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7PAYFPSY Psychology and Neuroscience of Psychosis - October 2023 > Cutting edge experimental therapeutics > Flashcards

Cutting edge experimental therapeutics Flashcards

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1
Q

What are some topics besides psychosis that neuromodulation is currently being studied for?

A

Besides psychosis, neuromodulation is being studied for conditions such as depression, OCD, and mood problems in people with psychosis.

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2
Q

Name five major neuromodulation techniques discussed in this module.

A

The five major neuromodulation techniques discussed are:
nial Magnetic Stimulation (rTMS)
Transcranial Direct Current Stimulation (tDCS)
Vagal Nerve Stimulation (VNS)
Trigeminal Nerve Stimulation (TNS)
Deep Brain Stimulation (DBS)

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3
Q

Which two neuromodulation techniques were primarily focused on in this module, and why?

A

The primary focus of this module was on
Repetitive Transcranial Magnetic Stimulation (rTMS) and
Transcranial Direct Current Stimulation **(tDCS) **
because they have the most substantial evidence base.

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4
Q

What are the two ways contemporary neuromodulation techniques are divided based on the targeted brain areas?

A

The two ways of categorizing neuromodulation techniques are

“top-down” techniques, which target higher and more complex brain regions,
and
“bottom-up” techniques, which involve external nerves outside the brain.

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5
Q

Give examples of top-down neuromodulation techniques.

A

Top-down neuromodulation techniques include
rTMS (Repetitive Transcranial Magnetic Stimulation),
tDCS (Transcranial Direct Current Stimulation), and
DBS (Deep Brain Stimulation).

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6
Q

**

Give examples of bottom-up neuromodulation techniques.

A

Bottom-up neuromodulation techniques include
VNS (Vagal Nerve Stimulation) and
TNS (Trigeminal Nerve Stimulation).

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7
Q

How are neuromodulation techniques categorized as either noninvasive or invasive?

A

Neuromodulation techniques are categorized
as** noninvasive** when applied externally to the body (e.g., the skull or neck) and
as invasive when they require cutting through the skin and potentially bone (e.g., DBS or Vagal Nerve Stimulation).

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8
Q

TMS

Explain the background physics of Transcranial Magnetic Stimulation (TMS).

A

TMS is based on Faraday’s Law of Electromagnetic Induction. A magnetic coil is placed above the skull, and when it turns on and off, it induces electrical currents within the brain, which can activate neurons due to the brain’s electrochemical nature.

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9
Q

How does slow TMS affect neurons, and what is the typical stimulation rate for slow TMS?

A

Slow TMS, typically applied at less than 1 Hertz (less than once per second), tends to inhibit underlying neurons. When applied for a period and then removed, the neurons underneath are less likely to fire for some time.

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10
Q

How does fast TMS affect neurons, and what is the typical stimulation rate for fast TMS?

A

Fast TMS, with a stimulation rate greater than 5 Hertz (more than five times a second, typically around 10 Hertz), tends to be stimulatory to underlying neurons. When the TMS coil is removed, the stimulated area is more likely to fire.

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11
Q

What is the size of the area directly underneath the TMS coil?

A

The area directly underneath the TMS coil is about half a centimeter in diameter, approximately the size of a penny or a cent.

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12
Q

What is the potential problem associated with the small diameter of effective activation in TMS?

A

The potential problem is that if someone or the coil moves even slightly during TMS application, it can result in hitting different parts of the brain due to the small diameter of effective activation.

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13
Q

What is meant by “superficial penetrants” in the context of TMS?

A

“Superficial penetrants” refer to the fact that TMS coils primarily affect the top centimeter of the cortex or brain due to various barriers such as the thickness of the skull and hair.

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14
Q

How is TMS coil placement typically done, and what are the drawbacks of manual placement?

A

TMS coil placement can be done manually, measuring on the skull using anatomical landmarks. The drawback is that manual placement introduces inaccuracies.

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15
Q

What is computer-guided application of TMS, and why is it more accurate than manual placement?

A

Computer-guided application of TMS involves a computer system that tracks the coil’s position in real space compared to the person’s head and helps size it appropriately. It is more accurate than manual placement.

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16
Q

What happens when the TMS coil turns on and off, and how can it be done in two different ways?

