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133 Cards in this Set
- Front
- Back
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Life time prevalence of Panic disorder
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4.7%
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Life time prevalence of specific phobia
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12.5%
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Life time prevalence of social anxiety disorder
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12.1%
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Life time prevalence of Generalized anxiety disorder
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5.7%
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Life time prevalence of OCD
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1.6%
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Panic disorder criteria
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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 |
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Panic attack physical symptoms
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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!!! |
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What is cardinal sign of a panic attack?
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HYPERVENTILATION
Hyperventilation --> hypocapnia & alkalosis --> decreased cerebral blood flow --> dizziness, confusion, derealization |
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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 |
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General anxiety disorder symptoms
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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 |
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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 |
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Social phobia/social anxiety description
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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 |
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What is common underlying fear in social phobia?
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Fear of being judged/scrutinized
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Epidemiology of social phobia?
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Lifetime Prevalence: 3-5%
******No difference between men and women******* Typical onset in late childhood/early adolescence Risk factors: Lower socioeconomic status, educational level |
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Course and outcome of social phobia?
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Course tends to be chronic
few seek help |
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What is cognitive theory of panic disorder?
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Confusion of normal somatic sensation...
Somatic sensations -->catastrophic thoughts about their meaning -->autonomic arousal/more thoughts --> PANIC |
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What is the role of the amygdala in fear conditioning?
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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! |
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Explain the fear network and panic disorder
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Potential deficit in cortical processing pathways --> misinterpretation of sensory information (bodily cues) --> inappropriate activation of fear network
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What is the role of the hippocampus in fear disorder?
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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 |
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What portions of the brain are part of the "fear network"?
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Prefrontal cortex
Insula Thalamus Amygdala Amygdalar projections to brainstem and hypothalamus |
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What are neurotransmitter abnormalities associated w/ panic disorder?
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↓ 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 |
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What is the neurotransmitter abnormality associated w/ panic disorder and noradrenergic dysregulation
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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 |
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What is the GABA impact on panic network??
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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! |
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What are the different neurotransmitters that are targeted in theories of panic disorder?
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GABA
Noradrenergic (alpha) Serotonin All theories claim a lack of any of these three lead to increased fear network |
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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 |
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What are the environmental contributions to anxiety disorders?
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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 |
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What is the most common type of mental disorder?
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anxiety disorders! (as a group)
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What % of people have addiction problems?
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• 25% of the U.S. population has a diagnosis of drug abuse or addiction
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what is DEFINITION of drug addiciton?
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• 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!!!!!! |
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What is the "reward circuitry" in the brain?
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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. |
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What are some of the long-lasting abnormalities of addiction?
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• Reduced responses to natural rewards.
• Sensitized responses to drugs of abuse and associated cues. • Impaired cortical control over more primitive reward pathways. |
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What are some cortical changes in addiciton?
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hypofrontality” in the frontal (limbic) cortex
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What drugs can treat opioid overdose?
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Two classic antagonists used for overdose:
Naloxone Naltrexone |
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Is the addiction of opiates related to the physical dependence or the tolerance associated with them?
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no, its largely independent from these actions
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What causes the addiction from stimulants?
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• 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) |
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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 |
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Which part of the brain is responsible for physical dependence & withdrawal?
(i.e. which part has an upregulation of cAMP-CREB pathway) |
Locus Coeruleus
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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 |
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What are treatments for drug addiction
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Replacement therapy
Antagonist therapy Antideppressants Behavioral therapy --> high rate of relapse |
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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 |
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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 |
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How long would an untreated course of depression last?
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6-13 months
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how long would a treated course of depression last?
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3 months
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Consequences of untreated depression?
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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 |
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What is the monoamine deficiency hypothesis for Major depressive disorder?
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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 |
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Explain glutamate dysfunction theory in MDD?
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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 |
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Explain Neuroendocrine dysregulation theory of MDD?
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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) |
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What are some structural changes seen in depression?
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Reduction in gray matter volume in hippocampus & prefrontal cortex!!!!
-->Relative lack of cortical regulation of the limbic system during adversity |
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What changes in glial cells are evident in depressed patient?
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reduction in GLIAL CELL DENSITY AND NUMBER
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What is the role of BDNF in depression?
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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 |
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What is heritability in depression?
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Heritability: 37%
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What gene is linked to depression?
