PS365 WLU Test 3 Emotion + Mood and Psychotic Disorders (not everything is on it!)

Ekman Faces

Created by Paul Ekman. The six core emotions: Anger, Happiness, Sadness, Fear, Disgust

Facial Action Coding System (FACS): To systematically study these expressions, Ekman and his colleague Wallace Friesen developed the Facial Action Coding System. This system provides a way to describe and code every observable facial muscle movement.

What is an Emotion?

- "I have a gut feeling I know what emotions are"

- "I know in my heart this is what an emotion is"

Damasio - separating reason from emotion is a fallacy

Somatic marker hypothesis: our emotions guide decision-making.

Somatic markers (e.g., rapid heart beat) are processed in the ventromedial prefrontal cortex (VMPFC) and the amygdala

- Visceral feelings often accompany emotions

- Automatic? Perhaps but not entirely devoid of conscious control.

James-Lange theory!

Every emotion is associated with a physical response to a stimulus

- So are emotions just a form of conditioned response?

- Quadriplegics experience emotion in the absence of visceral sensations

Cannon-Bard theory

- Emotions are perceived when the thalamus transfers information to skeletal muscles, autonomic nervous system AND the neocortex

- Some form of cognitive evaluation is required - not just stimulus-response pairing

Emotion and Survival

- The brain has evolved around reward-and-punishment systems (feelings) designed to maximize survival.

- A form of conditioning

Network involving orbitofrontal cortex and the limbic system

- Linking cognition with visceral feelings

Damasio - heart rate and gut feelings (somatic sensations, interoception) linked to cognitive evaluations - somatic marker hypothesis

James-Lange Theory Example

Stimulus (Growling dog) > Physiological Arousal (Increased heart rate) > Emotion (fear)

Cannon-Bard Theory

👉 When you experience a stimulus, your emotion and your physiological reaction happen at the SAME time, not one after the other.

1. Stimulus → The Growling Dog

The picture of the growling dog represents a threatening stimulus.

Your brain notices the danger.

2. The Thalamus (the grey brain area)

The thalamus is shown because, according to Cannon-Bard, it quickly sends signals in two directions at once:

- One signal to the amygdala / emotional centers → producing fear

- Another signal to the body (autonomic system) → producing physiological arousal (like increased heart rate)

This is why you see two arrows coming from the brain: one going up to the fear expression, and one going down to the heart.

3. Emotion and Physiological Arousal Happen Simultaneously

- Emotion (Fear) → the yellow scared face

- Physiological Arousal → the heart beating faster

Both happen at the same time, not one after the other.

Context Dependency of Emotion

- Schacter & Singer (1962) induced physiological arousal chemically

- Modified context (rude vs. pleasant experimenter)

- Different emotions reported depending on context

Physiological Signatures

- Physiological signatures for specific emotions (slideshow image)

Fear and Emotional Learning: Amygdala

- Destruction of the central nucleus of the amygdala eliminates all emotional conditioning

Three stages of emotion?

- Sensory Processing

Your brain receives incoming information from the environment and begins interpreting what the stimulus is.

- Low Road (Subcortical)

A fast, automatic emotional pathway where the thalamus sends signals straight to the amygdala, triggering quick reactions before conscious thinking.

- High Road (Cortical)

A slower, more deliberate pathway where the thalamus sends the stimulus to the cortex for detailed analysis before producing an emotional response.

Purpose of Emotion - Four functions of emotions:

- Immediate responses to stimuli (fight or flight)

- Influencing social behaviours (response to others)

- Communication of intent (giving someone the eye!)

