Cognitive models in psychosis Flashcards
(121 cards)
What brain structures are dopaminergic neurons found in?
Mid brain structures
Substantia Nigra [SNc]
Ventral Tegmental area [VTA]
Where do the dopaminergic neuron axons, located in the SNc and VTA, project to?
The axons project to the
- striatum,
including the caudate nucleus, putamen,
- ventral striatum, or nucleus accumbens, shown with a red line and the green line.
The dorsal and ventral prefrontal cortex are also projected too, and you can see that here displayed with the blue lines.
What found in post-mortem studies of patients with schizophrenia suggests higher levels of dopamine?
higher receptive density of D2 receptors
What is the relationship between the sensitisation of the mesostriatal dopamine system and psychotic symptoms in schizophrenia?
The sensitisation of the mesostriatal dopamine system, which includes dopaminergic pathways in the brain, has been linked to the severity of psychotic symptoms in schizophrenia. This suggests that the more the dopamine system is dysregulated, the more severe the psychotic symptoms are likely to be.
What role does dopamine D2 receptor antagonism play in the treatment of schizophrenia?
Dopamine D2 receptor antagonism is fundamental in the treatment of schizophrenia as it has been shown to significantly improve psychotic symptoms. Antagonists block the D2 receptors, countering the effects of dopamine dysregulation that contribute to psychosis.
What evidence supports the link between striatal dopamine dysregulation and schizophrenia?
Robust evidence from molecular imaging studies indicates that dis-regulated striatal dopamine is implicated in schizophrenia. These studies show that alterations in the function of the striatal dopamine system are associated with the presentation and severity of psychotic symptoms.
What has PET imaging revealed about L-DOPA uptake in patients with schizophrenia compared to controls?
PET imaging studies have demonstrated that L-DOPA, a precursor to dopamine, is taken up more rapidly in patients with schizophrenia than in control subjects. This finding supports the hypothesis that patients with schizophrenia may produce more dopamine.
What are the different neurotransmitter pathways that are thought to impact the negative and positive symptoms found in schizophrenia and what are the aims of the treatment in each case?
what are the 4 dopamine pathways?
Mesolimbic Pathway:
Mesocortical Pathway:
Nigrostriatal Pathway:
Tuberoinfundibular Pathway:
Give an overview of the Mesolimbic Pathway:
Originates from the ventral tegmental area (VTA).
Projects to various limbic structures, including the nucleus accumbens, part of the ventral striatum.
Often associated with the reward system of the brain, pleasure, and reinforcement; dysregulation in this pathway is implicated in the positive symptoms of schizophrenia and in addiction.
Give an overview of the Mesocortical Pathway:
Also originates from the VTA.
Projects to the prefrontal cortex, including the dorsolateral prefrontal cortex.
Involvement in cognitive control, motivation, emotional response; dysfunctions in this pathway are associated with the negative and cognitive symptoms of schizophrenia, such as blunted affect and impaired executive function.
Give an overview of the Nigrostriatal Pathway:
Originates from the substantia nigra, specifically the pars compacta region.
Projects to the striatum, which includes the caudate nucleus and putamen.
Plays a crucial role in the coordination of movement; degeneration of this pathway is a hallmark of Parkinson’s disease.
Give an overview of the Tuberoinfundibular Pathway:
Originates from the hypothalamus.
Projects to the pituitary gland.
Regulates the release of prolactin by inhibiting its secretion; antipsychotic drugs, which block dopamine, can disrupt this pathway and lead to elevated prolactin levels, resulting in side effects such as galactorrhea and amenorrhea.
What was the main observation in the response of dopamine neurons when monkeys received an unexpected weak liquid reward?
[study by Schultz and colleagues on dopamine release in response to stimuli and rewards in monkeys.]
The main observation was an increase in firing of dopamine neurons at the same time as the unexpected reward was given, indicating a surprise or salient event. This response to unpredicted primary rewards varies directly with the reward magnitude.
How does the dopamine response change during the course of learning when a reward is given as expected after a conditioned stimulus?
[study by Schultz and colleagues on dopamine release in response to stimuli and rewards in monkeys.]
During the course of learning, the dopamine response to the reward gradually decreases and a response to the conditioned stimulus that predicts the reward develops. The dopamine signal shifts from the reward to the predictor stimulus.
What happens to dopamine release when a conditioned stimulus is presented and the expected reward follows?
[study by Schultz and colleagues on dopamine release in response to stimuli and rewards in monkeys.]
There is a slight peak of dopamine release following the stimulus, reflecting the recognition that a reward is to come. However, when the expected reward is given, there’s no significant increase in dopamine release since there is no prediction error; the event occurred as expected.
Describe the dopamine response when a reward is predicted after a conditioned stimulus but is not given.
[study by Schultz and colleagues on dopamine release in response to stimuli and rewards in monkeys.]
Initially, there is a spike in dopamine release upon the recognition of the conditioned stimulus, but if the predicted reward does not follow, dopamine release decreases below normal levels, reflecting a negative prediction error.
What is the key message about the role of surprise in dopamine-mediated learning from Schultz’s study?
The key message is that the mismatch between what is expected and what actually occurs (surprise) drives learning. Dopamine release increases when events are better than expected, and there is a negative prediction error when events are worse than expected.
According to Miller’s hypothesis, how might an excessive supply of cerebral dopamine contribute to the positive symptoms of schizophrenia?
Miller proposed that in schizophrenic patients, an excessive supply of dopamine may facilitate the acquisition of associations between unrelated units of information, leading them to be treated as meaningful combinations. This can result in the formation of delusions and is associated with the positive symptoms of schizophrenia.
In the context of Miller’s hypothesis, how can aberrant salience lead to the formation of delusions in schizophrenia?
Aberrant salience occurs when a non-meaningful stimulus evokes dopamine firing, making it overly salient and attention-grabbing. This can lead individuals to form connections and seek explanations for these salient experiences, often resulting in the development of delusions.
What is a ‘delusion of reference’ as explained by Miller’s hypothesis, and how might it manifest in a patient’s experience?
A delusion of reference is an inference that a specific and unrelated stimulus is directly related to oneself. For instance, a patient might believe messages on TV are intended for them, assigning excessive salience to these messages and interpreting them as personally significant.
According to Miller’s hypothesis, how might antipsychotics affect the process of aberrant salience and its associated distress in schizophrenia?
Antipsychotics can block the aberrant salience of stimuli, supporting the extinction and unlearning of the associations that lead to delusions. However, they may also reduce the salience of normal events, potentially affecting motivation and normal emotional responses.
What is reinforcement-related speeding?
attributed to the anticipation of a potential reward on such trials leading to enhanced motivation and hence faster responding.
Faster reaction times in response to rewarding stimuli than neutral stimuli
In the reaction time study with psychosis and controls, with a reward and neutral type task, what difference was found? MURRAY
the difference was patients were significantly faster than controls on neutral trials.