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Psychosis and schizophrenia Flashcards

1
Q

Psychosis

A

Significant loss of contact with reality

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2
Q

Schizophrenia (SCZ)

A

Psychotic disorder characterized by major disturbances in thought, emotion, & behaviour

Disordered thinking
Ideas not logically related
Faulty perception and attention(things arent there or less important information)

Flat or inappropriate affect(not showing much emotion or appropriate emotion)

Bizarre disturbances in motor activity

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3
Q

Hallmark Symptoms

A
  • Delusions
  • Hallucination
  • Disorganized speech and/or behaviour
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4
Q

Positive & Negative Symptoms

A

Positive(+)
* Excess and/or distortion in normal range of behaviour and/or perception

Negative(-)
* Deficit of normally present behaviours

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5
Q

Positive Symptoms(+)

Excesses or distortions

A

Delusions
* Erroneous(false) beliefs
* Disturbance in content of thought
* Firmly held belief despite evidence

Hallucinations
* Sensory experience (any sensory modality) - hearing,visuan,sensation
* Seems real despite no external stimulus

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6
Q

Positive Symptoms: Examples

A

Delusions

– Thought insertion: someone else put thoughts in your head

– Broadcast thoughts: your thoughts are been showned to the world

– Thought withdrawal: someone taken certain thoughts out of your brain

– Made feelings: emotion caused by someone else

Hallucinations

– Voices talking about pt
or speaking pt’s thoughts aloud

– Voices arguing

– Voices commenting on pt’s actions

usually they experience audirory

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7
Q

Negative Symptoms(-)

Behavioural deficits

A

Reduced expressive behavior
* Alogia (minimal speech)
* Flat affect: no emotional response (externaly)

Reduced motivation/pleasure
* Avolition (minimal goal-directed activity)
* Anhedonia: not caring about things anymore
* Asociality: little interest with being with other people

  • Poorer prognosis: less likely to get better or symptoms worsens faster
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8
Q

Disorganization

A

Speech
* **Failure to make sense **(despite conforming to semantic and syntactic rules of speech) - content does not make sense

  • Disturbance in form (not content) of thought: musical

Behaviour

Catatonia:

Unusual complex movements

Catatonic immobility: not being able to move

Waxy flexibility: moving someone and they stay in that position

Inappropriate affect: acting innaproprly in the contex
ex:getting med because of someone laughing

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9
Q

Subtypes of Schizophrenia

A

Disorganized schizophrenia
* Disorganized speech & behaviour
* Flat/inappropriate affect

Catatonic schizophrenia
* Catatonic symptoms that may alternate with ↑ excitement

Paranoid schizophrenia
* Absurd, illogically organized beliefs
* Delusions of persecution
* Delusions of grandiosity
* Delusional jealousy
* Ideas of reference: something unrelated seeing as something specifically to you

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10
Q

Related Disorders

A

Schizophreniform disorder (brief)
* schizofrenia but lasted 6 months or less

Brief psychotic disorder (briefer)
* even brifier like couple of weeks

Schizoaffective disorder (+ mood)
* psychotic fetures in a mood disorder like in mania

Delusional disorder (delusions only)
* no hallucinations

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11
Q

Phases

A

1. Prodromal
* Obvious deterioration in role functioning (work,family)
* Change in personality (like schizotypal PD)

2. Active
* Psychosis

3. Residual
Improvement in positive symptoms & continued negative symptoms

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12
Q

Epidemiology

A

Lifetime risk 1%

Risk factors
* Father over 50 - when born
* Parents in dry cleaning business - when born?
* Severity: males > females

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13
Q

Age of Onset

A

Most common: ages 18-30

  • in man it peaks between 18 - 30 then it goes down
  • in women it peakes between 18 - 30 but it it peakes again in women between 45-49 (menopause)
  • estrogen might help prevent schizophrenia
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14
Q

Life Expectancy

A

Shorter

  • high risk for suicide
    20-40% attempt suicide
    10% complete suicide
    not necessarly during psychosis
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15
Q

Prevalence: SES

A

More prevalent in low SES groups

hypothesis for this
* stress of poverty causes the onset of schzofrenia
* people develop schziphroneia and then their ses lowers due to not beinga able to get a jod

casual directions

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16
Q

Factors Affecting Course

A
  • Gender: worst for man
  • Stress/Family environment
  • Expressed Emotion: means high levesls of hostility and critisim
  • Age of onset: older you are better the preognosis
  • Premorbid functioning: having more function before schizophrenia better to adjust later
  • Cognitive ability: higher IQ tends to do better
  • Access to treatment: really helps
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17
Q