- Subjective feelings (internal milieu)

Cortical Involvement in Emotion

- Perception of emotion (interpretation)

- Expression of emotion (facial, tonal)

- Experience of emotion (subjective)

Perception of Emotion

- Right hemisphere dominance for perceiving emotional expressions

- Emotion perception of facial expressions not affected by prosopagnosia

- Amygdala involved in eye perception, fearful faces

Expression of Emotion

- Right hemisphere dominance for emotional expressions

- Left side of the face perceived as more emotionally expressive

Negative emotions judged asymmetrically

Positive emotions judged symmetrically

- Most emotional expression cannot be faked unless the expresser is generating the emotion within themselves (e.g., method acting)

- A real smile involves Duchenne's

muscle, the lateral orbicularis oculi

(near the eye)

- Real and fake expression have

different neural mechanisms

Prosody - tone of voice

Affective prosody - emotional tone

"My mother-in-law is coming for dinner."

Propositional prosody - conveys semantic information

"What's that in the road ahead?"

"What's that in the road, a head?"

Experience of Emotion

Emotional valence and arousal

- Right hemisphere specialized for negative affect

Right hemisphere damage - euphoric indifference (inappropriate cheerfulness)

- Left hemisphere for positive affect

Left hemisphere damage - catastrophic reaction (emotional lability?)

Depression

Defining Symptoms:

- Chronic sadness

- Hopelessness

- Anhedonia

Common Symptoms:

- Changes in appetite

- Insomnia

- Lethargy

- Cognitive deficits

- Low self-esteem

- Suicidal thoughts

Depression in the Brain

- dlPFC hypoarousal

- ACC disconnected from dlPFC

- Subgenual cingulate cortex hyperactivation

- Hemispheric asymmetries

- Amygdala activation lasts longer

- Ventral striatum hypoarousal

- Hippocampus less active when encoding positive stimuli

Anxiety

Anxiety includes:

- Phobias

- General Anxiety Disorder

- Obsessive-Compulsive Disorder

- Post-Traumatic Stress Disorder

Two key dimensions of anxiety:

- Anxious apprehension (worrying)

- Anxious arousal (panic)

Anxiety in the Brain

Amygdala involvement in anxiety:

- Heightened response to individual triggers

- Hypersensitive to generally threatening stimuli

- Hippocampus smaller in PTSD patients

- vmPFC hyperactive for negative stimuli

- ACC overactive at rest and during threat

- Anxious apprehension associated with left frontal region

- Anxious arousal associated with posterior right hemisphere

Mood and Psychotic Disorders: Depression. Historical definitions of abnormality

Throughout history, whether a person's behavior is labeled abnormal often has depended on the cultural norms for appropriate behavior and the gender and ethnicity of the person.

Current definitions of abnormality focus on the person's ability to function in daily life and his or her level of distress and grasp of reality..

Since I will be talking in depth about how we diagnose and treat mental health disorders currently, I think its critical to briefly go over some of historical approaches taken to diagnose and treat for the mentally ill.

1. 18th century - Various behaviour patterns and mental states (delusions or hallucinations) were attributed supernatural causes - this resulted in so called "treatment", such as trepanning, exorcisms..

2.Then came the idea of the mind as an expression of brain activity, this approach to conceptualizing mental illnesses is reflected in the work of Franz Joseph Gall (later came to be known as phrenology) - basic tenets of Gall's system were: brain is the organ of the mind, and the brain is composed of separate innate faculties and the more we use a certain part of our brain, it grows in size... and as the skull takes its shape from the brain, the surface of the skull can be read as an accurate index of one's psychological aptitudes and tendencies.

Then we move into the era of mental asylums where there was an emphasis on reasoning over emotionality as the mark of socially acceptable way of behaving and thinking. Those who were seen to behave in ways that contracted with social norms were placed in mental asylums. A consequence of understanding mental health illnesses from biological point of view resulted in interventions such as, ECT (electroconvulsive therapy), frontal lobotomies, insulin coma therapy, bloodletting were used as treatment.

how we view mental illness impact treated

Patient Studies & Psychotherapy

3) Steps towards a biological understanding of abnormality

Patient studies that further revealed the important role of the brain in contributing to behaviour - Paul Broca (lesion in the inferior frontal lobe cause deficit to speech)

Cark Wenicke (lesion in the left temporal cortex causing a deficit to understanding speech)

4) 1890s - Psychotherapy began with the practice of psychoanalysis by Sigmund Freud, then later in the 1920s behaviorism became the dominant way of understanding and shaping human behavior - prominent influencer: skinner and Watson (classical and operant conditioning) - starting around the 1950s. Major influencers like Carl Rogers and then later Aaron Beck developed person-centered cognitive therapies that aimed to challenge a person's distorted thinking patterns through the development of a supportive and empathetic therapeutic relationship.

