Schizophrenia Flashcards
what is psychosis
cluster of disorderds, delusions, hallucinations and/or loss of contact with reality
schizophrenia is a type of psychosis
annual cost of schizophrenia
$65 billion anually
historical background of schizophrenia
haslam - a form of insanity, pinel working at same time
Kraeplin - dementia praeox (premature loss of mind). focused on onset and outcomes. combined symptoms which had been considered separate - spotte shared similar underlying features
Bleuler - introduced term schizophrenia meaning splitting the mind
facts about schizophrenia
- course
- gender
generally chronic
16-25 yo onset = young phenomena
moderate-to-severe lifelong impairment
life expectancy is slighty less than average - suicide, poverty, homelessness etc
equal gender distribution but women =better long term prognosis and different onset (men diagnosed earlier and women later)
rule of thirds in schizophrenia
1/3 = psychotic then back to functioning 1/3 = stay psychotic but just about independent 1/3 = downwards spiral
recent findings about schizophrenia
not a single disorder
8 genetically based variations
symptoms include clusters linked to different variations
DSM5 schizophrenia
2 or more -delusions -hallucinations -disorganised speech -disorganised or catatonic behaviour -negative symptoms (eg flat affect) impaired functioning 6 months (1 month of active symptoms)
dimensional assessment of schizophrenia
used to have subtypes but elimiated for DSM5 focus on symptom pattern and severity dimensions -hallucinations -delusions -disorganized speech -psychomotor behaviour (catatonia) -negative syptoms -cognition -depression -mania
positive symptoms of schizophrenia
active manifestations of abnormal behaviour or distortions of normal behaviour
delusions (90%)
hallucinations
types of delusions
somatic grandeur persecution manifestation delusion - strong belief that are misinterpreted as reality
what are hallucinations
sensory events without environmental input
auditory are the most common (can be any sensory modality)
normal volume, known, external, negative
brain studies of auditory hallucinations
broca’s area is active - speech production not wernicke’s (hearing bit)
= its their own inner voice
negative symptoms of schizophrenia
absence or insufficiency of normal behaviour
avolition (apathy) - inability to initiate and persist in activities
alogia - a relative absence of speech
anhedonia - inability to experience pleasure or engage in pleasureable activities
flat affect - show little expressed emotion, but may still feel emotion
define associative splitting
a separation among basic functions of human personality seen by some as the characteristic feature of schizophrenia
does not mean multiple personalities
capgras and cobards
Capgras - friend / family member has been replaced by a double
cobards - person believes they are dead, delusions
disorganised symptoms of schizophrenia
severe and excessive disruptions in
speech
affect - inappropriate eg crying at a funeral
behaviour
speech disordered in schiophrenia
cognitive slippage - ilogical and incoherent
tangentiality - going off on a tangent
loose associations or derailment
behaviour disordered in schizophrenia
disruption in goal directed behaviour
devline in routine daily functioning
catatonia - spectrum from wild agitation, waxy flexibility to complete immobility
can you spot schizophrenia signs in at risk children
studied at risk kids eating luncha nd interacting
then followed up 2 years later
those who later went on to develop schizophrenia typically displayed a less poisitve and more negative affect = so emotional affec could be a way to spot schizophrenia potentail in at risk children
how did we use to classify schizophrenia
paranoid
disorganized - silly, immature emotionality
catatonic - alternate mobility, excited agitation
dropped for DSM5
but in practice clinics often their own way of categorizing based on symptoms to aid recovery eg positive symptoms = good prognosis, largely negative or disorganised = poor prognosis
problems with diagnosis of schizophrenia
heterogeneity of symtoms
-symptoms change as dis develops
-schizophrenics can slip back into reality
treatment response varies
unitary disorder?