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Short/short allele for the serotonin transporter
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Bipolar criteria?
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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 |
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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) |
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Is the neurobiology btw manic or depression different?
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No they have same neurobiology
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Explain endocrine dysfunction of bipolar?
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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 |
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What is heritability of bipolar?
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VERY HIGH HERITABILITY (65%)
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What are some of the systems implicated in MDD?
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MONOAMINES (traditional target)
(more recently): the stress-related neuropeptides amino acid neurotransmitters neurotrophic factors |
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What is definition of dementia?
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*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 |
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Diagnostic criteria for dementia/
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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 |
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Who is more likely to be effected by dementia: men or women?
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women
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What is duration of dementia?
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varies from 6 months to 15 years
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Risk factors for dementia
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age (#1)
Gender (female) Vascular (hypertension, CV disease, obesity, diabetes, hyperlipidemia, cerebrovascular disease, CHF, A fib) Environmental factors (alcohol, diet?) Genetics |
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Factors associated w/ cognitive resilience?
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Education
Gender (men more resilient) Social networks Cognitive stimulating activities Conscientiousness exercise |
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Explain cortical vs subcortical dementia differences?
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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 |
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What are major etiologies of dementia?
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Primary neurodegenerative disorders
Infections Vascular and traumatic Toxic-Metabolic and nutritional Psychiatric Additional causes Mixed (Alzheimer’s + Vascular) |
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What is most common cause of dementia?
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1) alzheimers
2) Lewy bodies 3) vasculature |
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Alzheimer's specific features?
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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 |
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Neuropathology of AD?
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Amyloid plaques, neurofibrillary tangles
Neuronal loss (entorhinal cortex, hippocampus, select populations of neocortical pyramidal cells, cholinergic neurons in the nucleus basalis) |
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APOE Gene and alzheimers?
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APOE E4: Increased risk of AD
APOE E2: May provide protection from AD |
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Dementia with Lewy Bodies core features?
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(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 |
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Vascular dementia presentation?
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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. |
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Frontal lobe dementias?
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THINK ABOUT IF SOMEONE W/ 55 PRESENTS W/ DEMENTIA!!!
VERY DISINHIBITED, INAPPROPRIATE, FRONTAL LOBE DISEASE |
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Frontal lobe dementia findings?
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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 |
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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 |
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Creutzfeldt-Jakob dementia presentation?
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Peak incidence: 60-64 years
Rapidly progressive dementia Myoclonus, extrapyramidal signs, cerebellar signs, gait abnormalities Uniformly fatal- typically 6-9 months from onset |
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What is difference between ADL & IADL?
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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 |
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What are aspects of management of dementia?
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non pharmacological (education, care giver support, etc)
pharm: Anticonvulsants, SSRIs for behavioral disturbance, cholinesterase inhibitors, NMDA antagonists |
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Describe Delirium (also how differs from dementia)?
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*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) |
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What enzyme is the target of most FDA-approved Alzheimer’s drugs.
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Acetylcholinesterase!
Ergo drugs |
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What two genes are linked to cause Alzheimer's?
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APP1 (amyloid precursor protein) on chromosome 21
and Presenilin 1 often cause errors in γ-Secretase |
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What gene is linked to increase risk of alzheimers?
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Apolipoprotein E
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What is the difference between amyloid fibrils and oligomers?
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Oligomers – small aggregate of subunits aggregated (Floating soluble amyloid toxins) - little toxic dots
Amyloid fibrils are extracellular; beta-sheets that are protease resistent |
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What is the importance of amyloid fibrils?
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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 |
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What is importance of oligomers?
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These are Floating soluble amyloid toxins ... little dots that are thought to be actual source of toxicity
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Can AB lowering therapies improve cognitive function?
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No. they can only improve amyloid burden, but not cognitive function
Theory: this is b/c oligomers aren't impacted! |
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Why is passive immunotherapy (IVIg) being used for alzheimers??
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naturally occurring antibodies against oligomers!
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What is the prevalence of schizophrenia?
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*Leading cause of disability in the world
* 1.1% of Americans (2.4 million) have experienced or will experience a schizophrenic episode |
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What is the course of schizophrenia?
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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 |
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What genetic factors contribute to schizophrenia and what is the heritability?
