Psychopathology Prepjet Flashcards
ASD Risk Factors
risk factors for ASD include male gender, family history of ASD, certain medical conditions (e.g., fragile X and Angelman syndromes), birth before 26 weeks of gestation, advanced parental age, and exposure to certain environmental toxins during prenatal development (Gialloreti et al., 2019). Note that, despite extensive research, a link between ASD and childhood vaccinations has not been established (e.g., Hviid et al., 2019).
ASD Protective Factors
Prognosis for this disorder is best when the person has an IQ over 70, functional language skills by age five, and an absence of comorbid mental health problems
Research on ASD
Studies have linked ASD to structural abnormalities in the cerebellum and amygdala and a lower-than-normal level of serotonin synthesis that contributes to abnormal brain development (Boucher, 2009; Wenzel, 2017). The studies have also linked ASD to higher-than-normal blood levels of serotonin, but the relationship between increased levels of serotonin in the blood and decreased serotonin synthesis in the brain is not well understood (e.g., Yang, Tan, & Du, 2014). Family, twin, and adoption studies support a genetic etiology (e.g., Vierck & Silverman, 2011).
ADHD and statistics of male to female
ADHD is twice as common in males than females during childhood but the gender difference decreases somewhat in adulthood when the ratio of males to females is about 1.6:1. Up 80% of school-age children with ADHD continue to meet the diagnostic criteria for the disorder in adolescence, and up to 30% continue to do so into adulthood
ADHD comorbidity statistics in children
most studies have found oppositional defiant disorder to be the most common comorbid disorder followed by, in order, conduct disorder, an anxiety disorder, and a depressive disorder
ADHD and brain abnormalities in adult
Structural neuroimaging studies have found that overall brain volume and the volumes of the caudate nucleus, putamen, nucleus accumbens, amygdala, and hippocampus are smaller in people with ADHD
children and adolescents with this disorder have delayed cortical maturation (especially in the prefrontal cortex), while adults have reduced cortical thickness.
ADHD and brain abnormalities in children
children and adolescents with this disorder have delayed cortical maturation (especially in the prefrontal cortex), while adults have reduced cortical thickness. Functional neuroimaging studies have identified hyper- or hypoactivation in several brain networks. For example, these studies have found that children with ADHD often exhibit hypoactivation in the frontoparietal network, which consists of the dorsolateral and anterior prefrontal cortex, anterior cingulate cortex, lateral cerebellum, caudate nucleus, and inferior parietal lobe
What does a diagnosis of Tourettes include?
The diagnosis of Tourette’s disorder requires at least one vocal tic and multiple motor tics that may occur together or at different times, may wax and wane in frequency but have persisted for more than one year, and had an onset before 18 years of age.
Tourettes d/o and neurotransmitter and treatment?
Tourette’s disorder has been linked to dopamine overactivity, a smaller-than-normal caudate nucleus, and heredity. Treatment may include an antipsychotic drug (e.g., haloperidol) and medication for comorbid conditions – e.g., serotonin for obsessive-compulsive symptoms and methylphenidate or clonidine for ADHD. Behavioral treatments include comprehensive behavioral intervention for tics (CBIT), which consists of psychoeducation, social support, and habit reversal, competing response, and relaxation training
Age of onset for Communication Disorder (stuttering) and recovery
The onset is usually between two and seven years of age. Sixty-five to 85% of children recover from dysfluency, with the severity of symptoms at age eight being a good predictor of persistence or recovery. The treatment-of-choice is habit reversal training which incorporates several strategies including competing response training that, for this disorder, is regulated breathing.
Learning d/o
diagnosis of this disorder requires difficulties related to academic skills as indicated by the presence of at least one of six symptoms that last for at least six months despite the use of interventions that address difficulties: inaccurate or slow and effortful word reading; difficulty understanding the meaning of what is read; difficulties with spelling; difficulties with written expression; difficulties mastering number sense, number facts, or calculation; and difficulties with mathematical reasoning.
Prevalence of Learning Disorder
About 5 to 15 percent of school-age children have a specific learning disability and approximately 80% of these children have a reading disorder (American Psychiatric Association, 2018). Of the reading disorders, dyslexia is the most common type; of the types of dyslexia, dysphonic dyslexia is most common.
Brief Psychotic Disorder: what’s the timeline for the required diagnosis?
diagnosis of brief psychotic disorder requires the presence of one or more of four characteristic symptoms for at least one day but less than one month, with at least one symptom being delusions, hallucinations, or disorganized speech.
Schizophreniform and the time for the diagnosis?
diagnosis requires the presence of at least two of five characteristic symptoms for at least one month but less than six months, with at least one symptom being delusions, hallucinations, or disorganized speech.
Schizophrenia Diagnosis?
The diagnosis of schizophrenia requires the presence of an active phase that lasts for at least one month and includes at least two of five characteristic symptoms, with at least one symptom being delusions, hallucinations, or disorganized speech. (The other two characteristic symptoms are grossly disorganized or catatonic behavior and negative symptoms). There must also be continuous signs of the disorder for at least six months that may include prodromal and/or residual phases in addition to the required active phase. Prodromal and residual phases consist of two or more characteristic symptoms in an attenuated form or negative symptoms only.
Concordance rate for Schizophrenia?
