College aantekeningen
Notes for EUR 3.4 Depression and Psychosis
All articles and book chapters from 2019-20 are covered.
[Meer zien]Voorbeeld 4 van de 77 pagina's
Voorbeeld 4 van de 77 pagina's
In winkelwagengesponsord bericht van onze partner
Voorbeeld van de inhoud
Week 1: SchizophreniaPart 1: What is schizophrenia?
1. What is schizophrenia (DSM 5)?
a. Etiology
b. Symptomology
2. What is the difference to dementia?
Walker, E., Kestler, L., Bollini, A., & Hochman, K. M. (2004). Schizophrenia:
Etiology and Course. Annual Review of Psychology, 55(0), 401–430.
Introduction
• Schizophrenia is complex – no single factor discovered that characterises all patients
• Extremely debilitating
o Many first diagnoses between ages of 20-25; disrupts important stage of life
(independence from parents, intimate relationships, life and career goals)
o Profound neg impact on opportunities for attaining social and occupational success →
devastating for adult life course
• Occurs in all countries and across cultures and ethnic groups
• Current article: up-to-date overview of the status of scientific knowledge and theory about
schizophrenia
o Clear consensus that schizophrenia is a brain disease.
o Questions regarding nature of the etiological process: what neural abnormalities and
how are they triggered?
• Three themes:
o Etiology of schizo involves interplay between vulnerabilities and environmental
factors
o Illness does not emerge from specific deficit in specific region but dysfunction of
circuits that are comprised of multiple brain regions
o Brain maturational processes play a critical role in the etiological process
History and • Kraeplin first to differentiate schizophrenia (referred to as dementia praecox)
phenomenology • Schizophrenia: splitting of the mind (Bleuler, 1911)
o Reconceptualised dementia praecox as the group of schizophrenias, which reflects
contemporary view that schizophrenia is heterogenous group of disorders with varied
eitologies but similar clinical presentations
• Schneider, 1959 → dramatic changes to diagnostic conceptualisation:
o First-rank symptoms: diagnostic of schizophrenia (including types of hallucinations
and delusions that characterise the signs of psychosis)
o eg- thought insertion, thought broadcasting, thought withdrawal etc
o more detailed and specific than Bleuler’s conceptions
• 1980s → emphasis on negative/positive symptom distinction
o Positive symptoms: involve an excess of ideas, sensory experiences or behaviour
(eg- hallucinations, delusions and bizarre behaviours0. Emphasised by Schneider’s
first-rank symptoms.
o Negative symptoms: involve a decrease in behaviour (eg- blunted effect, anhedonia
and amotivation). Emphasised by Bleuler.
• Variety of diagnostic systems through 20th century meant that research progress somewhat
stunted. Most of these were unified under DSM.
DSM-5 Diagnosis (most widely used):
• Schizophrenia is main diagnostic category. Occurs when there is a range of symptoms
covering cognitive, behavioural and emotional dysfunction and also impaired occupational or
social functioning.
o At least two of the following are present for a significant amount of time during a
one-month period:
▪ delusions
▪ hallucinations
▪ disorganized speech
▪ highly disorganized or catatonic behaviour
▪ negative symptoms such as diminished emotional expression
, o ability to function in one or more major areas is markedly diminished (work, self-care,
interpersonal relationships)
o continuous signs of the disturbance last for at least 6 months (including prodromal and
residual phases).
o disorder is not directly attributable to substance or medication, not better explained by
another mental disorder
Subtypes of schizophrenia described in DSM 5
• paranoid:
o preoccupation with delusions or hallucinations,
o but there is no disorganised speech, disorganised or catatonic behaviour or
flat/inappropriate affect
o this subtype has best prognosis
• catatonic:
o dominated by postural and/or movement abnormalities, mutism and echolalia
• disorganised:
o prominently: disorganized speech, disorganized behaviour and flat/inappropriate
affect (but the criteria for catatonic are not met)
o worst prognosis
• undifferentiated: when patient doesn’t meet criteria for previous subtypes but does meet
criteria for schizophrenia.
Two other diagnostic categories
• residual:
o for individuals who previously met criteria in the past, but no longer do
o applied when there is a prominence of negative symptoms but not prominent
delusions, hallucinations, catatonic symptoms or disorganised speech/behaviour.
