Exam 3 Flashcards

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1
Q

National Comorbidity Survey-replication found ? % of population met criteria for OCD during their lifetime

Worldwide prevalence is ?%

Does it occur equally in all ethnic groups?

A

1.6%
1-3%
Yes

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2
Q

How does DSM-5 classify OCD differently vs. DSM-4? Why did the DSM committee decide to change classifiation?

A

DSM-4 as anxiety

New category “Compulsive and related disorders” “OCD and related disorders”. Still next to anxiety though

Treatment options different anxiety vs. OCD. Different subcategories. Differences in DSM-5 vs. DSM-4.

Fear not central to OCD. Repetitive thoughts and actions. Other things different too, like response to medication.

Serotonin helps more people with anxiety. Different neural circuits and response to pharmacological treatment.

Differs from anxiety disorders in course of illness, comorbidity, genetic risk/biomarkers, personality correlates, cognitive-emotional processing, treatment response.

Repetitive behaviors (cognition or body-focused actions)

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3
Q

DSM-5 OCD criteria (including 2 specifiers)

A

A. Obsessions, Compulsions or Both
B. O/C are time consuming (1 hour+) OR cause lots of distress/impair social/occupations/other functioning
C. not attributable to substance or medical condtion
D. not better explained by symptoms of another mental disorder
Specifiers: 1) insight 2) tics (those with tics have more severe symptoms)

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4
Q

? % of those with OCD have poor insight which is related to worse severity and poorer treatment outcomes

A

2-4%

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5
Q

Obsessions and their compulsions (7)

A
  1. Fear contaimintion (clean/wash)
  2. Pathological doubt (repetitive checking)
  3. Sexual/violent (repetitive undoing thoughts)
  4. Fear cause harm (repeated checking)
  5. Symmetry/exactness (ordering and arranging things)
  6. Religious obsessions (religious rituals/excessive praying)
  7. Superstitious obsessions (Superstitious rituals e.g., repeating activities a certain number of times)
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6
Q

Body Dysmorphic Disorder

(Criteria, clinical features, preferred treatment)

A

Preoccuption with perceived defects or flaws in physical appearance that leads to repetitive behaviors or mental acts in response to the apparent concerns

Poor insight, dermatologists/cosmetic surgeons to address defects, symptom onset during teens, waxing/waning course

CBT and SSRIs

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7
Q

Excoriation (skin-picking)

(Criteria, clinical features, preferred treatment)

A

Recurrent skin picking leads to lesions. Repeated attempts to decrease or stop skin picking.

More common in females. Symptom onset at beginning of puberty.

Habit reversal therapy. Limited studies on pharmacotherapy

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8
Q

Hoarding Disorder

(Criteria, clinical features, preferred treatment

A

Persistent difficulty discarding or parting with possessions because of urge to save/not discard. Accumulation where space not used as intended.

75% patients comorbid mood/anxiety
Sig. distress or impariment
Symptom onset 11-15
Hoarding progressively worsens

Behavior thearpy (remove hoarded items, reduce accumulation new things), no data support pharmacotherapy.

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9
Q

Trichotillomania (hair-pulling disorder)

(Criteria, clinical features, preferred treatment)

A

Recurrent pulling of hair from any part of the body resulting in hair loss. Repeated attempts to decrease or stop hair pulling

More common in females. Onset puberty.

Habit reversal therapy. Mixed/poor response to SSRIs.

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10
Q

Treatment Resistant OCD

A

DBS, psychosurgery for this

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11
Q

Types of Assessment for OCD(4 types)

A

Diagnostic Interview (SCID)
Clinician Administered Interview (Y-BOCS)
Family Report
Self-report questionnaire

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12
Q

Describe the Yale-Brown OCD scale

(2 advantages)

A

Most widely used OCD scale, measure of severity

First generate target symptoms list with patient, allows clinician and patient to agree on symptoms rated. Follow up with specific questions about obsessions/compulsions.

