337 Schizophrenia Flashcards

1
Q

dementia praecox

A
  • Emile Kraeplin’s conceptualization of schizophrenia (the first to propose groupings of psychotic syndromes)
  • early dementia: begins at an early age, then progressive deterioration of cognitive abilities
  • Kraeplin began the conceptualization of BP and schizophrenia as distinct forms of dysfunction (despite overlap in genes, etiology, symptoms)
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2
Q

Eugen Bleuler

A
  • contemporary of Kraeplin; people with DP didn’t always show linear deterioration over time and could emerge later in life
  • primary deficit was loose associations (disorganized thinking came first, but caused the other positive symptoms)
  • first to use the term ‘schizophrenia’ for split mind (shattered cognitive ability, not DID)
  • considered schizophrenia a group of disorders
  • led to a more broad definition which increased rates of prevalence as people in N. America preferred Bleuler’s conceptualization over Kraeplin’s more narrow one
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3
Q

six major signs/symptoms of Schz

A
  • disturbances in perception
  • content of thought
  • form of thought
  • affect
  • motoric
  • relating
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4
Q

disturbances in perception

A
  • hallucinations: no stimulus is present but a perception occurs (vs. illusion in which a stimulus is present but misperceived)
  • hallucinations can be ‘positive’ (seeing things that aren’t there) or ‘negative’ (not seeing something that is there)
  • hallucinations occur in the same time and physical space as other (real) perceptions so makes them difficult to differentiate
  • can occur in all sensory modalities
  • hearing your own thoughts (but perceived as someone else), voices talking about you (poor prognosis), voices narrating your behaviour
  • somatic passivity experiences: bodily sensations imposed by external forces
  • voices could be misinterpreting your own thoughts
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5
Q

misinterpreted self-talk study

A
  • Ps reading words into a microphone that immediately transmitted those words in a distorted voice into their headphones
  • people with schizophrenia with auditory hallucinations more likely to make misattributions about their own speech to someone else
  • also much more likely to make these misattributions if the words they were saying were derogatory
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6
Q

disturbances in content of thought

A
  • delusions: false belief based on an incorrect inference, firmly believed despite contradictory evidence
  • mild end: over-valued ideas (false belief, but can entertain the possibility that it could be false; common in schizotypal PD and prodromal schz)
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7
Q

common delusions

A
  • controlled by an outside force: lost the ability to act volitionally in the world
  • grandiose: famous, important, royalty
  • jealousy: partner being unfaithful
  • nihilistic: belief that oneself or the world doesn’t exist
  • persecutory: people scheming, plotting, out to get you
  • of reference: someone or some event is trying to signal something significant to you
  • somatic: something is wrong with a part of your body
  • often have multiple fragmented delusions
  • thought withdrawal: vacuum sucking out your thoughts
  • thought insertion: planted in your mind or they belong to someone else
  • thought diffusion/broadcasting: other people hearing their thoughts while they can’t necessarily hear their own
  • made impulses: external force causing you to do things without intent, acts aren’t always conscious
  • made feelings: external force giving you affective experiences
  • made volitional acts: attributing your motivation to do something to some external force
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8
Q

disturbances in form of thought

A
  • formal thought/speech disorder
  • derailment: similar to loose associations (can’t follow the logic) but no pressured speech
  • word salad (extreme): no logical or grammatical structure, words not even recognizable
  • alogia: poverty of speech or content of speech (not conveying information)
  • neologisms: making up new words or giving existing words new meaning
  • blocking: related to thought withdrawal, stops speaking abruptly
  • illogical thinking
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9
Q

disturbances in affect

A
  • blunted/flat (anhedonia is common, can be difficult to distinguish profound anhedonia in MDD from flat affect): blunted expression of affect though they might still have rich inner experiences of emotion
  • inappropriate affect: laughing in the wrong situations
  • difficulty perceiving emotions: identifying or tracking others’ emotional changes
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10
Q

