Session 12 - psychosis Flashcards
what is the definition of psychosis?
- presence of hallucinations or delusion but the patients have a lack of insight (don’t believe they’re unwell)
- this isn’t a diagnosis but a set of symptoms
what are hallucinations?
- the perception of a stimulus without an actual stimulus
- can be in any sensory modality
- auditory = very common
- olfactory = often seen in depression
what are visual hallucinations often caused by?
they’re usually organic so caused by a problem with the brain or eyes eg. SOL, Lewy body dementia
What are hallucinations in the ‘normal’ population known as?
- hypnogogic - experienced when going to sleep
- hypnopompic - experienced when waking up
what are delusions?
- a fixed, false believe which is unshakeable and outside of cultural norms
- eg. think they’re being spied on by the police
- unshakable - even if you showed them proof that what they’re saying isn’t true, they will still believe it
who first used the term Schizophrenia?
Eugen bleuler
what are the first rank symptoms?
- auditory hallucinations
- passivity experiences
- thought withdrawal, broadcast or insertion
- delusional perceptions
- somatic hallucinations
what are auditory hallucinations?
- thought echo - hearing thoughts aloud
- running commentary
- third person - voices referring to the patient in third person and conversing with each other about the patient
what are passivity experiences?
patient believes an action or feeling is caused by an external force
what is thought withdrawal, broadcast or insertion?
- thought withdrawal - thoughts are being taken. out of the mind
- thought broadcast - belief that everyone knows what the patient is thinking
- thought insertion - believed that thoughts are being implanted by others
what is delusion perception?
- attribution of a new meaning to a normally perceived object
- eg. red traffic light means aliens are coming
what are somatic hallucinations?
- mimics feeling from inside the body
- eg. the sense of being touched when no one is there.
what are the positive and negative symptoms and what do these mean?
Positive symptoms - something added
- delusions, hallucination, thought disorder (problem with organisation of thoughts), lack of insight
Negative symptoms - symptoms that take away from the patient
- under activity, low motivation, social withdrawal, emotional flattening, self neglect
What is the dopamine theory of schizophrenia?
- evidence for the involvement of dopamine in schizophrenia
- drugs that increase dopamine levels (eg. amphetamines) induce psychosis
- drugs that antagonise dopamine treat psychosis (esp those acting at D2 receptors - those with the strongest affinity to D2 receptors are most clinically effective)
what are the different dopamine pathways in the brain?
- mesocortical pathway
- mesolimbic pathway
- nigrostriatal pathway
- tuberoinfundibulnar pathway
what is the mesolimbic pathway?
- from the ventral tegmental area to the limbic structures and the nucleus accumbens
- overactive in schizophrenia
what is the mesocortical pathway?
- from the ventral tegmental area to the frontal cortex and the cingulate cortex
- this pathway is responsible for negative symptoms
- it’s underactive in schizophrenia
what are the brain changes in schizophrenia?
- enlarged ventricles
- reduced grey matter w/ reduced brain weight
- decreased temporal lobe volume → changes in temp lobe → auditory hallucinations
- reduced size of limbic structures and prefrontal cortex
what is the neuropathology of schizophrenia?
- decreased pre-synaptic markers
- decreased oligodendrocytes
- fewer thalamic neurones
- together these changed lead to a theory of aberrant connectivity which causes schizophrenia
apart from changes in the dopamine pathway, what other areas in the brain are affected in schizophrenia?
- involvement of the limbic system - they have a role in regulating emotional behaviour
- possible role of the basal ganglia - movement disorder features. even untreated patients can present with motor symptoms
what is the nigrostriatal pathway?
- it goes from the substania nigra pars compaca to the striatum (caudate nucleus and putamen)
- the basal ganglia is connected to this pathway
what type of symptoms does blockage of dopamine in the nigrostriatal pathway cause?
- extra pyramidal side effects → parkinsonism
- if taking anti psychotics for a long period of time can get tardive dyskinesia - where the face, body or both make sudden, irregular movements that can’t be controlled - eg. sticking out tongue or blinking excessively
- can also get akathisia - inability to stay still
what are the typical antipsychotics and eg?
- haloperidol
- they block D2 receptors in ALL CNS dopaminergic pathways
- but their main action as antipsychotics is on the mesolimbic and mesocortical pathways
- side effects come from antagonising D2 receptors in other pathways eg. nigrostriatal - Parkinsonism
what are atypical antipsychotics and eg?
- clozapine
- lower affinity for D2 receptor
- however milder side effects as they rapidly dissociate from the D2 receptor
- they also block 5HT2 receptors - so have some action on the serotonin pathway
why do we get Parkinsonism if we over treat a patient with a typical antipsychotic?
there’s decreased dopamine so increased inhibition on the thalamus so less glutamate going to excite the cortex
what are some side effects of antipsychotics?
- typical antipsychotics - Parkinsonism because of involvement of substantia nigra. they get rid of postitive symptoms but not negative
- atypical antipsychotics - impaired glucose tolerance, weight gain, diabetes, prolonged QT, hypercholesterolaemia, galactorrhea
- sexual dysfunction side effects due to lack of dopamine to inhibit prolactin production so hyperprolactinaemia
what can happen to the movement of an untreated schizophrenic patients and why does this occur?
- can develop catatonia - extreme end of schizophrenia where movement is impoverished
- more than two weeks, one or more of; stupor/mutism, excitement, posturing, negativism, rigitdity, waxy flexibility, command automatism
- less GABA binding so loss of inhibitory effect
- rarely occurs bc we treat early
what is the tuberoinfundibular pathway?
- from the arcuate and periventricular nuclei of the hypothalamus to the infundibular region of the hypothalamus
- in this pathway dopamine feeds back to the pituitary
why can you get hyperprolactinaemia when taking antipsychotics?
- affects the tuberoinfundibular pathway
- dopamine normally inhibits prolactin release from he pituitary
- DA antagonists which lower dopamine, lead to loss of dopamine’s inhibitory function and therefore increased prolactin levels
- this can lead to - amenorrhoea, galactorrhoea, decreased fertility, reduced libido and long term can lead to osteopenia/osteoporosis
what are some of the challenges in treating schizophrenia?
- patents tend to lack insight - can affect compliance with treatment
- therefore medication can be given in different ways such as a depot injection which is long acting and releases the antipsychotic slowly.
- it can be also be given PO or short acting IM
what are the factors associated with good prognosis?
- no family history
- good premorbid function
- actue onset
- mood disturbance
- prompt treatments
- maintenance of motivation
what are the long term complications of schizophrenia?
- mortality is twice as high as general population
- shorter life expectancy
- higher incidence of CVS disease, respiratory disease and cancer - partly due to medicine given and also life choices eg. smoking, less likely to have healthy lifestyle
- 9x greater suicide risk that general population
- 2x greater risk of violent death than general population
- substance misuse is common and many patients make (contributing to CVD)