  1. Used to select target symptoms for treatments.
  2. You can measure Improvement not just if they have symptoms or not
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13
Q

In controled trials of YBOCS, a decrease of ?% or greater is accepted as indicating clinically meaningful response (global improvement indicating much or very much improved)

A

35%

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14
Q

Neural Circutry of OCD

A

Cortico-striatal-thalamic-cortical loops (CSTC)

for cognitive and other associated features of OCD we are still learning about how constructs such as error monitoring is related to circuitry

OFC, prefrontal cortex, caudate/putamen, striatal/striatum, thalamus.

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15
Q

Basal Ganglia in OCD: the parts

A

Caudate Nucleus, Putamen, Globus Pallidus, subthalamic nucleus, substantia nigra

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16
Q

Striatum

A

Caudate nucleus and putamen

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17
Q

Ventral striatum

A

Nucleus accumbens, ventral part of caudate and putamen, olfactory tubercle

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18
Q

Basal Ganglia 5 Functions

A
  1. Movement Regulation: initaiton, execution, termination voluntary/involuntary movements
  2. Learning and memory: procedural memory
  3. Reward learning: link certain behaviors with positive outcomes
  4. Emotional processing: context of reward and motivation
  5. Cognitive control: cognitive control, including ability to inhibit unwanted thoughts and behaviors and to shift attention between tasks and stimuli
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19
Q

CSTC loops in OCD specifics you need to know

A

Basal ganglia and frontal cotex operate together to learn optimal behaviors and execute goal-directed behaviors

Motivation and emotional drive is coupled with planning and congitive components to plan an action, and then the movement itself are reflected in the organization, physiology, and connections between areas of frontal cortex and projections to striatum

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20
Q

Direct vs. Indirect Pathways: bridging collaterals between these pathways may permit modulation of what?

A

information transmission

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21
Q

OCD treatment

A

first line evidence based or something idk there are stars on the slide

  1. CBT (exposure and response prevention(ERT)#)
  2. Pharmacotherapy (SSRI: fluoxetine,paroxetine, sertraline#) (also: Clomipramine (tricyclics) and antipsychotics(risperidone/aripiprazole))
  3. TMS
  4. DBS
  5. Psychosurgery

ERT: most effective if you stick with it

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22
Q

How does ERT work?

A

Start with YBOCS, then treatment planning, psychoeducation about OCD

Systematic repeated and prolonged exposure to feared stimlui in vivo and imaginal
* In vivo: exposure in real life (in the session)
* Imaginal: ask patient to imagine in detail the distressing thoughts/situation (homework)
* Subjective units of distress (SUDS) ratings

Elimiation of rituals: abstain from ritual, patient learns that feared consequence does not occur

12-16 weeks. 50% report continued symptoms

Sympathetic nervous system up, but can only spike for so long.

Effective but high drop out rates

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23
Q

DBS for OCD

A

Electrode in brain, pulse generator under clavicale (computer and batter, lead wire all implanted)

The DBS lead goes through the putamen and caudate nucleus down to the nucleus accumbens.

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24
Q

rDoC in OCD (gillian paper- error related negativity). Why is it useful?

A

Error related negativity and error monitoring as constructs “performance monitoring”.

Functional sig of ERN seems to be priming defense responses and encouraging avoidance behavior.
ERN enhancement is not specific to OCD, social anxiety disorder and depression.

ERN good cognitive transdiagnostic marker for treatment predictions rather than neuroimaging (expensive and impractical) for most clinics to use diagnostically (at least for now)

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25
Q

rDoC in OCD: what are other constructs/paradigms in OCD? How do you measure them?

A

Goal selection, updating, representation, maintenance.

Measure by devaluation task. (an association with feared outcome is no longer present yet individuals with OCD have been show to continue behavior)

Larger response when they make an error relative to those that don’t. EEG signal. OCD = greater error related negativities.

Press button, don’t change when the rules switch

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26
Q

Test question: rDoC experiment for OCD rDoC?

A

Something related to a circuit.