A

When the TMS coil turns on and off, it causes depolarization in the brain cells underneath. This can be done in two different ways: slowly, at one Hertz or about once per second, and fast, at around 10 Hertz.

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17
Q

Why are longer-term changes important in TMS therapy, and how do they differ between slow and fast TMS?

A

Longer-term changes are important in TMS therapy because immediate effects would have limited value. Slow TMS tends to produce inhibition after the tool is removed, while fast TMS tends to produce stimulation after removal.

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18
Q

What is the ultimate goal of TMS therapy in terms of brain function changes?

A

The ultimate goal of TMS therapy is to induce immediate changes in brain function and then take the tool away to induce longer-term changes. This allows the therapy to have lasting therapeutic effects.

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19
Q

Immediate Effects: When TMS is applied, it…

A

…stimulates specific brain regions or neural pathways. This stimulation can lead to immediate changes in the excitability of neurons in the targeted area. Neurons may become more or less active depending on the type and frequency of TMS applied.

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20
Q

What is TMS?

A

Transcranial Magnetic Stimulation is abbreviated as TMS. It is a non-invasive neurostimulation technique that uses magnetic fields to induce electrical currents in the brain.

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21
Q

What are the two primary types of TMS?

A

Two primary types of TMS are Slow TMS (inhibition) and Fast TMS (stimulation).

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22
Q

How does Slow TMS affect brain activity?

A

Slow TMS inhibits brain activity in the stimulated region, leading to a temporary decrease in neuronal firing.

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23
Q

What is the impact of Fast TMS on brain activity?

A

Fast TMS stimulates brain activity in the targeted region, causing an increase in neuronal firing.

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24
Q

Name two processes influenced by TMS-induced changes.

A

TMS-induced changes influence processes like long-term potentiation (LTP) and long-term depression (LTD).

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25
Q

How does TMS affect gene expression related to neuronal plasticity?

A

TMS can modulate gene expression associated with neuronal plasticity, enhancing the brain’s ability to adapt.

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25
Q
A
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26
Q

What is one challenge in understanding the full effects of TMS?

A

One challenge is that TMS can have effects on distal brain regions, which are not fully understood due to the complexity of brain connectivity.

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27
Q

True or False: TMS is considered a non-invasive brain stimulation technique.

A

True. TMS is non-invasive, as it does not require surgery or penetration of the skull.

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28
Q

What are the potential side effects of TMS treatment?

A

Potential side effects of TMS treatment include mild discomfort, headache, and scalp irritation.

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29
Q

What is the primary target in the brain for rTMS in the treatment of depression?

A

In the treatment of depression, rTMS is most commonly applied to the left dorsolateral prefrontal cortex.

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30
Q

What principle underlies the use of rTMS in depression treatment?

A

The principle is that in depression, there is underactivation of certain brain areas, such as the dorsolateral prefrontal cortex and limbic regions.

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31
Q

How long does a typical rTMS session last, and what is the pulse pattern used?

A

A typical rTMS session lasts about half an hour and involves a pulse pattern of 4 seconds of stimulation followed by 26 seconds off, repeated throughout the session.

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32
Q

What level of evidence supports the effectiveness of rTMS in depression treatment, according to the European expert consensus statement in 2014?

A

According to the European expert consensus statement in 2014, rTMS is graded as level A, indicating a definite antidepressant effect.

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33
Q

Is rTMS recommended as a treatment for depression by NICE?

A

Yes, NICE recommends rTMS as an effective treatment for depression.

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34
Q

How is rTMS applied to treat auditory verbal hallucinations (voices) in psychosis?

A

rTMS is typically applied to the temporoparietal junction to target the overactive speech network associated with auditory verbal hallucinations in psychosis.

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35
Q

What is the primary goal of applying slow rTMS to treat auditory verbal hallucinations?

A

The goal of applying slow rTMS to treat auditory verbal hallucinations is to inhibit the overactive speech network in the brain.

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36
Q

What is the key difference in how tDCS affects the brain compared to rTMS?

A

tDCS enhances brain plasticity and makes brain regions more susceptible to subsequent inputs, while rTMS directly stimulates or inhibits brain cells.

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37
Q

How is tDCS applied to the scalp, and what is the typical current used?

A

tDCS involves the application of a small direct current through saline-soaked electrodes on the scalp, with a typical current of one to two milliamps.

