Test 5: Personality, Schizophrenia, and Neurocognitive Disorders Flashcards

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1
Q

What are the three personality disorder clusters? And the disorders?

A

A) Odd or eccentric: Paranoid, schizoid, schizotypal
B) Dramatic or erratic (emotional): antisocial, borderline, histrionic, narcissistic
C) Anxious or fearful: avoidant, dependent, obsessive-compulsive

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2
Q

What are the statistics of personality disorders?

A
  • Prevalence: ~1% general population
  • Origins: thought to begin in childhood
  • Course: Chronic if untreated, may transition into a different personality disorder
  • Comorbidity: its the rule not the exception
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3
Q

What are the statistics concerning gender for personality disorders?

A

More common traits:
- Men: aggression and detachment
- Women: submission and insecurity
More common disorders:
- Men: antisocial
- Women: histrionic

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4
Q

What are the personality disorders under study?

A
  • Sadistic: enjoy inflicting pain
  • Passive-aggressive: defiant, undermine authority
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5
Q

What are the clinical features of paranoid personality disorder?

A
  • Pervasive and unjustified mistrust and suspicion
  • Few meaningful relationships, sensitive to criticism
  • Poor quality of life
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6
Q

What are the causes of paranoid personality disorder?

A
  • Not well understood, may involve early learning that people and the world are dangerous or deceptive
  • More often found in people with experiences: prisoners, refugees, people with hearing impairments, older adults
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7
Q

What are the treatment options for paranoid personality disorder?

A
  • Few seek professional help on their own
  • Focus: development of trust
  • Cognitive therapy to counter negativistic thinking
  • Lack of good outcome studies
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8
Q

What are the clinical features of schizoid personality disorder?

A

Pervasive pattern of detachment from social relationships
- Very limited range of emotions in interpersonal situations
- Resembles autism

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9
Q

What are the causes of schizoid personality disorder?

A
  • Etiology unclear (scarce research)
  • Childhood shyness or abuse/neglect
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10
Q

What are the treatment options for schizoid personality disorder?

A
  • Few seek professional help on their own
  • Focus: value of interpersonal relationships
  • Building empathy and social skills
  • Lack of good outcome studies
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11
Q

What are the clinical features of schizotypal personality disorder?

A
  • Behaviors and dress is odd and unusual
  • socially isolated and highly suspicious
  • Magical thinking (superstitious), ideas of reference, and illusions
  • Many meet criteria for major depression
  • Some conceptualize this as resembling a milder form of schizophrenia
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12
Q

What are the treatment options for schizotypal personality disorder?

A
  • Address comorbid depression (on 30-50% pts)
  • Main focus on developing social skills
  • Medical treatment is similar to that used for schizophrenia
  • treatment prognosis generally poor
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13
Q

What are the clinical features of antisocial personality disorder?

A
  • failure to comply with social norms
  • violation of the rights of others
  • irresponsible, impulsive, and deceitful
  • lack of conscience, empathy, and remorse
  • “sociopathy,” “psychopathy” typically refer to this disorder or very similar traits
  • charming, interpersonally manipulative
  • substance abuse common, 60% diagnosed abuse various substances
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14
Q

What are potential causes of antisocial personality disorder?

A
  • early histories of behavioral problems including conduct disorder
  • “callous-unemotional” type of conduct disorder more likely to evolve into antisocial PD
  • families with inconsistent parental discipline and support
  • families often have histories of criminal and violent behavior
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15
Q

What are neurobiological contributions to antisocial personality?

A
  • Underarousal hypothesis: cortical arousal in too low - so seek stimulation from activities too fearful or aversive for most
  • Cortical immaturity hypothesis: cerebral cortex is not fully developed
  • Fearlessness hypothesis: fail to respond to danger cues
    – Psychopaths less likely to give up when goal becomes unattainable
  • Gray’s model: inhibition signals are outweighed by rewards signals
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16
Q

What might contribute to the development of antisocial personality?

