Dysfunction associated with psychiatric disorders (+ Schizophrenia) Flashcards
1
Q
Why classify psychiatric dysfunction (mental illness) into types? BROAD ANSWER
A
Broadly: to seek similarities and differences among patient groups
2
Q
Why classify psychiatric dysfunction (mental illness) into types? 4 SPECIFIC
A
- To guide treatment choices
- To allow clinicians to communicate
- To serve parties who require a diagnosis (e.g., insurance, CFA, legal system)
- To permit research (via categorization): into causes, treatment responsiveness, prognosis
3
Q
Classification of psychiatric disorders
A
- Primarily via the Diagnostic and Statistical Manual of Mental Disorders (APA)
- Atheoretical (not dependent on theory)
- Operationalist (meaning of a scientific concept depends upon the procedures used to establish it)
- Categorical
4
Q
DSM-I (1952) and DSM-II (1968):
Diagnosis of mental illnesses over time (process of DSM development)
A
- Heavy on psychodynamics (mental illness as “personality reactions” to stress)
- Intended to support data collection, particularly among WWII vets
5
Q
1960s - psychiatry’s “crisis of legitimacy”
Diagnosis of mental illnesses over time (process of DSM development)
A
- Argued that psychiatry was harmful & a means to control non-conformists
- Held that mental illness was a myth
- RESULT - major changes made to establish the DSM-III (1980) and DSM-IV (1994): exhaustive overhaul, attempted to standardize diagnosis
6
Q
DSM-5 (2013)
Diagnosis of mental illnesses over time (process of DSM development)
A
long process of working groups and reviewing current evidence, better attempts to control conflicts of interest
7
Q
DSM-5 definition of mental disorders (3)
A
- Characterized by clinically significant disturbance in an individual’s cognition, emotion regulation, or behavior that…
- reflects a dysfunction in the psychological, biological, or development processes underlying mental functioning, and
- is associated with significant distress or disability in social, occupational, or other important activities.
8
Q
DSM-5 explicit exclusions
A
- An expectable or culturally approved response to a common stressor or loss, such as the death of a loved one, is not a mental disorder.
- Socially deviant behavior (e.g. political, religious, or sexual) and conflicts that are primarily between the individual and society are not mental disorders unless the deviance or conflict results from a dysfunction in the individual, as described above.
9
Q
Criticisms of the DSM (5)
A
- Level of detail
- Overlap
- Authority
- Comparator
- Heterogeneity of criteria
10
Q
Level of detail
Criticism
A
“there are almost 24,000 possible symptom combinations for panic disorder in DSM-5, compared with just one possible combination for social phobia”
11
Q
Overlap
Criticism
A
- For many diagnoses, 2 people could be diagnosed with no overlapping symptoms
- High overlap between some diagnoses e.g., PTSD & MDD
12
Q
Authority: Who judges distress/impairment?
Criticism
A
Clinician vs self vs unclear
13
Q
Comparator
Criticism
A
- “decreased need for sleep…” and “more talkative than usual…” (to self)
- “excessive or inappropriate guilt…” (normative)
- “feelings of worthlessness” (none)
14
Q
Big picture trend:
A
Normative assumptions
- Normative: Evaluation of right or wrong, Ought, should
- Descriptive: What is or would be
15
Q
What were some controversial illnessess/components of the DSM?
A
- Masturbation (19th c.)
- Drapetomania – an “illness” causing black slaves to attempt escape
- Homosexuality: a disorder in DSM-I and DSM-II, removed for DSM-III following protests by gay activists and internal pressure from the “Gay PA”
16
Q
Deinstitutionalization
A
- Movement, starting in the 1950s and 1960s, to replace long-stay psychiatric facilities with community mental health services
- Possible with antipsychotic drugs such as chlorpromazine
- Without adequate support, people with mental illness are at higher risk of incarceration, being unhoused - “balloon theory”
17
Q
Mental illness and violence
A
- In the absence of substance use disorder, people with mental illness are not more violent than others from their same neighbourhoods (i.e., controlling for poverty, etc.)
18
Q
Schizophrenia
A
19
Q
Schizophrenia: DSM-5 criteria - A
A
2+ of the following:
- Delusions
- Hallucinations
- Disorganized speech (e.g., frequent derailment or incoherence)
- Grossly disorganized or catatonic behaviour
- Negative symptoms (i.e., diminished emotional expression or avolition)
20
Q
Schizophrenia: DSM-5 criteria - B
A
Level of functioning in one or more major life areas is below the level achieved prior to the onset
21
Q
Schizophrenia: DSM-5 criteria - C
A
Continuous signs of the disturbance persist for at least 6 months
22
Q
Schizophrenia: DSM-5 criteria - D
A
Schizoaffective disorders (bipolar I, depression with mania) have been ruled out
23
Q
Schizophrenia: DSM-5 criteria - E
A
Not attributable to the physiological effects of a substanceor another medical condition.
24
Q
How is Schizophrenia = “splitting of the minds”?
A
- Not between two personalities (i.e., dissociative identity disorder)
- Instead, between personality, memory, emotion, perception, etc.
25
Symptoms of schizophrenia: 3 categories
1. Positive symptoms
2. Negative symptoms
3. Cognitive abnormalities
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Positive symptoms
## Footnote
Symptoms of schizophrenia: 3 categories
mental phenomena that do not occur in healthy people
27
What can positive symptoms include?