Relationship to Person with Schizophrenia
Concordance Rate
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%
Schizophrenia and the neurotransmitters involved in it (DOPAMINE HYPOSTHESIS)?
ccording to the original dopamine hypothesis, schizophrenia is due to high levels of dopamine or hyperactivity of dopamine receptors. Evidence for this hypothesis is provided by research showing that amphetamines increase dopamine activity and produce schizophrenia-like symptoms, while drugs that decrease dopamine activity reduce or eliminate these symptoms. A revised version of the dopamine hypothesis (Kuepper, Skinbjerg, & Abi-Dargham, 2012) predicts that the positive symptoms of schizophrenia are due to dopamine hyperactivity in subcortical regions of the brain (especially in striatal areas), while the negative symptoms are due to dopamine hypoactivity in cortical regions (especially in the prefrontal cortex).
Brain abnormalities in Schizophrenia
Brain abnormalities associated with schizophrenia include enlarged ventricles and hypofrontality, which refers to lower-than-normal activity in the prefrontal cortex and is believed to contribute to the disorder’s negative and cognitive symptoms
Better prognosis for Schizophrenia include:
A better prognosis for schizophrenia is associated with female gender, an acute and late onset of symptoms, comorbid mood symptoms (especially depressive symptoms), predominantly positive symptoms, precipitating factors, a family history of a mood disorder, and good premorbid adjustment.
Worse prognosis for Schizophrenia include:
anosognosia (a lack of insight into or awareness of one’s disorder) is associated with non-adherence to treatment and an elevated risk for relapse. Patients whose family members are high in expressed emotion are also at increased risk for relapse. Expressed emotion refers to the emotional response of family members to a patient with schizophrenia or other mental disorder, and families high in expressed emotion are characterized by high levels of criticism and hostility toward and emotional overinvolvement with the patient
Schizophrenia across countries and prognosis:
The research has identified variations in the onset, course, and prognosis of schizophrenia across countries. For example, there’s evidence that patients living in non-Western developing countries are more likely than those living in Western industrialized countries to experience an acute onset of symptoms, a shorter course, and a higher rate of remission (e.g., Hopper & Wanderling, 2000). The studies have also found that an “immigrant paradox” applies to schizophrenia, alcohol use disorder, and a number of other psychiatric disorders. It occurs when “newly arrived immigrants have better health outcomes than much more acculturated immigrants (with longer US residence) or even US born natives of the same ethnicity”
Dx for Schizoaffective:
The diagnosis of schizoaffective disorder requires concurrent symptoms of schizophrenia and a major depressive or manic episode for most of the duration of the illness, but with the presence of delusions or hallucinations for two or more weeks without mood symptoms
Delusional Disorder
This diagnosis requires that (a) the person have one or more delusions for a duration of at least one month and (b) the person’s overall functioning has not been markedly impaired except for any direct effects of the delusion. The DSM-5 distinguishes between the following subtypes: (a) erotomanic (the person believes that another person is in love with him/her); (b) grandiose (the person believes he/she has great but unrecognized talent or insight); (c) jealous (the person believes his/her spouse or partner is unfaithful); (d) persecutory (the person believes he/she is being conspired against, spied on, poisoned, or maliciously maligned); and (e) somatic (the person’s delusion involves bodily functions or sensations)
Heredity for BIPOLAR disorder
twin studies report concordance rates of .67 to 1.0 for monozygotic twins and about .20 for dizygotic twins (Dubovsky, Davies, & Dubovsky, 2003).
Seasonal Affective Disorder is due to what and how is it treated?
seasonal affective disorder (SAD), and its symptoms include hypersomnia, overeating, weight gain, and a craving for carbohydrates. It’s been linked to a lower-than-normal level of serotonin and a higher-than-normal level of melatonin, which is a hormone that plays an essential role in the sleep-wake cycle. SAD is often responsive to phototherapy which involves exposure to bright light that suppresses the production of melatonin
Whats the prevalence rate for depression between male and female (child and as adults)?
During childhood, the rates of depression are similar for boys and girls; however, the rate for females increases in early adolescence while the rate for males remains fairly stable. Explanations for this gender difference incorporate the impact of biological and psychological factors. For example, there’s evidence that the increase of hormonal levels at puberty sensitizes females but desensitizes males to the stress of negative life events (Allen, Barrett, Sheeber, & Davis, 2006). The higher rate for females persists into adulthood, with female adolescents and adults having a rate that is 1.5 to 3 times higher than the rate for male adolescents and adults.
Whats the etiology of depression?
twin studies have found that the concordance rate for unipolar depression is about .50 for monozygotic twins and .20 for dizygotic twins
What parts to the brain is associated with depression?
Major depressive disorder has also been linked to lower-than-normal levels of norepinephrine and serotonin and increased levels of cortisol in the hypothalamic-pituitary-adrenocortical (HPA) axis, which plays an important role in the body’s reaction to stress
Describe Lewinsohns social reinforcement theory:
Lewinsohn’s (1974) social reinforcement theory describes depression as the result of a low rate of response-contingent reinforcement for social behaviors due to a lack of reinforcement in the environment and/or poor social skills. This results in social isolation, low self-esteem, pessimism, and other characteristics of depression that, in turn, further decrease the likelihood of positive reinforcement in the future