Lecture 14 Flashcards
What did Palombo say about podcasts?
● How do I pick a “good” podcast?
● How can I trust the information?
○ Is the guest an expert in that topic? (what are their credentials, are they speaking on a topic that they have expertise in. )
○ What kind of literature are they discussing? (is it a one off finding or is it a pattern in the literature. )
● Pay close attention to what you read in popular books too—if something catches your interest, read the original sources!
What do we use to diagnose disorders?
You may have heard of the “DSM” or Diagnostic and Statistical Manual of Mental Disorders by the American Psychiatric Association. It is used to diagnose and classify mental health conditions using a common language and set of criteria (i.e., standardization). The DSM is not a fixed document as it is updated every so often to reflect new knowledge and to adjust terminology. They are currently at Version 5. (this is adjusted to reflect new knowledge we have in the field and to adjust the terminology. It has faced well-deserved criticism over the years. )
● DSM has faced important and well deserved criticism over the years.
● It is important for mental health professionals to continue advocating for inclusive and affirming (supportive) language in the DSM.
What do we know about memory and post traumatic stress disorder?
● Intrusive memories or flashbacks (can feel like it is happening now)
● Avoidance of reminders (cues) of the trauma
● Possible fragmentation for aspects of the memory (evidence of completely
forgetting trauma is less clear)
● Memory of trauma feels self defining
● Nightmares of the trauma memory (Video) nightmares are a core feature of PTSD
● Reduced memory for neutral, every day material
characterized by changes in memory folllowing exposure to a traumatic event. For some individuals the memories fee llike they are happening again now. It isn’t just that the memories are strong, it is that for some individuals they come in the form of flashbacks where you feel like you are experiencing the event in the here and now. Individuals can be avoidant because they don’t want to think of the cues that trigger the event. There is possible fragmentation for aspects of the memory. For some individuals, the memory feels incomplete. This is controverisal. The memory of trauam feels self-difining. For some individuals, they feel that
There can be reduced memory for neutral everyday material.
Many people who experience traumatic events wil have some of these symptoms but not everyone will go on to experience PTSD. What might be different about someone who gets a diagnoses of PTSD vs. someone who doesn’t is their interfering with their daily life. Sometimes when someone is given a diagnoses, it involve just reaching that threshold whereas others don’t because they are just below. A lot of researchers choose to look at this continuously.
LISTENING TO RECORDING OF THIS LECTURE FOR PODCAST AND VIDEO ON PTSD PLEASE DO IT OR YOU WILL FAIL
What are the definitional challenges in the DSM relating to PTSD?
● But what is a trauma?
● Hard to define
● Definition has changed with different versions
● Current DSM: Exposure to actual or threatened death, serious injury, or
sexual violence (personally experienced or witnessed)
● Why is the addition of “witnessed” important?
the definition of trauma has changed with different versions of the DSM.
we have very powerful imagination systems so when we are witnessing something we can form a memory of what it would be like if it were to happen to us.
What causes PTSD?
● Unclear
● Only a subset of people exposed to trauma develop PTSD
● There could be predisposing biological or cognitive factors
in her research about the plane crash the rate was about 50%. The event was really similar across people, but only some people get PTSD. It isn’t just about how severe the trauma was.
What is the relationship between PTSD, Sleep and Dreams?
● During certain stages of sleep, memories are consolidated, particularly emotional ones
● During rapid eye movement (REM) sleep, noradrenaline (NE) levels dramatically drop.
(we’ve heard about the fact that this plays a role in arousal, is released from the brain stem and plays a role in the amygdala.)
○ Some research suggests that this allows the brain to process emotional memories, without the same intensity (thereby taking away the emotional charge).
○ One hypothesis is that in PTSD, this process is altered: NE does not decrease as much during REM sleep, leaving in the charge of emotional memories. Manifests as intrusive memories and nightmares
LISTEN TO THE The Matt Walker Podcast sleep and PTSD with Dr. Charan Ranganath.
Can CS-US linking be a model for PTSD?
● Fear conditioning has been used as a model for PTSD
● According to this theory, neutral stimuli become associated with strong fear responses.
● Unconditioned Stimulus (US): A vicious dog bite, which naturally evokes fear.
● Conditioned Stimulus (CS): The sight of that dog (a previously neutral stimulus).
● After the trauma: The person now fears dogs (conditioned response; CR).
● The CS-US linkages may be stronger in those with PTSD
this is heavily studied in non-human animals to try to understand the neurobioloy of fear conditioning and how it might be altered in clinical conditions.
