms of functionality.
o Exaggerated symptoms (delusions, overconfidence…).
o Usually includes psychosis.
• Bipolar I – At least 1 maniac episode.
o Bipolar Disorder Type I = Depression + Hypomania + Mania.
o Bipolar Disorder Type II = Depression + Hypomania.
• Rapid Cycling – 4 mood changes within a year.
2. Clinical characteristics.
Major depressive episode: .

Depressive symptoms: ≥5 symptoms during the same 2-week period that are a change from
previous functioning; depressed mood and/or loss of interest/pleasure must be present;
exclude symptoms clearly attributable to another medical condition.

Additional required criteria:

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Maniac episode:
Manic symptoms: during period of mood disturbance and increased energy/activity, ≥3 of the
following symptoms (4 if the mood is only irritable) present to a significant degree and are a
noticeable change from usual behaviour.

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Hypomanic episode:
Manic symptoms: during period of mood disturbance and increased energy/activity, ≥3 of the
following symptoms (4 if the mood is only irritable) present to a significant degree and are a
noticeable change from usual behaviour.

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3. Causal factors.
Causal Factors in Major Depressive Disorder:
• Genetic implication - Monozygotic vs Dizygotic.
• Stress/epigenetics – Expression of proteins.
• SAD – Seasonal Affective Disorder.
• Postpartum depression – Hormonal changes and psychosocial factors.
.

Affective disorders are very common:

• ≈5% suffer from unipolar affective disorder at some point.

• ≈1% from bipolar.
Genetics: Concordance rate higher for bipolar than unipolar.

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Causal factors in affective disorders:

• Stressful experiences:
o Evidence linking stress and affective disorders in sparse.
o Extreme stress is more likely to cause post-traumatic stress disorder (PTSD)
than depression.

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• Seasonal Affective Disorder (SAD):
.

o Wintertime depression and lethargy.

o Probably due to reduction of sunlight.
Causal factors in bipolar disorders:

• High heritability (89-90%).

• Many different genes implicated.
• Coding for Calcium channels.
• Coding for some proteins at nodes of Ranvier.

4. Brain and major affective disorders.

Brain & depression:
• Gray matter reduction.
o Prefrontal cortex.
o Hippocampus.
o Amygdala.
o Cingulate cortex.
• White matter reduction.
o Frontal cortex.
• fMRI studies.
o Atypical activation in frontal, cingulate, and insular cortices.
o Amygdala.
o Striatum.
o Thalamus.
BRAIN DIFFERENCES ASSOCIATED WITH BIPOLAR DISORDERS.

• MRI: reductions in Grey Matter volume.

- Medial prefrontal cortex.
- Left anterior cingulate.
- Left superior temporal gyrus.
- Prefrontal regions.
- Hippocampus.
• Meta-analysis fMRI studies: atypical activation and functional connectivity in:
- Frontal cortex
- Medial temporal lobe
- Basal ganglia

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BRAIN PATHOLOGY AND BIPOLAR AFFECTIVE DISORDER.

MEDIAL TEMPORAL LOBE (MTL).

• Hippocampus. .

• Connected areas:
o Entorhinal cortex.
o Perirhinal cortex.
o Para hippocampal cortex.

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Stress:

• Diathesis-stress model of depression.

- Diathesis = genetic susceptibility.
- Diathesis + Stress = depression.
- Support is indirect: depressed people...

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o Tend to release more stress hormones.
o Fail dexamethasone.
Suppression test – normal negative feedback on stress hormones not functioning
in many depressed patients.
HPA AXIS:

• Hippocampus has many glucocorticoid receptors.

• Following stress:
- Dendrites of pyramidal cells are shorter and less branched.
- Adult neurogenesis of granule cells reduced.
• Effects blocked with adrenalectomy; produced with corticosteroids.
STRESS AND THE HIPPOCAMPUS.

