WEEK 1: NOTHING AS PRACTICAL AS A GOOD THEORY
A COGNITIVE APPROACH TO PANIC – CLARK
Panic anxiety is qualitatively different from non-panic anxiety; it responds to imipramine, which blocks the
reuptake of serotonin.
Panic attack: an intense feeling of apprehension or impending doom, suddenly onset and associated with a
range of distressing physical sensations; breathlessness, chest pain, choking, dizziness, tingling hands and feet,
etc. Panic attacks occur in both phobic and non-phobic anxiety disorders. The attacks can occur in feared or
safe situations and can be identifiable or out of the blue.
In patients, panic attacks can be provoked by a wide range of pharmacological and physiological agents, often
with a history of panic (but not always). Why are these agents panic-inducing? Possible explanations:
Certain biochemical changes have a direct panic-inducing effect, so individuals who are vulnerable to
the agents have a biochemical disorder.
The agents do not have a direct panic-inducing effect, but only provoke panic if the bodily sensations
are interpreted in a particular fashion: cognitive theory of panic.
So, this theory proposes that panic attacks result from catastrophic misinterpretations of certain bodily
sensations. Individuals perceive these sensations as much more dangerous than they really are, which ends in a
vicious circle that culminates in a panic attack. Agents that provoke the sensations can be external (e.g. a
feared situation) or internal (e.g. breathlessness).
Two types of panic attacks within individuals with an anxiety history:
1. Heightened anxiety with the anticipation of an attack, e.g. in a feared situation.
2. No anticipation, but sudden anxiety as a result of e.g. a certain topic that is being discussed.
Occasionally, panic attacks are triggered by sensations which aren’t even a part of an anxiety response, such as
blurred sight. Patients perceive them as dangerous, then further reinforce their belief and start to panic.
In some patients, the panic-triggering sensations and their interpretations remain constant over time. In others,
both the sensations and interpretations can change over time. This depends on e.g. what illnesses they have
information about.
Research on panic attacks shows that the following statements fit the cognitive theory model:
Patients who suffer from panic attacks are dominated by thoughts which relate to the catastrophic
interpretation of bodily sensations.
A bodily sensation is one of the first things which individuals notice during an attack.
Hyperventilation plays an important role in the production of panic attacks.
Lactate can have panic-inducing effects because of the bodily sensations.
CBT can help patients think of alternative non-catastrophic interpretations to prevent a panic attack.
Drugs can help reduce certain bodily sensations, which can prevent panic attacks. However, stopping
the drug treatment can end up in misinterpretation of the sensations and thus panic attacks again.
Biological factors also increase an individual's vulnerability, in three ways:
1. A change in bodily processes leads to changes in bodily sensations.
2. Deficiencies in auto receptors can lead to higher noradrenaline in patients, so they perceive
more threat.
3. Varying levels of pCO2 as a result of the menstrual cycle can lead to hyperventilation.
EMDR: EYE MOVEMENTS SUPERIOR TO BEEPS IN TAXING WORKING MEMORY AND REDUCING VIVIDNESS OF
RECOLLECTIONS – VAN DEN HOUT
EMDR: eye movement desensitization and reprocessing; often used for PTSD patients to reduce vividness and
emotionality of negative (future) memories. Some therapists use beeps as well, but their effect is inferior to the
effect of eye movements. Also, EMDR seems equally effective as CBT on treating PTSD.
,Since working memory (WM) resources are limited, a secondary task makes recalling harder and makes
memories less vivid and emotional. In case of EMDR, this secondary task is eye movement. Memories are not
only blurred during the eye movements, but also during recollections directly after the eye movements.
Alternative secondary tasks can be effective as well, such as counting or drawing a complex figure. Simple tasks
like finger tapping does not have beneficial effects, since it is hardly taxing.
Three subsystems within WM:
1. Central executive: divides attention between tasks, selects retrieval strategies, activates memories and
inhibits distractions.
