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133 Cards in this Set

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Life time prevalence of Panic disorder
4.7%
Life time prevalence of specific phobia
12.5%
Life time prevalence of social anxiety disorder
12.1%
Life time prevalence of Generalized anxiety disorder
5.7%
Life time prevalence of OCD
1.6%
Panic disorder criteria
Recurrent unexpected panic attacks
Anticipatory anxiety:
≥ 1 month of concern about having additional attacks, worry about the implications of the attacks, or change in behavior related to anticipatory anxiety (avoidance)
Not substance induced
± Agoraphobia
Panic attack physical symptoms
Palpitations
Sweating
Trembling or shaking
Feelings of choking
Chest pain or discomfort
Nausea or abdominal distress
Paresthesias
Chills or hot flashes
Derealization or depersonalization
Dizzy, unsteady, lightheaded, faint
Dyspnea or air hunger, frequent sighing

HYPERVENTILATION!!!
What is cardinal sign of a panic attack?
HYPERVENTILATION

Hyperventilation --> hypocapnia & alkalosis --> decreased cerebral blood flow --> dizziness, confusion, derealization
Epidemiology of panic disorder?
Lifetime risk?
Male: female ratio?
age of onset?
Lifetime Prevalence:
2-3% of women, 0.5-1.5% of men

Females > Males (2-3:1)

Age of Onset:
Young adults/3rd decade but can be as late as 6th decade
Women have greater rise in panic disorder during childbearing years
General anxiety disorder symptoms
Excessive anxiety and worry, most days, for > 6months

Difficult to control the worry

>3 of the following symptoms:
Restlessness/keyed up
Easily fatigued
Poor concentration
Irritability
Muscle tension
Sleep disturbance

Impaired functioning
General anxiety disorder epidemiology?

Lifetime risk?
Male: female ratio?
age of onset?
Lifetime prevalence: 4-7%
Females> Males
Onset early 20s but can develop at any age
Chronic course
Symptoms fluctuate in severity over time
¼ develop panic disorder
Social phobia/social anxiety description
Fear of 1 or more social or performance situations in which exposed to unfamiliar people or to possible scrutiny by others

Exposure to fear situation provokes anxiety
*****Recognition that fear is unreasonable*****

Avoid situations or endure with intense anxiety/Functional impairment
Duration of > 6months in those under age 18
What is common underlying fear in social phobia?
Fear of being judged/scrutinized
Epidemiology of social phobia?
Lifetime Prevalence: 3-5%

******No difference between men and women*******

Typical onset in late childhood/early adolescence


Risk factors: Lower socioeconomic status, educational level
Course and outcome of social phobia?
Course tends to be chronic

few seek help
What is cognitive theory of panic disorder?
Confusion of normal somatic sensation...

Somatic sensations -->catastrophic thoughts about their meaning -->autonomic arousal/more thoughts --> PANIC
What is the role of the amygdala in fear conditioning?
Fearful response to conditioned stimulus (animals) // Panic attack (humans)

Panic originates in abnormally overactive amygdala fear network
&
Prefrontal cortex cannot shut down amygdala fear response!
Explain the fear network and panic disorder
Potential deficit in cortical processing pathways --> misinterpretation of sensory information (bodily cues) --> inappropriate activation of fear network
What is the role of the hippocampus in fear disorder?
Formation of contextual memory

May be important for phobic avoidance, which in part arises from an association of panic attacks with the context in which they occurred
What portions of the brain are part of the "fear network"?
Prefrontal cortex
Insula
Thalamus
Amygdala
Amygdalar projections to brainstem and hypothalamus
What are neurotransmitter abnormalities associated w/ panic disorder?
↓ 5HT1A receptor binding in cingulate cortex

Serotonin has an inhibitory impact on fear network, hence lack of serotonin leads to increased fear network

--> hence why SSRIs treat panic disorder
What is the neurotransmitter abnormality associated w/ panic disorder and noradrenergic dysregulation
Panic disorder associated with increased activity and sensitivity of noradrenergic system

Locus coerulues (that makes norepi) have increased noradrenergic transmission


If give patients an alpha antagonist they have more panic attacks --> but don’t know for sure
What is the GABA impact on panic network??
Gaba also an inhibitory system

Benzodiazepines bind to GABA-A receptor and decreased binding to this receptor lead to panic disorder
Ergo felt there are FEWER GABA-A RECEPTORS --> LESS GABA-->PANIC!
What are the different neurotransmitters that are targeted in theories of panic disorder?
GABA
Noradrenergic (alpha)
Serotonin

All theories claim a lack of any of these three lead to increased fear network
What is heritability of panic disorder?