Prognosis

A

Poorer outcome

  • Delay in treatment of 1st episode
  • Delay in treatment of acute exacerbations: sever symptoms
  • Males
  • History of birth complications
  • More severe hallucinations & delusions
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18
Q

Etiology: Bio

Genes

A

Most important in etiology!!
~ 80% of risk

  • Environmental factors modulate expression of symptoms
  • Inherit a tendency for schizophrenia
  • Do not inherit specific forms of schizophrenia
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19
Q

Family & Twin Studies

A
  • their children are 10 times more likely to have it
  • DZ twin are 12 times more likely
  • MZ twins are 44 times more likely
  • this shows both the importance of genes but also the enviroment (genes just explain half)
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20
Q

Adoption Studies

A

Adopted children with bio mother (SCZ +) 17% developed SCZ

Children adopted w/i same agency (bio mom SCZ –) 0 developed SCZ

Children of women (SCZ +)
Higher frequency other mental health problems

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21
Q

Genetic Markers*

A

Behavioral Markers

Smooth-Pursuit Eye Movement
* Tracking deficits are related with People with SCZ & relatives - similar genetic markers

22
Q

Etiology: Bio

Brain Structure and Function

A

Abnormalities

  • Attentional and working memory deficits
  • Impaired social cognition: not being able to recognize others emotions,speech eyc
  • Loss of brain volume
  • ** Reduced White matter**: less myanation - help your thoughts move quicker and less impulsive
  • Compromised cytoarchitecture: cells migration so it is more organized but with SCZ is disorganized
  • Disrupted brain development in adolescence: ex due to injury or stressors
23
Q

Decreased brain volume

A

Enlarged ventricles (spaces in between)

may be related to Negative symptoms?

24
Q

Brain Structure

A

Reduced volume of the thalamus
* Gateway for processing all incoming sensory info(deciding where it goes)
* Disorganized perception & thoughts?

Abnormalities in temporal lobe areas
(e.g., hippocampus & amygdala)
- regions of emotion which can cause emotion disregulation