Research gained momentum

First, paper and pen neuropsychological test measures were used to identify the brain basis of abnormal behaviour, and then later the advent of imaging allowed us observe "brain in action", and then the introduction of antidepressants further highlighted the role of chemical imbalances in the brain as the root cause of abnormality.

All these later approaches heavily emphasize the biological underpinning of mental health disorders, and this view was then reflected in the treatment approaches taken by clinicians.

The introduction of Drugs to Psychiatry - Diagnostic Approach: In the 1980's, mainstream American psychiatry shifted its focus to a biomedical view of mental health, from a psychosocial one

Psychiatry as a medical discipline began in Western Europe and in North America. At that time, two approaches to the practice of psychiatry was present. The first was the German-British one that saw mental illness as mainly genetic diseases, and an American one that was influenced by psychoanalytic thinking where psychological understanding of disorders of the mind was emphasized. In the 1980s, mainstream American psychiatry underwent a shift, moving away from its psychoanalytic influences to a biomedical focused one due to several political reasons, increased government involvement in mental health research and policy making, pressure from insurance companies and medical professionals from other fields to demonstrate the scientific legitimacy of psychiatric practices and the marketing of various drugs as "anti-depressants" and "anti-psychotics", as psychiatry became a drug intensive specialty, pharmaceutical companies formed alliances with psychiatric professions. However, the first DSM conceptualized mental health symptoms as dynamic conditions or as reaction to difficult life problems, psychotherapy was considered to be the best treatment. There was not a categorical approach to group different set of symptoms or behaviors into discrete categories with different labels

Its important to note that, psychiatry as field remained divided between biological psychiatrists and Freudians who rejected the biomedical model, in response to the threats posed by external members to its status as a legitimate branch of scientific medicine, psychiatry embraced the biomedical model. Shortly after publication of the DSM-111, the APA launched a marketing campaign to promote the biomedical model in media.

Psychiatry benefit from the perception that, like other medical disciplines, it too had its own valid disease-specific treatment.

The introduction of Drugs to Psychiatry - Diagnostic Approach

Psychiatry joined forces with the pharmacological industry as both shared a common interest in promoting a biomedical model of mental health

Biomedical model to mental health

The basic tenants of the biomedical model to mental health is that...

The dominant model of disease today in the Western world is a biomedical model. It assumes diseases to be fully accounted for by deviations from the norm of measurable biological variables. Within this framework, there is very little room for the social, psychological, and behavioural factors underlying illnesses.

This position was also echoed by former president of the APA, Paul Applebaum, who noted, "our brains are biological organs by their very nature. Any mental disorder is in its essence a biological process".

According to this diagnostic model, the ultimate goal is to develop precise therapeutic agents that specifically targets the disease etiology without harming the organism.

Psychiatrists & Pharmaceutical

- Policy change to APA in 1980

- Medical education & outreach programs

- NIMH allocating greater funds to research following the biomedical model

- NAMI connects with the pharma industry

A policy change by the APA in 1980 allowed drug companies to sponsor "scientific" talks, for a fee at its annual conference. This brought in revenue!

The APA began working together with drug companies on medical education, media outreach, and congress lobbying.

Under the direction of biological psychiatrists from the APA, the NIMH took up the biomedical model and began systematically directing grant funding towards biomedical research, while withdrawing funds from community-based psychosocial treatment.

The NAMI dedicated to reducing mental health stigma by blaming mental disorder on brain disease instead of social or environmental factors (poor parenting), formed ties with the APA, NIMH, and the drug industry.