What is heritability of social anxiety disorder?


What is heritability of GAD?
panic disorder: 0.28 - 0.43

Social Anxiety Disorder = 0.10-0.30

GAD = 0.15 - 0.20
What are the environmental contributions to anxiety disorders?
Disruptions of early attachment and childhood trauma may be associated with the later development of panic disorder

Those with panic disorder may be more susceptible to the effects of trauma than those without panic disorder

80% of patients with panic disorder report major stressors in previous 12 months

Interaction between life stress + genetic susceptibility --> panic disorder
What is the most common type of mental disorder?
anxiety disorders! (as a group)
What % of people have addiction problems?
• 25% of the U.S. population has a diagnosis of drug abuse or addiction
what is DEFINITION of drug addiciton?
• Loss of control over drug use.
• Compulsive drug seeking and drug taking despite horrendous adverse consequences.
• Increased risk for relapse despite years of abstinence

Addiction is caused by drug-induced changes in reward or reinforcement!!!!!!
What is the "reward circuitry" in the brain?
ventral tegmental dopamine neurons project onto limbic portions of the brain

Nucleus secumbens
Hippocampus, etc
Prefrontal cortex

• Rewards activate the neurons
• Expectation of rewards activates the neurons
• Absence of expected rewards inhibits the neurons
• Unexpected rewards activate the neurons even more.
What are some of the long-lasting abnormalities of addiction?
• Reduced responses to natural rewards.

• Sensitized responses to drugs of abuse and associated cues.

• Impaired cortical control over more primitive reward pathways.
What are some cortical changes in addiciton?
hypofrontality” in the frontal (limbic) cortex
What drugs can treat opioid overdose?
Two classic antagonists used for overdose:
Naloxone
Naltrexone
Is the addiction of opiates related to the physical dependence or the tolerance associated with them?
no, its largely independent from these actions
What causes the addiction from stimulants?
• The net effect of stimulants is the same: to increase monoaminergic transmission.


- Tolerance to some effects (euphoria, tachycardia)

- Sensitization to other effects (activation, paranoia, psychosis, irritability)
Explain the mechanism for opiate tolerance & dependence?

(key this is on exam)
When morphine is added to cells that express opiod receptors, there is found to be a decrease in cAMP b/c Gi linked receptors decrease cAMP.

If morphine was maintained, cAMP levels returned to normal so if you removed the morphine, there was a rebound effect --> shot upwards above normal level of cAMP

Meanwhile, CREB induction is opposite that of cAMP, so when cAMP rebounds, CREB crashes down

--> this is showing tolerance & withdrawl
Which part of the brain is responsible for physical dependence & withdrawal?

(i.e. which part has an upregulation of cAMP-CREB pathway)
Locus Coeruleus
Which part of the brain is responsible for dysphoria during early withdrawal?


(i.e. which part has an upregulation of cAMP-CREB pathway)
Ventral tegmental area
Antagonist therapy
What are treatments for drug addiction
Replacement therapy
Antagonist therapy
Antideppressants
Behavioral therapy --> high rate of relapse
Depression criteria

symptoms and duration?
>5 symptoms must be present for >2 weeks:

Sad mood
Anhedonia—lack of interest/pleasure
Sleep disturbance-insomnia/hypersomnia
Change in Appetite
Low energy/fatigue
Psychomotor agitation or retardation
Impaired concentration
Guilty feelings, self-blame
Suicidal/thoughts of death
Depression epidemiology?
Lifetime risk?
Men vs women?
age?
Lifetime prevalence of 15% across different populations
1 in 4 Women
1 in 8 Men

Can occur throughout the lifespan
Peaks of onset in 3rd and 7th (& beyond) decades