psychomotor disturbances

A
  • catatonia (much rarer now)
  • catalepsy/waxy flexibility: patients immobile but you can move them and they’ll stay in that position
  • stupor: immobile and unresponsive to the environment (but no brain damage)
  • posturing: assuming strange positions on their own
  • mutism (still sometimes common)
  • catatonic excitement: looks like psychomotor agitation, but looks purposeless and avolitional
  • catatonic negativism: immobile and resisting attempts to be moved
  • echolalia: senseless and avolitional repetition of auditory input
  • echopraxia: avolitional repetition of movements
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11
Q

disturbance in relating

A
  • very withdrawn
  • preoccupied with a fantasy world that only they can see, others don’t interact with (when supplemented by hallucinations, can be terrifying)
  • disordered volition: aimless and purposeless (has overlap with MDD)
  • anhedonia
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12
Q

positive vs. negative

A
  • positive: presence of symptoms that shouldn’t be there (hallucinations, delusions, inappropriate affect)
  • negative: absence of things that should be there (blunted affect, alogia, avolition)
  • positive responds better to meds, negative hard to treat
  • very few people have only negative symptoms
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13
Q

schizoaffective disorder

A
  • poor reliability, still controversial (thought of as a residual category)
  • not a very distinct diagnosis, but also not just an atypical form of mood disorder or schizophrenia
  • prognosis is better than schizophrenia, but worse than mood disorders
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14
Q

prevalence rates schizophrenia

A
  • 0.7-1%
  • 1.4:1 male to female ratio
  • women tend to present with more symptoms of depression (can explain gender prevalence differences)
  • female sex hormone (estrogen) may be protective
  • child-onset before age 13 is very rare
  • prevalence rates increase for boys and girls in teens (more for boys)
  • prevalence peaks again for women in late 40s (menopause, less estrogen)
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15
Q

Schz in childhood (under 13)

A
  • very rare, more common in boys
  • always insidious onset which makes it hard to tell where actual onset begins
  • usually early speech and language problems (noticeable differences in social, cognitive, motoric deficits)
  • delayed motor development, poor coordination (not reaching motor milestones like crawling, difficulty with smooth pursuit)
  • unlikely to remit
  • higher rates of schizotypal and Schz in relatives (higher genetic loading for child-onset)
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16
Q

course of Schz

A
  • only 20-30% able to live independently
  • another 20-30% have persistent moderate impairment and Sx
  • the last 50% have lifelong severe impairment
  • minority have periods of recovery
  • Schz has poorer prognoses and more impairment than other psychotic and nonpsychotic disorders
  • more benign course in countries that are not yet industrialized (demands of industrialized countries may make it difficult to find somewhere to exist OR because babies with fetal/birth complications are less likely to survive)
  • tend to die younger (even 20 yrs younger)
  • death by suicide is most common, then cardiovascular disease (smoking very common bc it manages sx, antipsychotics can have health-related side effects)
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17
Q

good prognostic indicators

A
  • good premorbid adjustment (had friends)
  • acute onset (less than 1 month)
  • manic and depressive symptoms
  • confusion or disorientation during psychotic episodes)
  • family history of mood disorders
  • patients with 5 good indicators = 80% had more positive outcomes
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18
Q

bad prognostic indicators

A
  • poor premorbid adjustment
  • insidious, gradula onset
  • negative symptoms (esp. blunted affect)
  • family history of Schz
  • lower IQ
  • patients with many bad indicators = 40% had positive outcomes
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19
Q

Schz comorbidity

A
  • substance abuse (alcohol and nicotine)
  • substances could trigger it (esp. ones that mimic symptoms, but also marijuana)
  • suicide risk (20% attempt, 5% complete) especially for young men (good premorbid functioning may have more pronounced risk)
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20
Q

schizophrenia and violence

A
  • perception of dangerousness and violence that isn’t founded
  • very slight increased risk population-wide (this could be driven by higher rates of substance use)
  • aggression more common in younger males with a history of violence (tendency to stop taking meds, toward impulsivity, substance abuse)
  • higher likelihood that people with Schz are likely to be victims of violence or will commit suicide
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21
Q