• Prolonged stress can also be harmful to the hippocampus and can affect memory.
• Cortisol enhances metabolic activity in the body.
• When metabolic activity is high in the hippocampus, the neurons are more sensitive to
damage by toxins or over-stimulation.
• Stress also impairs the production of new hippocampal neurons (impaired neurogenesis).
Depression hypothesis:

• Monoamine theory of depression:

- Underactivity of serotonin and norepinephrine synapses.
o Consistent with drug effect.
o Depression untreated with drugs may result in proliferation of monoamine
receptors (up-regulation), providing support for the monoamine theory.
- Problem with theory – not all respond to monoamine agonists.
- Depression & underactivity at 5HT and NE synapses.
- MAO-Inhibitors, Tricyclics SSRI and SNERI = 5HT and/or NE agonists.
- Autopsy studies show rHT & NE receptors abundant in
non-treated patients (post-mortem → Up-regulation.
Why up-regulation? Defense mechanism against
scarcity of neurotransmitters.
- Monoamine agonists not effective for most patients:
.

Slightly > placebo.

GABA, Glu and Ach also play a role in depression.

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• Neuroplasticity theory:
- AD drugs immediately produce increased transmission at monoaminergic synapse BUT
therapeutic effects take weeks → agonistic effects are not the main therapeutic
mechanism.
- Decreased neuroplasticity can be the critical mechanism, so depression = reduced brain

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neuroplasticity.

- Support for the neuroplasticity theory:

o Stress and depression and disruption of neuroplastic processes (BDNF synthesis,
HPC neurogenesis).

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THEORIES OF BIPOLAR DISORDER.

• No clear understanding.
• Lack of animal models.
• Neurotransmission (GABA, glutamate, monoamines).
• BDNF.
• HPA dysregulation.
Current hypotheses:

• HPA axis dysregulation.

• Circadian rhythms disruption (in patients and relatives).
• Neurotransmission (GABA, glutamate, monoamines).
• Lower BDNF levels.

2.1.1. Brain stimulation therapy.

TREATMENT OF DEPRESSION WITH BRAIN STIMULATION.

• Repetitive transcranial magnetic stimulation.

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Major Depressive Disorder: Depression is also associated with prefrontal cortex activity.

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• Deep brain stimulation.

Treatment of depression with brain stimulation: 2008 study found that chronic electrical
stimulation near the anterior cingulate gyrus helped relieve depression in treatment-resistant
patients.
• Electroconvulsive therapy (ECT): is an electrically induced seizure that is used for the
treatment of severe depression.
For patients who have not responded to antidepressant medication or are suicidal.
Applied every other day for a period of two weeks.
- Side effects: memory loss (minimized if shock is localized to the right hemisphere)
.

(drawback: high risk of relapse).

- Regular, non-strenuous exercise is recommended.
o Increases blood flow to the brain.
o Affects 5HT pathways.
o Contributes to regulate HPA axis negative feedback mechanism.
o Increases BDNF production.
o Active people are less likely than sedentary people to become depressed, though
this research is correlational.
PSYCHOTHERAPY IS AN ALTERNATIVE TO MEDICATION.
- Shown to be equally effective for all levels of depression, with three exceptions:
o Drugs work better for dysthymia: long-term, lifelong condition of unhappy mood.
o Antidepressants ineffective for sufferers of childhood neglect or abuse.
o Psychotherapy more likely to reduce relapse months or years later.
- Researchers show that people improve most with a combination of drugs and
psychotherapy.

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- 33% to 50% of patients do not respond well to either antidepressants or psychotherapy.

- Antidepressants and psychotherapy have overlapping effects:
o Increase metabolism in same brain areas.
o Changing thoughts change brain chemistry.
OTHER TREATMENTS FOR AFFECTIVE DISORDERS.

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• Sleep deprivation:
- More than 50% of depressed patients improved after one night of sleep deprivation.
- Depression returns with normal sleep pattern.
- Not explained by any current theory.
A night of total sleep deprivation is the quickest method of relieving depression. Benefit is
brief and increases sensitivity to pain.

Depression usually returns again after the next night’s sleep.