Only 50% receive any treatment and only 20% correct treatment
How long would an untreated course of depression last?
6-13 months
how long would a treated course of depression last?
3 months
Consequences of untreated depression?
Suicide (30% attempt, 15% complete)
Divorce/relationships affected
Decreased productivity/Inability to work
Poor hygiene
Can’t care for children
Decreased quality of life
Effects on caregivers
Medical comorbidities
What is the monoamine deficiency hypothesis for Major depressive disorder?
Acute increases in synaptic monoamines by antidepressants produce secondary neuroplastic changes that involve transcriptional and translational changes


once thought depression was the result of a deficiency of monoamines but found that a depletion of monoamines doesn't cause depression in normal subjects

--> more serotonin in synapse helps those w/ depression but isn't cause
Explain glutamate dysfunction theory in MDD?
Chronic stress --> Excess glutamate

Hyperactivation of NMDA type glutamate receptors on neurons and glial cells

End result is atrophy and death of neurons and glial cells

NMDA antagonist --> rapid antidepressant effect
Explain Neuroendocrine dysregulation theory of MDD?
People w/ depression have high levels of cortisol, thought is there is less negative feedback…
Negative feedback system doesn’t work well…

shows hippocampal damage (but other disorders show this)
What are some structural changes seen in depression?
Reduction in gray matter volume in hippocampus & prefrontal cortex!!!!

-->Relative lack of cortical regulation of the limbic system during adversity
What changes in glial cells are evident in depressed patient?
reduction in GLIAL CELL DENSITY AND NUMBER
What is the role of BDNF in depression?
BDNF = expressed abundantly in brain and involved in txn of genes for Serotonin destruction… levels of BDNF are effected by stres & cortisol

High cortisol --> low BDNF
What is heritability in depression?
Heritability: 37%
What gene is linked to depression?
Short/short allele for the serotonin transporter
Bipolar criteria?
At least 1 week of an abnormally and persistently elevated, expansive, or irritable mood
plus

Inflated self esteem/grandiosity
Decreased need for sleep
More talkative
Flight of ideas/racing thoughts
Distractibility
Increased goal-directed activity/psychomotor agitation
Excessive involvement in pleasurable activities with
high potential for painful consequences
Impaired functioning/need hospitalization/psychotic
Bipolar epi?
prevalence?
Men vs women
Age?
Lifetime prevalence: 0.5-1%
Equal prevalence in men and women
Mean age of onset: 21 years (18-44)
Is the neurobiology btw manic or depression different?
No they have same neurobiology
Explain endocrine dysfunction of bipolar?
Hypothalamic-pituitary-thyroid axis dysregulation
Hypothalamic-pituitary-adrenal axis dysregulation
Loss of sensitivity of glucocorticoid receptors --> impaired feedback inhibition in HPA axis --> elevated levels of corticosteroids
Cortisol may lead to increase in inflammatory cytokines and disrupt immune response
What is heritability of bipolar?
VERY HIGH HERITABILITY (65%)
What are some of the systems implicated in MDD?
MONOAMINES (traditional target)

(more recently):
the stress-related neuropeptides
amino acid neurotransmitters
neurotrophic factors
What is definition of dementia?
*Clinical syndrome marked by progressive cognitive impairment in clear consciousness.
*Cognitive deficits represent a decline from a previous level of functioning
*Involves multiple cognitive domains
*Significant impairment in social or occupational functioning
Diagnostic criteria for dementia/
Development of multiple cognitive deficits manifested by both:
1) Memory impairment
2) ≥ 1 of the following cognitive disturbances:
- aphasia (language disturbances)
- apraxia (motor dysfunction, strength okay)
- agnosia (cannot recognize things)
- disturbance in executive functioning
Who is more likely to be effected by dementia: men or women?
women
What is duration of dementia?
varies from 6 months to 15 years
Risk factors for dementia
age (#1)
Gender (female)
Vascular (hypertension, CV disease, obesity, diabetes, hyperlipidemia, cerebrovascular disease, CHF, A fib)
Environmental factors (alcohol, diet?)
Genetics
Factors associated w/ cognitive resilience?
Education
Gender (men more resilient)
Social networks
Cognitive stimulating activities
Conscientiousness
exercise
Explain cortical vs subcortical dementia differences?
1. Cortical
--> Prominent memory impairment, language deficits, apraxia, agnosia, and visuospatial deficits
-->Feature motor signs
2. Subcortical
--> Dementia features greater impairment in recall memory, decreased verbal fluency without anomia, bradyphenia, depressed mood, affective lability, apathy, and decreased attention/concentration, and decreased attention/concentration
-->Lack motor signs