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38
Q

pulses

what’s the difference between these two?

A
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39
Q

TMS

A
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40
Q

what neuromodulation technique would you use for depression and why?

A
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41
Q

depression

What is the underactivation model of depression?

A
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42
Q

What’s a typical TMS protocol for hallucinations?

A
43
Q

What effect size did a recent Meta-analyses find for the effectiness of TMS for hallucinations?

A
44
Q

What is the principle behind these studies and what are they testing?

A

The key principle is re-regulating dysfunctional fronto-limbic impulse control.

45
Q

What are the three psychological treatments that have a long history of development and evidence collection that are widely recommended ?

A
46
Q

What is the aim of family therapy and why was it developed?

A
47
Q

What was cognitive remediation developed in response to?

A

cognitive problems.

48
Q

What difficulties did those that went on to develop psychosis demonstrate years prior to an acute episode?

A

severe cognitive difficulties

49
Q
A
50
Q

What can be predicted by the severity of cognitive difficulties?

A

The cost of health and social care.

51
Q

Individuals with poor working memory recover less in the area of….

A

social functioning

52
Q

What is working memory important for?

A
53
Q
A
53
Q

What is Cognitive remediation therapy?
- a _____ therapy
- helping someone…..
- teaching individuals how to make….
- the therapist ensures that the …..

A
54
Q
A
55
Q

Explain massed practice

A
56
Q

Explain Errorless learning

A
57
Q

What is scaffolding in learning?

A
58
Q

What happens when psychiatric rehabilition is added to cognitive remediation?

A
59
Q

What was the outcome of the McGurk 2015 study with those who received CRT and a second course of supported employment?

A
60
Q

What did Each 2010 find about grey matter volume between people with a FPE in those who had CRT and those that didn’t?

A
61
Q
A
62
Q

How much of the variance between CRT and work quality outcome is not accounted for by Cognitive Flexibility, Memory and Planning and why might this be?

A
63
Q

How many synaptic connections and neurons does 1mm voxel of cerebral cortex have ( a standard fMRI unit)

A
64
Q

What is the first step in dopamine synthesis?

A

The first step in dopamine synthesis is the conversion of the amino acid tyrosine to L-dopa (dihydroxyphenylalanine) by the enzyme tyrosine hydroxylase.

65
Q

What enzyme converts L-dopa to dopamine in dopamine synthesis?

A

The enzyme aromatic L-amino acid decarboxylase (AADC) converts L-dopa to dopamine in the process of dopamine synthesis.

66
Q

What is the primary method of dopamine recycling in the brain?

A

Dopamine recycling primarily occurs through reuptake by dopamine transporters (DAT) on presynaptic neurons. This process involves the reabsorption of dopamine back into the neuron that released it.

67
Q

What are the two main types of dopamine receptors, and what are their functions?

A

There are two main types of dopamine receptors: D1 receptors and D2 receptors.

D1 receptors are primarily excitatory and are involved in promoting cellular processes related to reward, motivation, and motor function.
D2 receptors are inhibitory and play a role in modulating neurotransmitter release, especially in the context of motor control and cognitive function.

68
Q

What is the role of negative feedback in D2 receptors?

A

D2 receptors, when activated, can provide negative feedback to reduce further release of dopamine. This helps regulate dopamine levels in the synaptic cleft and prevent excessive stimulation of postsynaptic neurons.

69
Q

In the context of dopamine recycling, what part of the process is targeted by cocaine?

A

Cocaine primarily targets the dopamine transporter (DAT), inhibiting its function. This leads to an accumulation of dopamine in the synaptic cleft, intensifying dopamine signaling.

70
Q

Where are D1 receptors predominantly located in the brain?

A

basasl ganglia neurons and striatum

71
Q

What is the primary target of amphetamine in the brain related to dopamine regulation?

A

The primary target of amphetamine in the brain is the inhibition of the Vesicular Monoamine Transporter (VMAT). This inhibition leads to increased release of dopamine from vesicles into the synaptic cleft, resulting in heightened arousal and alertness.

72
Q

How do typical antipsychotic medications (e.g., haloperidol) primarily affect dopamine receptors?

A

Typical antipsychotic medications primarily block D2 dopamine receptors, leading to a reduction in dopamine signaling. This helps alleviate symptoms of psychosis but can also lead to side effects.