But…not found in all patients

25
**Brain Function**
**Hypofrontality** * **Reduced neural connectivity** * less activation * (excessive synaptic pruning?) Major Dopamine pathway (Prefrontal cortext inhibits DA in limbic system) **Working memory** * Representing sensory info to guide behavior * Disorganized behavior & speech, thought disorder
26
**Hearing hallucinations**
**Broca’s area:** Speech production (speaking) **Wernicke’s area:** Language comprehension (hearing) what was found is that in hearing hallucinations was being activated by the **speech production area**(Brocas) not the hearing one(Wernicke) they are hearing their own inner voice but not recognizing as their own own voice
27
**Original DA Hypothesis**
Schizophrenia related to an DA excess Drugs that increse DA (dopamine) * Result in schizophrenia-like behaviour e.g., Amphetamine, L-Dopa for Parkinson’s disease Drugs that reduce DA Reduce schizophrenia-like behaviour e.g., Neuroleptics Do not treat negative symptoms
28
Revised DA Hypothesis
* **Negative symptoms** **decrese** **DA** in **cortical regions** (underactivity at D1 receptors) * **Positive symptoms** **increse DA** in **subcortical regions pre-synaptic** (too much produced and released into synapse results overactivity at D2 receptors)
29
Dopaminergic Pathways*
**Mesolimbic Pathway** (positive symptoms) increse dopamine **Mesocortical Pathway** (frontal cortext) (negative symptoms) when a disfunction happens/decrese activity in the mesocortical pathway it can act as a cheeck that it increses meolimbic pathway/positive symproms
30
**Glutamate**
**decrese Glutamate** (e.g., PCP and “special K” create schizophrenia-like symptoms) Underactivity at NMDA receptors DA receptors also inhibit glutamate activity, so... Too ↑ DA activity => too ↓ glutamate activity
31
# **Etiology: Bio** **Neurodevelopmental Hypothesis**
“Silent lesion” **Abnormalities lie dormant until normal developmental processes expose problems** So...neuropathology before SCZ onset
32
Neurodevelopmental
Neuromotor, cognitive & behavioral abnormalities * **Smaller head circumference at birth** * **Slower to reach developmental milestones** * **Higher rates of left-handedness** Congenital minor physical & craniofacial anomalies * Velocardial Facial Syndrome
33
Neurodevelopmental
Gestational & perinatal exposures * **Viral infection**( 2 trimister) * **Early nutritional deficiencies & maternal stress** (1 trimister) * Pregnancy & birth complications
34
Gestational & perinatal (think: stress)
1st trimester maternal starvation Dutch Hunger Winter of 1944/1945 schizophrenia 2 more likely **Obstetric complications premature birth, hypoxia** higher rates of schizophrenia Maternal viral infections 1957 Helsinki influenza (2nd trimester) higher rate of schizophrenia
35
# **Later Environmental Stressor** **Cannabis**
People with schizophrenia are twice as likely as the general population to smoke cannabis
36
**Cannabis: Diathesis-Stress**
heavy use of weed during adolescence when u already have a disposition are more likely to develop schizophrenia more specif val val gene depending on your genotype and canabis use
37
General Diathesis-Stress Model
genetic factors,prenatal and perinatal events,brain vulnerability + stress, developmental maturation processes (syanptic prunning,different connedction)= psychosis
38
“doomed from the womb”?
no No environmental factor necessary or sufficient
39
Etiology: “Multiple-Hit” Model*
1. Gene, Virus, Toxins, Nutrition, Birth injury, Psychological, Stressors impacts... 2. Brain development from conception to early adulthood (e.g., neuron formation, migration, synaptic pruning) impacts... 3. Anatomical & functional disruption in neuronal connectivity & communication impacts... 4. Cognitive dysmetria (dysregulation of information processing in the brain) impacts... 5. Impairments in higher-order cognitive processes (e.g., attention, memory, language, emotion) impacts... 6. Symptoms of schizophrenia (e.g., hallucinations, delusions, negative symptoms, disorganized speech
40
Etiology: Psychosocial
**Psychological Stress** increse Relapse rate * Migration * Urbanization * Lowest SES Sociogenic hypothesis Social-selection theory “downward drift”
41
Migration
**Risk for developing schizophrenia:** 1st generation migrants: 2.7 2nd generation migrants: 4.5 From developing vs. developed countries: 3.3 From areas with predominantly black population: 4.8 Potential explanations? Diagnostic bias? No Selective migration? No Discrimination and social defeat? (chronic stressful experience of outsider status)
42
Etiology: Psychosocial
**Family** Outdated: “Schizophrenogenic mother” **Current** **Expressed emotion – relapse (3.7x)** (in families) **Criticism** **Hostility** **Emotional over-involvement**
43
stress is very important in the development of schizophrenia
both biological stressors but also external/social stressors
44
# **Treatment (Bio)** Treatment: Response
33% continue to have symptoms and problems even after treatment 12% need long-term institutional care 38% function well 15-25 years later (i.e., can manage symptoms) 10-15% fully recover (symptoms remit > 2 yrs, good social functioning) **No “cure"**
45
Treatment: Bio (Historical)
**Insulin coma** Serious risks, little success **ECT** Minimally effective **Prefrontal lobotomy** Controversy about cognitive deficits **Institutionalization**
46
Treatment: Bio (Current)
**Antipsychotic Medication** Mechanism: **Block DA receptors** * 1st generation “Conventional” antipsychotics * 2nd generation **“Atypical”** antipsychotics
47
Range of Response
**1+ psychotic episodes** * Relatively rapid return to normal functioning * **Good prospects for recovery** **Years of recurrent psychotic relapses** * Periods of remission * **Varying degrees of residual impairment** **Failure to respond**
48
**Conventional** Antipsychotics
60% show remission within 6 weeks **Better response: Positive symptoms** Worse response: Negative symptoms & Social functioning **Side effects problematic** (cause discontinuation) * **Tardive dyskinesia**: motor dysfanction * **Extrapyramidal side effects (EPS)**: muscle spasemous,motor problems
49
**Atypical** Antipsychotics
Reduce symptoms in **30% of drug-resistant patients**(people who tried the conventinal antipsychotics) **No tardive dyskinesia or EPS** But...weight gain, drowsiness, diabetes, agranulocytosis possible (fatal)
50
**Treatment: Psychosocial**
**CBT** * Reframe positive symptoms * Identify triggers for symptoms * Improve social skills * **Reduce relapse** * **Not helpful for negative symptoms** **Cognitive remediation** * Improve cognitive functioning - improving working memory,recall - help maintain brain connections **Other individual** * CBT + life skills
51
Treatment: Psychosocial
**Family Therapy** * Provides families with communication skills * Reduces high levels of **expressed emotion** **Case Management**: having someone make sure you are doing what u need to (go to work,school,therapy) **Social and Living Skills Training** **Vocational rehabilitation**

psyc 300 (15 decks)

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