is it distinct from normal experince? yes
one of the most studied disorders but still not well understood
delusional disorder
delusions without other major schizophrenia symptoms
may show other negative symptoms
types of delusions = erotomanic (soulmate belief), grandiose (JC picked me), jealous (spout is cheating), persecutory (gov is after me), somatic
so a persistent belief that is contrary to reality. delusions are long standing and persisting
rare
late onset
more females than males
do function
aspects of hereditable personality traits
brief psychotic disorder
one or more positive symptoms of schizophrenia
usually precipitated by extreme stress or trauma
lasts less than a month
schizotypal personality disorder
odd beliefs and behaviour but reality testing generally intact
may reflect a less severe form of schizophrenia
schizophreniform disorder
schizophrenic symtpms for less than 6 months
associated with good premorbid functioning
2/3 go on to develop schizophrenia
schizoaffective disorder
schizophrenia with mood disorder symptoms during the psychosis
so need 2 weeks without mood symptoms major mood episode
shared psychotic disorder
a psych disturbance in which inidividuals develop a situation similar to that of a person whom they share a close relationship
in DSM5 included under delusional disorder
atteniated psychosis syndrome
a diagnosis under study that would be given to a person who is beginning to experience one or more of the symptoms of schizophrenia, such as hallucinations or delusions but is aware these are unusual experiences
high risk of developing schizophrenia - may be an prodomal stage
early schizophrenia signs
more severe symptoms first occur in late adolescence / early adulthood but may even be signs in early childhood
physical abnormalities
poor motor coordination
mild cognitive and social problems
but cannot be sure a child will develop schizophrenia
prodomal stage
perios of 1-2 years before serious symptoms of schizophrenia occur but when less severe but unusual behaviours start to appear
schizotypal personality disorder
a personality disorder involving a pervasive pattern of interpersonal deficits featuring acute discomfort with and reduced capacity for close relationships as well as cognitive or perceptual distortions
culture and schizophrenia
some argue it isnt real and just a derogatory label for people who behave outside of cultural norms
but emotional pain = it is real
course and treatment outcomes vary from culture to culture (worse outcomes in Asis)
in london blacks = more likley to be detained against their will etc
natural course of schizophrenia
premorbid
prodromal
onset / deterioration
chronic / residual
genetic influences from family studies
inherit a tendency for schizophrenia - any type not a specific type
schizophrenia increases risk in other family members. also more severe = more risk
genetic influences from twin studies
risk in MZ twins rhighest
so definitley genes but also big environment
genetic influences from adoption studies
risk remain high in adopted children with a biological parent suffereing from schizophrenia
but highly supportive / good adoption fmaily = protective
summary of genetic research
risk increases as a function of genetic relatedness
multiple genes involved
one need not show symptoms of schizophrenia to pass on relevant genes
schizophrenia has a strong genetic component, but genes alone are not enough
paternal age = more cell divisions in sperm
Genain quads
4 women, all schizophrenic. same genetics and same dysfunctional family
but different onset, symptoms, course and outcomes
de novo mutations
gene mutations that occur as a result of a mutation in a germ cell
how can identical siblings have different environmens
different prenatal and faimly experiences = unshared environemtns
eg diff treatment by fam
different nutrients in womb as have to compete for them
differeing traumatic birth experiences
implicated genes / chromosomes
15 / 23 have been implicated neuroreglin 1 = NMDA, GABA, Ach receptors synaptic plasticity DA metabol G72 - regulates glutamatergic activity mylenation, glial function
smooth pursuit eye movement
tracking a moving object visually with head kept still
tracking is impaired in persons with schizophrenia including their relatives
offspring of twins study
identical twin pairs plus frat twin pairs
wanted to determine relative likelihood childs risk
data showed you can have genes that predisopose you to schizophrenia, not show dis yourself, but still pass dis onto your children
what genetic methods can we use
genetic linkage studies - known genes as marker points
endophenotyping - find basic processes that contribute to the behaviours or symptoms of the dis and find the gene / genes that cause these difficulties (eg smooth eye pursuit movements)
dopamin hypothesis
overactivity of dopamine DA neurons in the brain causes schizophrenia