Game where the rules switch.
Congitive systems, cognitive control, goals updating selection and maintenance. Circuit: CSTC.
different diagnoses

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27
Q

Rats and OCD

A

Basal ganglia similar to animals

Frontal cortex inactivated, more checking behavior

Light = food. Check more often. in this case, checking wastes time

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28
Q

Monkeys and OCD

A

Closer resembalance to human brain. Cortex of human not covered by rat. Rat 28% human brain volume, monkey 60-70% depending on species

Humans only correlation of activity. Monkey gets drug effect on brain and changes.

Juice reward. Normally get the new rule, but not if OFC is inactivated. Then more repetitive behaviors. Learn, but hard to switch back. Go on responding to behavior even if not rewarded anymore. Some patients with OCD see change in OFC and first degree relatives.

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29
Q

Reaction to trauma is highly variable. Name how variable.

Because of this variability, how is clinical distress put in the DSM-5? How do we treat trauma patients?

Where is trauma in general in DSM-5?

A

Anxiety/fear, anhedonia/dysphoric, externalizing anger/aggression, dissociative symptoms

Clinical distress related to trauma has own category in DSM-5

Don’t ask patients how they react, because react many different ways

30
Q

Where is DSM-5 chapter on general trauma?

A

DSM-5 chapter place between OCD and dissociative disorders

31
Q

Types of trauma (general) disorders

A

Reactive attachment, disinhibited social engagement disorder, PTSD, acute stress disorder, adjustment disorders

32
Q

history of PTSD

A

Medical diagnosis in 1980. Vietnam War

Shell shock during WWI

“Environmental” but inhereited component

More common in women

33
Q

DSM-5 additional criteria for PTSD (F., G., and H.)

A

F. Duration: Symptoms >1 month
G. Distress/Impairment: Clinical sig distress, social/ocupational/other important functioning impairment
H. Not attributable to another disorder: independent of physiological effects of a substance (e.g., medication, alcohol) or other condition

34
Q

Criterion A for PTSD

How do you assess? Like what is the name of the assessment?

A

Exposure

Actual/threatened violent death, serious injury/accident or sexual violence.

  1. Directly exposed to trauma
  2. Eyewitness (in person) to others directly exposed
  3. Learning of direct exposure to trauma of close family member/friend
  4. Repeated or extreme exposure to aversive details of traumatic event (e.g. viewing human remains or repeatedly exposed to details of child abuse) in person or via work related media

Life events checklist

35
Q

Criterion B for PTSD

A

Intrusion Symptoms

1+ symptom

At least one intrusion symptom:
1. Recurrent, involuntary, distressing trauma memories
2. Recurrent, distressing trauma-related dreams
3. Dissociative reactions/flashbacks related to trauma
4. Intense or prolonged psychological distress to trauma reminders
5. Marked physiological reactions to trauma reminders

36
Q

PTSD general criterion

A

A. Exposure
B. Intrusion
C. Avoidance
D. Negative congition/mood
E. Hyperarousal
F. Duration
G. Distress/Impairment
H. Not attirbuable to another disorder.

37
Q

Criterion C for PTSD

A

Avoidance

1+ symptom:
1. Avoidance/efforts to avoid distresing internal trauma reminders (memories, thoughts, feelings)
2. Avoidance or efforts to avoid distressing external trauma reminders (people, places, activities)

38
Q

Crierion D for PTSD

A

Negative Mood and Cognition

2+ symptoms
1. Amnesia for important parts of trauma exposure
2. Persistent exaggerated negative beliefs about self/others/world
3. Persistent distorted trauma related cognitions leading to inappropriate blame of self/others
4. Persistent negative emotional state (fear, horror, anger, guilt, shame)
5. Loss of interest or participation in sig activities
6. Detached/estranged feelings from others
7. Persistent loss of positive emotions (e.g., happiness satisfaction and love)

39
Q

Criterion E for PTSD

A

Hyperarousal

2+ marked alterations in trauma related arousal and reactivity

  1. Irritability and angry outbursts with little/no provocation
  2. Reckless/self-destructive behavior
  3. Hyperviligance
  4. Exaggerated startle
  5. Concentration problems
  6. Sleep Problems
40
Q