A
  • Genetic influences: history of antisocial behavior or criminality in parents
  • Developmental influences: high-conflict childhood (in at risk children)
  • Impaired fear conditioning: children not learn to fear aversive consequences of negative actions
  • Biological-environmental: early antisocial behavior alienates peers who would be role models, antisocial behavior and family stress mutually increase one another
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17
Q

What are potential treatment options for antisocial personality disorder?

A
  • few seek treatment on their own
  • antisocial behavior is predictive of poor prognosis
  • emphasis is placed on prevention and rehabilitation
  • often incarceration is the only viable alternative
  • may need to focus on practical (selfish) consequences
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18
Q

What are the clinical features of borderline personality disorder?

A
  • unstable moods, behaviors, and relationships
  • impulsivity, depression, fear of abandonment, very poor self-image
  • self-mutilation and suicidal gestures
  • comorbidity rates are high with other mental disorders, particularly mood disorders
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19
Q

What are the rates of comorbid disorders with borderline personality disorder?

A
  • 1 in 5: depressed (suicide attempts - 6%)
  • 2 in 5: bipolar criteria
  • 2 in 3: substance abuse
  • eating disorders: 25% bulimia pts have borderline PD
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20
Q

What are the causes of borderline personality disorder?

A
  • strong genetic component: also linked to depression genetically
  • high emotional reactivity may be inherited
  • may have impaired functioning of limbic system
  • early trauma/abuse increase risk
  • high shame, low self-esteem
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21
Q

What is the triple vulnerability for borderline personality disorder?

A
  • generalized biological vulnerability: reactivity
  • generalized psychological vulnerability: lash out when threatened
  • specific psychological vulnerability: stressors that elicit borderline behavior
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22
Q

What are the treatment options for borderline personality disorder?

A
  • few good outcome studies
  • antidepressant medications: short-term relief
  • dialectical behavior therapy: most promising focusing on
    – dual reality of accepting difficulties and need for change
    – interpersonal effectiveness
  • distress tolerance to decrease reckless/self-harming behavior
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23
Q

What are the causes of histrionic personality disorder?

A
  • etiology unknown due to lack of research
  • often co-occurs with antisocial PD feminine variant of antisocial trait?
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23
Q

What are the clinical features of histrionic personality disorder?

A
  • overly dramatic and sensational
  • sexually provocative (may be)
  • impulsive and needs to be center of attention: manipulative (often)
  • thinking and emotions perceived as shallow
  • more commonly diagnosed in females
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24
Q

What are the treatment options for histrionic personality disorder?

A
  • Focus on attention seeking and long-term negative consequences
  • Targets may also include problematic interpersonal behavirors
  • Little evidence that treatment is effective
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25
Q

What are the clinical features of narcissistic personality disorder?

A
  • Exaggerated and unreasonable sense of self-importance
  • Preoccupation with receiving attention
  • Lack sensitivity and compassion for others
  • High sensitivity to criticism; envious and arrogant
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26
Q

What are the causes of narcissistic personality disorder?

A
  • Causes largely unknown
  • Failure learn empathy as child
  • sociological view: product of “me” generation
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27
Q

What are the treatment options for narcissistic personality disorder?

A
  • Focus on grandiosity, lack of empathy, unrealistic thinking
  • Emphasize realistic goals and coping skills for dealing with criticism
  • Little evidence efficacy
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28
Q

What are the clinical features of avoidant personality disorder?

A
  • Extreme sensitivity to others opinions
  • Highly avoidant most interpersonal relationships
  • Interpersonally anxious and fearful of rejection
  • Low self esteem
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29
Q

What are the causes of avoidant personality disorder?

A
  • May be linked to schizophrenia; occurs more often in relatives of people with schizophrenia
  • experiences of early rejection
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30
Q

What are the treatments of avoidant personality disorder?

A
  • similar to social phobia
  • focus: social skills, entering anxiety-provoking situations, increase social contact
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31
Q

What are the clinical features of dependent personality disorder?

A
  • Reliance on others for major and minor life decisions
  • Unreasonable fear of abandonment
  • Avoidance of disagreement
  • Unable make decision
  • Clingy and submissive
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32
Q

Causes of dependent personality disorder?

A
  • Not well understood/poor research
  • Linked to early disruptions in learning dependence
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33
Q

What are the treatment options for dependent personality disorder?