2. Visuospatial sketchpad: processes visuospatial information.
3. Phonological loop: processes verbal information.
Eye movements should affect the VSSP and verbal tasks should load the PL. Also, tasks in general load the CE as
well. However, it is not sure to what extent every component is loaded by certain tasks.
Research shows that eye movements affect memory by taxing the CE during recall. Binaural stimulation
(hearing two frequencies at once) seems to tax the CE to a certain degree. In reducing vividness of memories,
binaural stimulation has less of an effect (1/3) compared to eye movements.
PSYCHIATRIC SYMPTOMS AS PATHOGENS – VAN DEN HOUT
Disorders are typically seen as the causes of their symptoms, which is not true (in case of psychopathology). A
symptom should not be seen as ‘output’, but as ‘input’ that causally contributes to other symptoms. So a
psychosis does not lead to hallucinations, but the occurrence of hallucinations may predict a psychosis.
Explanandum: the phenomenon to be explained. Explanans: the explanation itself. These two terms should be
defined independently (e.g. ‘She is depressed, because she is sad all the time’ is a tautology and thus wrong!).
All disorders are defined entirely by symptoms. There is no other way to establish a disorder than to assess
symptoms. The presence of a psychiatric disorder in the absence of symptoms is logically impossible.
Thus far, specific biological markers that predict psychopathology have not been found. There are no genes or
combinations of genes that lead to e.g. a brain tumor. However, who knows what insights may be found in the
future.
Comorbidity rates are high; half of individuals who meet diagnostic criteria for one disorder, meet the criteria
for a second disorder as well. Why do disorders co-occur so often, when they have distinct profiles? One might
argue, looking for any specific disorder is misguided. Perhaps we should concentrate on symptoms and forget
about their clusters in the DSM.
Network theory: symptoms causally contribute to other symptoms. So, in stead of explaining depression in
terms of sadness, we could argue: stressor -> depressed mood -> insomnia -> fatigue -> concentration
problems. Network theory can also be used to explain these disorders:
Panic disorder: 1) bodily sensations and 2) intense fears reinforce each other and lead to panic attacks.
OCD: the general fear of being guilty for having acted in an irresponsible way is an explanans of the
heterogenous symptoms of OCD: 1) involuntary thoughts and 2) exaggerated uncertainty.
Psychopathology states: And network theory states:
1. Symptoms are clustered reasonably consistent … since a specific symptom (e.g. sleeplessness) is more
likely to induce fatigue than agoraphobia.
2. Co-morbidity is widespread … and can be explained by bridge symptoms:
overlapping complaints that fuel other symptoms of
two or more disorders.
3. Underlying biological markers have not been … so their existence does not have to be assumed in
found yet. the future.
The idea that psychopathological symptoms are not caused by a disorder, but are the disorder, was formulated
by Eysenck: one of the founding fathers of CBT. So, if you take away the symptoms, you cured neurosis.
, To explain the occurrence of OCD, Van dan Hout states that familiarity leads to uncertainty: the perseveration-
uncertainty effect. The more familiar you are to e.g. a gas stove, the easier you will miss out on details and the
more you will check if the gas is actually turned off. This may lead to compulsions.
Network theory’s contributions to experimental psychopathology are:
Giving a solid concept for symptom -> symptom processes.
Powerful empirical clues about what symptom -> symptom associations are central.
Experimental psychopathology’s contributions to network theory are:
It researches causality between symptoms and delivers insightful data for the network theory.
It researches certain symptom -> symptom associations that need more than common sense to be
understood.
It enriches and refines the DSM, which the network theory can use to derive its associations from.
WEEK 2: ASSOCIATIVE LEARNING
CLASSICAL CONDITIONING AND THE ACQUISITION OF HUMAN FEARS AND PHOBIAS – DAVEY
Although classical conditioning has a negative history in the press, it has now been recognized as a fundamental
learning process. Contemporary models are able to specify the conditions under which associative learning is
likely to occur. Also, the models include the non-associative processes that modulate the strength of a
conditioned response, so that theorists can explain complex phenomena of fears and phobias.
