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Serper Final > Schizophrenia: Class Notes > Flashcards

Schizophrenia: Class Notes Flashcards

1
Q

Schizophrenia, History: Kraeplin

A

SZ consists of a large range of symptoms
o Conceptualized as one disorder, but it is most likely multiple disorders

Emil Kraepelin, 1904
• A student of Wundt’s experimental lab
• Later became the chief psychiatrist in Estonia
• Father of modern European psychiatry

Created an illness classification system
• Which was the first since Hippocrates
• Both believed illness was due to bodily imbalance

First used the term “dementia praecox” to label SZ
• Translated meant an early onset of deteriorating mental functioning
• Used term to distinguish SZ from bipolar – which was previously grouped

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2
Q

Schizophrenia, History: Bleuler

A

Eugen Bleuler, 1911

Noticed dementia praecox occurred at different ages, and some people recovered

Guided by a desire to be like Freud and his tendency to use metaphors

Believed the underlying problem stemmed from “loose associations”
o Which led to a “split mind”
• Hence the name “schizophrenia”

Failed to properly operationalize “loose associations”
o Led to an abstract construct of the disorder in the US

The US followed Bleuler’s definition, while Europe continued to rely on Kraepelin’s more specific definition

**U.S. thus experienced a surge in hospitalizations due to SZ over-diagnosis, and increase in lobotomies

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3
Q

Schizophrenia as “Salience Disorder”

A

Current trend is a push to relabel schizophrenia as “salience disorder”

Salient = ability to focus on appropriate stimuli

Hallucination may reflect the inability to recognize the subjective value of experiences from an internal representation/source

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4
Q

Schizophrenia: Onset and Prevalence

A

In DSM-III, age 34 was the cut off for being able to obtain a diagnosis of SZ

Current DSM does not have a cut off age (but geriatric onset is very rare)

SZ typically develops around puberty

Lifetime prevalence ~ 1%

Some evidence of gender differences
o Men typically demonstrate more severe cases
o It has been argued estrogen serves as a protective factor

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5
Q

Risk factors: Age of Father

A

Possibly due to degeneration of sperm

Similar link with autism

Potentially encourages social deficits

No specific cutoff age, but 40+ is considered at risk
(Similar to mothers 40+ and link to Down Syndrome)

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6
Q

Risk Factors: Immigration status; Marriage

A

Affects more immigrants, but cause vs effect?
o Could be more people with SZ flee their native countries due to persecution

Marriage
• Common for men with antisocial personality disorder to marry women with SZ

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7
Q

Risk Factors: Prenatal

A

Prenatal infection
o Increase in SZ following a flu epidemic

Exposure to a feline virus increases one’s chance

Rhesus (Rh) incompatibility

Blood types of the mother and child are different

Winter month births
o This trend reflects still-born trends

Some propose the same complication that would kill the fetus may lead to an increased chance of SZ

Poor prenatal care
o Malnutrition and maternal stress

Pregnancy and/or birth complications

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8
Q

Neurodevelopmental factors

A

Dormant, prenatal, brain lesions only arise during puberty

Disorganized neuroarchitecture

Neurons of the brain are strung together in irregular patterns

Complicated, impractical, tangle

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9
Q

Other Biological Factors

A

*Note: not all those diagnosed with SZ display these abnormalities

**Abnormalities are not required to diagnosis SZ

Decreased brain volume

Decreased volume of the thalamus
o Thalamus and irregular temporal lobe are linked with hallucinations

Increased ventricles – which is correlated with negative symptoms

Irregularities in the frontal lobe

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10
Q

The dopamine hypothesis:

A

Dopamine mediates the salience of environmental events and internal representations

Increased DA D2 receptors activity

Complicated link though: blocking D2 may increase D1

Drugs that block dopamine help control symptoms in those with SZ
o But current meds only target D2 receptors and only treat the positive symptoms

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11
Q

Dopamine Hypothesis: Pathways

A

4 major dopamine pathway, but 2 key in SZ

  • Mesolimbic
  • Mesocortical

Nigrostriatal
Tuberoinfundibular

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12
Q

Flaws to Dopamine Hypothesis

A

There is no genetic link to dopamine production

There is no consistent therapeutic effect of regulating dopamine

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13
Q

Glutamate Hypothesis

A

Nearly half of all neurons in the brain and nearly all of them in the cerebral cortex use glutamate