Connected by their complementary motives, the APA, NIMH, NAMI and the pharma industry helped to strengthen the "biologically-based brain disease" concept of mental disorder in American culture.

A good example of their collaboration - in the 2009 NIMH brochure on OCD, consumers were encouraged to seek help from a doctor who may prescribe antidepressant, antianxiety, and or beta-blockers as treatment options.

NIMH (National Institute of Mental Health)

NIMH allocating greater funds to research following the biomedical model, while withdrawing funds from community focused, psychosocial treatment program

NAMI (National Alliance on Mental Illness)

How did Drug Companies promote a biomedical model of mental health?: DTC drug advertisements and Language used to describe psychotropics

Direct to consumer drug advertisements (only legal in American and New Zealand) inform the public that depression and other mental disorder may be caused by a chemical imbalance in the brain that can be correct with medication - pharma companies spend a lot of money annually on DTC ads ($4.7 billion in 2010) to educate consumers about mental disorders and encourage them to request medications from their physicians. This is one approach that pharma companies take to pathologize normal human experience/ unnecessary symptom labelling (one example of lowering the symptom threshold)... ordinary processes or reactions to events seen as medical problems

Reframing routine human conditions, such as, unhappiness or boredom as depression in milder forms

Promoting a drug prescribed to treat ADD in children to ADD in adults

social anxiety disorder -FDA approved paraoxtine to treat SAD: marked by extreme shyness, fear of public speaking, eating in front of people, using the public washroom

The language used to describe the psychiatric medications has evolved to reflect the biomedical model. SSRI are called anti-depressants not only simplifies the condition, but also ignores the harmful side effects associated with the medication. The drug becomes known mainly as a mood-stabilizer and not for the many side effects that comes up with taking the drug

At the end.. Address the question of how yes, pharma companies did play a critical role in creating new diagnostic labels and lowering symptom thresold

Alternative Answers

DSM classifies mental health illnesses

- Statistical infrequency

- Violation of norms

- Personal distress

- Disability or dysfunction

- Unexpectedness

The disorders in the DSM is defined by specific sets of behaviours and not by etiology, because we do not yet have specific biomarkers for specific mental illnesses.

As we change our understanding of what constitutes as an "abnormal behavior" (shaped by societal norms, impediment to our daily functioning, level of personal distress), we can also expect to see fluctuations in the number of diagnoses and to symptom threshold.

Therefore, clinical care guidelines in psychiatry are vulnerable to subjectivity because the absence of biological markers for mental disorders increases clinical uncertainty.

Clinical Depression

. One of the most common mental health illnesses (~1 in 10 adults)

• First episode of depression that a person experiences is often tied to a severe life stress, such as a bereavement or job loss, but subsequent depressive episodes may appear to be decoupled from discrete life stressors

• One issue that complicates research on depression is the vast array of symptoms, subtypes, and variations

• Depression is a mood disorder characterized by chronic feelings of sadness and hopelessness and loss of interest or pleasure in activities that once were enjoyed

Common Symptoms

•Poor appetite or overeating

•Insomnia

•Hypersomnia

•Low energy

•Slowed thinking and action

•Low self-esteem

•Poor concertation and difficulty making decisions

•Suicidal thoughts

As you can see these symptoms encompass many domains of functioning, including affect, motivation, cognition, and regulation of the body's homeostatic systems.

Variations of Depression

•A milder state of chronic depression lasting at least two years has been termed dysthymia

• Depression can also be seasonal with a typical onset during mid-fall as the days become shorter

• Depression can also be interspersed between periods of mania

During mania, the person often experiences euphoria, rushes of energy, reckless impulses to engage in excessively in pleasurable activities such as sex, and shopping, irritability, racing thoughts, and a sense of grandiose power.

When mania occurs, either alternating with a depressive episode or occurring alone, a person is described as having bipolar disorder.

