schizophrenia Flashcards
what is the most common psychotic disorder?
schizophrenia
what is schizoaffective disorder?
schizophrenia and bipolar disorder
key characteristics of schizophrenia?
- Early onset (late adolescence)
- Prevalent
- Disabling and chronic - chronic relapsing disorder
is schizophrenia a condition to do with mood?
not a condition of mood, but perception of thoughts –
- mental state out of touch with reality, associated with delusions and hallucinations
- abnormalities of perception, thought & ideas
- profound alterations in behaviour (bizarre and disturbing alienation)
prevalence of schizophrenia
1% of population
ethnicity and gender have no effect
schizophrenia – 4 phases?
- The prodrome
- Active phase
- Remission
- Relapse
Cycles between remission and relapse common
what can szn patients tell?
patients can sometimes tell when a relapse is coming
prodrome phase
Late teens/early twenties: often mistaken for depression or anxiety. Can be triggered by stress
active phase
Onset of positive symptoms. Differentiation of what is and isn’t real becomes difficult. Usually lasts for 4-6 weeks
remission
Treatment return to ‘normality’, can last for years
3 classes of schizophrenia symptoms
positive, negative, cognitive
-two or more symptoms must persist for at least 6 months to be classed as schizophrenia
positive symptoms?
present in the onset
Hallucinations (e.g. visual, auditory)
Delusions
Disorganised thought/speech
Movement disorders
negative symptoms?
kick in later, more pronounced
Social withdrawal Anhedonia Lack of motivation Poverty of speech Emotional flatness
cognitive symptoms?
very often present later on in life
Impaired working memory
Impaired attention
Impaired comprehension
what are hallucinations?
when a perception is experienced without stimulus (positive symptoms)
Most commonly auditory - patients hears Voices talking about them (3rd person) Voices talking to them Voices giving a running commentary Voices echoing their thoughts (thought echo)
Patients may engage in a dialogue with the voices or obey their commands
what are delusions?
fixed, unshakable belief - not consistent with cultural/ social norms
-often paranoid or persecutory
Motor, volitional and behavioural disorders in schizophrenia
-Bizarre postures, strange mannerisms
-Altered facial expression – grimacing
-State of catatonia – motionless, mute, expressionless, uncomfortable or contorted postures
-extreme hyperactivity (destructiveness, walk round naked)
Impulsive behaviour – violent acts; murder w/o reason
schizophrenia - killing?
people can become violent, and they often do not feel regret after killing due to their emotional flatness
Formal thought disorder
- Disturbances in thinking → unintelligible speech
- Derailment of speech
- Loosening of associations; failure to follow train of though to its conclusion
- Poverty of speech (speech fails to convey sense/information)
- Manifests as distorted or illogical speech - neologisms, new words formed
social withdrawal
Patients withdraw from their families and friends, spend a lot of time on their own.
- Lack of initiative or motivation
- Do not want to do anything
- No longer interested in things that used to interest them
cognitive deficits
- Deficits in SELECTIVE attention, problem solving and memory
- Blunted affect
- Decreased responsiveness to emotional issues
- Expression is inappropriate to circumstances
lack of insight
no/lack of understanding what’s wrong.
-patients usually do not accept that any thing is wrong or that treatment is necessary
The aetiology of schizophrenia
genetics
-SCZ isn’t directly inherited, but can ‘run in families’
‘Candidate’ risk genes:
Gene deletions
Gene mutations
environmental factors
- Pregnancy/birth complications
- Stress
- Drug use
-current thinking is that a person needs both to manifest the disease
what do twin studies show?
shows that there is a genetic component to the disease
Not inherited, but there IS a risk
50% chance of developing schizophrenia if one twin diagnosed
candidate risk genes?
COMT
DISC1
GRM3
-Possessing these abnormal genes doesn’t mean you will definitely get schizophrenia – similarly, some people who have schizophrenia do not have these genetic abnormalities
-Increased vulnerability of developing SZN
influenza
Finnish study reported a spike in schizophrenia for people who were foetuses during the 1957 influenza epidemic
Pregnancy/birth complications association with schizophrenia
Low birth weight
Premature birth
Asphyxia during birth
-caused of early life stress, associated with a slightly higher risk of developing schizophrenia
name some causes of stress….
-Moving country
-Early-Life Bereavement
-Loss of >1 first-degree relative further increased risk
-Loss of job/home/relationship
-Physical/emotional/sexual abuse
The mechanism by which stress may trigger schizophrenia is unknown
Drug Use
Cannabis is number 1 used drug of abuse other than alcohol
Early use of cannabis is a big risk factor
which pathway is involved in producing positive symptoms of szn?
dopamine hypothesis of schizophrenia
Hyperactivity of mesolimbic dopaminergic pathway, increased release of dopamine.
amphetamine?
increases dopamine dramatically in the mesolimbic pathway, and has been shown to play a role of psychotic like symptoms
which pathway is involved in producing negative symptoms of szn?
Low activity of mesocortical pathway
what do we need to do to the pathways to treat szn?
increase DAergic transmission (D1) in mesocortical regions, decrease DAergic transmission (D2) on mesolimbic regions
evidence against the dopamine hypothesis of schizophrenia
you would expect to find high levels of dopamine in the CSF, but this hasn’t been found
Brain Structure Abnormalities
scans have been looked at of twins, one of whom suffers with schizophrenia - clear structural abonormalities
- enlarged lateral ventricles – smaller hippocampus
- reduction of gray matter
- size of the brain is slightly smaller
hypofrontality?
Reduced activity in frontal cortex and Reduced blood flow to the frontal cortex
-hypofunction
glutamate/NMDA hypofunction hypothesis
- decreased glutamate
- low levels of NMDA receptor/glutamate in pre frontal cortex is associated with the negative szn symptoms
- mice, genetically removed NMDA receptors and mice produced szn-like episodes
Glutamate excitatory on GABAergic neurons
DA inhibitory on GABAergic neurons
Too little glutamate, too much DA – uninhibited sensory input to limbic regions (NAc, Hi, Amy)
Hyperactivity of serotonin receptors
Many antipsychotics antagonise 5-HT receptors
5-HT activates DA pathways
5-HT2A antagonism – may contribute to antipsychotic effect, may reduce movement disorder side effects
main current theory?
Over stimulation of mesolimbic D2 receptors
Hypoactivity of frontal cortical D1 receptors
Reduced prefrontal glutaminergic activity
5HT involved
why would anti-psychotics cause a loss of reward?
because they affect d2 receptors everywhere
2 types of antipsychotics?
typicals
-‘first generation’
First developed in the 1950s
Mainly antagonise D2 receptors
atypicals
-‘second generation’
First developed in the 1980s
Mainly antagonise D2 and 5-HT2A receptors
why would anti-psychotics have endocrine effects?
because there are d2 receptors in the brain, and dopamine binds and decreases prolactin release
antipsychotics are d2 receptor blockade, therefore causing increased PRL levels, so breast swelling, lactation and impotence
why might anti-psychotics cause hypotension?
due to the alpha adrenoceptor blockade
why do anti-psychotics cause decreased pleasure?
dopamine receptors involved in reward system