● A person relives the memory, which reinforces the CS-US connection. What is more, new thoughts get linked to the memory, creating more CS stimuli. This makes the memory stronger.
if you have a formerly neutral cue, you are creating new opportunities to think about that. If you think about your trauma a lot in the living room, the condiiliving room itself becomes a cue.
Is there a theory of PTSD beyond CS-US linking?
● Another prominent theory of PTSD suggests that PTSD is associated with an overgeneral fear response. A person with PTSD may show a conditioned response to all breeds of dogs.
this generalization gradient is bigger. Ex: a person with PTSD may show a conditioned response to all breeds of dogs.
Can the strong conditioned response in PTSD be extinguished?
Can the Strong Conditioned Response be Extinguished?
● In PTSD there may be more difficulty breaking the CS-US link.
● Not clear if this idea best captures PTSD.
you can use extinction to sever the relationship between CS and US. Some would argue this is just harder in people with PTSD like stickiness in terms of exxtinction. Some debate on this theory for sure.
What are limitations of the popular models of PTSD?
● Largely based in non-human animal work, where the focus is on implicit (non- declarative) memory. They do not provide a full understanding of PTSD in humans, which also involves declarative, episodic memory. They also do not account for other memory differences (e.g., reduced memory for neutral material).
this allows us to probe the neurobiology we otherwise wouldn’t be able to do in humans. There are limitations though, We know in PTSD people have these vivid episodic memories they relive. Can an animal model help us explain something like flashbacks?
you start with a strong CS US connection and then you repeat this and see stronger connections.
the amygdala, the hippocampus and the prefrontal cortex are often talked about in relation to PTSD but she doesn’t know whether or not she should hang her hat on that. Hippocampal volume differences might be a vulnerability factor in development of PTSD.
What are theraperutic approaches to PTSD?
● There are different types of therapies with different theoretical traditions and practices but many involve memory. The goal is to reduce the emotional impact of traumatic memories in a way that diminishes their negative impact.
relating to therapy, there is a lot of focus on memory. The therapies often try to reduce the emotional impact of the traumatic memory. propranalol, psychotherapy etc. One example: an interesting body of work looked at using a stimuli to interrupt the consolidation process. Some researchers are going to emergency rooms and they are having individuals exposed to a trauma in the last few hours play tetris. One idea is that these intrusive memories that develop and stick around in individuals with PTSD invovle a lot of evocative imagery. The researchers are saying what if we mess with that? What if we give you other stimuli. These studies have shown that when individuals play tetris, later on their symptoms of PTSD are reduced. These researchers are rooting their ideas in memory theory.
How do you conduct research to understand PTSD?
Some theories are challenging to test because we do not have a baseline. We often study people after a trauma has occurred. Why is this a limitation to understanding causes and mechanisms?
some of the ideas of the challenges are that the data is collected retrospectively, it is collected after the fact. This is a limitation because if you are looking at say brain volume, you don’t know what is before or after. Is it a vulnerability factor or is it a result? Often studies with PTSD involve no trauma exposed control group, trauma exposed group with a diagnosis of PTSD and another without PTSD diagnosis.
Another example comes up when thinking about studying different kinds of memory with PTSD. One observation we see is that folks with PTSD also perform slightly lower on tests relating to declarative memory that have nothing to do with trauma. There’s interpretive challenges (maybe someone is thinking about their PTSD because they know the study is about PTSD and then this is making them perform worse in the moment).
Could look at changes before and after therapy. These studies are challenged by the fact that sometimes an individual is not diagnosed but has similar symptoms.
What is substance use disorder?
● Substance Use Disorder refers to a maladaptive pattern of substance use that leads to clinically significant impairment or distress.
● Addictive substances (e.g., drugs) target different neurotransmitter systems in the brain.
How does operant conditioning relate to substance use disorder?
● One learning model to understand drug use or substance use disorder is operant or instrumental conditioning.
● But classical conditioning is also highly relevant. Let’s visit these in turn.
How do drugs change neuro transmission WATCH VIDEO
DRAW DIAGRAM
First: A Primer on How Drugs Change Neurotransmission
(B) Amphetamine works by causing dopaminergic neurons to make and release more dopamine (1). Cocaine works by blocking the reuptake of unused dopamine molecules (4). Both drugs thus increase the amount of dopamine in the synapse, increasing the chance that dopamine molecules will activate receptors on the postsynaptic neuron (2).
this is what happens from drugs.