PTSD diagnosis specifiers (hint: there are 2)

A

With dissociative symptoms - in addition to stressor, persistent or recurrent symptoms of depersonalization or derealization. Must not be attributable to a substance or another medical condition

Specify if with delayed expression- diagnostic criteria not met until at least 6 months after the event (although onset of some symptoms might be immediate)

41
Q

5 steps to PTSD assessment

A
  1. Tramatic event (threat to life/limb)
  2. Trama exposure (directly, witnessed, loved one, aversive details)
  3. Meets symptom critieria (1+ intrusion, 1+ avoidance, 2+ cogn/mood, and 2+ arousal)
  4. > 1 month
  5. Distress/impairment
42
Q

3 measures to assess for PTSD (which is the gold standard)?

A

Gold standard = Clinician Administered PTSD Scale (CAPS) –> clinican asks about DSM-5 criteria and examples of symptoms. Provides diagnosis as well as symptom severity

SCID- clinician administered, diagnosis only

PTSD Checklist (PCL-5): self-report of symptom severity, correlated with CAPS

43
Q

How is PCL-5 scored? What is the cut off?

A

Trick question.
1. Total symptom severity score 0-80 summing scores for 20 items
2. DSM-5 cluster severity scores
3. PTSD diagnosis by 2= moderately or higher a symptom endorsed and at least 1 B item, 1 C item, 2 D items, 2 E items

Cut off suggested around 31-33.

44
Q

Did the PTSD Fenster et al. paper take an rDoC or DSM-5 approach?

A

Paper organized by DSM-5 criteria

  1. Intrustions - persistent reexperiencing trauma
  2. Avoidance - active/passive
  3. Negative mood- memory/beliefs/negative emotions/detacahment
  4. Hyperarousal
45
Q

Criterions B: Intrustions BRAIN NETWORKS

A

Nightmare, unwanted memories, reexperience trauma

Undermodulation

Cortex (PFC/rACC) not inhibiting limibic system (amygdala)

PTSD: increased amygdala/insula activity
decreased mPFC/rACC activity

Failure of PFC and rACC to downrgulate visceral experience of trauma (amygdala)

May play a role in imparied fear extinction (vmPFC)

46
Q

Criterion C: Avoidance (BRAIN AREAS and NETWORKS)

A

Persistent, effortful avoidance of distressing/trauma related stimuli (2 symptom: thoughts/feelings or people/places/things)

May be associated with imparied fear extinction learning

Cortex/hippocampus - intrusions

Amygdala, hippocampus, cingulate cortex
RAT: IL, NAcc, LA

DISRUPTED POSTERIOR DMN. Less connectivity between PCC & Hippocampus in PTSD = more avoidance

47
Q

Criterion D: Altered mood and cognition (BRAIN AREAS and NETWORKS)

A

Heterogenous group of symptoms; includes memory deficits, distorted beliefs, persistent negative emotions, diminished interest in reward, constricted emotional experience, social detachment symptoms

Symptoms might overlap with depression. Circuits include those for memory, emotional regulation, reward.

Smaller hippocampal volume

mPFC, cingulate, Thalamus, amygdala, hippocampus
RAT: (IL, NAcc, BLA, hippocampus)

48
Q

Criterion E: Arousal (BRAIN AREAS and NETWORKS)

A

Includes hypervigilance, irritability, aggressiveness, reckless behavior, exaggerated startle, concentration difficulty, sleep disturbance

vmPFC, OFC, dACC, PAG, Locus Corelleus (LC?)
Overactive salience network

49
Q

What is found through a meta analysis of PTSD neural circuits?