• schizophreniform disorder:
o when symptoms do not meet the 6-month criteria
o often made as a prelude to schizophrenia diagnosis (although some will recover
completely and not suffer further psychosis
• diagnostic boundaries of schizophrenia are still unclear
• also boundaries between schizophrenia and mood disorders are obscure
o many schizophrenics show marked signs of depression
o depressive symptoms sometimes present before the onset of schiz; also frequently
occur in combination with marked psychotic symptoms
o → schizoaffective disorder: hybrid between mood disorders (bipolar disorder or
major depression with psychotic features) and schizophrenia. Prognosis somewhere
between that of mood disorder and schizophrenia
▪ depressive subtype: if mood disturbance only includes depressive episodes
▪ bipolar subtype: where symptoms of the disorder includes manic episodes
Cognitive and • performance deficits on cognitive tasks from both simple to complex
socioemotional • not merely the side-effects of treatment → apparent in first-episode patients
aspects of • deficits at early stages of sensory processing
schizophrenia o eg- slower in initial processing of visual/auditory stimuli (assoc with less brain
activation in thalamus, PFC, parietal lobe etc)
o eg- inhibited prepulse inhibition, where startle response is not reduced via exposure to
a pre-stimulus (as it would be in normal)
• impairments in responding to stimuli
o due to both deficit in speed of response selection and execution of motor responses
o most common: deficits in manual motor speed and coordination
• impairments in higher level cognitive functions
o verbal and spatial memory, attention
o executive functions (eg- abstract reasoning and planning). These cog abilities are
subserved by frontal lobes and are predictive of prognosis
• deficits in thinking about social phenomena
o impaired ability to comprehend and solve social problems
o may be due to limitations in more basic cog processes (eg- memory and reasoning),
however these cannot fully account for social-cog deficits
o abnormal expressions of emotion in both faces and verbal communication (less
intense facial expression, more neg expressions, less accurate than normal
comparisons in labelling)
, • UNRESOLVED QUESTION: whether schizophrenia is assoc w/ decline in cog functioning
following clinical onset. True for some patients.
• Deficits in cog functioning
o Not specific to one sensory modality, stage of information processing or cognitive
domain (eg- planning, memory, abstract reasoning)
o Instead, impairments are generalised
o Aggregated data obscures substantial individual differences in performance (eg- some
patients are average or above; some patients are outside range for normals)
▪ Suggestion that there are no specific or unique cognitive deficit in
schizophrenia; they may be secondary consequences of one or more etiologic
contributing factors.
The origins of vulnerability
The genetics of • Vulnerability to the illness can be inherited:
schizophrenia o risk for schizophrenia is elevated in individuals who have a biological relative with
the disorder → closer genetic relative (eg- parents, siblings) = greater likelihood
o evidence from genetic studies using twin, adoption and family history methods
▪ Monozygotic twins (MZ), share 100% of genes → 25-50% of cotwins will
also develop illness
▪ Dizygotic (DZ) twins share about 50% genes → 10-15% of DZ cotwins are
also diagnosed with the illness
• Adoption studies
o Show that schizophrenia can run in families due to genetic factors, rather than the
environmental influence of being exposed to mental illness
▪ Eg- biological relatives of adoptees with schizophrenia found to also have
higher rates of schizophrenia than the adoptive relatives who raised them)
o BUT, genetics may act in concert with environmental factors → genetic vulnerability
mainly expressed in assoc w/ disruptive adoptive environments (consistent with the
diathesis-stress model)
• Disorder involves multiple genes, rather than a single gene
o Array of genes acting together, or numerous single susceptibility genes acting
independently
o Potential candidate genes: 5-HT2a, D3 receptor gene, several chromosomal regions,
22q11 deletion (25% with this abnormality have schizophrenia)
• Significant overlap in the genes that contribute to schizophrenia, schizoaffective disorder and
manic syndromes. There may genetic vulnerabilities to psychosis in general, and the
expression of these can take the form of schizophrenia or affective psychosis (depending on
other inherited and acquired risk factors).
• Hard to estimate relative magnitude of the inherited and environmental contributors to etiology
of schizophrenia
• Do not know whether genetic vulnerability is present in all cases of schizophrenia
• Also, do not know whether genetic predisposition to schizophrenia is always expressed
(unexpressed genetic vulnerabilities may be common in general population)
Prenatal and • Events that adversely affect fetal development are now considered as potential
postnatal factors environmental triggers of genetic vulnerability.
o They are also sufficient to produce vulnerability to schizophrenia
• Prenatal events
o Obstetrical complications (OCs), including pregnancy problems + labour/delivery
complications. Those most linked to hypoxia (fetal oxygen deprivation) were most
strongly linked to later schizophrenia.
o Maternal infection: higher rate of schizophrenia after flu epidemic or exposure to
rubella. “season of birth” effect – disproportionate births after winter.
o Prenatal maternal stress: assoc with greater risk for schizophrenia and general
psychopathology in offspring (eg- mothers who lost spouse or divorced during
pregnancy). Mechanism likely stress hormones disturbing fetal neurodevelopment.
• Postnatal events
o Head injuries, particularly if sustained in early childhood
• Questions: whether OCs and postnatal brain trauma act independently to increase risk for
schizophrenia, or act in conjunction with a genetic vulnerability
• More likely that genetic vulnerability involves increased sensitivity to prenatal complications
and/or postnatal brain trauma
, • Less likely that prenatal and postnatal brain insults act independently of genetic vulnerabilities
→ such effects would entail complex interactions among factors
Course and prognosis
• Assuming that genetic and obstetrical factors confer the vulnerability for schizophrenia, the
diathesis (tendency) must be present at birth
• BUT, schizophrenia typically diagnosed in late adolescence or early adulthood (males
typically four years earlier than females on average)
• → This raises interesting questions about developmental course prior to the clinical onset
Premorbid • Evidence that signs of schizophrenia are (subtly) visible before diagnosis
development • Comparison of children who will develop schizophrenia to those with healthy adult outcomes
= deficits apparent as early as infancy
• Cognitive functioning: children perform below healthy siblings and classmates on measures
of intelligence and achievement. Poorer grades in school. Magnitude of deficit more
pronounced in adolescence.
