Chapter 16: Psychological Disorders Flashcards
Psychological Disorders
A pattern of behavioral or psychological symptoms that impact multiple life areas and/or create distress for the person experiencing these symptoms.
DSM-IV: approximately 26.2 million Americans over age of 18 meet criteria for a psychological disorder (2005).
Schizophrenia
“Split Mind”
Disturbances in reason, emotion, perception, social relationships.
Loss of contact with reality.
Inability to function in daily life.
Positive symptoms: –Hallucinations –Delusions & Paranoia –Disorganized speech (e.g., word salad) –Disorganized behavior Negative symptoms –Social and emotional withdrawal –Absence of normal cognition or affect (e.g., flat affect, poverty of speech) Cognitive symptoms –Poor "executive functioning" –Inability to sustain attention –Problems with working memory
Concordance Rate: Risk increases with genetic similarity.
Many genes, on many different chromosomes, contribute to Schizophrenia.
~1% of world’s population
2.5 million Americans in a given year.
Equally split between genders, males have earlier onset (18-25, usually).
Schizophrenia:
Positive symptoms
–Hallucinations
–Delusions & Paranoia
–Disorganized speech (e.g., word salad)
–Disorganized behavior
Schizophrenia:
Negative symptoms
–Social and emotional withdrawal
–Absence of normal cognition or affect (e.g., flat affect, poverty of speech)
Schizophrenia:
Cognitive symptoms
–Poor “executive functioning”
–Inability to sustain attention
–Problems with working memory
Genetics of Schizophrenia
Many genes, on many different chromosomes, contribute to Schizophrenia.
Risk increases with genetic similarity
A Possible Genetic Marker
A majority of schizophrenic patients and ~50% of their relatives show abnormal intrusions of saccades in smooth pursuit tasks.
Schizophrenia:
Prenatal Factors
Low socio-economic groups Abnormal fetal development Birth complications Maternal exposure to viruses during pregnancy –Seasons
Schizophrenia:
Paternal Age
Sporadic Schizophrenia
Damaged sperm: mechanisms to ensure correct DNA translation impaired in older men resulting in “de novo” mutations.
Diathesis-Stress Model of Schizophrenia
Diathesis: Genetic predisposition & vulnerability.
Stress: Life stressors can trigger disorder.
Schizophrenia:
Brain Structure & Function Abnormalities
Enlarged ventricles. Cellular disorganization. Decreased activation of the frontal lobe. Decreased hemispherical symmetry. Adolescent loss of gray matter.
Schizophrenia:
Cellular Abnormalities in Hippocampus
Hippocampus is smaller in individual with schizophrenia
Neurons in the hippocampus are disorganized.
Schizophrenia:
Hypofrontality
Lower activity in the frontal lobes; associated with negative symptoms (e.g., social withdrawal).
Lower levels at rest and during difficult cognitive tasks.
Decreased hemispheric asymmetry; ambiguous handedness; disease might be related to a failure in normal brain lateralization.
Schizophrenia:
Adolescent Loss of Gray Matter
Cortical gray matter growth at puberty.
Gray matter loss extends into 20s.
Schizophrenic teens loose large amount of gray matter.
The Dopamine Hypothesis
Drugs that increase dopamine produce positive symptoms even in people without the disorder.
Drugs that reduce dopamine (typical neruroleptics) reduce positive symptoms.
Therefore, Schizophrenia may be caused by excess dopamine
Problems with Dopamine Hypothesis
Different time course for speed at which drugs block dopamine receptors (hours) and behavioral effects (weeks).
25% of patients do not respond to dopamine antagonists.
Atypical antipsychotic drugs (e.g. clozapine) suggest other receptors and transmitters involved (serotonin).
The Glutamate Hypothesis
PCP, Ketamine (NMDAR antagonists) produce symptoms similar to schizophrenia.
Therefore, schizophrenia symptoms may be related to the reduced activity of glutamate.
schizophrenia Hypothesis
schizophrenia symptoms may be related to the reduced activity of glutamate.
Schizophrenia may be caused by excess dopamine
Tardive dyskinesia
Tardive dyskinesia is a difficult-to-treat and often incurable form of dyskinesia, a disorder resulting in involuntary, repetitive body movements. In this form of dyskinesia, the involuntary movements are tardive, meaning they have a slow or belated onset. This neurological disorder most frequently occurs as the result of long-term or high-dose use of antipsychotic drugs, or in children and infants as a side effect from usage of drugs for gastrointestinal disorders.
