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Clinical neuroscience > Lecture 22- Psychosis > Flashcards

Lecture 22- Psychosis Flashcards

1
Q

Definition of psychosis

A
  • Disorder of the mind
  • The presence of hallucinations or delusions
  • Describes symptoms, not a diagnosis in itself
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2
Q

Hallucinations

A
  • Perception without a stimulus
  • Can be in any sensory modality
  • Visual hallucinations are usually organic (caused by problem with brain (SoL) or eyes)
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3
Q

Delusions

A
  • Delusion – a fixed false belief, which is unshakeable.
  • Outside of cultural norms.
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4
Q

Schizophrenia quick facts

A
  • Patients with schizophrenia don’t have a split mind or personality
  • Patients with schizophrenia are generally no more ‘dangerous’ than any other patient.
  • 5% of violent crimes are committed by patients with severe mental illness, which means that 95% are committed by ‘normal people’!
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5
Q

First Rank Symptoms of schizophrenia

A
  • Auditory hallucinations
  • Passivity experiences
  • Thought withdrawal, broadcast or insertion
  • Delusional perceptions
  • Somatic hallucinations
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6
Q

Positive symptoms of schizoprehnia

A
  • Delusions, hallucinations, thought disorder, lack of insight
  • Added symptoms

The positive symptoms are so called because they are thinking or behaviour that the person with schizophrenia did not have before they became ill and so can be thought of as being added to their psyche

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7
Q

Negative symptoms:

A
  • Underactivity, low motivation, social withdrawal, emotional flattening,
  • Self neglect
  • Symptoms that take away from the patient
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8
Q

auditory hallunications

A
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9
Q

thought withdrawal, broadcast or insertion

A
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10
Q

passivity experiences

A
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11
Q

delusional perception

A
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12
Q
A
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13
Q

somatic hallucinations

A
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14
Q

All patients with Schizophrenia are different

A
  • While patients with Schizophrenia might have the same cluster of symptoms e.g. delusions, hallucinations, absence of insight.
  • How each patient experiences these symptoms will be completely different e.g.
    • Delusions MI5 are following them
    • Delusions witchcraft is being performed on them
    • Delusions family are poisoning them
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15
Q

Pathophysiology of Schizophrenia

A
  • Dopamine pathways
  • Brain changes
  • Limbic system
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16
Q

Dopamine (DA) theory of Schizophrenia

A
  • Drugs e.g. amphetamines which cause the release of DA induces psychotic symptoms.
  • All medications that antagonise DA receptors, help treat psychosis & those with the strongest affinity to D2 receptions are most clinically effective.
17
Q

how many DA (dopaminergic) pathways in the brain?

A

4

18
Q

4 dopamine pathways of the brain

A
  1. The Mesolimbic Pathway.
  2. The Mesocortical Pathway.
  3. The Nigrostriatal Pathway. …
  4. The Tuberoinfundibular (TI) Pathway.
19
Q
A
20
Q

Mesolimbic pathway

A
  • From Ventral tegmental area to Limbic structures (amygdala, septal area, hippocampal formation) and Nucleus accumbens
  • Thought to be overactive in schizophrenia
21
Q

Mesocortical pathway

A
  • From the ventral tegmental area to frontal cortex and cingulate cortex
  • Thoughts to be underactive in schizophrenia
22
Q
A
23
Q

tuberoinfundibular pathways

A

from arcuate and periventricular nuclei of hypothalamus to the infundibular region of the hypothalamus

24
Q

nigrostriatal parthways

A

from the substantia nigra pars compacta to striatum (caudate nucleus and putamen)

25
Q

Brain changes in schizophrenia

A
  • Enlarged ventricles
  • Reduced grey matter (with reduced brain weight)
  • Decreased temporal lobe volume (auditory hallucinations)
  • Reduced hippocampal formation, amygdala, parahippocampal gyrus and prefrontal cortex
26
Q

Neuropathology of Schizophrenia

A
  • Decreased pre-synaptic markers
  • Decreased oligodendroglia
  • Fewer thalamic neurons
  • Together these changes have led to a theory of “aberrant connectivity” causing schizophrenia
27
Q

treatment of schizophrenia

A

typical and atypical antipsychotics

28
Q

Typical antipsychotics block..

A
  • Block D2 receptors (dopamine) in all CNS dopaminergic pathways
    • Main action as antipsychotics is on mesolimbic and mesocortical pathways.
  • But side effects come from antagonising D2 receptors in other pathways e.g. parkinsonism
29
Q

how do atypical antipsychotics differ from typical antipsychotics

A
  • Lower affinity for D2 (dopamine) receptors
    • Milder side effects as dissociate rapidly from D2 receptor
  • Also block 5HT2 (serotonin) receptors – less parkinsonism
30
Q

parinsonism side effects from taking typical antipsychotics results from

A

drug antagonising nigrostriatal pathway (1/4 DA pathways)–> lack of dopamine in basal ganglia= extrapyramidal side effects e.g. parkinsonims

less dopamine= less movement

31
Q

basal ganglia and movement

A
32
Q

Importance of dopamine- awakenings

A

Between 1915 and 1926, 5 million people worldwide suffered from Acute Encephalitis Lethargica, or ‘sleepy sickness’ .One third died in the acute stages. Many survivors lived on for decades in ‘sleepy’ states- akintetic.

Dopamine was used to promote movement with astonishing results.

33
Q

what can result from untreated psychosis

A

catatonia

34
Q

catatonia

A

Catatonia is a neuropsychiatric behavioural syndrome that is characterized by abnormal movements, immobility, abnormal behaviours, and withdrawal.

More than two weeks, one or more of

  • Stupor / mutism
  • Excitement
  • Posturing
  • Negativism
  • Rigidity
  • Waxy flexibility
  • Command automatism
35
Q

So if dopamine promotes movement, why do untreated patients develop catatonia?

A

Probably due to less GABA binding so loss of inhibitory effect

36
Q

Hyperprolactinaemia & antipsychotics

A
  • Dopamine normally inhibits prolactin release from the pituitary.
  • DA antagonists, which lower DA lead to loss of DA’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
37
Q

Difficulties treating people with SCZ

A
  • Lack insight (cant see they aren’t well)
  • Medications therefore often not taken.
  • Medications can be given in different ways: PO (inc orodispersible), short acting IM, depot
38
Q

Prognosis

A
  • Earlier someone is treated the better the prognosis.
  • Moderately good long term global outcome in about 50%
  • Good prognostic factors
    • Absence of family history
    • Good premorbid function
    • Acute onset
    • Mood disturbance
    • Prompt treatment
    • Maintenance of initiative and motivation
  • Mortality is twice as high as in general population
  • Shorter life expectancy
  • Higher incidence of CVS disease, respiratory disease and cancer
  • Suicide risk is 9x higher than in general population
  • Death from violent incidents in 2x as high
  • About 50% have a substance misuse problem
  • Higher rate of cigarette smoking

Clinical neuroscience (30 decks)

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