PSY 346 Presentation DiathesisStress Model of Schizophrenia Nov 202003

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PSY 346 Presentation Diathesis-Stress Model of
Schizophrenia Nov 20/2003
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Diathesis-Stress

• Diathesis Predisposition for disease that may be
  genetic, and encompasses cognitive sets, chronic
  feelings of helplessness, past experiences, and
  overall psychological hardiness.

• Stress An environmental/life event that disrupts
  homeostasis and occurs when the situation is
  appraised as exceeding the persons adaptive
  resources. Stress is moderated through the use
  of coping strategies, resilience to stress
  strategies, social support, emotional release,
  and exercise.

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Diathesis-Stress Model

• The interaction between a constitutional
  predisposition and an environmental trigger that
  affects the course rather than the cause of
  schizophrenia

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Schizophrenia is Characterized by

• Cognitive distortions (inability to maintain
  focused thought, too much extraneous sensation)
• Brain malfunctioning (elevated dopamine and
  serotonin levels, and excessively large vesicles)
  
• Symptoms include both positive and negative
  symptoms.

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Positive Symptoms

• the behavior a person actually displays
• delusions (inappropriate or unwanted beliefs or
  thoughts) that are firmly held personal beliefs
  that have no basis in reality (paranoia believe
  others are persecuting/conspiring against you)
• hallucinations (perceiving in the absence of an
  external physical stimulus) such as hearing
  voices (instructing you, carrying on conversation
  with you)
• bizarre behavior or inappropriate affect (out of
  proportion emotional response)

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Negative Symptoms

• lack of expected functioning slow deterioration
  of functioning
• withdrawal from society (exacerbate their
  isolation)
• less sociable (dulled emotions, inappropriate
  emotions, and change in speech)
• exhibit catatonia (long periods of being
  virtually motionless)

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Causes

• Genetic Factors MZ twins have a 50 chance of
  schizophrenia diagnosis
• Environmental Factors Influenza received during
  the 2nd trimester of pregnancy and relationship
  between socioeconomic status (monetary deficits
  may be due to their condition)

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Schizophrenia

• Developmental events and precursors include
  elevated rates of soft neurological signs and
  birth complications, slow habituation and high
  baseline autonomic activity, high rate of
  developmental disorders of speech/language and
  overall and specific cognitive deficits. Brain
  morphological studies and intelligence testing
  provide further evidence of deterioration.

• Early Onset Schizophrenia (EOS) is a rare
  disorder with a prevalence of 1/10 000 before the
  age of 12 (increases dramatically around
  puberty/early adolescence). It can be understood
  as a progressive-deteriorating developmental
  disorder.

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• Positive symptoms increased linearly with age,
  whereas negative symptoms were most frequent on
  early childhood and adolescence.
• Negative symptoms at the beginning of the episode
  could be potentially hidden by the positive
  symptoms and probably became evident after the
  disappearance of the positive symptoms as a
  result of neuroleptic treatment.

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Neurobiological and Psychological Changes During
Puberty and Adolescence

• Myelination of the association cortex and the
  limbic cortex. This is a risk factor because
  neocortical and limbic circuits might not attain
  adequate function until adolescence.
• Maturation of the prefrontal cortex responsible
  for executive functions in the fronto-temporal
  network
• The role of gonadal hormones (estrogen increases
  the frequency of synapses in the rat hippocampus,
  androgens increase the synaptic elimination in
  the rat)
• Decline of cerebral plasticity
• Changes in the dopaminergic innervation and
  periadolescent synaptic pruning

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Morphology

• Brain Morphology shows a decreased total cerebral
  volume, decreased gray matter volume, increased
  ventricular volume and decreased midsaggital
  thalamic area (midsaggital area of the corpus
  callosum was significantly increased). There
  exists a strong correlation between negative
  symptoms and total cerebral volume.

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Schizophrenia reflects a great degree of social
impairment resulting in deficit. The concept of
childhood attentional deviance has three
particular dimensions of relevance, which
include social sensitivity, social indifference,
and social isolation, which can be further
explained by

• Attentional deficit at an early age which may be
  an important link to later social dysfunctioning.
• Attentional impairment may be primary to the
  social deficit
• Attentional deficit seems to remain stable
  throughout development
• Attentional deficit can be tested reliably at
  approximately 2.5 years (relationship between
  attentional dysfunction and social skills becomes
  significant at mid-adolescence when they first
  display their social deficits)

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Manifestation

• The manifestation of schizophrenia at an early
  age is not a sudden phenomenon, but is the result
  of many factors that contribute to etiology, age
  at onset, symptomatology, course, and outcome.

• Obstetric complications are not developmental
  precursors, rather they are events that might
  have great impact on future development. The
  same applies to other stable traits such as
  attentional dysfunction or event related
  potentials that can be looked at as a stable
  vulnerability marker for schizophrenia. Other
  influences that change over time include
  speech/language ability, scholastic performance,
  intelligence, and transient symptoms of pervasive
  development.

