Lecture 14 - Schizophrenia and Affective Disorders Flashcards
Describe a brief overview of SZ
- Affects approx. 1:300 people (roughly 24 million)
- Onset is most often during adolescence and 20s (onset typically earlier in men)
- Considered to be a type of psychosis: a loss of contact with reality
- A “split mind”, a break in reality (Bleuler, 1911)
What are positive symptoms of SZ?
(Something you gain) hallucinations, thought disorder, delusions (persecution, grandeur, control)
What are negative symptoms of SZ?
(Something you lose) flat emotional response, speech poverty, lack of initiative and persistence, anhedonia (lack of interest), social withdrawal
What are cognitive symptoms of SZ?
(General symptoms) difficulty sustaining attention, low psychomotor speed, deficits in learning and memory, poor problem solving, poor abstract thinking
Describe symptoms in general
- Persecution e.g. government following me
- Grandeur e.g. I am Jesus
- Control e.g. believing microchip controlling them
- Hallucinations are not the same as delusions (mistake in perceptions vs mistake in belief)
- Not everyone with SZ will show all at once
What are the neurology symptoms of SZ?
- Ventricular enlargement is one of the earliest and most consistent findings in SZ
- The ventricles of patients with SZ are approx. 130% the size of normal controls
- Ventricles are the fluid-filled cavities within the brain that play important roles in supporting and protecting neural tissue, regulating cerebrospinal fluid (CSF) flow, and providing buoyancy to the brain.
- Discordant = one has it, one doesn’t (discordant twin study)
What are other physical symptoms of SZ?
- If schizophrenia has a biological basis, it should correlate with other biological traits
- Schiffman found this to be true, with those with more minor physical anomalies being more likely to develop the condition
- Schiffman et al. (2002)
- Two or more hair whorls, epicanthus (folds on inner eye), hand lines
- No single one is a predictor of schizophrenia
What causes SZ?
- We’re not completely sure
- Clear link with genetics – polygenic trait?
- Clear link with environmental factors
- Interaction between genetic make up and environmental interaction best predictor
- Don’t know exact genes or exact environmental factors yet
- Combined, this suggests a genetic predisposition
Describe the heritability of SZ
- Biggest chance is between twins, not parents (suggests strong genetic link)
- % drops drastically (polygenic in nature)
- Husband/wife higher than general population (suggests an environmental factor)
Describe the relationship between heritability and the environment in SZ
- Monozygotic twins
- Monochorionic (sharing a single placenta) vs. dichorionic (separate placentas)
- Davis et al. (1995) found monochorionic concordance was 60% and dichorionic concordance was 10.7% (pre-natal environment is an environment e.g. one side may get inflamed, one side may not etc.)
What are some other environmental factors involved in SZ?
- Cannabis use
- Prenatal infection e.g. one sac became inflamed, and one didn’t
- Birth month e.g. more likely to get infection in winter months
- Childhood trauma
- Chronic stress
- Individuals have no control over these
What is the dopamine hypothesis?
- People with SCZ have overactivity in dopamine neurons in midbrain (mesolimbic system) (nearly double)
- Hypothesis originated from observations made in the 50s and 60s using antipsychotic medications which antagonize dopamine receptors, alleviating psychotic symptoms in individuals with schizophrenia (e.g. Chlorpromazine)
- Dopamine agonists induce positive symptoms (e.g., amphetamine)
- Talking and art therapies too
Why do dopamine agonists induce positive symptoms?
- Activity of dopamine neurons in the accumbens strongly reinforce behaviour (reward/pleasure/satisfaction)
- Fibiger (1991) – paranoid delusions caused by activity in Amygdala (Amygdala – fear responses, learning emotional responses)
- Snyder (1974) – schizophrenics report elation at the start of a schizophrenic episode
- This causes a reinforced belief spiral (positive symptoms chemically rewarded)
- Ventral tegmental area (midbrain) -> dopamine -> nucleus accumbes/amgydala
What did Stahl (2018) show?
- Still an emerging picture
- New evidence from drug research (psychedelics/hallucinogens/LSD/PCP etc.)
- NMDA theory: glutamate hypoactivity in regions involved with cognition and executive function (e.g., prefrontal cortex)
- Serotonin theory: serotonin dysfunction may disrupt typical cognitive abilities prompting the SCZ development
- Note: Higher order! All happening in the frontal lobes (where dopamine neurons don’t typically go)
- NMDA is a glutamate receptor (suggests separate but perhaps complimentary systems, quite complicated and we still don’t know)
What are some other treatments of SZ?
- Non-medication treatments also available e.g. CBT and art therapy
Describe a brief overview of affective disorders
- Affective disorder = categorized as a mood disorder, identified by disruptions in emotions
- Why is Schizophrenia not an affective disorder?
- While there can be some overlap in symptoms and comorbidity between schizophrenia and affective disorders (e.g., SZ can feature both psychotic symptoms and mood episodes), these conditions are generally considered distinct entities due to their unique clinical presentations, neurobiological underpinnings, and treatment approaches
What are the main types of affective disorders?
Bipolar disorder
- Alternating periods of mania and depression
- 1% of the population afflicted at some point in their life
- Equally frequent in men and women
Unipolar disorder (MDD – major depressive disorder)
- Depression without mania
- 2 or 3 times more likely in women than men
Seasonal affective disorder (SAD)
- Depression typically associated with the onset of winter months (linked with external cues)
- Some cases of mania without depression, but rare
What are the primary symptoms of affective disorders?
- Depression – low energy levels, anhedonia, loss of appetite for food and sex, sleeping problems, constipation
- Mania – euphoria, delusional, poor attention span, lack of sleep, grandeur
Describe the neurology and physiology of affective disorders
- Currently unclear – no consistent neurological markers across conditions
What causes affective disorders?
- We’re not completely sure
- Clear link with genetics – polygenetic trait?
- Clear link with environmental factors (e.g. basic needs not met = trigger depression)
- Again, this suggests a genetic predisposition
What is the heritability of affective disorders?
- Gershon et al. (1976) found MZ concordance was 69% and DZ concordance was 13%
- Price (1968) – concordance is the same whether twins are raised apart or together
- Rosenthal (1971) – 10 times more likely to suffer from affective disorder if a close relative also does
What is the monoamine hypothesis?
- Suggests depression is caused by faulty activity on monoamine neurons, e.g.:
- Deficiencies in serotonin (thought to play a role in modulating mood)
- Norepinephrine imbalance (plays a role in the bodies stress response)
- Dopamine dysfunction (plays a role in reward and pleasure pathways)
- Monoamine neurons = neurotransmitter modulators
What are treatments of affective disorders?
Drugs (table in notes)
- Suggests its probably/primarily a serotonin or norepinephrine interaction
- Non-medication treatments are also available
- No one-size-fits-all