- More practical solution: go to sleep earlier so that he patient gets eight hours of sleep.
o Relieves depression for a week, sometimes longer.
- Disruption of sleep patterns is common in depression. Typically fall asleep but awaken
early and are unable to get back to sleep.
- Enter REM sleep within 45 minutes and have an increase average number of eye
movements during REM sleep.
- Lifelong trait of depressed people: Sleep disorders experienced during adolescence
increase the likelihood of depression.
.

• Exercise:
- Helps reduce depression.
- Increases adult hippocampal neurogenesis.
- Findings suggests that depression may be caused by reduced adult hippocampal
neurogenesis.

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2.1.2. Pharmacological treatment.

ANTIDEPRESSANT DRUGS.

• Monoamine oxidase inhibitors.

• Tricyclic antidepressants.
• Selective monoamine reuptake inhibitors.
• Atypical antidepressants.
• NMDA-Receptor antagonists.
• Effectiveness.

As long as NT is in the synapse, it is “active” – activity must somehow be turned off.

• Reuptake: scoop up and recycle NTs.

• Enzymatic degradation: a NT is broken down by enzymes.
DISCOVERY OF ANTIDEPRESSANT DRUGS.
Monoamine oxidase inhibitors (MAOIs) – Iproniazid.

• Prevent breakdown of monoamines.

• Must avoid foods high in tyramine – “cheese effect” → ↑ Tyramine = ↑ NE = ↑ blood
pressure.
• Tyramine is found in small amounts on protein-containing foods.
- Cured meats (dry-type summer sausages, pepperoni, and salami...).
- Fermented cabbage (sauerkraut and kimchee).
- Soy, fish, and shrimp sauces.
- Yeast-extract spreads, such as Marmite.
- Improperly stored foods or spoiled foods.
- Broad bean pods, such as fava beans.
.

Tricyclic antidepressants – Imipramine.

• Block reuptake of serotonin and norepinephrine.

• Safer than MAOIs.

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SELECTIVE MONOAMINE REUPTAKE INHIBITORS.

Selective serotonin-reuptake inhibitors (SSRIs), for example:

• Include Prozac, Paxil, Zoloft, and others.

• No more effective than tricyclics, but side effects are few and they are effective at treating

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other disorders.
Selective norepinephrine-reuptake inhibitors (SNRIs) are also effective.

EFFECTIVENESS OF DRUG ON THE TREATMENT OF AFFECTIVE DISORDERS.

2002 study: results are about the same for MAOIs, tricyclic, and SSRIs; about 50% improve, compared
to 25% of controls.
2008 study: meta-analysis indicated that placebo was about 82% as effective as anti-depressants in
severely depressed individuals. Drugs even less effective for mild to moderately depressed
individuals.

Mood stabilizers.
Lithium:
• Calm guinea pigs?
• Effects on maniac patients.
Anticonvulsants.
Antipsychotics.
All act against mania.
Some act against depression.
Some against both.
They do not eliminate all symptoms.
Severe side effects discourage adherence.

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3. Introduction against anxiety.

3.1. Anxiety disorders.
Anxiety – fear in the absence of threat.

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Anxiety disorder – when anxiety interferes with normal functioning.

• Accompanied by physiological symptoms: tachycardia, hypertension, sleep disturbances,

nausea, etc.
The most prevalent psychiatric disorders:

• Generalised anxiety: extreme feelings of anxiety about many different activities.

• Specific phobias: anxiety about particular objects.
.

• Panic disorders: rapid onset of attacks of extreme fear and severe symptoms of stress.
Clinical characteristics:

Separation anxiety disorder:

A. Developmentally inappropriate and excessive fear or anxiety concerning separation from
those to whom the individual is attached, as evidenced by at least three of the following:
1. Recurrent excessive distress when anticipating or experiencing separation from home
or from major attachment figures.
2. Persistent and excessive worry about losing major attachment figures or about possible
harm to them, such as illness, injury, disasters, or death.
3. Persistent and excessive worry about experiencing an untoward event (e.g.- getÝng
lost, being kidnapped, having an accident, becoming il) that causes separation from a
major attachment figure.
4. Persistent reluctance or refusal to go out, away from home, to school, to work, or
elsewhere because of fear of separation.
5. Persistent and excessive fear of or reluctance about being alone or without major
attachment figures at home or in other setÝngs.
6. Persistent reluctance or refusal to sleep away from home or to go to sleep without
being near a major attachment figure.
7. Repeated nightmares involving the theme of separation.
8. Repeated complaints of physical symptoms (e.g., headaches, stomach-aches, nausea,
vomiting) when separation from major attachment figures occurs or is anticipated.
Selective mutism:
A. Consistent failure to speak in specific social situations in which there is an expectation for
speaking (e.g., at school) despite speaking in other situations.
B. The disturbance interferes with educational or occupational achievement or with social
communication.
C. The duration of the disturbance is at least 1 month (not limited to the first month of school).

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D. The failure to speak is not attributable to a lack of knowledge of, or comfort with, the spoken
language required in the social situation.
E. The disturbance is not better explained by a communication disorder (e.g. childhood-onset
fluency disorder) and does not occur exclusively during the course of autism spectrum
disorder. schizophrenia, or another psychotic disorder.

Specific phobia:
A. Marked fear or anxiety about a specific object or situation (e.g., flying, heights, animals,
receiving an injection, seeing blood).
Note: In children, the fear or anxiety may be expressed by crying, tantrums, freezing, or
clinging.
B. The phobic object or situation almost always provokes immediate fear or anxiety.
.

C. The phobic object or situation is actively avoided or endured with intense fear or anxiety.
D. The fear or anxiety is out of proportion to the actual danger posed by the specific object or
situation and to the sociocultural context.
E. The fear, anxiety, or avoidance is persistent, typically lasting for 6 months of more.
F. The fear, anxiety, or avoidance causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
G. The disturbance is not better explained by the symptoms of another mental disorder,
including fear, anxiety, and avoidance of situations associated with panic-like symptoms or
other incapacitating symptoms (as in agoraphobia), objects or situations related to
obsessions (as in obsessive-compulsive disorder): reminders of traumatic events (as in
posttraumatic stress disorder): separation from home or attachment figures (as in
separation anxiety disorder); or social situations (as in social anxiety disorder).
Social anxiety disorder (social phobia):
A. Marked fear or anxiety about one or more social: situations in which the individual is
exposed to possible scrutiny by others.
Examples include social interactions (e.g., having a conversation, meeting unfamiliar
people), being observed (e.g., eating or drinking), and performing in front of others (e.g.,
giving a speech).
Note: in children, the anxiety must occur in peer setÝngs and not just during interactions
with adults.
B. The individual fears that he or she will act in a way or show anxiety symptoms that will be
negatively evaluated (i.e., will be humiliating or embarrassing: will load to rejection or
offend others).
C. The social situations almost always provoke fear or anxiety.
Note: in children, the fear of anxiety may be expressed by crying. tantrums, freezing,
dinging, shanking, or failing to speak in social situations.
D. The social situations are avoided or endured with intense fear or anxiety.
E. The fear or anxiety is out of proportion to the actual threat posed by the social situation and
to the sociocultural context.
F. The fear, anxiety, or avoidance is persistent, typically lasting for 6 months or more.

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G. The fear, anxiety, or avoidance causes clinically significant ds-tress of impairment in social,
occupational, or other important areas of functioning.
H. The fear, anxiety, or avoidance is not attributable to the physiological effects of a substance
(e.g., a drug of abuse. a medication) or another medical condition.
I. The fear, anxiety, or avoidance is not better explained by tie symptoms of another mental