Decreased glutamate leads to negative and cognitive symptoms of SZ, including sensory processing deficits

Early trials of glutamate agonists seem to yield similar results of antipsychotics

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14
Q

Glutamate Hypothesis: NMDA gateway

A

NMDA(R) (glutamate receptor) antagonists increase negative and cognitive symptoms

Glutamate regulates other neurotransmitters that are affiliated with SZ – NMDA is known as the gateway receptor

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15
Q

SZ Categories of Symptoms

A

Delusions/hallucinations

Negative affect

Disorganized speech/behavior

Hospitalization occurs if the individual is a risk to self or others

*Just having the symptoms does not lead to hospitalization

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16
Q

Delusions

A

Disturbances in content of thought

Fixed and firmly held despite clear contradictory evidence

Erroneous beliefs

Self-reference

Alien control (aka made impulses)

Thought control

thought broadcast

Grandiosity (though it’s more popular in bipolar)

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17
Q

Hallucinations

A

Sensory experiences that seem real but occur in the absence of any external perceptual stimuli

Can occur in any sensory modality (taste, sight, smell, etc.)

~70% of hallucinations involve auditory hallucinations

10-20% are visual hallucinations
• Which are typically distorted images – not clear-cut

Some evidence hallucinations may be the inability to identify thoughts/ideas as internally-generated
• source monitoring errors

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18
Q

Difference between hallucinations and illusions

A

Illusions are caused by real-world stimuli

Hallucinations are typically negative

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19
Q

Disorganized Speech

A

Failure to make sense of speech–despite conforming to semantic and syntactic rules of speech

Includes disturbances in form, not content, of thought

Differs from manic “flight of ideas”
• With flight of ideas, the speech, while confusing, is understandable when broken down

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20
Q

Disorganized Behavior

A

Impairments of goal-directed activity

Occurs in all areas of daily-functioning

Catatonia – frozen

Catatonia Stupor = cannot be physically moved

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21
Q

Negative Symptoms

A

Avolition (loss of motivation)

Anhedonia (loss of interest)

Flat affect

Alogia (aka poverty of speech; using few words and a lack of spontaneity)

**Important to note flat affect is in terms of expression
• Independent of internal feelings

Overall loss or decrease in normally-present behaviors

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22
Q

Altered Neurocognitions

A

Working memory

Attentional functioning

Speech production

Eye tracking

*Degree to which these are dysfunctional are the best predictors of real-life functioning following discharge

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23
Q

Expressed Emotions (E. E.)

A

Expressed emotions (E.E.) of the families which includes

  1. Emotionally overinvolved
  2. Overly critical
  3. Hostile

Increased EE is related to increased rate of relapse following discharge

In such cases, patient is better living alone following discharge

EE can be reduced via psychoeducation

Some argue that EE may not only encourage relapse, but it can encourage SZ’s appearance in the first place

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24
Q

Risk Factors: Low SES

A

*SZ 8x more likely in low SES, possibly due to:

Poor nutrition

Lack of access to appropriate healthcare

Increased stress

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25
Q

Schizoaffective Disorder

A

Includes mood symptoms

But the psychotic symptoms are independent of the mood

If they are dependent, then it’s bipolar or depression with psychotic features

26
Q

Schizophreniform Disorder

A

Active symptoms for less than 6 months, with impaired functioning

Typically turns into SZ

27
Q

Delusional Disorder

A

Only well-developed delusional symptoms are present, and the individual is still able to function

28
Q

Shared Psychotic Disorder

A

When two people share a delusion, not SZ

One is typically the alpha and one is the beta (and follows along)

29
Q

Brief Psychotic Disorder

A

Occurs after a traumatic event and naturally fades away

The individual is not likely to have another episode

30
Q

SZ Treatment: History, Dorothea Dix

A

Dorothea Dix advocated for better treatments

Increase in psychiatric institutes in the late 19th century in reaction to her work, but there were few treatments

Castration, lobotomy, near-death experiences, hydrotherapy

31
Q

SZ Treatment: 1950’s

A

Real change began in the 1950s

Creation of the first psychiatric drug – Thorazine

First used to treat allergies

Affects the D2 receptors

Has many side effects including sedation (like most allergy medication)

32
Q

SZ Treatment: 1960’s

A

Development of Haldol

The Community Mental Health Act – in an attempt to move treatment to the community

  • Released many patients from hospitals without building community health centers
  • Patients were now on the streets
33
Q