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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 |
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Explain the neurodevelopmental hypothesis in relation to schizophrenia
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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) |
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Explain structural brain abnormalities in relation to schizophrenia
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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. |
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explain neurotransmitter abnormalities in relation to schizophrenia
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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 |
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Explain disconnectivity syndrome in relation to schizophrenia
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Oligodendrocytes were sick and producing STRANGE MYLIN SHEATHES!!!
NOT NEUROTRANSMITTER DISEASE!!! Oligodendrocytes produce mylin, if oligodendrocyte abnormalities there are conduction abnormalities |
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Positive symptoms of schizophrenia
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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) |
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Negative symptoms of schizophrenia
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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) |
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Cognitive symptoms of schizophrenia
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Attention
encoding (2o memory) constructional apraxia verbal fluency |
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Diagnostic Criteria for OCD
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*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 |
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Difference btw OCD and other anxiety disorders
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Different from psychosis KNOW ITS FROM THEIR OWN HEAD!!! Have insight!
Pyschosis --> think someone is implanting thoughts in their brain |
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Treatment options for OCD
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1)SSRI
2) Cognition behavioral therapy |
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Etiologic hypotheses for OCD
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1) Neurotransmitter based (serotonin & glutamate)
2) Circuit based: cortico-basal ganglia - thalamo-corticol loop 3) infection triggered autoimmune process |
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What neurotransmitter is implicated in OCD?
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1) Serotonin (based on clinical usefulness of SSRI)
2)Glutamate (the glutamate transmitter gene is implicated and there is evidence of increased CSF glutamate) |
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What is the only gene that has been implicated in OCD
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glutamate transporter gene SLC1A1
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How does OCD relate to huntingtons or the orbitofrontal-subcortical pathway?
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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. |
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What is rational of DBS?
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Put a lesion in the Ventral Capsule/Ventral Striatum --> 3/4 improve!
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What is dementia?
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Clinical syndrome marked by progressive cognitive impairment in clear consciousness.
Involves multiple cognitive domains Significant impairment in social or occupational functioning |
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What are major diagnostic features of dementia?
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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 |
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What is difference btw subcortical and cortical dementia syndromes?
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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 |
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If patient is falling down w/ dementia and having hallucinations, and REM sleep disturbances what disease is most likely?
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Dementia with Lewy Bodies
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If a 55 year old presents with dementia what is most likely?
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Frontotemporal dementia...
Pick's disease! |
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If a patient with dementia has urinary incontinence and an abnormal gait, what is most likely?
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Normal Pressure Hydrocephalus
Treatable!!!! |
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What fits on axis I of the DSM-IV
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Clinical disorders, including major mental disorders, and learning disorders, Substance Use Disorders
considered more “biological" |
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What fits on axis II of the DSM-IV
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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)
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What fits on axis III of the DSM-IV
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Acute medical conditions and physical disorders
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What fits on axis IV of the DSM-IV
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Psychosocial and environmental factors contributing to the disorder
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What fits on axis V of the DSM-IV
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Global Assessment of Functioning or Children’s Global Assessment of Functioning for children and teens under the age of 18
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Describe Personality Disorder Cluster A
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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. |
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Describe Personality Disorder Cluster B
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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. |
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Describe Personality Disorder Cluster C
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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. |
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Describe schizotypal characteristics?
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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 |
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What sort of type of personality has problems w/ memory or getting to the office from the elevator?
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Schizotypal
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What group has higher hertiability? Axis I or II disorders?
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Both have similar level of heritability
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What is neurobiolgoy behind schizotypal personality disorder?`
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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 |
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Borderline PD Characteristics
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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 |
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Borderline mnuemonic
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IMPULSIVE
Impulsive Moodiness Paranoia or dissociation under stress Unstable self-image Labile intense relationships Suicidal gestures Inappropriate anger Vulnerability to abandonment Emptiness (feelings of) |
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What disorder has high rates of childhood trauma or abuse?
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Border line personality disorder
(but its a low predictor) |
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Neurobiology of Borderline?
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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 |
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Neurobiology of Borderline with neurotransmitters?
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Abnormalities in serotonergic function associated with aggression and suicidal behavior
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Treatment of Borderline personality disorder?
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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 |
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Describe avoidant?
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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. |
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What's an early sign of avoidance?
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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
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What is the brain imaging in Avoidant?
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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 |
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What is tx for avoidant?
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Target of most psychotherapy but controlled studied
Short term social skills training diminish symptoms Antidepressant medications help with social anxiety |