Cortical:
Alzheimer's
Pick's disease
Creutzfeld-Jakob disease

Subcortical dementia:
due to HIV
Parkinson's
Huntington's
muliple sclerosis
What are major etiologies of dementia?
Primary neurodegenerative disorders
Infections
Vascular and traumatic
Toxic-Metabolic and nutritional
Psychiatric
Additional causes
Mixed (Alzheimer’s + Vascular)
What is most common cause of dementia?
1) alzheimers
2) Lewy bodies
3) vasculature
Alzheimer's specific features?
Onset btw 40 &90, usually after 65
Memory impairment + 1 other cognitive effect (aphasia, apraxia, agnosia,executive dysfunction)

Early impairment: short term memory & language

Death typically 8-10 years after onset
Neuropathology of AD?
Amyloid plaques, neurofibrillary tangles

Neuronal loss (entorhinal cortex, hippocampus, select populations of neocortical pyramidal cells, cholinergic neurons in the nucleus basalis)
APOE Gene and alzheimers?
APOE E4: Increased risk of AD
APOE E2: May provide protection from AD
Dementia with Lewy Bodies core features?
(1) fluctuating cognition with pronounced variations in attention and alertness
(2) recurrent visual hallucinations***
(3) spontaneous parkinsonism

FALLS, DELUSIONS & REM SLEEP DISORDERS --> DIFF THAN ALZHEIMERS
Vascular dementia presentation?
Onset acute if large or strategic vascular event, more insidious if smaller subcortical/small vessel infarcts
Course may be static if no further events, or progressive with stepwise decline if more events.
Can have continued gradual decline even without clearly defined vascular events.
Frontal lobe dementias?
THINK ABOUT IF SOMEONE W/ 55 PRESENTS W/ DEMENTIA!!!

VERY DISINHIBITED, INAPPROPRIATE, FRONTAL LOBE DISEASE
Frontal lobe dementia findings?
Restricted to frontal and anterior temporal lobes


Neurons enlarged, vacuolar, extensive gliosis
Include characteristic Pick inclusion bodies, neurofibrillary tangles and ballooned cells, all containing tau protein
Normal pressure hydrocephalus

Signs, imagine, timing, and tx?
"wet wobbly, wacky"

Abnormal gait (often initial symptom)
Urinary incontinence
Dementia

Imaging: enlarged ventricles disproportionate to cortical atrophy

Develops over weeks to months

tx: remove CSF via LP
Creutzfeldt-Jakob dementia presentation?
Peak incidence: 60-64 years
Rapidly progressive dementia
Myoclonus, extrapyramidal signs, cerebellar signs, gait abnormalities
Uniformly fatal- typically 6-9 months from onset
What is difference between ADL & IADL?
Activities of daily living vs independent activites of daily living

(the latter = more complicated) - i.e. telephone, shopping, laundry, transportation, food prep, house keeping, finances
What are aspects of management of dementia?
non pharmacological (education, care giver support, etc)

pharm: Anticonvulsants, SSRIs for behavioral disturbance, cholinesterase inhibitors, NMDA antagonists
Describe Delirium (also how differs from dementia)?
*Develops over SHORT PERIOD OF TIME

*Sensorium clouded
*agitated or stupor
*REVERSIBLE (often)
*common when on meds/in hospital

Delirium can also present with cognitive impairment but must distinguish it from dementia as it is usually reversible and associated with worse clinical outcomes


(delusions)
What enzyme is the target of most FDA-approved Alzheimer’s drugs.
Acetylcholinesterase!