(A) A presynaptic dopamine- producing neuron releases dopamine into a synapse (1). These molecules activate dopamine receptors on the postsynaptic neuron (2). Unused molecules are broken down (3) and taken back into the presynaptic neuron, a process called reuptake (4).
A is what happens in our brains naturally.
What is the role of dopamine in the brain?
● The incentive salience hypothesis of dopamine function states that one role of dopamine is to signal how much the animal “wants” a particular outcome— that is, how motivated the animal is to work for it
○ According to this hypothesis, an ability to motivate responding—is reduced in dopamine-depleted animals. Dopamine does not have as much to do with “liking” something (the so called pleasure idea). “Liking” is linked to opioid receptors.
this debunks a common myth that dopamine is a pleasure chemical. It was less to do with liking but more to do with wanting or motivation.
Animals with depleted dopamine will not lever press for food but they will consume it if its freely available (still “like” food). Animals with increase dopamine will lever press more. This is operant conditioning.
● S = The lever
● R = The act of lever pressing
● O=Thefood
● Drugs that affect the dopamine system change the manner of responding “R”.
How do you know if an addiction will form?
● It is not known whether a particular individual who starts using a particular drug will form an addiction, and it is also hard to know how difficult it will be for a particular individual to respond to treatment.
● Some theories of learning and memory can help us answer these questions and ultimately help individuals live better lives.
● In the last slide we saw the role of S-R-O (operant conditioning). What about classical conditioning?
Example: Tolerance to Addictive Drugs
● Classical Conditioning might help us understand certain symptoms, such as cravings.
○ Environmental cues (people, places, etc.) act as CSs associated with the drug (the US).
○ The intense craving felt in response is the CR resulting from the body’s conditioned compensatory response of lowering the levels of the brain chemicals enhanced by the drug in anticipation of the drug’s arrival.
○ Example: if the drug typically speeds up heart rate, your body will compensate by decreasing heart rate and breathing (other examples, lowering blood pressure, body temperature) or vice versa in response to environmental cues (CSs).
Conditioned Compensatory Response in the Lab
○ Inject adrenaline (US) à heart rate increase (UR).
○ Repeat the procedure in the same testing chamber (CS).
○ Eventually, CS comes to produce a decrease in heart rate (CR) that helps maintain homeostasis (balance) against expected adrenaline injection.
○ Testing chamber evokes a CR that weakens the overall effects of the drug.
○ Needle can also be a CS!
Implication: A New Location is Not a Strong CS!
Familiar drug taking location (park bench)
Novel drug taking location (hotel)
the probability of someone having an overdose is much higher in a novel location vs. a familiar location.
What is the study on rodents and overdoses in new locations?
In first-time dose rats, large heroin dose
led to (a group of rodents who have been given a dose of heroin for the first time) :
* 96 percent fatal overdose.
In rats with small dose before larger
dose in the same location (in rats who have had the drug before) :
- only 32 percent overdose.
In rats with small dose before larger dose in a different location (now you see double the percentage of overdose) :
* 64 percent fatally overdose.
Implications
● This study demonstrates the risk of overdose is higher when the drug is taken in a novel environment (e.g., hotel). This is because the novel environment lacks the environmental cues (CSs) to initiate compensatory responses.
the body hasn’t readied itself to offset the use of a drug.
how do you extinguish a drug habit?
● Substance use can be partially reduced through Pavlovian extinction: repeated nonreinforced exposure to experimentally manipulated cues that had previously been paired with administration of alcohol or drugs
Outside of the Laboratory?
● Outside the laboratory it can be difficult to extinguish a habit.
○ Cue-exposure therapy should be conducted in as many different contexts as
possible, including contexts where original habits were formed.
(this has to be done with the outside world in mind. You can’t just do it to the onfines of the lab. )
○ It should be spread out over time, rather than conducted all at once.
(should used spaced practice. This will make the unlearning of the CS-US much stronger.)
What is parkinson’s disease?
● In Parkinson’s Disease, there is a loss of dopamine input to the basal ganglia from the brainstem, leading to profound movement impairments.
● Learning is also affected, especially procedural learning and operant or instrumental conditioning.
this is a neurological condition that affects the brain’s basal ganglia system and dopamine. Parkinson’s is known for the motore symptoms but there are cognitive impairments as well.
Why This is Important
● Understanding patterns of spared and impaired memory can help with rehabilitation.
we talked abotu this in the context of amnesia. It is really the implicit learning in memory that is affected. So if we are trying to get them to remember something we will focus less on the implicit things.