A
  • Efficacy treatment is lacking
  • Therapy typically progresses gradually due to lack of independence
  • Target skills fostering confidence and independence
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34
Q

What are the clinical features of obsessive-compulsive personality disorder?

A
  • Excessive and rigid fixation on doing things the right way
  • Highly perfectionistic, orderly emotionally shallow
  • Unwilling to delegate
  • Difficulty with spontaneity
  • Often interpersonal problems
  • Obsessions and compulsions are rare
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35
Q

What are the causes of obsessive-compulsive personality disorder?

A

Not well known, weak genetic contribution

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36
Q

What are the treatments of obsessive-compulsive personality disorder?

A
  • Little data
  • Address fears related to the need for orderliness
  • Target rumination, procrastination, and feelings of inadequacy
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37
Q

What is psychosis and how does it relate to schizophrenia?

A
  • Psychosis: gross departure from reality
  • Schizophrenia: a pervasive type of psychosis characterized by disturbed thought, emotion, and behavior
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38
Q

What are the types of schizophrenia symptoms?

A
  • Positive: “additional”
    – active manifestations of abnormal behavior
    – distortions or exagerations of normal behavior
  • Negative: “absence” of normal behavior
  • Disorganized: erratic speech, emotions, and behavior
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39
Q

What are the symptoms in the “positive” symptoms cluster?

A

1) Delusions: “basic feature of madness”
- gross misrepresentations of reality
- most common: of grandeur or persecution
2) Hallucinations:
- experiencing sensory events without environmental input
- Can involve all senses but most common is auditory
- SPECT: neuroimaging shows that in auditory hallucinations the Broca’s area–involved in speech production (broken speech) is active

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40
Q

What are the symptoms in the “negative” symptoms cluster?

A

Absence or insufficiency of normal behavior
- Avolition (apathy): lack of initiation & persistence
- Alogia: relative absence of speech
- Anhedonia: lack of pleasure, indifference
- Affective flattening: little expressed emotion

41
Q

What is more concerning avolition?

A

This person may experience
- no eye contact in conversation
- limited/halted speech
- stops participating in events or gatherings & no enthusiasm in special occasions/events
- avoids making or receiving phone calls
- trouble starting/completing projects
- fails to make appointments (Dr, tax preparer)

42
Q

What are the symptoms in the “Disorganized” symptom cluster?

A

Confused or abnormal
1) Speech
- cognitive slippage: illogical & incoherent speech
- tangentiality: “going off on a tangent”
- loose associations: conversation in unrelated directions
2) Affect:
- inappropriate emotional behavior
3) Behavior:
- variety of unusual behaviors
- Catatonia

43
Q

What is catatonia?

A
  • immobility or agitated excitement
  • considered its own disorder or as a symptom when comorbid
  • stuporous (retarded) catatonia:
    – Stupor: immobility during which people may hold rigid poses
    – Mutism: inability to speak as well
    – Waxy flexibility: maintain positions after being placed in them by someone else
    – Mimicking: maybe partial and they may repeat meaningless phrases or speak only to repeat what someone else says
    – Stereotypy: stereotyped, repetitive movements
  • Excited catatonia: bizarre, non-goal directed hyperactivity and impulsiveness
  • severe and quite rare
44
Q

What were the subtypes of schizophrenia?

A
  • Previously divided based on content of psychosis
  • No longer used
  • Included: paranoid, catatonic, residual (minor symptoms persist after past episode), disorganized (many disorganized symptoms) and undifferentiated
45
Q

What is schizophreniform disorder?

A
  • Psychotic symptoms 1-6 months (>6 mo schizophrenia)
  • Associated with relatively good functioning
  • Most resume normal life
  • Lifetime prevalence: ~0.2%
46
Q

What is schizoaffective disorder?

A
  • Symptoms of schizophrenia and major mood episode
  • Psychotic symptoms occur outside mood disturbance as well
  • Prognosis similar to schizophrenia
  • No not tend to get better on own
47
Q

What is delusional disorder?