Features
Tardive dyskinesia is characterized by repetitive, involuntary, purposeless movements. Some examples of these types of involuntary movements include:
Grimacing
Tongue movements
Lip smacking
Lip puckering
Pursing of the lips
Excessive eye blinking
Rapid, involuntary movements of the limbs, torso, and fingers may also occur. In some cases, an individual’s legs can be so affected that walking becomes difficult or impossible. These symptoms are the opposite of patients who are diagnosed with Parkinson’s disease. Parkinson’s patients have difficulty moving, whereas tardive dyskinesia patients have difficulty not moving.
Respiratory irregularity, such as grunting and difficulty breathing, is another symptom associated with tardive dyskinesia, although studies have shown that the prevalence rate is relatively low.
Tardive dyskinesia is often misdiagnosed as a mental illness rather than a neurological disorder,[8] and as a result patients are prescribed neuroleptic drugs, which enhance the probability that the patient will develop a severe and disabling case, and may even experience a shorter survival period.
Cause
Tardive dyskinesia was first described in the 1950s shortly after the introduction of chlorpromazine and other antipsychotic drugs. However, the exact mechanism of the disorder remains largely uncertain. The most compelling line of evidence suggests that tardive dyskinesia may result primarily from neuroleptic-induced dopamine supersensitivity in the nigrostriatal pathway, with the D2 dopamine receptor being most affected. Neuroleptics act primarily on this dopamine system, and older neuroleptics, which have greater affinity for the D2 binding site, are associated with high risk for tardive dyskinesia. The D2 hypersensitivity hypothesis is also supported by evidence of a dose-response relationship, withdrawal effects, studies on D2 agonists and antagonists, animal studies, and genetic polymorphism research.
Treatment of Schizophrenia
No effective treatments prior to about 1950.
Discovery of chlorpromazine (Thorazine).
Neuroleptics have greater effects on positive than negative symptoms.
Typical antipsychotics block dopamine throughout brain
Tardive dyskinesia.
Atypical antipsychotics (clozapine) acts on serotonin receptors; can produce reduction in both positive and negative symptoms (e.g., flattened affect).
Repeated Transcranial Magnetic Stimulation (rTMS) reduces auditory hallucinations
Mood Disorders
Mood is altered in a way that affects daily life.
More profound than “feeling blue” or “feeling hyper”.
Long-lasting, consistent, and interferes with daily life.
Major Depressive Disorder (MDD)
Symptoms: •Depressed mood for at least 2 weeks •Loss of pleasure in normally enjoyable activities •Sleep disturbances •Eating alterations •Lack of energy or restlessness •Difficulty concentrating •Feelings of hopelessness, worthlessness •Suicidal thoughts
The “Common Cold” of Mental Disorders.
MDD affects 1 in 5 Americans at some point in their lives.
Prior to adolescence, boys and girls are equally likely to experience depression.
In adults, women are about twice as likely as men to be diagnosed with MDD
–Biological difference?
–In adults, sex difference may be related to fluctuations in female hormones (e.g., PMS, PMDD, postpartum depression, menopause)
Most patients experience 5–6 episodes during their lifetimes.
The risk for major depression increases with age in men, whereas women experience their peak risk between the ages of 35 and 45.
Prevalence of Affective / Mood Disorders
12% of men & 21% of women will report depression in lifetime.
Depression recurs in 35% of patients and is unremitting in 15% of patients.
Genetics of Depression
Concordance rate between identical twins is 40% versus 11% for fraternal twins.
Adoption studies support a role for genetics in depression, with a similar rate for twins reared apart.
Brain Changes in Depression
Structural abnormalities in several brain areas:
–Decreased volume of hippocampus and orbitofrontal cortex
–Increased amygdala volume
Functional changes:
–Decreased ACC activation
–Increased blood flow in PFC
and amygdala.
Emotional Dysregulation
Sleep Disturbances in MDD
- Enter first cycle of REM sleep faster.
- NMREM: Decrease in stages 3 & 4 (deep sleep) and increase in Stages 1 & 2
- Selective waking during REM decreases depression.
