13- Schizo Flashcards
History
Emil Kraepelin => Recall medical model / classification of “syndromes”
Refined unitary concept of “psychosis” into two distinct syndromes:
- Dementia Praecox = dx with progressive deterioration (Unlike other dementias, begins at early age)
- Manic Depression
=> Differentiated BP and Schz as distinct dx but evidence now for common genetic vulnerability and continuum of dysfunction
Eugen Bleuler (1857 –1939) => Swiss psychiatrist, contemporary of Kraepelin
Argued against notion that this phenomena was best characterized as dementia (deterioration) praecox (early onset) => Did not always deteriorate + Could emerge at later age
=> In 1911, used the term “schizophrenia” for the first time aka “schizo” (to split, or crack) “phren” (mind)
- Dx characterized primarily by loss of association between thought processes, emotion, and behavior
- Caused by neurobiological disease process
- Gives rise to secondary sx ex: hallucinations, delusions
- Distinction from “multiple personality disorder” => Or dissociative identity disorder (DID) in DSM-5
Schizo DSM-5 Criteria
Need at least TWO of the following:
- Delusions*
- Hallucinations*
- Disorganized speech*
- Grossly disorganized or catatonic beh
- Negative symptoms
=> With marked functional impairment, sx present for 6 months and includes at least one month of active symptoms
- Ruled out other disorders ex: unipolar, bipolar, schizoaffective disorder
- Not attributable to substance use
Delusions
Dx of thought content
- False belief based on an incorrect inference
- Firmly held despite contradictory evidence
- Delusions are extreme end of continuum
- Mild end: over-valued ideas => False belief, but willing to entertain the idea that it’s false (Common in schizotypal PD + prodromal (low sx lvl) schizo)
Ex:
- Thought broadcasting
- Thought insertion
- Grandiose delusions
- Delusions of jealousy
- Nihilistic delusions (nothing is real, everyone is dead)
- Persecutory delusions (ex: under cover agents)
- Delusions of reference (everything in your env is for you)
- Religious delusions
- Somatic delusions
Hallucinations
- Continuum from illusions to hallucinations
- Can occur in all sensory modalities => Auditory*, visual, olfactory, tactile, gustatory
=> Auditory: Perceived as distinct from one’s own thoughts, Speak at normal conversational volume, Often reflect voices of people they know, Most often derogatory
Are they really hearing voices though? => Alternative explanation: Do they misinterpret their own self talk?
=> Study: Sample of Schizophrenic patients with hallucinations, Schizophrenic patients without hallucinations, Healthy controls
Participants read complimentary, derogatory, or neutral adjectives + Recorded them, altered pitch, and played it back to them then ask if source is self, someone else, or unsure
Results:
- Schz w/ hallucinations more likely to misidentify their distorted speech as belonging to someone else
- Especially likely if derogatory words (vs. neutral or complimentary)
- Not just uncertain, but rather positively misidentifying
=> Misattribution of sensory experience + Lots of support for this with brain imaging studies
Disorganized Speech and Catatonic Beh
Also disorder of thought form
- Communicates words and sounds, but
doesn’t make sense - Loosening of associations or “derailment”
- Word salad
- Alogia (don’t speak aka poverty of speech)
- Neologisms (make up words)
- Blocking (talk…. then stop)
Catatonic Beh => Psychomotor deficits ranging agitation to immobility with unpredictable movements
Problems with everyday activities ex: dressing, hygiene
- Catatonia => Stupor (rigid posture), Waxy flexibility (can mold them), Much rarer now than 100 years ago
Negative and Positive Sx
Neg Sx (absence of ~):
Affect => Blunted/flat affect
- Appear emotionally unexpressive and nonresponsive, but physiological measures reveal heightened reactivity
- Inappropriate affect (don’t match sit)
- Problems perceiving others’ emotions
Motivation => kind of overlap with depression
- Very socially withdrawn
- Anhedonia
- Avolition => no motivation to do things in a goal-directed way
Positive vs. Negative Symptoms
- Positive = presence of sx that shouldn’t be there ex: hallucinations, delusions, inappropriate affect => tend to respond better to medz
- Negative = absence of something that should be there ex: blunted affect, alogia, avolition, anhedonia => often very hard to treat (poorer prognosis with negative sx)
Schizoaffective Dx
People with schizophrenic features AND a severe mood dx => Mood disorder can be unipolar or bipolar
- Need to have delusions or hallucinations for at least 2 weeks in the absence of mood episode