A

Key feature: delusions contrary to reality
- lack positive and negative symptoms
- Types:
1) Erotomanic: someone higher is in love or attracted to you
2) Grandiose: they are someone other than who they are (supernatural/celebrity)
3) Jealous: sexual partner is unfaithful
4) Persecutory: they or someone close to them are being mistreated / spied on
5) Somatic: believing bones are glass
- Better prognosis than schizophrenia
- Very rare: 26-60/100,000
- Later onset: 35-55
- Somewhat more common in females (55%)

48
Q

What is the psychotic disorders due to other causes?

A
  • Psychosis resulting from substance use, medications, or medical conditions
  • Knowing the cause is important for treatment of the underlying cause
  • Includes:
    1) substance/medication-induced psychotic disorder
    2) psychotic disorder associated with another medical condition
49
Q

What is the brief psychotic disorder?

A
  • positive or disorganized symptoms
  • lasting less than 1 month
  • briefest duration of all psychotic disorders
  • typically precipitated by trauma or stress
50
Q

What is the attenuated psychosis syndrome?

A
  • attenuate = debilitate
  • a condition in need of further study
  • individuals at high risk for developing schizophrenia or beginning to show signs of schizophrenia
  • intention: focus attention on those benefit early intervention
  • tend have good insight into own symptoms
51
Q

What are the prevalence, onset, and life expectancy statistics of schizophrenia?

A
  • Prevalence: 0.2- 1.5% worldwide population
  • Onset: often early adulthood (but can develop at any time)
    – childhood cases extremely rare but not unheard of
    – chronic (generally): moderate-to-severe lifetime impairment
  • Life expectancy: slightly less than average: increased risk suicide and accidents, self care may be poorer
52
Q

What are the gender and cultural facture statistics of schizophrenia?

A
  • Affects men and women equally
    – Females: better longer long-term prognosis
    – Males; slightly earlier onset
  • Cultural factors: psychotic behaviors not always pathologized, found in similar rates in all cultures
53
Q

What is the course of schizophrenia?

A

Prodromal phase (initial symptoms)
- 85% experience
- 1-2yrs before serious symptoms
- less severe, yet unusual symptoms:
– ideas of reference, magical thinking, illusions, isolation, marked impairment in functioning, lack of initiative/interests/energy

54
Q

What does the research indicate about the causes of schizophrenia?

A
  • Can be inherited: greater risk the closer the family member with schizophrenia
  • Healthy environment is a protective factor
55
Q

What is the dopamine hypothesis of the neurobiological influences of what causes schizophrenia?

A

Partially caused by overactive dopamine
- Evidence: dopamine agonists (inc) result in schizophrenic-like behavior, antagonists (dec) reduces behavior (neuroleptics, L-Dopa)
- Problem: many neurotransmitters are likely involved

56
Q

What are the neurobiological influences other than the dopamine hypothesis of what causes schizophrenia?

A

1) Structural and functional abnormalities in the brain:
- Enlarged ventricles, reduced tissue volume
- Hypofrontality: less active frontal lobes (major dopamine pathway)
2) Viral infections: influenza epidemics during prenatal development (inconclusive)
3) Marijuana: increase risk in at-risk
*Conclusions: reflects diffuse neurobiological dysregulation, but structural and functional brain abnormalities are not unique to schizophrenia

57
Q

What are the psychological and social influences on schizophrenia?

A
  • Stress: (may) activate underlying vulnerability, increase risk of relapse
  • Family interactions: High expressed emotion (EE)–criticism, hostility, and emotional over-involvement/intrusiveness–associated with relapse
58
Q

What is the medical treatment of schizophrenia?

A
  • Historical: generally ineffective & barbaric: insulin coma induction, psychosurgery, ECT
  • Antipsychotic (neuroleptic) medications: 1950s,
    – first line treatment
    – most reduce/eliminate positive symptoms,
    – primarily affect dopamine system but also serotonergic & glutamate
  • Experimental: Transcranial Magnetic Stimulation (block auditory hallucinations)
59
Q

What are the common side effects of antipsychotic medications?