Cognitive signature of depression

•Memory and attention are biased towards negative events and interpretations, contributing to rumination

• Executive functions (e.g., mental set shifting, emotional regulation, cognitive control) are impaired

• Many sub-regions of the frontal lobe have been identified as functioning atypically in depression

• These regions include brain systems involved in cognitive control, DLPFC and ACC

Posterior Cortical Regions & DMN

• In addition to the frontal lobes, posterior parts of the cortex, especially in the right hemisphere are affected by depression

• Because depression is often characterized by excessive self-focus and rumination, it seems plausible that DMN could be altered in depression; possibly strong functional connection with subgenual frontal cortex.

• Amygdala over activation towards negative events

• Reduced activity in reward pathway

Cognitive deficits in depression include difficulties on tasks of spatial function, implicating the right hemisphere.

In addition, reduced activity in the posterior right hemisphere could contribute to the lethargy and fatigue seen in depression, as this region is thought to play a role in maintaining levels of arousal and vigilance.

Panic Disorder: Recurrent unexpected panic attacks

A panic attack is an abrupt surge of intense fear or intense discomfort that reaches a peak within minutes.

Criterion A: Recurrent unexpected panic attacks

Criterion B: At least one of the attacks followed by 1 month of persistent worry about additional panic attacks or their consequences (eg., losing control, having a heart attack)

Panic attack is a symptom that can occur in the context of any anxiety disorder as well as any other mental disorders, such as, depression, PTSD, substance use. Unexpected and expected panic attacks

Roughly mention about that it falls under the broad umbrella category of anxiety disorders, and differentiate the two

Panic attacks: emotion evoked by the perception of an actual danger that causes major sympathetic activation with small effects on the HPA axis Diff to Anxiety: emotional state related to a potential threat (mostly activating HPA)

At least 1 of the attacks has been followed by at least 1 month of at least 1 of the following: Persistent concern or worry about additional panic attacks or their consequences (e.g. - losing control, having a heart attack, "going crazy").

Criterion C: Disturbance not attributable to the physiological effects of a substance or an underlying medical condition

Criterion D: Disturbance not explained by another mental disorder

- Social anxiety disorder

- GAD

- Separation anxiety disorder

Recurrent: more than one unexpected panic attack

An Important distinction between expected and unexpected panic attacks

Expected panic attacks are attacks for which there is an obvious cue or trigger, such as a situation in which panic attacks typically occur (e.x: social gathering)

Unexpected refers to a panic attack for which there is no obvious cue or trigger at the time of occurrence (e.x: nocturnal panic attacks)

Nocturnal panic attack: waking from sleep in a state of panic

Why is this question important to address?

1. Evaluate the utility in each of these frameworks in explaining panic attacks that result from expected relative to unexpected cues

2. Treatment approaches

•Whether pharmaceuticals or therapy would be suitable as an effective intervention

It is important to delineate the different reasoning as to why panic attacks occur? (biological inherent false alarm or a type of cognitive appraisal of the person that triggers the attack because it helps to evaluate the utility in each of the frameworks that I will describe in explaining panic attacks that result from expected vs. unexpected cues.

Evidence for a catastrophic interpretation of threat: Clark's framework (maladaptive schema) Part 1

Here, individuals may anticipate a catastrophic outcome from a mild physical symptom or medication side effect (e.g: thinking they may have a hear disease or that a headache means presence of a brain tumor).

This cognitive model that I just described by Clarke conceptualized panic attacks as a result of a maladaptive schema or a cognitive framework influencing information processing, in that the individually preferentially attends to danger cues, interprets ambiguous cues as threatening, and selectively remembers cues relevant to fear.

According to Clarke, panic attacks result from a catastrophic interpretation pf physical sensations. The catastrophic interpretation involves perceiving physical sensations as more dangerous than they are, and as indicative of an immediate , impending disaster. These sensations are the physical symptoms experiences in the event of a panic attack (e.x: palpitations, breathlessness, and dizziness). For example, a person may interpret a sudden difficulty in thinking as evidence of an impending loss of control and insanity.