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disorder, such as panic disorder, body dysmorphic disorder, or autism spectrum disorder.
J. It another medical condition (e.g. Parkinson’s disease, obesity, disfigurement from burns or
injury) is present, the fear, anxiety, or avoidance is clearly unrelated or is excessive.
Panic disorder:
A. Recurrent unexpected panic attacks. A panic attack is an abrupt surge of intense fear or
intense discomfort that reaches a peak within minutes, and during which time four (or
more) of the following symptoms occur:
Note: The abrupt surge can occur from a calm state or an anxious state.
1. Palpitations, pounding heart, or accelerated heart rate.
2. Sweating.
3. Trembling or shaking.
4. Sensations of shortness of breath or smothering.
5. Feelings of choking.
6. Chest pain or discomfort.
7. Nausea or abdominal distress.
8. Feeling dizzy, unsteady, light-headed, or faint.
9. Chilis or heat sensations.
10. Paraesthesia’s (numbness or tingling sensations).
11. Derealization (feelings of unreality) or depersonalization (being detached from
oneself).
12. Fear of losing control or "going crazy".
13. Fear of dying.
Panic attach specifier:
Note: Symptoms are presented for the purpose of identifying a panic attack; however, panic attack is
not a mental disorder and cannot be coded. Panic attacks can occur in the context of any anxiety
disorder as well as other mental disorders (e.g. depressive disorders, post-traumatic stress disorder,
substance use disorders) and some medical conditions (e.g., cardiac, respiratory, vestibular,
gastrointestinal). When the presence of a panic attack is identified, it should be noted as a specifier
(e.g. "posttraumatic stress disorder with panic attacks"). For panic disorder, the presence of panic
attack is contained within the criteria for the disorder and panic attack is not used as a specifier.
A. An abrupt surge of intense fear or intense discomfort that reaches a peak within minutes,
and during which time four (or more) of the following symptoms occur:
.

Note: The abrupt surge can occur from a calm state or an anxious state.
1. Palpitations, pounding heart, or accelerated heart rate.
2. Sweating.
3. Trembling or shaking.

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4. Sensations of shortness of breath or smothering.

5. Feelings of choking.
6. Chest pain or discomfort.
7. Nausea or abdominal distress.
8. Feeling dizzy, unsteady, light-headed, or faint.

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9. Chis or heat sensations.
10. Paraesthesia’s (numbness or tingling sensations).
11. Derealization (feelings of unreality) or depersonalization (being detached from
oneself).
12. Fear of losing control or "going crazy."
13. Fear of dying.
Agoraphobia:
A. Marked fear or anxiety about two (or more) of the following five situations:
1. Using public transportation (e.g., automobiles, buses, trains, ships, planes).
2. Being in open spaces (e.g., parking lots, marketplaces, bridges).
3. Being in enclosed places (e.g., shops, theatres, cinemas).
4. Standing in line or being in a crowd.
5. Being outside of the home alone.
B. The individual fears or avoids these situations because of thoughts that escape might be
difÏcult or help might not be available in the event of developing panic-like symptoms or
other incapacitating or embarrassing symptoms (e.g., fear of falling in the elderly; fear of
incontinence).
C. The agoraphobic situations almost always provoke fear or anxiety.
D. The agoraphobic situations are actively avoided, require the presence of a companion, or
are endured with intense fear or anxiety.
E. The fear or anxiety is out of proportion to the actual danger posed by the agoraphobic
situations and to the sociocultural context.
F. The fear, anxiety, or avoidance is persistent, typically lasting for 6 months or more.
G. The fear, anxiety, or avoidance causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
H. If another medical condition (e.g., inflammatory bowel disease, Parkinson's disease) is
present, the fear, anxiety. or avoidance is clearly excessive.
I. The fear, anxiety, or avoidance is not better explained by the symptoms of another mental
disorder-for example, the symptoms are not confined to specific phobia, situational type:
do not involve only social situations (as in social anxiety disorder); and are not related
exclusively to obsessions (as in obsessive-compulsive disorder), perceived defects or flaws
in physical appearance (as in body dysmorphic disorder), reminders of traumatic events (as
in posttraumatic stress disorder), or fear of separation (as in separation anxiety disorder).