SZ Treatment: Haldol

A

Still a high dosage medication but lacked the sedating effects of Thorazine

Had many extrapyramidal symptoms (EPS)

Long term use: risk of tardive dyskinesia

34
Q

SZ Treatment: Haldol EPS

A

EPS=movement disorders and tardive-like symptoms

Blocked dopamine receptors throughout the brain, thereby mimicking the symptoms of Parkinson’s

Increase in acetylcholine and norepinephrine :

Muscle rigidity

Slowed movements

Resting tremors

Dystonia (muscles locked)

Akathisia (inability to sit still)

To deal with the side effects, additional drugs were administered to reduce the EPS

Lower ACH and remove the cholinergic effects

Add beta-blocker to decrease norepinephrine and remove akathisia

35
Q

SZ Treatment: Tardive dyskinesia

A

Includes spasmodic, gross, motor-movements

Not due to EPS, but rather due to long-term usage of 1st generation antipsychotics

Due to years of chronic dopamine depletion, new, more sensitive, dopamine receptors are created
*More sensitive receptors = more easily fired

36
Q

SZ Treatment: Late 1980s, early 1990s – development of 2nd generation antipsychotics

A

2nd generation antipsychotics aka “atypicals”

Atypicals have, generally, less severe side effects, but are no more efficient that 1st generation antipsychotics

Less restrictive on the dopamine systems

Controls the system just enough and then releases hold to reduce symptoms

Clozapine– “first and best” according to Serper

37
Q

SZ Treatment: Psychological Approaches

A

In conjunction with medication:

Family therapy

Case management
• Supervisor is in contact 24 hours a day
• Known as the Assertive Community Model (ACT)

Social skills Treatment
• Difficult to generalize skills however

Cognitive remediation
• Attempt to increase attention and memory by treating the brain like a muscle

Cognitive behavioral therapy
• For delusions and psychosis

Other forms of individual treatment

38
Q

DA Theory in SZ: L-Dopa

A

L-dopa and D-amphetamine can cause psychosis-like state in healthy humans and exacerbate symptoms of schizophrenia

39
Q

DA Theory in SZ: postmortem studies

A

Postmortem studies showed abnormalities in DA indexed in SZ

*Though data always confounded by drugs

40
Q

DA Theory in SZ: Neuroimaging Studies

A

SZ patients when psychotic demonstrate:

Heightened synthesis of DA

Heightened DA release in response to an impulse

Heightened level of synaptic DA

41
Q

DA Theory in SZ: DA Deficiency

A

SZ = DA deficiency disorder

Inadequate stimulation of the dopamine D1 receptors

Administration of a D2 antagonist–(blocks DA auto receptors) results in:

  • Increased DA release
  • Increased stimulation of D1 receptors

Antipsychotic drugs increased the metabolism of DA when administered to animals

42
Q

DA Theory in SZ: Amphetamines

A

Amphetamine increases synaptic monoamine levels and can induce psychotic symptoms

Reserpine – effective for treating psychosis – blocks the reuptake of DA and other monoamines

Clinical effectiveness of antipsychotic drugs was directly related to their affinity for DA receptors

*Proposal: excess in dopaminergic neurotransmission

43
Q

DA Theory in SZ: Abnormal regulation of the DA system

A

DA mediates the salience of environmental events and internal representations
* e.g. pleasure, reward, reinforcement, prediction error

A dysregulated hyperdopaminergic state leads to stimulus-independent DA release

This leads to an aberrant assignment of salience to one’s experience

44
Q

DA Theory in SZ: Prominence

A

DA model has been the leading neurochemical hypothesis of SZ for the last 40 years

**Current medications functioned primarily to block DA D2 receptors

45
Q

Glutamate Theory in SZ

A

NMDA (Glutamate receptors) agonists produce negative and cognitive symptoms of SZ

Induce neuropsychological and sensory processing deficits

Dysregulation of brain DA systems through changes in Glu mechanisms results in positive symptoms of SZ

Currently no approved medication for negative and cognitive symptoms

NMDA receptors appear to be a potential site for therapeutic intervention in SZ

46
Q

SZ and affect

A

Deficits in affective EXPRESSION define the disorder

*Not deficits in affective experience

Lack of affect is poor prognostic indicator

The more affect an individual has, generally, the easier it is to treat the disease
e.g. paranoia is highly treatable due to affective component