Clark suggested a sequence of events that results in a vicious cycle which culminates in a panic attack. As shown on the slide, a trigger stimulus, internal or external, is perceived as a threat leading to a state of apprehension. This state is then accompanied by a variety of bodily sensations which are interpreted in a catastrophic fashion. Catastrophic interpretations lead to further increases in apprehension and bodily sensations culminating in a panic attack.

Clarke also suggested that the perception of physical sensations and catastrophic interpretations does not need to be conscious. Unconscious perceptions and interpretations would explain spontaneous panic attacks when the individual is awake or sleep, like in the case of a nocturnal panic attack.

Evidence for a catastrophic interpretation of threat: Clark's framework (maladaptive schema) Part 2

Overall, the cause is assumed to be an inability to appraise the physical symptoms more objectively during a panic attack.

Recommended treatment following this framework: CBT - identify the patient's catastrophic interpretations pf physical sensations; and suggesting alternative noncatastrophic interpretations of these sensations that is more in touch with reality; testing the validity of alternative interpretations through discussion, graded exposure to the perceived threat

Barlow's integrative model of Panic attacks

•Barlow's model of panic attacks claims that some individual possess biological and psychological vulnerabilities to develop panic attacks in the absence of a real threat.

•These false alarms occur as a function of stressful life events and are facilitated by negative affect.

Integrated: some individuals may be biologically predisposed to viewing physical sensations or life events are extremely catastrophic.

The learned alarms - through repeated pairing of stressful life events and negative affect (classical condition), interceptive cues may become associated with the initial panic attack and result in subsequent attacks (learned alarms).

It it's the initial association of an initial false alarm with somatic cues that may be particularly crucial in the development of panic attacks specific to situations.

Some individuals experience a panic attack, and subsequently become anxious in anticipation of having another attack. The vulnerability for developing anxious apprehension may lar dormant unless activated by certain psychological vulnerabilities and experience. One of them is t that emotions and situations in general are uncontrollable (lack of perceived control) . As a result of the false alarm and individuals low perception of control, they may begin to experience anxious apprehension about having future panic attacks.

- Dysregulation of the HPA axis

Etiology

Combined Approach - one that integrates the biological predispositions and the cognitive appraisals of the individual

•Biological factors may act as predisposing factors

•Stressful life events may act as precipitating factors

. One's appraisal of the situations may then maintain the occurrence of the panic attacks

Schizophrenia

Early neurocognitive theories of schizophrenia placed heavy emphasis on the left hemisphere probably due to the prevalence of auditory hallucinations and deficits of verbal memory. But there is little reason to suspect that schizophrenia affects only one hemisphere of the brain.

First episode psychoses commonly occur in teenage years where association cortices are becoming more heavily myelinated. So one could consider schizophrenia to be both a neurodevelopmental disorder and a disorder of higher level association cortices.

What is schizophrenia?

"A large group of disorders, manifested by characteristic disturbances of language and communication, thought, perception, affect, and behaviour which last longer than six months."

Schizophrenia is a serious mental illness that affects how a person thinks, feels, and behaves. People with schizophrenia may seem like they have lost touch with reality, which can be distressing for them and for their family and friends.

DSM

2 or more of the following characteristic symptoms:

Delusions; hallucinations; disorganized speech; grossly disorganized or catatonic behaviour; negative symptoms

Social/Occupational Dysfunction

•Duration: continuous signs for at least 6 months

Exclusion Criteria: medical/drug, other psychiatric or developmental disorders

DSM-V = diagnostic and statistical manual of American Psychiatric Association

Characteristic symptoms--these define the disease

Social/occupational dysfunction: for a significant portion of time since onset of symptoms, one or more major areas of functioning have been affected--interpersonal relationships, work, school, self-care--markedly below level achieved prior to onset.