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Generalised anxiety disorder:

A. Excessive anxiety and worry (apprehensive expectation), occurring more days than not for
at least 6 months, about a number of events or activities (such as work or school
performance).
B. The individual finds it difÏcult to control the worry.
C. The anxiety and worry are associated with three (or more) of the following six symptoms
(with at least some symptoms having been present for more days than not for the past 6
months):
Note: Only one item is required in children.
1. Restlessness or feeling keyed up or on edge.
2. Being easily fatigued.
3. DifÏculty concentrating or mind going blank.
4. Irritability.
5. Muscle tension.
6. Sleep disturbance (difÏculty falling or staying asleep, or rest-less, unsatisfying sleep).
D. The anxiety, worry, or physical symptoms cause clinically significant distress or impairment
in social, occupational, or other important areas of functioning.
E. The disturbance is not attributable to the physiological effects of a substance (e.g., a drug of
abuse, a medication) or another medical condition (e.g., hyperthyroidism).
F. The disturbance is not better explained by another mental disorder (e.g., anxiety or worry
about having panic attacks in panic disorder, negative evaluation in social anxiety disorder
(social phobia), contamination or other obsessions in obsessive compulsive disorder,
separation from attachment figures in separation anxiety disorder, reminders of traumatic
events in posttraumatic stress disorder, gaining weight in anorexia nervosa, physical
complaints in somatic symptom disorder, perceived appearance flaws is; body dysmorphic
disorder, having a serious illness in illness anxiety disorder, or the content of delusional
beliefs in schizophrenia or delusional disorder).
Causal factors:
ETHOLOGY OF ANXIETY DISORDERS.
There is good evidence for a genetic contribution. However, no specific genes have been linked to
anxiety disorders.

The role of life experiences is also critical.

Genetic contributions:

• Heritability estimates 30-50%.

• Higher concordance for MZ twins.
• No specific genes linked.

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Neural bases:
Based on analysis of therapeutic drug effects.

• GABAA receptors.
• Serotonin receptors.
•

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Overlapping of involved brain areas (comorbidity of anxiety and depression).
- Hippocampus.
- Amygdala.
- Medial prefrontal cortex.
GABA.

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.
5HT.

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OVERLAPPING AREAS.

Pharmacological treatment:

• Benzodiazepines (GABA agonists). .

- Anxiolytic + hypnotic + anticonvulsants + muscle relaxants.

- Very addictive.
• Serotonin agonists (buspirone).
- Selective agonist of 5-HT1A.
- Not an SSRI.
- More specific than benzodiazepines.
- Side effects: dizziness, nausea, headache, insomnia.
• Antidepressant drugs.
- Consistent with comorbidity depression and anxiety.
- Atypical antipsychotics and anticonvulsants also effective against some anxiety disorders.
ANIMAL MODEL OF ANXIETY.
Assess anxiolytic potential of drugs: assume that defensive behaviours triggered by fear, and that fear
and anxiety are comparable.

• Elevated-plus-maze test: time in open arms indicates less anxiety.

• Defensive-burying test: time burying is measure of anxiety.
• Risk-assessment test: time freezing and assessing risk indicate anxiety level.
Validated by effectiveness of benzodiazepines, but not all anxiety treated with such drugs.

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4. Tourette syndrome.
• A disorder of tics (involuntary movements) or vocalizations.
• Begins in childhood.
• Major genetic component.
• Many also have signs of ADHD and/or OCD.

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• No animal models, no genes identified, imaging difÏcult due to ties.
• Patients tend to have smaller caudate nuclei.
Tic disorders:
Note: A tic is a sudden, rapid, recurrent, nonrhythmic motor movement or vocalization.
Tourette's Disorder:

A. Both multiple motor and one or more vocal tics have been present at some time during the
.

illness, although not necessarily concurrently.

B. The tics may wax and wane in frequency but have persisted for more than 1 year since first tic
onset.
C. Onset is before age 18 years.
D. The disturbance is not attributable to the physiological effects of a substance (e.g., cocaine)
or another medical condition (e.g., Huntington's disease, post viral encephalitis).
HERITABILITY OF TOURETTE’S SYNDROME.
Concordance:

• 50% for MZ.

• 10% for DZ.
Neural bases:

• Brain areas.
- Caudate nucleus.
- Prefrontal cortex.
• Neurotransmitters.
- Dopamine.
- GABA.
• Lack of postmortem studies.

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Treatment:

• Education: concentration + effort.

• Comorbidities.
• ADHD.
• OCD.

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• Both. .

• Neuroleptics used but not clearly effective.