Ergo drugs
What two genes are linked to cause Alzheimer's?
APP1 (amyloid precursor protein) on chromosome 21

and Presenilin 1

often cause errors in γ-Secretase
What gene is linked to increase risk of alzheimers?
Apolipoprotein E
What is the difference between amyloid fibrils and oligomers?
Oligomers – small aggregate of subunits aggregated (Floating soluble amyloid toxins) - little toxic dots

Amyloid fibrils are extracellular; beta-sheets that are protease resistent
What is the importance of amyloid fibrils?
3% of all Alzheimer’s is completely genetic and the causative genes are either the amyloid precursor per se or the enzymes that act upon it

The only forms of Alzheimer’s disease where we know the cause ALL begin with amyloid-related genes

The rationale is that drugs that succeed with genetic Alzheimer’s will succeed in common forms
What is importance of oligomers?
These are Floating soluble amyloid toxins ... little dots that are thought to be actual source of toxicity
Can AB lowering therapies improve cognitive function?
No. they can only improve amyloid burden, but not cognitive function

Theory: this is b/c oligomers aren't impacted!
Why is passive immunotherapy (IVIg) being used for alzheimers??
naturally occurring antibodies against oligomers!
What is the prevalence of schizophrenia?
*Leading cause of disability in the world

* 1.1% of Americans (2.4 million) have experienced or will experience a schizophrenic episode
What is the course of schizophrenia?
Premorbid (youth -15)
Prodromal (15-20)
Progression (20-45)
Stable relapsing (45-60)

positive symptoms decrease w/ age
Negative symptoms increase w/ age

Uncommon to see in someone over the age of 40 develop...

Correlates with MYLINATION OF FRONTAL CORTEX & REORGANIZATION OF SYNAPTIC CONNECTIONS IN FRONTAL CORTEX
What genetic factors contribute to schizophrenia and what is the heritability?
family studies show schizophrenia prevalence is about 6-8% in first degree relatives & adopted away children from mothers w/ schizo have 16% risk (vs 1%)

Twin studies -50%

Sadly, not mendelian genetics, numerous snps for schizophrenia and also these snps are shared w/ other disorders as well
Explain the neurodevelopmental hypothesis in relation to schizophrenia
It suggests that the etiology of schizophrenia may involve pathologic processes, caused by both genetic and environmental factors, that begin before the brain approaches its adult anatomical state in adolescence.

(i.e. 2 hit hypothesis - maldevelopment during early brain development & adolescence) combine to produce scizophrenia

(example, viral disease during pregnancy or famine increases risk)
Explain structural brain abnormalities in relation to schizophrenia
Macroscopic
1)enlarged ventricles
2) shrunken temporal gyri
3)decreased coherence of white matter tracts

Microscopic
1) hippocampal changes volume low (oddly, siblings are btw schizo & control) --> possibly from hypoxia?
2)increased cortical cell density

Decreased neuropil hypothesis:
Reduction of dendritic arbors and axons in the schizophrenic cortex results in a thinner cortex with cells that are more densely packed.
explain neurotransmitter abnormalities in relation to schizophrenia
1)DOPAMINE HYPOTHESIS:

*All antipsychotic neuroleptic drugs can block DA receptors and the potency of a neuroleptic drug to displace the binding of spiroperidol from striatal membranes is correlated with these drugs’ clinical potency

*Administration of dopaminergic drugs can mimic or worsen some schizophrenic symptoms

*DA is a modulator of symptom severity not etiological event

2) GLUTAMATE HYPOTHESIS
*PCP model --> induces schizo
*block NMDA --> decrease GABA--> excess GLUTAMATE!

--> also less GABA transporter

overall: hypo GABA --> excess glutamate
Explain disconnectivity syndrome in relation to schizophrenia
Oligodendrocytes were sick and producing STRANGE MYLIN SHEATHES!!!

NOT NEUROTRANSMITTER DISEASE!!!

Oligodendrocytes produce mylin, if oligodendrocyte abnormalities there are conduction abnormalities
Positive symptoms of schizophrenia
Hallucinations
(false perceptions through hearing, touch, taste, smell, or vision)

Delusions
(false beliefs inexplicable in terms of the patient’s cultural background)

Formal thought disorder
(illogical and often disjointed but fluent speech)

Behavioral disorganization
(bizarre behavior)
Negative symptoms of schizophrenia
Alogia
(poverty of speech per se or of speech content)

Affective blunting
(impairment in emotional expression reactivity, and feeling)

Avolition
(characteristic lack of energy, drive, and interest)