A

PFC-amygdala alterations (PFC doesn’t regulate amygdala, which leads to intrusions, fear extinction deficits, and emotional regulation deficits)

Hippocampal.amygdala-cingulate alterations (avoidance and fear extinction deficits)

Medial PFC, reward circuitiry (mood alterations)

Disrupted DMN

Overactive salience network/insula (hyperviligance)

PTSD: more amygdala and midACC (fear memories), less vmPFC and IFG (hippocampus)

lateral and ventromedial PFC low in activation

50
Q

What is hard about putting DSM criteria for PTSD into RDoC domains?

A

So many can apply!

For example, Intrusive memories = Negative valence systems (loss), cog (attention, memory, perception, control, etc.), and arousal (arousal)

Distress due to trauma cues = negative valence system (potential threat/sustained threat) and congitive systems (cog control)

Marked physiological reactions = negative valence (acute threat) and arousal and regulatory systems (arousal)

I’m not listing them all. Life is too short for that.

51
Q

Why are traumatic memories such a thing in PTSD?

A

Emotionally arousing experiences (good or bad) tend to be remembered. Fear condition circuitry

52
Q

How do you ameliorate effects of negative memories?

A

Fear extinction
Reconsolidation interference (memory conslidation)
Memory suppression
Future: erase memories
Optogenetic manipulation?

For this test, only discuss fear extinction

53
Q

ESSAY QUESTION: A review of fear condition. What regions? What happens? How does it work?

A

UCS (shock) depolarizes lateral nucleus of amygdala call, NT depolarization diffuses form UCS spine to CS spine, strengthing connection of spines.

Circuit: Sensory cortices, thalamus, lateral/central amygdala.

UCS/CS paired. CS only small signal.

Thalamus, auditory, and somatosensory regions –> Lateral Amygdala –> Central nucleus of amygdala –> other regions (freezing, blood pressure, hormones)

54
Q

What is fear extinction: the process by which [blank] is weakened?

What actually happens? Is a memory erased?

What happens during extinction recall?

A

previously learned fear stimulus and response to stimulus

Original fear memory NOT erased, new memory is formed, inhibits fear response

During extinction recall, new extinction memory retrieved

55
Q

How do you teach the rat the tone is no longer to be feared (fear extinction)?

What is the problem with fear extinction?

A

1) Fear Conditioning (tone is bad)- 2 animal groups
2) Extinction (only 1 group)
3) Consolidation
4) Extinction recall (green group freezing goes down fast this time than the other group)

Have to keep teaching or go back to fear response. If you don’t do any more testing, by day 14, ~100% back to freezing.

Moral: extinction INHIBITS but does not erase the fear memory

56
Q

Extinction circuitry in the rat vs. Fear circuitry in the rat

A

Extinction: IL (infralimbic) activates BLA, activates ITC, INHIBITS central amygdala

Fear: PL (prelimbic) activates BLA, ACTIVATES central amygdala

BLA = basolateral amygdala
ITC = intracalated cells
Infralimibic cortex (PL and IL?)

These are connections between mPFC and amygdala.

57
Q

What is influencing the fear and extinction circuits and why?(Besides amygdala, what part of the brain is influenced?)

A

Hippocampus (Contextual memory, e.g., if rat in a pink box for extinction, still scared in blue box)

CS –> Amygdala and Hippocampus
Hippocampus –> Infralimbic mPFC and Amygdala
Amygdala –> Infralimbic mPFC

What does vmPFC/Infralimbic mPFC do with these inputs? Weighs the context with the fear memory from amygdala. Then, it inhibits amygdala output, BUT outside CONTEXT, amygdala is uninhibitied.

58
Q

Does fear extinction erase a memory?

A

No, forms a new memory

59
Q

How does the new inhibitory memory from fear extinction compete with original memory?

A

Context dependent way

Retrieval of extinction should activate GABA inhibitory networks. When GABA blocked, fear expressed.

Extinction memory might be recalled in extinction/exposure context, but not necessarily in original acquisition context or completely new contexts

Hippocampal involvement related to contextual extinction memory recall.

60
Q

Why do relapses develop when you use fear extinction?

A

Difficulties in extinction memory recall and/or its (long-last) transfer beyond therapy context

61
Q

Retrival of extinction involves expression of an inhibitory memory and is context specific.