• Antipsychotics. D2 blockers.

• Support abnormalities in Basal Ganglia-Thalamus-Cortex feedback circuit.

TETRABENAZINE.
Blocks dopamine accumulation in presynaptic storage vesicles.

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5. Obsessive-compulsive disorder.
“OCD is characterized by the presence of obsessions and / or compulsions, Obsessions are recurrent
and persistent thoughts, urges, or images that are experienced as intrusive and unwanted, whereas
compulsions are repetitive behaviours or mental acts that an individual feels driven to perform in
response to an obsession or according to rules that must be applied rigidly. Some other obsessive-
compulsive and related disorders are also characterized by preoccupations and by repetitive
behaviours or mental acts in response to the preoccupations. Other obsessive-compulsive and related
disorders are characterized primarily by recurrent body-focused repetitive behaviours (e.g., hair
pulling, skin picking) and repeated attempts to decrease or stop the behaviours.”

Obsessive-compulsive disorder:
A. Presence of obsessions, compulsions, or both:
Obsessions are defined by (1) and (2):
1. Recurrent and persistent thoughts, urges, or images that are experienced, at some time
during the disturbance, as intrusive and unwanted, and that in most individuals cause
marked anxiety or distress.
2. The individual attempts to ignore or suppress such thoughts, urges, or images, or to
neutralize them with some other thought or action (Le., by performing a compulsion).
Compulsions are defined by (1) and (2):
1. Repetitive behaviours (e.g., hand washing, ordering, checking) or mental acts (e.g.,
.

praying, counting, repeating words silently) that the individual feels driven to perform
in response to an obsession or according to rules that must be applied rigidly.
2. The behaviours or mental acts are aimed at preventing or reducing anxiety or cis-tress,
or preventing some dreaded event or situation; however, these behaviours of mental
acts are not connected in a realistic way with what they are designed to neutralize or
prevent or are clearly excessive.
Note: Young children may not be able to articulate the aims of these behaviours or mental
acts.

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B. The obsessions or compulsions are time-consuming (e.g., take more than 1 hour per day) or
cause clinically significant distress or impairment in social, occupational, or other important
areas of functioning.
C. The obsessive-compulsive symptoms are not attributable to the physiological effects of a
substance (e.g., a drug of abuse, a medication) or another medical condition.

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D. The disturbance is not better explained by the symptoms of another mental disorder (e.g.,
excessive worries, as in generalized anxiety disorder, preoccupation with appearance, as in
body dysmorphic disorder: difÏculty discarding or parting with possessions, as in hoarding
disorder, hair pulling, as in trichotillomania (hair-pulling disorder): skin picking. as in
excoriation [skin-picking] disorder: stereotypies, as in stereotypic movement disorder,
ritualized eating behaviour, as in eating disorders; preoccupation with substances or
gambling. as in substance-related and addictive disorders; preoccupation with having an
illness, as in illness anxiety disorder, sexual urges or fantasies, as in paraphilic disorders;
impulses, as in disruptive, impulse-control, and conduct dis-orders: guilty ruminations, as in
major depressive disorder, thought insertion or delusional preoccupations, as in
schizophrenia spectrum and other psychotic disorders; or repetitive patterns of behaviour,
as in autism spectrum disorder).
Neural bases:

• Brain areas.
- Basal Ganglia.
- Prefrontal cortex.
• Neurotransmitters.
- Dopamine.
- Serotonin (Base in pharmacology: clomipramine, ISRS).
- Combination.

Treatment:

• Clomipramine – TRYCICLIC ANTIDEPRESSANT.

• ISRS/SNRIs – not like in depression, more time.

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CLOMIPRAMINE TABLETS.

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6. Post-traumatic stress disorder.
• Panic Attack.
- Initial real threat.
- Un-adaptative association.
- Thousand-yard stare.
Posttraumatic stress disorder:
Note: The following criteria apply to adults, adolescents, and children older than 5 years.
For children 6 years and younger, see corresponding criteria below.
A. Exposure to actual or threatened death, serious injury, or sexual evidence in one (or more)
of the following ways:
.