- Symptoms of mood episode present for at least 50% of the total duration of illness
- Not attributable to effects of substance
=> Issues:
- Poor reliability
- Controversial since introduction in 1933
- Not clearly a distinct dx
- Prognosis is somewhere between schizophrenia and mood dx
- Long-term prognosis for schizoaffective > schizophrenia
Epidemio
Prevalence Rates & Gender Differences
- Lifetime prevalence rate about .7% to 1%
- M:F ratio is about 1.4:1
- Males tend to have more severe sx
- Some gender difference may be accounted for by bias in dx => Women also presenting with depressive sx and less severe psychotic sx more likely to be diagnosed with something else
- Female sex hormones (estrogen) may also be protective => Postmenopausal, estrogen decreases *Late-onset schizophrenia more common in women
Age of Onset => Most onset in late adolescence and early adulthood (18 to 30)
- Gender differences in onset
- Schizophrenia in childhood rare
- Extremely rare to see onset before age 13
- More common boys
Course => Study: Followed 208 patients for 20 years
- 22% had very bad outcomes (continually psychotic)
- 52% had intermediate outcomes (symptoms, but not continually psychotic)
- 22% had improved
=> Many attempts to re-examine these data have
found same pattern of findings
- More insidious onset associated with poorer outcomes (vs. acute onset)
- Course is very heterogeneous => Probably because dx is heterogeneous
=> Variation as function of country
- Studies consistently find better outcomes for ind with schizo in developing countries
- Despite poorer countries having less access to mental health resources and services ex: less likely to be on antipsychotic medz
Unclear why, but have proposed cultural explanations => Greater dependence on social network
Comorbidity and Violence
Subs abuse very common =>
- Especially alcohol and nicotine
- Nicotine may play self-medicating role
- Subs can also trigger sx => improve fcting & improve cognitive deficits that axe ass with attention, memory, sensory processing
=> Average life expectancy is approx. 20 years shorter than general population
Suicide
- About 20% will make at least one attempt
- 5% die by suicide
- Especially young men
- Some evidence that those with best premorbid functioning more at risk
=> Common perception that people with schizophrenia are dangerous and aggressive
Likely a slight increase in risk (population wide)
Aggression more common if:
- Male
- History of violence
- Non-adherence to taking meds
- Impulsive personality traits
=> Link between schizophrenia and aggression is probably best accounted for by substance use *Substance use alone increases risk of aggression
Majority of people with schizophrenia more likely
to be victims of violence or suicide
Etiology - Genes and Env
Schizophrenia has long been known to run in families => Risk increases with increasing genetic similarity and Also find higher rates of schizotypal PD in families of person with schizo
Twin Studies
- Higher concordance rates for Mz twins than for Dz twins
- Meta-analyses suggest concordance rates of: Mz: 28% * Dz: 6% (Heritable, but not as heritable as bipolar)
Study: Offspring => Incidence rate of schizophrenia 17.4% (kids have High genetic risk + Low environmental risk)
Twin studies can also overestimate genetic heritability
Genetic Vulnerability
- Clear that genes play a role
- Attempts to identify “schizogenes” => Over 600 possible genes identified each making small contribution to outcome
- Also clear that genes don’t explain everything (not 100% concordance rates)
- Adoption studies demonstrate that the environment you are raised in matters => Adopted kids of biological parent with schizophrenia have heightened risk BUT no risk if they are raised in healthy adopted family env
*Genes are not deterministic
Shared Environment
- 2/3 of Mz twins are monochorionic (share placenta and blood supply)
- Dz twins are always dichorionic
- Schiz concordance rates for Mz twins that are monochorionic are higher than Mz twins that are dichorionic
Risk Factors (5)
1- Prenatal Viral Infections
- Mother’s exposure to viral infections during pregnancy
- Major epidemic of influenza in Finland => Increased risk of Schiz among children of moms who were at their second trimester at the time of the epidemic *But, can’t tell if moms were actually exposed or not
- Direct evidence: Measured antibodies for viruses during pregnancy => Found increased risk of later schizophrenia
=> What is the mechanism? New research looking at immune response
2- Season of Birth
- Small but significant increase in risk for people born in late winter, early spring (5-10% increase)