A

DRYNESS
- blurred vision
- dry mouth
- constipation
- drowsiness
- muscle spasms/tremors
- weight gain

60
Q

What are the development and aspects of antipsychotic medications?

A

1) first generation medications: acute & permanent side effects are common
- Parkinson’s-like side effects
- Tardive dyskinesia: involuntary movements (face, mouth, hands, etc)
- Problematic compliance (aversion to side effects, finances, dr relationship)
- Injectable antipsychotics may improve compliance
2) Second generation/ atypical psychotics
- may help pts unresponsive to other meds

61
Q

What was the historical precursors and current psychosocial treatment of schizophrenia?

A
  • Historical: psychodynamic therapy - NOT effective
  • Psychosocial approaches
    – Behavioral on inpatient units: reward adaptive behavior (self-care & socialization)
    – community care programs
    – social and living skills training
    – behavioral family therapy
    – vocational rehabilitation
62
Q

What is the illness management and recovery psychosocial treatment of schizophrenia?

A
  • Engages pt as active participant in care
  • Continuous goal setting and tracking
  • Modules: social skills training, stress management, substance use
  • Individual social skills training and family interventions reduce schizophrenic relapses (high EE)
63
Q

What are the cultural considerations for psychosocial treatment of schizophrenia?

A
  • Consider cultural factors that influence individuals’ understanding of own illness (supernatural beliefs)
  • Involve family and community as possible
64
Q

What is the prevention psychosocial treatment of schizophrenia?

A
  • identify at risk children (relatives)
  • foster supportive, stable environments
  • offer additional treatments at prodromal stages, including social skills training
65
Q

What are neurocognitive disorders and what are the three types?

A
  • Affected learning, memory, and consciousness
  • Most develop later in life
    Types:
    1) Delirium: temporary confusion and disorientation
    2) Mild neurocognitive disorder: early stages of cognitive decline
    3) Major neurocognitive disorder: broad cognitive deterioration affecting multiple domains
66
Q

How has the DSM perspective changed concerning neurocognitive disorders?

A
  • From “organic” mental disorders to “cognitive” disorders
  • Broad impairments in cognitive functioning
  • Cause profound changes in behavior and personality (what makes these general medical conditions often best treated by mental health professionals)
67
Q

What is the nature of delirium?

A
  • Central features: impaired conscientiousness and cognition
  • Onset: Develops rapidly (hrs, days)
  • Appear confused, disoriented and inattentive
  • Marked memory and language deficits
68
Q

What are the facts and statistics of delirium?

A
  • Up to 20% adults in acute care facilities
  • Greater prevalence: older adults, undergoing medical procedures, AIDS & Cancer patients
  • Full recovery often within several weeks
69
Q

What are the medical conditions or causes of delirium?

A
  • Dementia (50% involve temporary delirium)
  • Head injury/brain trauma
  • Infections (UTI)
  • Drug intolerance/withdrawal
  • Poisons
  • Immobility
  • Excessive stress
  • Sleep deprivation
70
Q

What are treatment and prevention options for delirium?

A
  • Treatment:
    – attention to precipitating medical problems
    – psychosocial interventions: reassurance/comfort, coping strategies, inclusion of pts in treatment decisions
  • Prevention:
    – address proper medical care for illness, and proper use and adherence to therapeutic drugs
71
Q

What is the nature of major and mild neurocognitive disorders?

A
  • Gradual deterioration of brain functioning: judgement, memory, language, advanced cognitive processes
  • Has many causes and may be irreversible
72
Q

What is the difference between major and mild neurocognitive disorders?

A
  • Major: new DSM-5 term for dementia
    – 1+ cognitive deficits that represent a decrease from previous functioning
    – substantiated by clinical assessment
    – interfere with daily independent activities
  • Mild: New DSM-5 classification for early stages of cognitive decline: able to function independently with some accommodations
73
Q

What is the prevalence and statistics of major neurocognitive disorders?

A
  • New case every 7 seconds
  • 65+: 5%, 85+: 20%
  • Mild: 70+, 10%
74
Q

What are the initial stages of major neurocognitive disorder?