1. Directly experiencing the traumatic evert/s).

2. Witnessing, in person, the event(s) as it occurred to others.
3. Learning that the traumatic events) occurred to a close family member or close friend. In
cases of actual or threatened death of a family member or friend, the events) must have
been violent or accidental.
4. Experiencing repeated or extreme exposure to aversive details of the traumatic events)
(e.g., first responders collecting human remains; police ofÏcers repeatedly exposed to
details of child abuse).
Note: Criterion A4 does not apply to exposure through electronic media, television, movies,
or pictures, unless this exposure is work related.
B. Presence of one (or more) of the following intrusion symptoms associated with the
traumatic events), beginning after the traumatic events) occurred:
1. Recurrent, involuntary, and intrusive distressing memories of the traumatic event(s).
Note: In children older than 6 years, repetitive play may occur in which themes or aspects
of the traumatic events) are expressed.
2. Recurrent distressing dreams in which the content and/or effect of the dream are related
to the traumatic event(s).
Note: In children, there may be frightening dreams without recognizable content.

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3. Dissociative reactions (e.g., flashbacks) in which the individual feels or acts as the
traumatic event(s) were recurring (Such reactions may occur on a continuum, with the
most extreme expression being a complete loss of awareness of present surroundings.)
Note: In children, trauma-specific reenactment may occur in play.
4. Intense or prolonged psychological distress at exposure to internal or external cues that
symbolize or resemble an aspect of the traumatic events).
5. Marked physiological reactions to internal or external cues that symbolize or resemble an
aspect of the traumatic events).
C. Persistent avoidance of stimuli associated with the traumatic event(s), beginning after the
traumatic events) occurred, as evidenced by one or both of the following:
1. Avoidance of or efforts to avoid distressing memories, thoughts, or feelings about or closely
associated with the traumatic event(s).
2. Avoidance of or efforts to avoid external reminders (people, places, conversations,
activities, objects, situations) that arouse distressing memories, thoughts, or feelings
about or closely associated with the traumatic event(s).
D. Negative alterations in cognitions and mood associated with the traumatic event(s),
beginning, or worsening after the traumatic event(s) occurred, as evidenced by two (or
more) of the following:
1. Inability to remember an important aspect of the traumatic event(s) (typically due to
dissociative amnesia and not to other factors such as head injury, alcohol, or drugs).
2. Persistent and exaggerated negative beliefs or expectations about oneself, others. or the
world (e.g., 1 am bad," "No one can be trusted," "The world is completely dangerous." My
whole nervous system is permanently ruined).
3. Persistent, distorted cognitions about the cause of consequences of the traumatic event(s)
tut lead the individual to blame himself/herself or others.
4. Persistent negative emotional state (e.g., fear, horror, anger, guilt, or shame).
5. Markedly diminished interest or participation in significant activities.
6. Feelings of detachment or estrangement from others.
7. Persistent inability to experience positive emotions (e.g. inability to experience happiness,
substation, or loving feelings).
E. Marked alterations in arousal and reactivity associated with the traumatic event(s),
beginning, or worsening after the traumatic event/s) occurred, as evidenced by two for
more) of the following:
1. Irritable behaviour and angry outbursts (with little [Link] provocation) typically expressed
as verbal or physical aggression toward people or objects.
2. Reckless or sell-destructive behaviour.
3. Hypervigilance.
4. Exaggerated startle response.
5. Problems with concentration.
6. Sleep disbalance (e.g., difÏculty falling or staying asleep or restless sleep).

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F. Duration of the disturbance (Criteria B, C, D, and E) is more than 1 month.

G. The disturbance causes clinically significant distress or impairment in social, occupational,
or other important areas of functioning.
H. The disturbance is not attributable to the physiological effects of a substance (e.g.,
medication, alcohol) or another medical condition.

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Neural bases:

• Brain areas.
- Hippocampus (less size).
- Amygdala.
• Neurotransmitters.
- Noradrenergic hyperactivation.

Treatment:

• Benzodiazepines? – Alcohol and drugs!

• Noradrenergic antagonist.

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