73
Q

What is the relationship between dopamine and schizophrenia, and how do antipsychotic medications address this relationship?

A

Schizophrenia is associated with excessive dopamine activity in certain brain regions. Antipsychotic medications help manage schizophrenia by reducing this excessive dopamine activity, particularly at D2 receptors.

74
Q

How do atypical antipsychotic medications (e.g., risperidone) differ from typical antipsychotic medications in terms of their impact on dopamine receptors?

A

Atypical antipsychotic medications have a broader receptor profile and often affect multiple neurotransmitter systems, including serotonin. They have a lower affinity for D2 receptors compared to typical antipsychotics, which can lead to fewer extrapyramidal side effects.

75
Q

What potential side effects are associated with antipsychotic medications due to their actions on dopamine receptors?

A

Common side effects of antipsychotic medications include extrapyramidal symptoms (such as tremors and rigidity), as well as changes in motor function and sometimes dyskinesias (abnormal involuntary movements) due to their impact on dopamine receptors.

76
Q

How does the use of antipsychotic medications relate to the regulation of dopamine levels in the brain?

A

Antipsychotic medications help regulate dopamine levels in the brain by targeting and modulating dopamine receptors. They aim to restore the balance of dopamine signaling, particularly in individuals with conditions like schizophrenia.

77
Q

What is an inconsistency in the dopamine model regarding the emergence of psychosis related to amphetamine and cocaine use?

A

An inconsistency in the dopamine model is that it takes repeated heavy use of very potent forms of amphetamine and cocaine, not a single exposure, for psychosis to emerge.

78
Q

What short-term effects do stimulants like amphetamine and cocaine have on dopamine release in the brain?

A

In the short term, stimulants cause a massive release of dopamine onto the target neurons in the cortex and basal ganglia. This initial release is associated with feelings of confidence, energy, and well-being.

79
Q

How does the pattern of dopamine release change with repeated exposure to amphetamine and cocaine, and why is repeated use associated with psychiatric risk?

A

With repeated exposure to the drugs, dopamine release actually decreases. It is this repeated use that carries psychiatric risk, even though the initial experiences are positive.

80
Q

What are the likely factors contributing to the development of addiction to amphetamine and cocaine, beyond just the dopamine system?

A

The development of addiction to amphetamine and cocaine likely involves plastic adaptations and multiple components of neuronal networks, including both biomechanical and structural changes. These changes are not only related to psychotic reactions but also to addiction itself.

81
Q

How do drugs, including both pro- and antipsychotic drugs, as well as addictive substances, impact the structure of neuronal networks in the brain?

A

Drugs, whether they are pro- or antipsychotic or addictive, have long-lasting effects on the structure of neuronal networks in the brain. This includes both biomechanical and structural changes, leading to alterations in the fine-grained structure of the nervous system.

82
Q

How do molecules like LSD impact consciousness, perception, thinking, and beliefs, and what is the primary neurotransmitter system involved?

A

Molecules like LSD demonstrate that higher consciousness, perception, thinking, and beliefs have an organic substrate. Their effects are attributed to very specific actions on serotonin signals in the nervous tissue.

83
Q

What was the goal in drug discovery related to psychosis, and how did it lead to the development of Risperidone and similar medications?

A

The goal in drug discovery was to find a compound to block the effects of LSD, followed by trials in people with schizophrenia. The success of this approach led to the development of medications like Risperidone. A molecule effective against a model psychosis could also be effective for endogenous psychotic illnesses such as schizophrenia.

84
Q

What distinguishes second-generation antipsychotic medications like Risperidone from older antipsychotics, and what neurotransmitter systems do they target?

A

Second-generation antipsychotic medications like Risperidone work on both dopamine and serotonin systems. While it was initially thought that the blockade of serotonin receptor 2A was important, it has become clear that the ability to block dopamine D2 receptors remains the critical mechanism.

85
Q

Which club drug is associated with eliciting bizarre changes in consciousness that resemble schizophrenic psychosis?

A

Ketamine is a club drug that can elicit bizarre changes in consciousness, resembling the picture of schizophrenic psychosis.

86
Q

What neurotransmitter system does ketamine affect, and what was the task in finding a compound to block its effects?

A

Ketamine affects the glutamate signaling system. The task was to find a compound that could block the effects of ketamine.