A
  • memory and visuospatial skills impairments
  • Facial agnosia: inability to recognize familiar faces (aka prosopagnosia/facial blindness)
  • Other symptoms: delusions, apathy, depression, agitation, aggression
75
Q

What are the later stages of major neurocognitive disorder?

A
  • Cognitive function continues to deteriorate
  • Total support needed for daily activities
  • Increased risk of early death because of inactivity and other illnesses
76
Q

What are the causes of neurocognitive disorders?

A
  • Frontotemporal
  • Vascular
  • With Lewy bodies
  • Substance/medication induced
  • Unspecified
    Due to:
  • TBI
  • HIV infection
  • Another medical condition
  • Multiple etiologies
  • Alzheimer’s Disease
  • Prion disease
  • Parkinson’s Disease
  • Huntington’s disease
77
Q

What are the clinical features of neurocognitive disorder due to Alzheimer’s disease?

A
  • Nearly half of neurocognitive disorders
  • Gradual and steady development (typically)
  • Memory, orientation, judgment, and reasoning deficits
  • Additional symptoms: agitation, confusion, combativeness, depression, anxiety
  • Definitive diagnosis only by autopsy
78
Q

What is the nature and progression of Alzheimer’s? (Survival, onset)

A
  • Early and later stages: slow
  • During middle stages: rapid
    (“Nun study” - analysis of nun’ journal writing over many years shows pattens of deterioration)
  • Post-diagnosis survival: 8 yrs
  • Onset: 60s/70s (“early onset” = 40s & 50s)
79
Q

What is the prevalence of Alzheimer’s disease?

A
  • 5 million Americans, several million worldwide
  • more common in less educated individuals
    – more educated declines more rapidly after onset
    – suggests education provides a buffer period of better initial coping
  • slightly more common in women:
    – possibly estrogen is protective
80
Q

What are the extent of deficits in Alzheimer’s Disorder?

A
  • Aphasia: difficulty with language
  • Apraxia: impaired motor functioning
  • Agnosia: failure to recognize objects
  • Difficulties with: planning, organizing, sequencing, abstracting information
  • Negative impact on social and occupational functioning
81
Q

What are the aspects of the vascular neurocognitive disorder?

A
  • Cause: blockage/damage to blood vessels
  • 2nd leading cause of neurocognitive disorder
  • Onset: sudden (ie stroke)
  • Variable patterns of impairment
  • Most require formal care in later stages
  • Cognitive disturbances
  • Obvious neurological signs brain tissue damage
  • Prevalence: 70-75, 1.5% 80+, 15%
  • Risk slightly higher in men
82
Q

What are the aspects of frontotemporal neurocognitive disorder?

A
  • Damage to frontal or temporal regions of the brain: personality, language, behavior
  • 2 Types of Impairment:
    1) decline in appropriate behavior
    2) declines in language

ie: Pick’s disease: pick bodies/cells inside nerve cells in the damaged areas of the brain

83
Q

What are the aspects of neurocognitive disorder due to Pick’s disease?

A
  • Rare: 5% all dementia diagnoses
  • Cortical dementia like Alzheimer’s
  • Early onset: 40s-50s
  • Little known about cause
84
Q

What are the aspects of neurocognitive disorder due to traumatic brain injury?

A
  • Leading cause: accidents
  • Symptoms at least 1 week after injury including executive functioning, learning, memory- most common
  • ie athletes experiencing repeated head blows
85
Q

What are the aspects of neurocognitive disorder due to Lewy Body Disease?

A
  • Lewy body: microscopic protein deposits that damage brain over time
  • Onset: gradual
    – impaired attention/alertness, visual hallucinations, motor impairment
86
Q

What are the aspects of neurocognitive disorder due to Parkinson’s Disease?

A
  • Degenerative brain disorder
  • Dopamine pathway damage
  • 1/1,000 worldwide
  • Chief difficulty: motor problems - tremors, posture, walking, speech
  • Not all with PD develop dementia
  • 75% survive 10+ yrs after diagnosis -
87
Q

What are the aspects of neurocognitive disorder due to HIV infection?