Sometimes delusion is grandiose, but person is not grandiose, lacks self-esteem
*this is more likely SZ than manic

47
Q

Eugen Bleuler

A

Loose Associations

Threads that run through consciousness that bind together thoughts, actions and behavior

Normals: tightly connected threads
SZ: associations loosen or break, causes a split mind

Split consciouness

Split between thoughts, feelings, behavior

–>Schizophrenia

48
Q

SZ: Monothetic Taxonomy

A

Bleuler’s concept of SZ

One symptom defines a disorder: loose associations
Vaguely defined

Anyone with symptom has disorder

Anyone with disorder has the symptom

*few others:
Pedophilia
Selective Mutism

Also possibly PTSD–traumatic event more criterion, but not alone

49
Q

Bleuler and Kraeplin USA and Europe

A

SZ dx
1930: 20% in NY and London

1955: 80% NY
still 20% London

Europe: Kraeplin

  • dementia praecox dx
  • narrow definition

USA: Bleuler

  • different construct of SZ
  • broad definition
  • translated into Enhligh
  • expanded Bleuler’s definition to ambulatory SZ, process SZ, reactive SZ etc
  • lot of people lobotomized were probably OCD, Bipolar, BPD–wide net
50
Q

Reserpine

A

Earliest drug used to treat SZ which was originally designed to control blood pressure

Inhibits D2 receptors

51
Q

DA Pathways: Mesolimbic

A

Affiliated with reward-related cognitions

Increased activation = positive symptoms of psychosis

52
Q

DA Pathways: Mesocortical

A

Affiliated with cognitive control

From the midbrain to the frontal cortex

Decreased activation = negative symptoms and cognitive deficits

53
Q

DA Pathways: Nigrostriatal

A

Involved with smooth motor movements

Destruction leads to Parkinson’s

54
Q

DA Pathways: Tuberoinfundibular

A

Linked with the pituitary gland

Regulates sex drive

55
Q

Glutamate Hypothesis: NMDA Antagonists

A

Recreational use of NMDA antagonists increase SZ-like behavior, both positive and negative symptoms

eg.
angel dust

ketamine

56
Q

Glutamate Hypothesis: Genetics

A

Genes affiliated with SZ impact glutamate

More specifically NMDA receptor expression or receptor sites and activation
*especially in the frontal cortex

Increase in enzymes that break down glutamate in those with SZ

Medication-free individuals with SZ display decreased NMDA binding at the hippocampus

57
Q

SZ and Low SES: Social Drift vs. Social Residual

A

Social drift – the illness causes one to descend in SES ladder

Social residual – the illness prevents one from ascending this ladder

58
Q

Tardive dyskinesia

A

Not due to EPS, but rather due to long-term usage of 1st generation antipsychotics

Due to years of chronic dopamine depletion, new, more sensitive, dopamine receptors are created

More sensitive = more easily fired

Includes spasmodic, gross, motor-movements

59
Q

2nd generation (atypicals) side effects

A

Obesity

Diabetes

Metabolic deregulation

Zyprexa tends to cause the most weight gain

Increase in prolactin release
*alterations of sex characteristics and libido

Agranulocytosis = deadly allergic reaction
o Destroys red blood cells in 1% of those with SZ

60
Q

DA hypothesis: Salience and Delusions

A

DA mediates the salience of environmental events and internal representations
* e.g. pleasure, reward, reinforcement, prediction error

A dysregulated hyperdopaminergic state leads to stimulus-independent DA release

This leads to an aberrant assignment of salience to one’s experience

Delusions may be cognitive effort by the patient to make sense of these aberrantly salient experiences

61
Q

DA hypothesis: Salience and Hallucinations

A

DA mediates the salience of environmental events and internal representations
* e.g. pleasure, reward, reinforcement, prediction error

A dysregulated hyperdopaminergic state leads to stimulus-independent DA release

This leads to an aberrant assignment of salience to one’s experience

Hallucinations may reflect the direct experience of the aberrant salience of internal representations

Antipsychotics dampen the salience of these abnormal experiences

If antipsychotic treatment is stopped, the dysregulated neurochemistry returns, and a relapse occurs

62
Q

DSM-5 Changes in SZ

A

At least 1 of core “positive symptoms” necessary for dx

Removal of subtypes (paranoid, disorganized, cationic)
*no distinctive pattern of tx response or course

Serper Final (9 decks)

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