Most traditional conditioning theories are based on processes found in animals. Classical conditioning is
mediated by CS-US associations in both humans and animals. However, there are some important dynamic and
procedural differences between conditioning in humans and animals.
Animals base their associations on situational information and on prior expectations (resulting only from prior
conditioning experiences). However, humans also have prior beliefs. So, some circumstances with a
combination of situational information and prior beliefs can lead to covariation bias: people’s tendency to
overestimate the association between a fear stimuli and negative outcomes. The same bias can occur in
animals, but purely based on expectancies from prior experiences (not on beliefs).
Another difference is that humans are more ‘prepared’ to associate certain stimuli with fear and trauma, such
as spiders and snakes. Humans are much more sophisticated in forming expectancies, since they have more
sources to get information from than animals. So, prior expectancies can influence the strength of conditioning
in humans, presumably by generating a covariation bias that influences the CS-US relationship.
Interesting phenomena in classical conditioning
Latent inhibition: it is much more difficult to condition an association between CS and US if the CS is already
presented alone a couple of times prior to the conditioning. So, if a US is already predicted by CS 1, the
exposure with both CS 1 and CS 2 results in little or no learning about the new component CS 2: blocking. So,
latent inhibition and blocking are examples of CS-US pairings failing to generate a conditioned response.
Sensory preconditioning: two completely unrelated neutral stimuli are presented to a subject together, e.g. a
buzz (CS1) and a light (CS2). This pairing will not evoke much of a response. However, if the buzz alone is
presented with food (US), it results in a conditioned response. Then, if only the light is presented without the
US, it results in the same conditioned response, since the subject already made the association between the
buzz and the light before.
Higher-order conditioning: one neutral stimulus is presented, e.g. a buzz, followed by an US, e.g. food. The buzz
forms a CR from being paired with a food. Then, another neutral stimulus, e.g. a light, is paired with the buzz.
As a result, the light becomes the CS that produces the CR. So, in sensory preconditioning you start with pairing
the two neutral stimuli together and in higher-order conditioning you end with pairing the two together.
Criticisms on classical conditioning
There are some criticisms on the classical conditioning model in case of phobias, such as:
A COGNITIVE APPROACH TO PANIC – CLARK
Panic anxiety is qualitatively different from non-panic anxiety; it responds to imipramine, which blocks the
reuptake of serotonin.
Panic attack: an intense feeling of apprehension or impending doom, suddenly onset and associated with a
range of distressing physical sensations; breathlessness, chest pain, choking, dizziness, tingling hands and feet,
etc. Panic attacks occur in both phobic and non-phobic anxiety disorders. The attacks can occur in feared or
safe situations and can be identifiable or out of the blue.
In patients, panic attacks can be provoked by a wide range of pharmacological and physiological agents, often
with a history of panic (but not always). Why are these agents panic-inducing? Possible explanations:
Certain biochemical changes have a direct panic-inducing effect, so individuals who are vulnerable to
the agents have a biochemical disorder.
The agents do not have a direct panic-inducing effect, but only provoke panic if the bodily sensations
are interpreted in a particular fashion: cognitive theory of panic.
So, this theory proposes that panic attacks result from catastrophic misinterpretations of certain bodily
sensations. Individuals perceive these sensations as much more dangerous than they really are, which ends in a
vicious circle that culminates in a panic attack. Agents that provoke the sensations can be external (e.g. a
feared situation) or internal (e.g. breathlessness).
Two types of panic attacks within individuals with an anxiety history:
1. Heightened anxiety with the anticipation of an attack, e.g. in a feared situation.
2. No anticipation, but sudden anxiety as a result of e.g. a certain topic that is being discussed.
Occasionally, panic attacks are triggered by sensations which aren’t even a part of an anxiety response, such as
blurred sight. Patients perceive them as dangerous, then further reinforce their belief and start to panic.
In some patients, the panic-triggering sensations and their interpretations remain constant over time. In others,
both the sensations and interpretations can change over time. This depends on e.g. what illnesses they have
information about.
Research on panic attacks shows that the following statements fit the cognitive theory model:
Patients who suffer from panic attacks are dominated by thoughts which relate to the catastrophic
interpretation of bodily sensations.