A

HIV-1 can cause neurological impairments and dementia in some individuals
- cognitive slowness, impaired attention, & forgetfulness
- apathy & social withdrawal
- typically occurs in later disease stages
- now occurs in <10% of individuals with HIV; because HAART (highly active, antiretroviral therapies) decrease risk

88
Q

What are the aspects of neurocognitive disorder due to Prion disease?

A
  • Misfolded protein sin the brain that reproduce and cause damage
  • No known treatment, always fatal
  • Can only be acquired though cannibalism or accidental transmission (blood transfusion)
  • ie: Creutzfeldt-Jakob disease
    – 1/1M
  • eating nerve tissue of mad cow diseased cows
  • MCD: slowly destroys brain and spinal cord of in cattle (Bovine Spongiform Encephalopathy)
89
Q

What are the aspects of substance/medication-induced neurocognitive disorder?

A
  • Prolonged drug use, especially in combination with poor diet
  • May be caused by alcohol, sedative, hypnotic, anxiolytic, or inhalant drugs
  • Brain damage may be permanent
  • Symptoms similar to Alzheimer’s
    – memory impairment, aphasia, apraxia, agnosia, disturbed executive functioning
90
Q

What are the brain features of Alzheimer’s disease?

A
  • Neurofibrillary tangles (strandlike filaments)
  • Amyloid plaques (gummy protein deposits between neurons)
  • Atrophy
91
Q

What are the biological processes and genetic Factors of Alzheimer’s Disease?

A
  • Many preliminary findings that need further research
  • Genes: Chromosome 21,19 (late onset), 14 (early onset), and 12
  • Deterministic genes: rare & inevitable (Beta-amyloid precursor gene, Presenilin-1 and -2 genes)
  • Susceptibility genes: more likely but not certain to develop Alzheimer’s
92
Q

What is an example of a susceptibility gene for Alzheimer’s disease?

A

ApoE4 gene
- chromosome 19
- late onset
- More prevalent in those with family history of Alzheimer’s
- More likely to produce cognitive decline in the context of a stressful environment

93
Q

What are the contributing psychosocial factors in Neurocognitive Disorders?

A
  • Psychological and psychosocial factors do not cause dementia directly but they may influence onset and course
  • Lifestyle factors: drug use, diet, exercise, stress
  • Environmental stressors: repeated head trauma
  • Cultural factors: ethnicity and lower SES
  • Educational attainment, coping skills social support
94
Q

What are the general facts about medical treatments for neurocognitive disorders?

A
  • Few primary treatments exist
  • Most attempt to slow progression of deterioration, but cannot stop it
  • Most not effective because we have no way to replace extensive brain damage
95
Q

What are specific medical treatments for neurocognitive disorders?

A
  • Future: glial cell-derived neurotropic factors, stem cells: may slow deterioration, vaccines
  • Some drugs target cognitive deficits:
    – Cholinesterase-inhibitors: Aricept, Exelon, Reminyl
    – long-term effects not well demonstrated
  • Exploratory: Ginkgo biloba to improve memory (findings mixed)
  • Associated symptoms: SSRIs (depression/anxiety), antipsychotics (agitation)
  • All: only modestly effective, short periods
96
Q

What are the effects of medical treatments of neurocognitive disorders?

A
  • Any gains in a person’s abilities are only temporary
  • Any improvement is to 6 months prior
  • Many patients discontinue medications because of expense or severe side effects
97
Q

What are the psychosocial treatments of neurocognitive disorders?

A

Aim:
- enhance lives of patients and families
- teach compensatory skills
- memory enhancement devices (memory wallets with statements about ones life)
*Cognitive stimulation can delay onset of more severe symptoms

98
Q

What are the psychosocial treatments for caregivers of neurocognitive disorders?

A
  • Instructions on how to handle problematic behavior: wandering, socially inappropriate behaviors, aggressive or rebellious behaviors
  • Treatment of mental health due to stress
99
Q

What are prevention measures for neurocognitive disorders?

A
  • Reduce risk in older adults:
    – use anti-inflammatory medications
    – control blood pressure
    – don’t smoke, active social life
  • Other targets:
    – increasing safety behaviors to reduce head trauma
    – reduce exposure to neurotoxins and use of drugs