heritability of schz

A
  • risk gets more and more elevated as you increase genetic overlap with a proband who has schz (Mz, Dz, kids, siblings, parents)
  • higher concordance in Mz twins than any other family member (28% vs. 6% in Dz) but still not as heritable as bipolar
  • offspring of the discordant co-twin (no schizophrenia with a twin who has it) is still much higher (17.4) so genetics playing a role
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22
Q

monochorionic vs. dichorionic twins with schz

A
  • monochorionic twins (Mz) share placenta and circulation & more likely to be schz-concordant than dichorionic Mz twins
  • dichorionic twins (Mz or Dz) do not share this environment
23
Q

endophenotypes

A
  • intermediate step between genotype and phenotype (closer to the genes than phenotype, but still linked to the phenotype)
  • needs to be present in the population of interest
  • must be heritable
  • must always be present (not just in the state of psychosis), not state-dependent
  • co-segregate with the illness within families
  • present at higher rates within affected families
  • amenable to reliable measurement
  • ideally specific to the illness of interest
24
Q

eye-tracking endophenotype

A
  • ability to track the overall shape of the wave, but lots of noise, herky-jerky patterns
  • most reliable lab correlate
  • also seen in unaffected siblings, stays stable over time (not due to having psychosis or treatment)
  • only 50% of people with schizophrenia display this pattern, but more specific to schizophrenia than any other endophenotype (only seen in schz or related disorders)
25
Q

risk factors: SES status

A
  • schz tend to have lower social class (causation vs. selection hypothesis)
  • selection hypothesis: family of origin doesn’t also have lower SES, only the person with schz (difficult to maintain a job, less education, more homelessness)
  • causation hypothesis: immigrants and their first generation descendents tend to have higher rates of schz but their countries of origin do not
  • selective immigration hypothesis: people with higher risk of schz are immigrating (goes against what we know abt immigration & their families of origin don’t have more schz)
  • stress theory of immigration: becoming a minority, dealing with stigma, finding jobs (kids also have to do this)
  • diagnostic bias: black people diagnosed with schz, white people with BP
26
Q

risk factor: paternal age

A
  • advanced paternal age at conception associated with higher risk
  • unclear what the cause/mechanism is
  • could be due to mutations in sperm cells (repeated mitosis)
  • or men who are older and having kids could be different in some way (schizotypal PD more likely to have kids when older?)
27
Q

risk factor: birth complications

A
  • breech delivery, prolonged labour, umbilical cord around neck = anoxia/hypoxia
  • anoxia also associated with DA sensitivity later
28
Q

risk factor: prenatal exposure

A
  • viral infections during 2nd trimester (mothers during an epidemic were more likely to have schizophrenic kids - ecological fallacy, not necessarily every mother came into contact with the flu)
  • antibodies during pregnancy (if you have the antibodies, you had the flu) = schizophrenia in kids - direct evidence
29
Q

risk factor: season of birth

A
  • kids born in late winter/early spring show a 5-15% increase in rates
  • true in both northern and southern hemisphere and their respective winters, and effect decreases as you approach the equator
  • viruses can cause fetal damage and these are more common in fall and early winter (2nd trimester)
30
Q

risk factor: malnutrition during pregnancy

A
  • dutch hunger winter = rates are 2x normal
  • could be a general lack of nutrition or a specific lack of folate or iron which are essential for brain development
  • replicated effect
31
Q

neurodevelopment during 2nd trimester

A
  • important period for neural migration (cells moving out to form the cortex and develop cortical organization)
  • could be a final common pathway conferring risk for schz
  • important for cortical connectivity, could result in cell death or thinner grey matter if disrupted (like by viruses, stress, malutrition)
  • disorganization in how cells are positioned (scrambled/nonparallel cytoarchitecture) and thinner cortices
  • creating a latent vulnerability that can be triggered by a stressor or substance
32
Q