Duration--to rule out other possibilities

i.e. drug abuse (amphetamines can produce a state that resembles paranoid schizo.)

i.e. may be manic if short term

Epidemiology

•Prevalence: approximately 1% of the population worldwide

• Greater among lower socio-economic classes in urban areas

Age of onset: a disease of the young

Males: 18-25

Females: 26-40

Cost: over $100 billion annually to Canada

lifetime risk the same in males and females

socioeconomic--tend to "drift" down

Cost-this is the approximate estimate of the direct and indirect costs of treating mental illness--the majority of that amount is due to schizo.

Suicide-10%, but 50% attempt

Prognosis-

1 in 3-severe deterioration ( institution, chronic medication)

1 in 3-good recovery-look after themselves, may need med.

1 in 3-in-between

Negative symptoms and Positive Symptoms

Positive symptoms represent behaviours we normally do not see in healthy individuals - the addition of behaviours in some sense. Auditory hallucinations and a variety of delusions - including what are referred to as "passivity phenomenon". Passivity phenomenon refer to delusions in which the person feels that their thoughts or actions are controlled by some external agent. Thoughts are being withdrawn or inserted into their heads for example. Delusions are most commonly of a paranoid type - the patient feels they are being monitored in some way but can take other forms (note: delusions of grandeur - I'm awesome at something - are more commonly observed in mania).

Hallucinations

Delusions

Incoherent speech

Thought disorders (insertion/withdrawal)

Incongruity of affect

Catatonia

Negative symptoms on the other hand represent a diminution of behaviors we would normally expect to observe in a neurotypical individual. Flattened affect and avolition represent affective and motivational changes whereas alogia - represents a cognitive deficit.

Affective flattening

Alogia

Anhedonia, apathy, avolition

A sociality

Attentional impairment

Frequency of Symptoms

Symptoms and Percentage

Lack of insight - 94%

Blunted affect - 82%

Asociality - 79%

Delusions - 73%

Unkemptness - 67%

Lack of interest - 65%

Auditory hallucinations - 64%

Apathy - 60%

Thought derailment - 58%

Suspiciousness - 51%

Neuropsychological deficits

Meta-analysis (204 studies):

•General and widespread deficits

Largest deficits in:

- Verbal memory, bilateral motor skill, performance IQ, WCST

- Memory, attention, language

Disorder of Association Cortex

Original focus was on left temporal and frontal cortices (auditory hallucinations)

No reason to suspect other association cortices (parietal - perhaps even medial temporal) are not equally affected

First episode in teenage years

- Disorder expresses itself when late myelinated areas come on-line

Subtypes of Schizophrenia

Paranoid

1. Acute onset

2. Auditory hallucinations, paranoid delusions

3. Most responsive to antipsychotic drugs

4. Intelligence relatively intact

5. Guarded, tense, potentially aggressive

Paranoid schizophrenia is the most common subtype. Patients can have a good prognosis with continued treatment. Onset is usually a little older (30s) and commonly involves delusions of persecution. These patients may appear tense, suspicious, and guarded in their social interactions. They can often hold down a job, but struggle to maintain social relationships as they can become hostile or aggressive. Intelligence tends to be more or less intact.

Simple

Gradual onset

Negative symptoms predominate

- Withdrawal from social activity

- Avolitional, flattened affect

Simple schizophrenia presents with a gradual onset and is characterized by a gradual withdrawal from all social activity and a corresponding lack of motivation and drive, and a flattening of affect.

The insidious onset of prominent negative symptoms and the lack of delusions, hallucinations, and thought disorder are the essential clinical features of simple schizophrenia.

Disorganized or Hebephrenic

1. Gradual onset

2. Inappropriate affect and pronounced thought disorder

3. Extremely poor contact with reality

4. Most severe type, less favourable prognosis

The disorganised subtype that was shown in the video of Heather, used to be referred to as Hebephrenic

Catatonic

Acute onset in adolescence

Catatonic motor symptoms with underlying thought disorder and delusions

Motor symptoms

- Stupor, rigidity, mutism

Least common

The Catatonic subtype is the least common of the four. These patients actually alternate between catatonia and extreme excitement/agitation. This form of schizophrenia has been known to respond well to ECT.