- Anti-depressions tend to decrease REM
Monoamine – Circadian Interaction
Monamines play essential role in regulation of sleep and wake cycles (e.g., serotonin and SAD).
Cortisol release by adrenal glands in response to both circadian rhythms and stress-related activity (HPA axis).
Links stress, circadian disruption, and development of depression.
Antidepressants and Neurogenesis
Antidepressants stimulate neurogenesis in the hippocampus
Blocking neurogenesis prevents the beneficial effects of antidepressants
Bipolar Disorder
In bipolar disorder, the individual alternates between periods of depression and mania
–Mania involves a distinct period of abnormally and persistently elevated expansive and/or irritable mood that includes excess energy and confidence that often lead to grandiose schemes
–Sustained overall-activity, talkativeness, increased energy , decreased need for sleep, and excessive involvement in pleasure seeking activities including sex and drugs are also common.
Affects men and women equally at about 1%.
Has an early onset
Concordance rates between identical twins may be as high as 85%
Complex heritability, families often display both schizophrenia and bipolar.
Dietary omega-3 fatty acids may provide protection
Anxiety Responses
A diffuse apprehension
Point of stress often vague in nature
Associated with feelings of uncertainty or unsettled concern
Warns of danger and activates fight-or-flight response
Elevated heart rate, blood pressure, blood glucose, and adrenalin release aid in survival
Pharmacotherapy
Anxiolytics: medication that relieves anxiety.
These drugs may include sedative-hypnotics, producing sedation to sleep to unconsciousness.
CNS depressants are a large class of compounds that include barbiturates, benzodiazepines, and the most common depressant of all: Alcohol
More GABA
More slowed down
Generalized Anxiety Disorder
Most common psychiatric disorder: lifetime prevalence of 10-30%
High co-morbidity with depression, up to 58%
Like depression, women 2X as likely to experience anxiety disorder
Concordance rates for twins range from 20-40%, depending on the disorder
Panic Attack
Intense fear or discomfort
Diagnosis: repeated attacks followed by at least one month of worrying about another attack
Prevalence: 2-3% of population
Co-morbidity with depression or other anxiety disorders
Treated with antidepressant medications.
Obsessive-Compulsive Disorder
Characterized by uncontrollable obsessions and compulsions which the sufferer usually recognizes as being excessive or unreasonable.
Obsessions are recurring thoughts or impulses that are intrusive or inappropriate and cause the sufferer anxiety.
Compulsions are repetitive behaviors or rituals performed by the OCD sufferer, performance of these rituals neutralize the anxiety caused by obsessive thoughts, though relief is only temporary.
Obsessive-Compulsive Disorder
Partly genetic, but birth trauma, infection and injury may also cause OCD
Increased activity in the basal ganglia and decreased activity in the orbitofrontal cortex
The orbitofrontal cortex is connected with the caudate nucleus and acts like the brain’s automatic transmission, allowing a person to ‘shift gears’ from one response to another. In the person with OCD, this process often gets stuck, which is why people with OCD may repeat the same behaviors over and over again.
OCD patients are low in serotonergic activity
Treat with SSRIs in conjunction with behavioral therapy.
Selective serotonin reuptake inhibitors (SSRIs)
treat Obsessive-Compulsive Disorder
Posttraumatic Stress Disorder (PTSD)
Recurrent dreams of trauma, flashbacks, hyper-arousal and avoidance of stimuli associated with trauma, high levels of vigilance and an impairment in daily functioning.
Lifetime prevalence: 1-10%
Natural disaster: 4-16%
War veterans: 30%
Sex assault victims: 50%
Prisoners of war: 50-75%
Some individuals appear more susceptible to PTSD
Other demonstrate higher rates resilience
Of those that do develop PTSD, 74% have family history of psychopathology
PTSD Etiology
Those susceptible to PTSD may have poor negative feedback of the HPA axis, due to smaller than normal hippocampus.
Combat veterans that developed PTSD have a smaller hippocampus, relative to combat veterans that do not develop PTSD.
Non-military twin also has small hippocampus, suggesting those that do develop PTSD may be susceptible due to impaired regulation of stress response.
A smaller hippocampus may also reduce ability of individual to “contextualize” memory, thus generalizing stress response to independent factors associated with traumatic experience.
Treatment of PTSD
Treatment consists of medication and/or cognitive-behavior treatment, including extinction therapy