- Viral infections most common in fall and early winter => Mom would be in second trimester of gestation for people born in late winter, early spring
- Others propose that lack of vitamin D exposure can influence prenatal brain developmental
3- Birth Complications
- Schiz more likely to have experienced birth complications than healthy controls ex: prolonged labor, preterm delivery, low birth weight, fetal distress, breathing difficulties
- All can result in hypoxia/anoxia
- Hypoxia/anoxia at birth can also result in structural brain changes and alter sensitivity to dopamine
4- Advanced Paternal Age
- Advanced paternal age at conception associated with increased risk of Schiz
- Evidence suggests this might best be accounted for by association between late fatherhood and schizotypal PD => Men with schizotypal PD more likely to marry late
5- Social Class
- Schizophrenics tend to have lower SES
Two competing hypotheses:
- Social causation
- Social drift
- Social drift: Family of schizophrenic not necessarily at low SES
- Social causation: Immigrants have higher rates of Schiz, but country of origin do not
Etiology - Neurocognitive (4)
1- Neurocognitive Impairments
- Frontal brain deficiency hypothesis
- Consistently see poor performance on neuropsychological tests that rely on frontal lobe ex: attention, language, memory
- Cognitive impairments appear early on => Low IQ risk factor for Schiz * Likely not just consequence of the illness (However, deficits can be magnified in acute phases)
Ex: Wisconsin Card Sorting Task => don’t have flexible thinking
2- Smooth Pursuit => deficits in smooth pursuit in Schiz patients
- Also see deficits in first-degree relatives of Schiz patients
- Stable over time
- Seems to not just be due to attentional dysfunction => Don’t find this in ADHD samples
3- Loss of Brain Volume
- Lots of evidence for decreased whole brain volume in schizophrenia (About 3% less volume than controls)
- Even in recent-onset (suggests not a result of tx)
- Progressive loss of gray matter after onset
- Progressive deterioration also continues for many years into the illness => Re: Kraepelin’s dementia praecox
4- Gray Matter Deficits
- Also evident in discordant Mz twins of schizophrenics
- Not explained by antipsychotic medz or other tx
- Not explained by damage from the illness itself
- May be a causal risk factor under genetic control
Dopamine Hypothesis
One of the most enduring theories of schizophrenia
- Therapeutic effects of antipsychotic drug on schizophrenic symptoms worked on dopamine system => Blocks dopamine D2 receptors
- Cocaine, amphetamines boost DA activity => Can result in psychosis, paranoia, distorted sense of reality
- L-DOPA for Parkinsons => Suggestive, but none provide direct evidence
Previously challenging to study
- One approach was to use postmortem brains
- Challenging because most people with Schiz are on antipsychotics
Technological advances with PET scans
- Too much dopamine synthesized and released into synapse
- Some evidence for increased D2 and D3 receptors (although more likely linked to treatment effects)
Revised dopamine hypothesis
- Excess DA transmission in striatum
- Reduced DA transmission in frontal lobes
How might DA influence schizophrenic sx?
Positive sx can be explained by increased DA activity
- Aberrant salience
- Increased DA may cause pts to attend more to
irrelevant stimuli - Patients may struggle to make sense of everyday experiences
Negative sx can be explained by decreased DA activity
- Anhedonia, avolition, alogia
- Cognitive impairments (working memory)
Etiology - Cannabis Use
People with schizophrenia are 2x more likely to smoke weed => Correlate? Or cause?
- Evidence that it predicts onset of Schiz => But could they just be in early stages of disorder? Significant effect even when controlling for childhood sx of psychosis
- THC increases DA synthesis
- Cannabis use exacerbates symptoms in people with Schiz
Etiology - Family Env (EE)
- “Schizophrenogenic mother”
- Expressed Emotion => Deinstitutionalization of patients (Some go home to live with parents/Some live solitary lives)
- Expressed emotion (EE) refers to caregiver’s attitudes toward child with mental dx
Three components:
- Criticism
- Hostility
- Emotional overinvolvement
=> Repeatedly shown to predict relapse *Regardless of characteristics of patients
- When EE is lowered, relapse rates decrease
- Suggests EE may at least play causal role in relapse
- Idea is that high EE increases stress for the patient
Vicious Cycle => Patient says something strange, High EE family more likely to criticize, Increases probability of another strange remark, Increases probability of more criticism