Etiology of Schizophrenia

Genetic

Environmental

Neuroanatomical

- CT and MRI show ventricular enlargement

- MRI demonstrates a variety of structural differences

Schizophrenia remains an ideopathic disease - we don't know its cause. But we can consider some thing about the genes, environment and neuroanatomical contributions to schizophrenia.

Although believed to play an important role, a definitive genetic abnormality has not yet been found.

In terms of environmental contributions, as mentioned there is evidence that higher rates of perinatal complications in winter months, and that complications with pregnancy or delivery may be causally related to schizophrenia.

There are numerous neuroanatomical findings including enlarged ventricles that are related to negative symptoms and are more evident in males.

Genetic = although believed to play an important role, a definitive genetic abnormality has not yet been found

-non-Mendelian inheritance pattern

environmental -higher rates of perinatal complications in winter months, and that complications with pregnancy or delivery may be causally related

-maternal exposure to influenza?

Neuroanatomical - ventricular enlargement related to negative symptoms; occurs more in males

thalamus-filter/gate for info reaching cortices

-viral infection? autoimmune disease?

PET: hypometabolism (resting PET)

PET: hypofrontality

PET: possible asymmetry - hyper right hemisphere vs. hypo left

PET: differences in neural networks used (Stroop eg)

Anatomical differences in schizophrenia

Ventricular size

Total brain volume

Grey matter in association cortices

Asymmetries?

[Image]

This shows the enlarged ventricles of a patient with schizophrenia alongside their monozygotic twin. Enlarged ventricles are indicative of reduced grey or white matter in the patient - but the cause of this reduction remains elusive.

Metabolic imaging also shows changes with a general finding of hypometabolism and in particular hypofrontality.

Dopamine (DA) Hypothesis

Excessive DA activity or unusually high responsiveness to DA in the mesolimbic/mesocortical DA system

Nucleus accumbens/parts of amygdala - thought to mediate memory, learning, affect, thought organization

Gating mechanism for consciousness?

- Stimuli ineffectively gated leads to overflow of information (misattribution of sources?)

limbic areas = nucleus accumbens, olfactory tubercle, parts of amygdala

these structures mediate:

believed limbic areas such as NA act as a gating mechanism that prevents consciousness from being inundated by various internal and external stimuli

-schizo may result from a failure of these mechanisms

The most prominent theory to explain schizophrenia over the past 50 years is known as the Dopamine hypothesis. The notion is that patients with schizophrenia may have either an excessive amount of DA in their system or may show a heightened responsiveness to it.

DA is particularly important for representing reward and value and via connections with the nucleus accumbens and the amygdala is thought to help regulate learning, emotion and the organisation of thoughts.

These connections may represent a kind of gateway to conscious experience. If stimuli are inefficiently gated this could lead to information overload and other aspects of cognitive dysfunction characteristic of schizophrenia such as source attribution errors - that is, schizophrenia patients may fail to accurately attribute the source of information (their own internal voices being attributed to something external).

Evidence for DA hypothesis

Antipsychotic drugs used to treat schizophrenia block DA receptors

Postmortem studies - higher # D2 and D4 receptors

Amphetamine psychosis resembles schizophrenia

- Amphetamine increases total level of DA in the system

- Amphetamine exacerbates symptoms of schizophrenia

1. amphetamines-- L-Dopa (any drug that increases DA) can produce a clinical state virtually indistinguishable from paranoid schizo.

2. mainly D2 receptors (target of action)

3. compared to healthy controls

problem--elevated because of the disease or treatment?

Limitations to Current Etiology

Antipsychotics treat mostly positive (e.g., hallucinations) but not negative symptoms

Antipsychotics block DA receptors rapidly, remission of symptoms occurs gradually (~weeks)

Enlarged ventricles/grey matter loss - hints at additional pathology

Low prefrontal DA activity