whole brain volume schz

A
  • tends to be decreased even in recent-onset people (suggests it’s not a result of treatment)
  • also see progressive loss of grey matter over time (progressive deterioration continues for many years into the illness)
  • consistent with Kraeplin’s DP
  • beginning in parietal and spreading to temporal and frontal (language and EF areas) until it gets to almost every region
  • not explained by just being ill or by antipsychotics, just a part of the course
  • some genetic mechanisms: inappropriate pruning of cells
33
Q

dopamine hypothesis

A
  • antispychotics block DA D2 receptors
  • cocaine, amphetamines boost DA activity and result in paranoia, psychosis, break with reality
  • L-DOPA for Parkinson’s increases DA and can cause hallucinations
  • hypoxia/anoxia = DA hypersensitivity
  • CSF studies haven’t always found increased DA metabolites (could be a receptor problem which is difficult to test bc antipsychotics alter DA receptor activity)
  • excess DA transmission in the striatum, reduced transmission in frontal lobes
  • aberrant salience: more DA = more attention toward irrelevant stimuli = difficulty integrating your sense of reality with others
  • failure to respond to meaningful reward cues (anhedonia and negative symptoms)
34
Q

dopamine hypothesis: dlPFC

A
  • activity in dlPFC heavily regulated by DA activity
  • region that is very important for working memory
  • working memory deficits seen in schz (and unique to schz, not seen in BP who were actively psychotic or healthy) even when in non-psychotic states, in schizotypal PD, and 1st degree unaffected relatives
  • could be a premorbid risk factor
35
Q

dopamine hypothesis: motor symptoms

A
  • abnormal orofacial movements and upper limb dyskinesia (also seen in childhood and can reliably distinguish kids who went on to develop schz)
  • DA strongly involved in motor systems
  • early premorbid indicator
36
Q

cannabis and schz

A
  • people with schizophrenia 2x more likely to smoke weed
  • but since there’s often insidious onset: maybe people with schz self-medicating premorbid symptoms with cannabis
  • prospective relationship even when controlling for premorbidity (still not definitive proof of causality)
  • THC increases DA synthesis: more DA and DA hypersensitivity correlated with how schz manifests
  • psychosis + consuming cannabis will exacerbate psychotic and cognitive symptoms (working memory, cognitive disorganization)
  • also see greater decreases in grey matter in patients using cannabis than those not using cannabis (still not causal; severe schz = using more, smoking weed because of the loss of grey matter)
37
Q

expressed emotion ins schz

A
  • families high on tendencies to express negative emotions
  • during deinstitutionalization, patients who went home had higher rates of relapse and worse symptoms (these families had more emotional overinvolvement and showing hostility)
  • well-replicated effect regardless of patient characteristics
  • when EE is lowered (family therapy), relapse rates decrease
  • EE could play a causal role (stress of being in this type of family, types of attributions people make about patients)
  • EE still nonspecific (worse outcomes for depression, BP, predicts better outcomes for BPD)
38
Q

components of EE

A
  • criticism: disapproval or dislike of the patient
  • hostility
  • emotional overinvolvment: no emotional distance from others’ emotional experiences, very intrusive
39
Q

Rosenfarb EE study

A
  • the types of reactions patients are eliciting from high-EE families
  • patients expressing somatic concerns, anxiety or depression, irritability, anger/hostility, unusual thinking, bizarre comments
  • in high EE families, patients are more likely to exhibit odd or disruptive bx which elicits criticism from the family, which makes it even more likely that the patient will respond with something else that is odd (defending their reality) and so on
40
Q

multiple hit model

A
  • no single etiological factor will explain the development of schz
  • example pathway: genetic factor + pre/perinatal factor = brain vulnerability + stressors + further disorganization of brain during maturation = psychosis
41
Q

non-psychotic voice-hearers

A

no experienced distress or other effects from auditory hallucinations (usually because their community experiences hallucinations as positive)

42
Q

catastrophizing auditory hallucinations hypothesis

A
  • voices at first seem neutral but they become ominous when you start to fight them and with others’ negative reactions
  • starting to interact with the voices = engaging in strange bx and rituals (these are attempts to make your reality coherent again)
  • catastrophic interpretations of hallucinations, so therapy should focus on how people think about their thoughts
43
Q