Anhedonia
(difficulty in experiencing interest or pleasure)
Cognitive symptoms of schizophrenia
Attention
encoding (2o memory)
constructional apraxia
verbal fluency
Diagnostic Criteria for OCD
*Recurrent unwanted and distressing thoughts (obsessions) and/or repetitive irresistible behaviors (compulsions)

*Majority have both obsessions and compulsions

*Insight present: acknowledged as senseless or excessive at some point during illness

*Compulsions usually reduce anxiety, but are not pleasurable

*Symptoms produce subjective distress, are time-consuming (> 1 hr/day), or interfere with function
Difference btw OCD and other anxiety disorders
Different from psychosis  KNOW ITS FROM THEIR OWN HEAD!!! Have insight!
Pyschosis --> think someone is implanting thoughts in their brain
Treatment options for OCD
1)SSRI
2) Cognition behavioral therapy
Etiologic hypotheses for OCD
1) Neurotransmitter based (serotonin & glutamate)
2) Circuit based: cortico-basal ganglia - thalamo-corticol loop
3) infection triggered autoimmune process
What neurotransmitter is implicated in OCD?
1) Serotonin (based on clinical usefulness of SSRI)

2)Glutamate (the glutamate transmitter gene is implicated and there is evidence of increased CSF glutamate)
What is the only gene that has been implicated in OCD
glutamate transporter gene SLC1A1
How does OCD relate to huntingtons or the orbitofrontal-subcortical pathway?
This signal could be caused by excess tone in the direct relative to the indirect orbitofrontal-subcortical pathway, resulting in increased activity in the orbitofrontal cortex, ventromedial caudate, and medial dorsal thalamus.

orbitofrontal-subcortical hyperactivity rivets attention and compels patients to respond with ritualistic behavior, and inability to switch to other behaviors.
What is rational of DBS?
Put a lesion in the Ventral Capsule/Ventral Striatum --> 3/4 improve!
What is dementia?
Clinical syndrome marked by progressive cognitive impairment in clear consciousness.

Involves multiple cognitive domains

Significant impairment in social or occupational functioning
What are major diagnostic features of dementia?
1) Memory impairment
2) ≥ 1 of the following cognitive disturbances:
- aphasia (language disturbances)
- apraxia (motor dysfunction, strength okay)
- agnosia (cannot recognize things)
- disturbance in executive functioning
What is difference btw subcortical and cortical dementia syndromes?
1. Cortical
a) Prominent memory impairment, language deficits, apraxia, agnosia, and visuospatial deficits
b) Feature motor signs

2. Subcortical
a ) Dementia features greater impairment in recall memory, decreased verbal fluency without anomia, bradyphenia, depressed mood, affective lability, apathy, and decreased attention/concentration, and decreased attention/concentration
b) Lack motor signs
If patient is falling down w/ dementia and having hallucinations, and REM sleep disturbances what disease is most likely?
Dementia with Lewy Bodies
If a 55 year old presents with dementia what is most likely?
Frontotemporal dementia...

Pick's disease!
If a patient with dementia has urinary incontinence and an abnormal gait, what is most likely?
Normal Pressure Hydrocephalus


Treatable!!!!
What fits on axis I of the DSM-IV
Clinical disorders, including major mental disorders, and learning disorders, Substance Use Disorders

considered more “biological"
What fits on axis II of the DSM-IV
Personality disorders and intellectual disabilities (although developmental disorders, such as Autism, were coded on Axis II in the previous edition, these disorders are now included on Axis I)
What fits on axis III of the DSM-IV
Acute medical conditions and physical disorders
What fits on axis IV of the DSM-IV
Psychosocial and environmental factors contributing to the disorder
What fits on axis V of the DSM-IV
Global Assessment of Functioning or Children’s Global Assessment of Functioning for children and teens under the age of 18
Describe Personality Disorder Cluster A
odd or eccentric disorders

Paranoid: irrational suspicions and mistrust of others

Schizoid: lack of interest in social relationships

Schizotypal: characterized by odd behavior or thinking.
Describe Personality Disorder Cluster B
dramatic, emotional or erratic disorders

Antisocial: pervasive disregard for the law and rights of others.

Borderline: extreme "black and white" thinking, instability in relationships, self-image, identity and behavior often leading to self-harm and impulsivity.