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Peak of manifestation occurs around puberty.
Three potential arguments include

• The possibility that certain genes that offer
  predisposition to schizophrenia could be
  activated during adolescence/puberty. There have
  been no obtained empirical results, but potential
  regions have been listed for gene susceptibility.
• Neurobiological/psychosocial maturation processes
  could either trigger the disorder or lower the
  threshold for the manifestation around
  puberty/adolescence
• Biological conditions (genetic risks, birth
  complications, neurosensory and neuromotor
  deficits) and developmental precursors (overall
  specific cognitive impairments, delayed
  speech/language development, poor adjustment in
  school) could accumulate and interact with each
  other and lead to a manifestation of a
  schizophrenic breakdown when a certain
  individually variable threshold is reached.

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Schizophrenia

• Pre-schizophrenic children reflect a reduced
  degree of success in social adjustment which
  progresses throughout childhood/adolescence into
  developmental gender impairment (reflecting an
  existing degree of impairment in the premorbid
  functioning)

• Developmental deviance and abnormalities in
  premorbid social interaction and language-related
  functions act to precipitate an earlier age of
  onset in schizophrenia. The effect of these
  factors on age of onset (more pronounced in
  adolescent cases than for adult onset patients)
  acts to influence social function and personality
  traits into adulthood

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Early Onset Schizophrenia (EOS onset prior to
age 18, mean 14.2) has been associated with

• Delayed motor/speech milestones (developmental
  deviance ranging from disruptive behavior to
  withdrawal) of spelling/reading and other related
  academic performances
• Poor childhood premorbid adjustment continuing
  throughout adolescence (particularly in males who
  show a greater vulnerability)
• Inclusion of schizophrenia spectrum traits
  reflecting the continual abnormalities of
  development regarding adjustment/personality
• Overall increased impairment in speech/language

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Late Onset Schizophrenia

• Late Onset Schizophrenia (LOS/AOS onset beyond
  18 years of age, mean 22.9) shares a number of
  clinical, neuropsychological, and nonspecific MRI
  characteristics with early onset schizophrenia.

• LOS is associated with
• a reduced dosage necessity of neuroleptic
  treatment
• larger thalamic volume (MRI)
• mild impairment in cognitive functioning

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Chromosomal Abnormalities

• schizophrenia onset emerges from the disruption
  of a particular locus
• provides a permissive genetic environment for
  mutations elsewhere in the genome to become
  expressed as psychotic illness

• The chromosomal abnormalities inherent in the
  complexity of the genetics of Schizophrenia may
  represent a linkage to a susceptibility locus
  such that

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GABA

• GABA function is decreased in brain areas of
  structural change (represented in MRI
  schizophrenics). The decreased levels of GABA
  are associated with negative symptoms, poor
  premorbid functioning (putative neurodevelopment)
  and with decreased dopamine and serotonin
  turnover. Lower plasma GABA levels were
  independently associated with larger
  ventricle-to-brain ratios, lateral prefrontal
  atrophy, and poor premorbid social functioning

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Substance Abuse Patterns in Schizophrenia

• Schizophrenia onsets might be precipitated by the
  onset of drug abuse (and to a lesser extent
  alcohol abuse) in persons directly exposed to
  schizophrenia predisposition. Age of onset is
  significantly lower for drug abusers compared to
  the control population. As many as 82.7 have a
  history of drug abuse habits within the time
  frame of the initial stage.

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Substance Abuse

• Alcohol abuse led to a small likelihood of
  premature precipitation of psychosis, by acting
  to trigger the first psychotic episode.
  Substance abuse is associated with an increase in
  positive symptoms especially hallucinations and
  psychotic thought disorders. It is also
  associated with a reduction in negative symptoms
  (affective flattening).
• Patients abuse drugs as a dysfunctional way of
  coping with the unpleasant phenomena of bluntness
  and indifference, and in so doing appear to
  accept the increase in positive symptoms.

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HPA Axis

• HPA function is characterized by hypersensitivity
  to stress and increased cortisol release in
  schizophrenia, which may be a triggering factor
  for the psychiatric symptoms. Furthermore
  dopamine activation stimulates the HPA axis
  through abnormal neurotransmission. The HPA axis
  acts as a potentiating system responsible for the
  moderation of the diathesis expression via its
  effects on DA-mediated circuitry. Thus any
  hippocampal damage or DA abnormalities render a
  state of hypersensitivity to stress. This is
  consistent with prenatal factors of
  schizophrenia.

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Conclusion

• Factors of both nature and nurture debates
  interact to construct our global depiction of the
  diathesis-stress model of schizophrenia
• Current trends in research reflect the more
  medicinal/pharmacological implications and have
  arisen so as to stress the role of correcting
  hormonal and genetic imbalances inherent in the
  affected predisposition group