A bodily sensation is one of the first things which individuals notice during an attack.
Hyperventilation plays an important role in the production of panic attacks.
Lactate can have panic-inducing effects because of the bodily sensations.
CBT can help patients think of alternative non-catastrophic interpretations to prevent a panic attack.
Drugs can help reduce certain bodily sensations, which can prevent panic attacks. However, stopping
the drug treatment can end up in misinterpretation of the sensations and thus panic attacks again.
Biological factors also increase an individual's vulnerability, in three ways:
1. A change in bodily processes leads to changes in bodily sensations.
2. Deficiencies in auto receptors can lead to higher noradrenaline in patients, so they perceive
more threat.
3. Varying levels of pCO2 as a result of the menstrual cycle can lead to hyperventilation.
EMDR: EYE MOVEMENTS SUPERIOR TO BEEPS IN TAXING WORKING MEMORY AND REDUCING VIVIDNESS OF
RECOLLECTIONS – VAN DEN HOUT
EMDR: eye movement desensitization and reprocessing; often used for PTSD patients to reduce vividness and
emotionality of negative (future) memories. Some therapists use beeps as well, but their effect is inferior to the
effect of eye movements. Also, EMDR seems equally effective as CBT on treating PTSD.
,Since working memory (WM) resources are limited, a secondary task makes recalling harder and makes
memories less vivid and emotional. In case of EMDR, this secondary task is eye movement. Memories are not
only blurred during the eye movements, but also during recollections directly after the eye movements.
Alternative secondary tasks can be effective as well, such as counting or drawing a complex figure. Simple tasks
like finger tapping does not have beneficial effects, since it is hardly taxing.
Three subsystems within WM:
1. Central executive: divides attention between tasks, selects retrieval strategies, activates memories and
inhibits distractions.
2. Visuospatial sketchpad: processes visuospatial information.
3. Phonological loop: processes verbal information.
Eye movements should affect the VSSP and verbal tasks should load the PL. Also, tasks in general load the CE as
well. However, it is not sure to what extent every component is loaded by certain tasks.
Research shows that eye movements affect memory by taxing the CE during recall. Binaural stimulation
(hearing two frequencies at once) seems to tax the CE to a certain degree. In reducing vividness of memories,
binaural stimulation has less of an effect (1/3) compared to eye movements.
PSYCHIATRIC SYMPTOMS AS PATHOGENS – VAN DEN HOUT
Disorders are typically seen as the causes of their symptoms, which is not true (in case of psychopathology). A
symptom should not be seen as ‘output’, but as ‘input’ that causally contributes to other symptoms. So a
psychosis does not lead to hallucinations, but the occurrence of hallucinations may predict a psychosis.
Explanandum: the phenomenon to be explained. Explanans: the explanation itself. These two terms should be
defined independently (e.g. ‘She is depressed, because she is sad all the time’ is a tautology and thus wrong!).
All disorders are defined entirely by symptoms. There is no other way to establish a disorder than to assess
symptoms. The presence of a psychiatric disorder in the absence of symptoms is logically impossible.
Thus far, specific biological markers that predict psychopathology have not been found. There are no genes or
combinations of genes that lead to e.g. a brain tumor. However, who knows what insights may be found in the
future.
Comorbidity rates are high; half of individuals who meet diagnostic criteria for one disorder, meet the criteria
for a second disorder as well. Why do disorders co-occur so often, when they have distinct profiles? One might
argue, looking for any specific disorder is misguided. Perhaps we should concentrate on symptoms and forget
about their clusters in the DSM.
Network theory: symptoms causally contribute to other symptoms. So, in stead of explaining depression in
terms of sadness, we could argue: stressor -> depressed mood -> insomnia -> fatigue -> concentration
problems. Network theory can also be used to explain these disorders:
Panic disorder: 1) bodily sensations and 2) intense fears reinforce each other and lead to panic attacks.