Therefore, retrival of extinction would be expected to activate what two things?

A
  1. Inhibitory networks
  2. Hippocampus
62
Q

What two brain regions make up the striatum?

A

Caudate Nucleus and Putamen

63
Q

First line pharmacological treatment for OCD is

A

SSRIs

64
Q

The CBT used as a first line treatment for OCD is

A

Exposure and response prevention

65
Q

Pretend little Albert no longer scared of the white rat. Describe the neural circuitry involved in this and NT and context.

A

**Extinction learning, consolidation, extinction recall.

Extinction Learning: tone no longer paired with rat

Consolidation: gene translation/transcription and long term structural brain changes to consolidate extinction memory

Extinction recall: little albert in same context, recalls white rat not predicting aversive stimulus

Fear conditioning: thalamic input–> basolateral amygdala (fear expression, conditioning, and response).

Extinction Learning: vmPFC/infralimbic cortex –> BLA (intercalated cells ITC, inhibit central amygdala’s fear response). Extinction inhibits fear circuit.

Hippocampus plays a role in contextual memory because learn fear in context. Fear extinction would not be learned in new context, fear would generalize.

66
Q

Describe Neurocircutry of OCD and its involvement in intrusive thoughts

A

Cortico-striatal-thalamic-cortical loop (direct and indirect pathways)

Direct: Cortex –> Striatum, more active –| substantial niagara and GP (internal). These usually inhibit thalamus, but now they aren’t so thalamus activates cortex even more. DECREASED FILTERING OF INTRUSIVE THOUGHTS. Net effect: excitatory

Indirect pathway: Cortex -> striatum –| GP (external), now not inhibit, so it DOES inhibit —| subthalamic nucleus (STN) –> SN/GP (internal) —–| Thalamus. Now SN/GP (internal) can inhibit thalamus, less irrelevant info given to cortex. Net effect inhibitory.

Balance between direct and indirect pathway in OCD is skewed (more excitatory net effect from direct pathway). Direct pathway might be overactive so thalamus is stimulating cortex back in loop to a greater extent.

There are more intrusive thoughts that are not related to a goal that would have otherwise been inhibited.

67
Q

PTSD vs. OCD. How would you know?

A

Must have been through trauma in the past and are doing this action to decrease anxiety of precieved threat from trauma event

To assess for PTSD, ask if they have been exposed to trauma of an actual or threatened violent death or serious injury or sexual violence. Many sure themselve,s eyewitness, learned about close relative, or repeated/extreme exposure to details.

1+ intrusion symptom: recurrent, involuntary distressing trauma memories
1+ avoidance symptom (internal thought/feelings OR external people/places/things)
2+ negative mood/cognitive symptoms (e.g., loss of interest or participation in activities)
2+ hyperarousal symptoms (hypervigiliance, concentration problems, trouble sleeping)

Symptoms must be for more than one month and impacting life/causing distress, and not better explained by medication, substance use, or other illness.

PTSD not OCD if symptoms AFTER traumatic event. Ask why they feel compelled to check front door is locked. Ex: done to prevent trauma (PTSD) or done to prevent imagined threat (OCD)?

68
Q

Other disorders in DSM-5 chapter “OCD and related disorders” include what?

What ISN’T included?

A

Included: Excoriation disorder, hoarding disorder, body dysmorphic disorder, trichotillomania

Not: Tic disorder

69
Q

In PTSD, resting state fMRI studies have shown…

A

Decreased posterior DMN

Increased Salience network

70
Q

Ways to disrupt negative memories. Name them. Is DBS included?

A

Disrupt negative memories by fear extinction, disruption of consolidation, memory suppression, and optogenetic erasure

NOT DBS

71
Q

True or false: experiencing trauma always leads to reaction of fear, helplessness, or horror

A

False

72
Q

Sites for DBS for OCD include…

Where is it NOT?

A

Subthalamic Nucleus (STN) and Nucleus Accumbens (NA)

NOT: GP, putamen, or substantia nigra