Histrionic: pervasive attention-seeking behavior, inappropriately seductive behavior and exaggerated emotions.

Narcissistic: pervasive pattern of grandiosity, need for admiration, and a lack of empathy.
Describe Personality Disorder Cluster C
anxious or fearful disorders

Avoidant: social inhibition, avoidance of social interaction.

Dependent: pervasive psychological dependence on others

Obsessive-compulsive: rigid conformity to rules, moral codes and excessive orderliness.
Describe schizotypal characteristics?
Magical thinking (aura, destiny, telepathy, even participating in magical rituals)

Disturbances in working memory (difficulty completing tasks)

Ideas of reference (i.e. belief that conversations and gestures of others hold significant personal meaning)

Unusual perceptual experiences

Odd thinking and speech, odd or peculiar behavior and/or appearance

Suspicious, lack of close friends, and excessive social anxiety

Inappropriate or extremely reserved emotional responses
What sort of type of personality has problems w/ memory or getting to the office from the elevator?
Schizotypal
What group has higher hertiability? Axis I or II disorders?
Both have similar level of heritability
What is neurobiolgoy behind schizotypal personality disorder?`
Runs in family with schizophrenia

SPD and SCZ show similar abnormalities in working memory and on various neurophysiological measures, including eye-tracking abnormalities and impaired startle prepulse inhibition

SPD and SCZ show temporal volume (STG), but SPDs have relative preservation of frontal lobe volume

Also reduced striatal (caudate and putamen) dopaminergic activity in SPD compared with SCZ, perhaps accounting for lack of full blown psychosis
Borderline PD Characteristics
Extreme emotional instability, especially anger
Hypersensitivity to interpersonal interactions-
especially perceived rejection
Self-injury done to “relieve” emotional pain
Dissociative symptoms
Impulsivity, especially impulsive aggression: verbal and physical
Unstable intense interpersonal relationships
Chronic feelings of emptiness, identity disturbance
Onset in adolescence, but symptoms evident from young childhood
Borderline mnuemonic
IMPULSIVE
Impulsive
Moodiness
Paranoia or dissociation under stress
Unstable self-image
Labile intense relationships
Suicidal gestures
Inappropriate anger
Vulnerability to abandonment Emptiness (feelings of)
What disorder has high rates of childhood trauma or abuse?
Border line personality disorder

(but its a low predictor)
Neurobiology of Borderline?
Anterior cingulate gyrus and orbital frontal cortex is small in borderline patients

Orbital frontal cortex doesn’t activate normally in borderline patients

Uncoupled Orbital frontal cortex and amygdala

High pain threshold but more intense amygdala/insula activation to painful stimuli
Neurobiology of Borderline with neurotransmitters?
Abnormalities in serotonergic function associated with aggression and suicidal behavior
Treatment of Borderline personality disorder?
Standard pyschotherapy makes them worse!!!!
Psychoanalytics are bad --> don’t do well reflecting on their early life (destabilizes, makes suicide and cutting worse) – 10% lifetime completion of suicide
>70% of patients engage in self harm
Borderline show illness over time…

SKILLS BASED TREATMENTS WORK!!!! -->BUT TAKE A LONG TIME
Describe avoidant?
Longstanding feelings of inadequacy; Subjective sense of being “socially inept”
Extreme sensitivity to what others think about them. Hypersensitivity to criticism, blushing easily.
Sensitivity results in inhibition, not aggressive response as in BPD or ASPD
Behavioral avoidance of work, school and any activities that involve socializing or interacting with others
Social isolation, with restricted interpersonal contacts
Unlike schizoid or schizotypal: They desire affection and acceptance and may imagine idealized relationships with others.
What's an early sign of avoidance?
During a "non stress test" in pregnancy, if it takes a while for the baby's heart rate to return to normal its a sign of avoidance
What is the brain imaging in Avoidant?
Heightened amygdala response to fear inducing stimuli, with decreased prefrontal modulation, and decrease connectivity between prefrontal cortex and amygdala

Note similar model to Borderline, specificity is under investigation
What is tx for avoidant?
Target of most psychotherapy but controlled studied
Short term social skills training diminish symptoms
Antidepressant medications help with social anxiety