* **Hallucinations**: **perceptions without sensory cause**
* **Often auditory** – voices, noises, music
* Command hallucinations have a high risk of harm including suicide
* **Delusions**: **beliefs that are not realistic or culturally appropriate**
* Can be quite varied
28
Negative Symptoms
## Footnote
Symptoms of schizophrenia: 3 categories
Negative symptoms **resulting from an impairment of normal
function**
29
What can Negative Symptoms include?
* Blunted emotional responses (“affective flattening”)
* Impoverished content of thought and speech (disturbed attention)
* Reduced social motivation
30
Schizophrenic speech
Grammar is **reasonably intact but content wanders or is incoherent** – “loosening of associations"
31
Common development of schizophrenia:
* ~0.5-1.5% of population
* Slightly more common in men
* Onset usually teens to early 30s
* Often preceded by a prodromal period
32
Risk factors of Schizophrenia
* Genetics
* Growing up in an urban environment
* 1st or 2nd trimester maternal infection or malnutrition
* Perinatal complications
* Cannabis or stimulant use
* Paternal age >35 years (at the point of conception)
33
Brain changes - Structural
* Widespread **decreased grey matter**, particularly in frontal and temporal cortices
* Pronounced **thinning of dorsolateral prefrontal cortex** (dlPFC) (critical for working memory)
34
Brain changes - Structural volume loss results in...
* ...enlarged ventricles (fluid filled spaces in the brain)
* Overall, volume loss is **not due to cell death** but rather **a reduction in cell processes (same number of cells but less axons and dendrites)**
35
Brain changes - Structural: Prefrontal Cortex
* Loss of dendritic spine density
* There is ONE cell that there is fewer of: **GABAergic interneuron**
36
Brain changes - Structural: Hippocampus
In the Hippocampus (in the medial temporal lobe), there is both:
* Atypical **layering structure**
* Atypical **neuron shape**
37
Brain changes - Functional
**Abnormal (often *hypo*active) frontal and temporal lobes** **including hippocampus** (same areas that are structurally affected)
38
Non-pharmacological treatments
**Cognitive Behavioural Therapy (CBT)** has shown some promise for the management of positive and negative symptoms when combined with medication
39
Pharmacological treatment
The most common treatments (for positive symptoms) are **antipsychotic drugs**
40
Pharmacological treatment: **TYPICAL antipsychotic drugs**
**Typical** (older)
* E.g., chlorpromazine (Thorazine), haloperidol (Haldol)
* **Act on dopamine**
* **Can have movement disorder side effects**
41
Pharmacological treatment: **ATYPICAL antipsychotic drugs**
**Atypical** (newer)
* E.g., olanzapine (Zyprexa), aripiprazole (Abilify)
* **Act on dopamine, serotonin, and other receptors**
* **Can have metabolic side effects (weight gain, diabetes...)**
42
Two theories of schizophrenia
1. Dopamine theory
2. Glutamate hypofunction theory
43
Dopamine theory
## Footnote
Two theories of schizophrenia
maybe schizophrenia is caused by too much activity at dopamine receptors
44
Dopamine theory - based on several findings:
1. **The brains of individuals with Parkinson’s disease have marked dopamine depletions**; and **antipsychotic drugs produce symptoms that are similar to Parkinson’s disease.**
2. **Drugs known to increase dopamine levels** (e.g., amphetamine, cocaine) **produce symptoms of schizophrenia** (maybe it's *too much* dopamine)
3. **The efficacy of an antipsychotic drug is correlated with the degree to which it blocks activity/tightly binds at dopamine D2 receptors.**
45
In the 80s and 90s, researchers began to realize that the theory had several major problems:
1. The **newer “atypical” antipsychotic drugs produce a wide variety of changes in the brain (NOT JUST FOCUSED ON DOPAMINE) and were just as good as traditional antipsychotics** (challenges a dopamine-only effect = something else is going on)
2. It takes 2-3 weeks for antipsychotic drugs to work on delusions/hallucinations, yet their effects on dopamine receptor activity are **immediate** (why is there a lag in improving symptoms?)
3. Most patients show no significant improvement to the first antipsychotic they are given.
46
Glutamate hypofunction theory
Finding: **phencyclidine** (PCP) and **ketamine** can **induce negative symptoms and psychosis and *act antagonistically upon NMDA receptors*** – a specific type of receptor for the neurotransmitter glutamate
* Basically: **we can produce something that looks like schizophrenia with these drugs, which we know act on glutamate**
* NMDA receptors allow calcium to enter the cell, which can cause many biological changes
* Glutamate = excitatory
* GABA = inhibitory
47
Glutamate hypofunction theory - how does it work?
1. Glutamate neuron (excitatory) may be in the medial PFC, frontal and temporal lobes
2. Glutamate neuron synapses on to the GABA neuron (inhibitory) - meaning the more it fires, the more it inhibits whatever its firing to
* HOW? through NMDA receptors for glutamate
* RESULT: send inhibitory GABA signals onto other neurons; the more excitatory a glutamate neuron is, the more GABA neurons inhibit the rest of the brain
48
Glutamate hypofunction theory - If glutamate signalling becomes abnormal, this can lead to..
1. **Less GABAergic transmission** (i.e., decreased inhibition of downstream cells = ***less*** **inhibition of the brain) leading to...**
2. **A widespread pattern of too much activity** (unbalanced excitation vs inhibition)
49
Glutamate hypofunction theory - what triggers the dysfunction?
* We don’t fully know!
* Could be considered a neurodevelopmental disorder with both genetic and environmental components
We *do* know that there is a big reduction in NMDA synapses in teens & twenties. This might reflect:
* Dysregulated plasticity (maybe weak synapses persist too long in childhood?)
* Excessive immune activation (microglia) and overly-aggressive synaptic pruning