support for dopamine hypothesis
drugs (eg neuroleptics) that block dopamine receptors reduce positive symptoms, acting on D1 and D2
amphetamines which increase dopamine = create positive symptoms
high number of D2 receptors in schizophrenic brains
so dopamine agonist = schizophrenic activity up, dopamine antagonist = schizophrenic activity down
problems with dopamine hypothesis
dopamine antagonists don’t treat negative symptoms
new drugs = poor dopamine antagonists but work really well
time lapse - immediately in brain but no improvement for 2 weeks
parkinsons
neuroleptics increase D2 receptors
PET scans = inconclusive
revised dopamine hypothesis
overactivity of dopamine neruson in the mesolimbic pathway may cause the symtptoms
-anitpsychotics which block dopamine receptors lessen positive symptoms
but
underactivity of dopamine neurons in the mesocortical pathway in the prefrontla cortex may cause negative symtoms
-anitpsychotics have little or no effect on the negative symptoms
and glutamate hypofunctioning - especially hallucinations
structural and funcitonal abnormalities in the brain
enalrged ventricels and reduced tissue volume = there has been atrophy
inverse relationshup between ventricle size and response to medication
abnormal neural migration (fetus brain)
gray metter loss in adolesence
hypofrontality - less active frontal lobes (major dopamin pathway)
what is the hypofrontality hypothesis
discordant twins = low blood flow only in afected twin
cognitive flexibility
-schizophrenics cant shift sttention to other criterion
-functional imaging = frontal lobe activity lower at rest esp in right hemisphere, does not increase during task
-drug treatment increased activation of frontal lobes
influenza and schizophrenia
individuals with schizophrenia and exposed to influenze prenatally = more likely to have enlarged ventricles
marijuana use and schizophrenia
chronic and early use of marijuana is a potential influence
high doses = increased lieklihood of developing schizophrenia
but also schizophrenics are more likely ot have a cannabis use disorder
but correlations = unclear why and how
stress and schizophrenia
may activate underlying vulnerabilty and/or increase risk of relapse
large city = increased risk
engage in combat in war = display temporary symptoms of schizophrenia
high number of stressful events reported in 3 weeks prior to showing disorder shown in many research centres but is retrospective
california earthquake study
assessed schizophrenics, bipolar and healthy controls
both patient groups = more stress related symtoms than controls
schizophrenics = lower leveles of self esteem and more liekly to engage in avoidance coping
schizophrenergic mother
obselete and unsupported theory
mum was cold, dominating and rejecting = caused schizophrenia in heroffspring
double blind communication
obselet, unsupported theory
practice of transmitting conlicting messages that was thought to cause schizophrenia = again all parents fault …
expressed emotion
hostility, criticism and over-involvement demonstrated by some families towards a fmaily member with a psych dis. can contribute to relapse
so high EE = see symptoms as controllable
cultural variations = variations in high EE
role of pscyh factors in schizophrenia
likely to exert only a minimal effect in producing schizophrenia
how did we used to treat schizophrenia
huge insulin doses = to induce comas
risk of serious illness and death
psychosurgery and ECT (we still use ECT in last ditch cases)
antipsychotic (neuropleptic meds)
dopamine atagonists are often the first line of treatment
most reduce or elimnate positive symptoms
acute and permament extrapyramidal and parkinson’s like symptoms are common
poor compliance is common
atypical (risperdal, olazapine) have better side effect profiles than Thorazine
what do we mean by extrapyramidal symptoms
work on neurotransmitter symptoms
akinesia - expressionless face, slow motor activity, monotomous speech
tardive dyskinesia - involuntary movements of tongue, face, jaw. tends to be from long term high does useage
dont tend to be reversible
one way tried to get round poor med compliance
inject every few weeks
still would just not rock up for next injection
psychosocial approaches for schizophrenia
behavioural (ie toekn economies) on impatient units
community care
social and living skills
behavioural family therapy
vocational rehabilitation
are usually a necessary part of treatment
self-help groups seem to do well (maybe just the kind of people who attend though)
ACT - wide ranging multidiscplinary training
sadly country differences ie lock up in some cultures
prevention of schizophrenia
identify and treat high risk children
instability of family rearing environment = can trigger onset
so poor parenting = strain on already vulnerability
attenuated psychosis syndrome might help
