Psychopathology: Schizophrenia Spectrum/Other Psychotic D/O Flashcards
Brief Psychotic Disorder Requirements
- 1+ of 4 sx: delusions, hallucinations, disorganized speech**, and grossly disorganized/catatonic bx
- 1-30 days
** = 1 of the symptoms must be one of these
What are delusions
false belief based on incorrect inference about external reality that is firmly held despite proof/evidence to the contrary
What are hallucinations
Perception-like experience with the clarity and impact of a true perception without the external stimulation of the relevant sensory organ
What are illusions
Actual stimulus is misperceived or misinterpreted
**Not to confuse with hallucination that does not have an actual stimulus
Schizophreniform D/O
- 2+ of 5 sx: delusions, hallucinations, disorganized speech**, grossly disorganized/catatonic bx + Negative sx (avolition, alogia, anhedonia)
- 1-6 MONTHS
** = 1 of the symptoms must be one of these
Schizphrenia
- 2+ of 5 sx: delusions, hallucinations, disorganized speech**, grossly disorganized/catatonic bx + Negative sx (avolition, alogia, anhedonia)
- 1+ MONTH of ACTIVE PHASE
*6+ MONTHS of Sx
Other phases include:
Prodromal Phase=2+ characteristics in a reduced form
Residual Phase=2+ characteristics in negative symptoms only
** = 1 of the symptoms must be one of these
Genetic factors/Concordance rates of 1st degree relatives (Gottesman, 1991)
Relationship to Person with Schizophrenia
Parent =6%
Biological sibling=9%
Child of one parent with schizophrenia=13%
Dizygotic (fraternal) twin=17%
Child of two parents with schizophrenia=46%
Monozygotic (identical) twin=48%
Concordance rates for discordant twins (twins in which only one twin has schizophrenia)
Discordant MONOzygotic twins = increased risk of schizophrenia being similar for offspring of affected and non-affected twins
Discordant DIzygotic twins = risk for offspring of affected twins was SIMILAR to risk for offspring MONOzygotic twins and GREATER than risk for non-affected twins
Discordant MZ twins have significant genetic liability that can be transmitted to children even though they do not manifest it themselves
Dopamine hypothesis for Schizophrenia
Due to HIGH levels of dopamine or HIGH activity of dopamine rceptors
AMPHETAMINES increase dopamine and produce schizophrenia-like symptoms.
Updated Dopamine hypothesis for Schizophrenia (Kuepper, Skinbjerg & Abi-Dargham, 2012)
Positive sx due to Dopamine HYPER activity in the SUBcortical regions of the brain (striatal areas–basal ganglia)
Negative sx due to Dopamine HYPOactivity in CORtical regions (prefrontal cortex)
Brain abnormality associated with Schizophrenia
*Enlarged Ventricals
* HYPOFRONTALITY=lower-than normal activity in prefrontal cortex (contribute to negatie sx)
* Dysfunction of Temporal-Limbic-Frontal network causes negative symptoms
* Disinhibition in striatum (caudate nucleus, putamen, and nucleus accumbens within basal ganglia) causes positive symptoms
Comorbid d/o with Schizophrenia
Anxiety D/O
OCD
Tobacco use (70-85% aka over half meet criteria for tobacco use d/o)
Onset of Schizophrenia
1st appears between late teens and early 30ths
Peaks early- to mid-20’s for men and late-20s for women
Course of Schizophrenia
Psychotic sx decrease with age.
Negative and cognitive sx persist
Better prognosis for schizophrenia
female gender
acute & late onset of sx
comorbid mood symptoms (esp Depression)
Premoninantly positive symptoms
Precipitating factors
Family Hx of mood disorder
Good premorbid adjustment