Schizophrenia 1 Flashcards

1
Q

What is schizophrenia

A

Family of disorders with 2 symptom categories
POSITIVE: gained behaviors, its how its diagnosed
(auditory hallucinations, delusions (paranoia) and thought disorder) = PSYCHOSIS
NEGATIVE: normal functions that are lost (blunted emotional response, poverty of pseech, social withdrawal, enhedonia, lack of insight, COGNITIVE DEFICITS

Schizophrenias can be very different clusters of symptoms (don’t often look alike)

1% of population has it
Onset after 18 and before 30 in men, but some women after menocause.

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2
Q

How was schizophrenia initially desrcribed?

A

Dementia praecox (early dementia) by Kraeplein and later by Bleuler as schizophrenia (split mind)

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3
Q

What are the diversity of symptoms in schizophrenia?

A

Positive ones used to diagnose
1/3 needed: hallucinations, delusions or disorganized speech.
- need to be ruled out by other conditions first
- many other symptoms (lack of insight into illness, can’t rationalize it, delusions, suspicioousness, paranoid, auditory and verbal hallucinations, flatness of affect.

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4
Q

What are the cognitive abnormalities in schiz?

A

Less dramatic than positive ones, can’t often see it, but are a big part of disorder. #1 predictor of long term outcomes (functioning leads to prognosis)
- psychotic severity is NOT related to cognitive severity

Many mediated by PFC

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5
Q

What are the 7 primary domains of cognition that are affected in schiz?

A
Speed of processing
working memory
learning (visual and memory) 
social cognition 
attention
reasoning and problem solving
verbal learning memory 

PFC mediated, and are impaired in schiz

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6
Q

Why do some schizophrenic people use nicotine?

A

Because it enhances cognition

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7
Q

What do twin brain activation studies show about cognitive abnormalities in schizophrenia?

A

When performing wisconsin card sort (heavily reliant on PFC), people with schizophrenia have way less activation in PFC at rest and during the task, but no different elsewhere.

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8
Q

How do genetics play a role in schizophrenia?

A

Odds of getting in increase as the relationship to family member goes up (50% in monozygotic twin, and both parents)

  • linked to dozens of genes and combinations
    1. COMP gene
    2. DISC1 gene: encodes for proetins needed in neural development and can induce cognitive imapirment in mice

not the only factor tho!

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9
Q

Describe how the early environment can lead to schizophrenia?

A
Perturbations during development
Perinatial complications 
- poor nutrition during pregnancy
- premature birth and low birth weight
- physical and immune stressors during pregnancy

Early developmental insults can lead to abnormalities in adulthood, and later stressors can trigger onset.

GEnetis increase sensitivity to these stressers in utero or later in life.
Won’t be diagnosed until they show the psychotic break.

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10
Q

What behaivors in infancy can predict schizophrenia?

A

Passivity, apathy, reduced responsiveness to verbal commands, temperament, poor sensorimotor performance (interview style research)

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11
Q

What happens in the brains of early onset psychotic schizophrenia?

A

In teens, brain makes a lot of neurons and synapses then prunes them, in people with this rare condition, too many synapses are pruned resulting in lost cortical grey matter.

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12
Q

Describe the development of schizophrenia in stages?

A

Early Stage: genetics + early insults (virus, toxin, poor nutrition and birth complications) = neural abnormalities from conception to adulthood (neuron formation, migration, pruning etc)

Latent Stage: early signs predicting schiz, see other abnormalities besides psychosis (motor abnormalities, apathy, withdrawal, attentional deficits)

Late stage: Excessive pruning in teenage years laesd to abnormal connnectivty and function + later environmetnal insults (stress, substance use, HPA axis) = greater impairment and positive symptoms.

Some brains just more suceptible to it.

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13
Q

What species get schizophrenia?

A

only humans ehehe

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14
Q

How is the hippocampus effected in schizophrenia?

A

Not lesioned or fewer cells, just disorganized wierd to get smaller. Shown by enlarged ventricles (other temporal lobe regions smaller too)

  • not correlated with time of onset or symptom duration
  • its not brain damage, its a change in neural organization occuring EARLY IN DEVELOPMENT that disrupts how brain processing information (making you develop it later in life)
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15
Q

How is the PFC affected in schizophrenia?

A

Pyramidal cells: reduced # of dendrites/spines and shorter basal dendrites
= fewer synaptic contacts
= reduces processing power, leads to hypofrontality

GABA interneurons: usually serve as filter for PFC (and hippocampus), with 1:80 ratio GABA to PFC neuron to mediate patterns of exitatory and inhibitory balance
= schizophrenics have less markers for gagba neurons: less neurons OR they are less effective.
= noisy cortex, reducing filtering and impairing functioning.

ITS THE PATTERNS OF ACTIVITY THAT ARE DISRUPTED
- too much where its not wanted and too little where its needed

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16
Q

What is the dopamine hypothesis of schizophrenia?

A

THEORY: schiz caused by abnormal dopamine transmission leading to overstimulation of D2 receptors.

1) Chlorpromazine is an antipsychotic that causes parkinsons, parkinsons are depleted in dopamine
2) Drugs that increase DA release induce psychotic symptoms
3) Chlorpormazine and antipsychotics block DA 2 receptors.

17
Q

What is support for the DA hypothesis of schizophrenia?

A

DA system more sensitive and is related to positive symptoms of schiz.

We know all drugs that can treat psychosis block D2 receptors
STUDY: What drives this increase of DA in schiz?
- Not receptor count (same # of them)
- Dop release yes!
When given amphetamine that induces DA release, ppl with schiz are more sensitive to it, so they release MORE dopamine in striatum and this release also increases positive symptoms of schizophrenia (positive correlation)

18
Q

What does dopamine do in schiz? Simple version unlikely to be testable.

A

Increase in DA makes you pay attention to things, hyperactive may make you pay attention to stuff you wouldn’tnormally focus on (aberrant salience attribution) that can lead to delusions (this weird thing happend so it must mean the FBI is after me) whereas normal people don’t may too much attention to coincidences or weird stuff.

Antipsychotics then don’t take away hallucinations or delusions they often jsut make them less bothersome.
They also don’t treat the whole disorder just the postive symptom part.

19
Q

How has the dopamine hypothesis for schiz been revised?

A

Dopamine imbalance hypothesis

  • neg symptoms due to reduced prefrontal DA
  • pos sypmtoms due to increased striatal and mesolimbic DA (hypersensitive)
  • because we see redcued PFC DA, its not as simple as MORE dopamine. Reduced PFC DA is driving other symptoms
  • drugs that increase PFC dopamine (like amphetamines) can imporove cognitive functions but make positive symptoms WORSE.