87
Q

What other drug, similar to ketamine, is mentioned in the lecture, and what kinds of states can both of these drugs produce?

A

Ibogaine, a molecule from a plant called Ibogaine, is mentioned. Both ketamine and Ibogaine can produce bizarre, trancelike, and mystical states.

88
Q

What is the significance of ketamine as a drug model of schizophrenia, and what symptoms and cognitive effects are associated with acute ketamine use?

A

Ketamine is considered a convincing drug model of schizophrenia. It can produce the full spectrum of schizophrenia symptoms, including negative symptoms like apathy and withdrawal. Acute ketamine use also produces marked detrimental effects on cognition, attention, concentration, memory, and thought organization.

89
Q

At the molecular level, what does ketamine block, and what is the role of this blocked receptor in synaptic plasticity and learning?

A

At the molecular level, ketamine blocks the NMDA receptor channel. The NMDA receptor is essential for synaptic plasticity and learning. When open, it allows calcium and sodium to enter the cell, leading to processes that strengthen the synapse. This strengthening process is known as long-term potentiation (LTP).

90
Q

What is an autoreceptor, and where is it located in relation to the release of neurotransmitters like glutamate?

A

An autoreceptor is a receptor located on the same terminal from which a neurotransmitter, in this case, glutamate, is released. It serves as a form of feedback control.

91
Q

Which molecule, mentioned in the lecture, was effective in blocking the effects of ketamine in animals and proceeded to human trials?

A

The molecule LY-023 was effective in blocking the effects of ketamine in animals and advanced to human trials.

92
Q

What ultimately happened in larger, better-designed trials for both Bitopertin and LY-023 in the context of schizophrenia treatment?

A

Larger trials for Bitopertin (involving 3600 patients) and further trials of LY-023 failed to find any therapeutic benefits in schizophrenia. The initial successes did not hold up in larger trials.

93
Q

What hypothesis is presented regarding the potential mismatch between the effects of ketamine and the traditional paranoid form of schizophrenia in patients?

A

The lecture suggests that perhaps the problem was with the ketamine model. While amphetamine can reproduce paranoid psychosis, the phenomenology of ketamine is different. Ketamine produces a dramatic effect on consciousness but may not resemble paranoid psychosis. The hypothesis is that glutamate drugs might have been targeted at the wrong patient group, focusing on paranoid psychosis rather than the self-absorbed catatonic form of schizophrenia.

94
Q

How is nitric oxide produced in the brain, and what signal triggers its production at glutamate synapses?

A

Nitric oxide is produced in the brain at glutamate synapses. Its production is triggered by the signal of calcium rushing through the NMDA channel. The enzyme responsible for synthesizing nitric oxide and the NMDA channel are attached to each other.

95
Q

What unique property does nitric oxide have as a neurotransmitter, and how does it affect nearby blood vessels?

A

Nitric oxide is a gas, a gaseous neurotransmitter, and it can diffuse in all directions after production. Some of the nitric oxide will reach nearby blood vessels, causing dilation of the vessel, leading to increased local blood flow. This phenomenon is the basis for the BOLD (Blood Oxygenation Level Dependent) response in functional MRI.

96
Q

How does nitric oxide communicate with other neurons and nerve terminals, and what is the term for this direction of information flow?

A

Nitric oxide signals to other neurons in the vicinity and nerve terminals. This direction of information flow, from the post-synaptic side to the pre-synaptic side, is termed retrograde transmission. It is a departure from the conventional pre- to post-synaptic information flow.

97
Q

What other retrograde signals have been discovered in addition to nitric oxide, and when was nitric oxide identified as the first retrograde signal?

A

Nitric oxide was the first retrograde signal to be discovered, which occurred in the early 1990s. Other retrograde signals, such as endocannabinoids (the brain’s own cannabis system), have also been identified.

98
Q

What are they trying to do by activating the nerve in Vagal Nerve stimulation?

A
99
Q

The activation of the vagal nerve alters the firing rate of ……

A
100
Q

By activating the vagal nerve, it can effect ….. and ……… (important for some people, in terms of depression)

A
101
Q

What does a typical VNS protocol look like?

A
102
Q

How does TNS work?

A
103
Q

What are the key issues with TNS?

A
104
Q
A

7PAYFPSY Psychology and Neuroscience of Psychosis - October 2023 (5 decks)

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