1st generation antipsychotics

A
  • neuroleptics
  • have extrapyramidal symptoms (EPS) bc they block all DA receptors: involuntary muscle movements, spasms
  • tardive dyskinesia (potentially permanent bc the brain adds more DA receptors in response to a lack of input): involuntary movements of lips, tongue, neck (which look bizarre and contribute to further alienation)
  • dramatic and rapid decrease in symptom severity (within 24hrs)
  • side-effects include drowsiness, dry mouth, extreme weight gain
  • the earlier you treat psychosis, the better it works (lasting effects if you treat first episode onset)
  • could contribute to loss of brain tissue
44
Q

2nd-generation antipsychotics

A
  • drowsiness, dry mouth, extreme weight gain
  • no EPS side-effects
  • equally effective as 1st gen (except clozapine which is better)
  • more expensive than 1st gen = restricted access
  • can result in metabolic syndrome, downstream diabetes, loss of white blood cells
  • could contribute to progressive loss of brain tissue
45
Q

psychosocial treatments for schz

A
  • family therapy as an adjunct (esp. for high EE)
  • psychoeducation is a major element: explaining what schz is, what causes it, helping them make different attributions abt behaviour
  • improve coping and problem-solving: how to relate to each other and regulate emotions
  • improve communication: reduce aggression and anger
46
Q

CBT for schz

A
  • may be helpful for positive symptoms, not so much for negative symptoms
  • goals: decrease intensity of positive sx, reduce relapse, decrease social disabilities
  • coping with hallucinations and delusions: changing the response you’re having can help decrease their intensity
  • VR environments where patients can practice chit-chat to increase their likelihood of having low-stakes positive interactions with strangers (has downstream positive effects on symptom severity)
47
Q

ABC model

A
  • activating event: voices or a real-life event
  • belief: what people think about the voice (usually these are negative)
  • consequence: emotions you’re having bc of the belief, behaviours you perform bc of it
  • try to intervene around the belief to separate feelings from what is actually happening
48
Q

thought suppression schz

A
  • trying not to think about something means you’re actively keeping the thought in mind and makes it come back stronger
  • main goals of CBT and ACT for schz is to stop fighting the thoughts, just to accept it and not let it affect your behaviour or feelings
49
Q

hearing voices network

A
  • peer support group for anyone who hears voices (which isn’t necessarily psychopathological in itself just because of statistical deviance, and the voices can be accommodated)
  • aims to reduce distress surrounding auditory hallucinations
  • evidence is anecdotal
  • evidence that they work better for people with lower social functioning: could just be providing social contact and an accepting environment to practice social skills
  • limited evidence for whether they reduce distress about the voices, but can reduce stress about voices, take away their power and control over your behaviour
50
Q

rules of engagement hearing voices network

A
  • trying to increase ability to be assertive with your voices
  • develop a contract for when you can engage with the voices or when you ignore them
  • tips for how to deal with the hallucinations like pretending to talk on the phone while you shout at them
  • selective listening: only engage with the voices when they say something positive (reward) and ignore when they say something negative (extinguish)
51
Q

cognitive and biological factors in schz from textbook

A
  • deficits in sensory gating (filtering out unnecessary stimuli)
  • deficits in verbal and spatial memory, EF, social cognition
  • enlarged brain ventricles (brain shrinking)
  • ‘leaky’ myelinated pathways indicating axonal damage (abnormal connectivity)
  • adolescence is a period of synaptic pruning, but it may go on too long and result in schz-prone brains
52
Q

premorbid vs. prodromal

A
  • premorbid: subtle and occur long before onset
  • prodromal: immediately precede onset (this is so common that there are criteria for identifying individuals who are at high risk for developing schz in the next two years
53
Q

phases of schz treatment

A
  • acute: reduce sx severity using meds
  • stabilization: to consolidate gains and attain a stable living condition
  • maintenance: when sx are in remission, prevent relapse and improve functioning