PSY 346 Presentation Diathesis-Stress Model of Schizophrenia Nov 20

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

2. 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 person�s adaptive resources. Stress is moderated through the use of coping strategies, resilience to stress strategies, social support, emotional release, and exercise.

3. Diathesis-Stress Model The interaction between a constitutional predisposition and an environmental trigger that affects the course rather than the cause of schizophrenia

4. 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.

5. 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)

6. 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)

7. 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)

8. Schizophrenia 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. 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.

9. 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.

10. 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

11. 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.

12. 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)

13. 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.

14. 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.

15. 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

16. 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

17. 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

18. Chromosomal Abnormalities The chromosomal abnormalities inherent in the complexity of the genetics of Schizophrenia may represent a linkage to a susceptibility locus such that: 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

19. 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

20. 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.

21. 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.

22. 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.

23. 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