• Abnormalities in social behaviour:
o less responsive in social situations, show less positive emotion, poorer social
adjustment.
o More negative facial expressions of emotion than siblings visible from first year (via
home movies), indicating schiz vulnerability subtly manifested in earliest
interpersonal interactions.
• Motor functions
o Delayed and abnormal motor development (eg- bimanual manipulation and walking)
o These motor deficits persist into clinical illness
o Motor deficits are also observed in children at risk for various disorders (including
learning). However is an important cue towards dysfunctional brain circuitry in
schizophrenia.
• At risk children usually don’t manifest diagnosable mental disorders until adolescence.
o Here, subtle signs of abnormality give way to pattern of escalating adjustment
problems (including depression, social withdrawal, irritability, substance abuse
problems).
o However, this developmental pattern not unique to schizophrenia → adolescence is
critical period for emergence of broad range of disorders.
• Behavioural risk factors sometimes observed in preschiozphrenic adolescents are subclinical
signs of psychotic symptoms:
o Defining features of Axis II disorders (namely schizotypal personality disorder)
o Symptoms: social anxiety/withdrawal, affective abnormalities, eccentric behaviour,
unusual ideas (eg- extrasensory phenomena) and unusual sensory experiences
o Unusual ideas and perceptions not severe or persistent enough to meet criteria for
delusions or hallucinations, but they are recurring
• Extensive research shows genetic link between SPD and schizophrenia (through twin and
family history studies)
o Also, longitudinal studies indicate that 20-40% of youth with schizotypal signs
eventually show an Axis I schizophrenia spectrum disorder
o Remainder either show other adjustment problems or a complete remission of
symptoms in young adulthood
o Adolescents w/ SPD manifest some similar functional abnormalities to schizophrenics
→ motor abnormalities, cognitive deficits and increased cortisol
Illness onset and • Onset of clinical symptoms can be abrupt or gradual → but is usually preceded by prodromal
course phase: escalating signs of behavioural dysfunction and subclincal psychotic symptoms
• Longer untreated psychotic episodes may be harmful for schizophrenia patients and result in a
worse course of illness
• Following clinical onset: varied course of illness
o Some experience full recovery (only 20-30% of patients will be able to lead relatively
normal lives; i.e., independent living and holding job)
o Majority experience debilitation (20-30% manifest continued moderate symptoms and
>50% experiencing significant impairment throughout adulthood)
• Chronicity of illness = suicide is leading cause of death among people with schizophrenia
• High rate of comorbidity (e.g., high rate of substance abuse)
• Determinants of course of schizophrenia:
o Poorer prognosis associated with male sex, gradual onset, early age of onset, poor
premorbid functioning, family history of schizophrenia.
Voordelen van het kopen van samenvattingen bij Stuvia op een rij:
Verzekerd van kwaliteit door reviews
Stuvia-klanten hebben meer dan 700.000 samenvattingen beoordeeld. Zo weet je zeker dat je de beste documenten koopt!
Snel en makkelijk kopen
Je betaalt supersnel en eenmalig met iDeal, creditcard of Stuvia-tegoed voor de samenvatting. Zonder lidmaatschap.
Focus op de essentie
Samenvattingen worden geschreven voor en door anderen. Daarom zijn de samenvattingen altijd betrouwbaar en actueel. Zo kom je snel tot de kern!
Veelgestelde vragen
Wat krijg ik als ik dit document koop?
Je krijgt een PDF, die direct beschikbaar is na je aankoop. Het gekochte document is altijd, overal en oneindig toegankelijk via je profiel.
Tevredenheidsgarantie: hoe werkt dat?
Onze tevredenheidsgarantie zorgt ervoor dat je altijd een studiedocument vindt dat goed bij je past. Je vult een formulier in en onze klantenservice regelt de rest.
Van wie koop ik deze samenvatting?
Stuvia is een marktplaats, je koop dit document dus niet van ons, maar van verkoper eur-lifesaver. Stuvia faciliteert de betaling aan de verkoper.
Zit ik meteen vast aan een abonnement?
Nee, je koopt alleen deze samenvatting voor €16,99. Je zit daarna nergens aan vast.
Is Stuvia te vertrouwen?
4,6 sterren op Google & Trustpilot (+1000 reviews)
Afgelopen 30 dagen zijn er 53022 samenvattingen verkocht
Opgericht in 2010, al 14 jaar dé plek om samenvattingen te kopen