OCD: the general fear of being guilty for having acted in an irresponsible way is an explanans of the
heterogenous symptoms of OCD: 1) involuntary thoughts and 2) exaggerated uncertainty.
Psychopathology states: And network theory states:
1. Symptoms are clustered reasonably consistent … since a specific symptom (e.g. sleeplessness) is more
likely to induce fatigue than agoraphobia.
2. Co-morbidity is widespread … and can be explained by bridge symptoms:
overlapping complaints that fuel other symptoms of
two or more disorders.
3. Underlying biological markers have not been … so their existence does not have to be assumed in
found yet. the future.
The idea that psychopathological symptoms are not caused by a disorder, but are the disorder, was formulated
by Eysenck: one of the founding fathers of CBT. So, if you take away the symptoms, you cured neurosis.
, To explain the occurrence of OCD, Van dan Hout states that familiarity leads to uncertainty: the perseveration-
uncertainty effect. The more familiar you are to e.g. a gas stove, the easier you will miss out on details and the
more you will check if the gas is actually turned off. This may lead to compulsions.
Network theory’s contributions to experimental psychopathology are:
Giving a solid concept for symptom -> symptom processes.
Powerful empirical clues about what symptom -> symptom associations are central.
Experimental psychopathology’s contributions to network theory are:
It researches causality between symptoms and delivers insightful data for the network theory.
It researches certain symptom -> symptom associations that need more than common sense to be
understood.
It enriches and refines the DSM, which the network theory can use to derive its associations from.
WEEK 2: ASSOCIATIVE LEARNING
CLASSICAL CONDITIONING AND THE ACQUISITION OF HUMAN FEARS AND PHOBIAS – DAVEY
Although classical conditioning has a negative history in the press, it has now been recognized as a fundamental
learning process. Contemporary models are able to specify the conditions under which associative learning is
likely to occur. Also, the models include the non-associative processes that modulate the strength of a
conditioned response, so that theorists can explain complex phenomena of fears and phobias.
Most traditional conditioning theories are based on processes found in animals. Classical conditioning is
mediated by CS-US associations in both humans and animals. However, there are some important dynamic and
procedural differences between conditioning in humans and animals.
Animals base their associations on situational information and on prior expectations (resulting only from prior
conditioning experiences). However, humans also have prior beliefs. So, some circumstances with a
combination of situational information and prior beliefs can lead to covariation bias: people’s tendency to
overestimate the association between a fear stimuli and negative outcomes. The same bias can occur in
animals, but purely based on expectancies from prior experiences (not on beliefs).
Another difference is that humans are more ‘prepared’ to associate certain stimuli with fear and trauma, such
as spiders and snakes. Humans are much more sophisticated in forming expectancies, since they have more
sources to get information from than animals. So, prior expectancies can influence the strength of conditioning
in humans, presumably by generating a covariation bias that influences the CS-US relationship.
Interesting phenomena in classical conditioning
Latent inhibition: it is much more difficult to condition an association between CS and US if the CS is already
presented alone a couple of times prior to the conditioning. So, if a US is already predicted by CS 1, the
exposure with both CS 1 and CS 2 results in little or no learning about the new component CS 2: blocking. So,
latent inhibition and blocking are examples of CS-US pairings failing to generate a conditioned response.
Sensory preconditioning: two completely unrelated neutral stimuli are presented to a subject together, e.g. a
buzz (CS1) and a light (CS2). This pairing will not evoke much of a response. However, if the buzz alone is
presented with food (US), it results in a conditioned response. Then, if only the light is presented without the
US, it results in the same conditioned response, since the subject already made the association between the
buzz and the light before.
Higher-order conditioning: one neutral stimulus is presented, e.g. a buzz, followed by an US, e.g. food. The buzz
forms a CR from being paired with a food. Then, another neutral stimulus, e.g. a light, is paired with the buzz.
As a result, the light becomes the CS that produces the CR. So, in sensory preconditioning you start with pairing
the two neutral stimuli together and in higher-order conditioning you end with pairing the two together.
Criticisms on classical conditioning
There are some criticisms on the classical conditioning model in case of phobias, such as:
