Chapter 15: Psychological Disorders


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Looking at problematic behaviors that interfere with life.

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Chapter 15: Psychological Disorders

  1. 1. Psychological Disorders
  2. 2. Substance Abuse <ul><li>Definition: </li></ul><ul><li>Maladaptive pattern of substance use leading to clinically significant impairment of distress </li></ul><ul><li>Synapses, Reinforcement, & Drug Use </li></ul><ul><li>Experiments showed dopamine release in the area of the nucleus accumbens was reinforcing </li></ul><ul><li>Most abused drugs & ordinary pleasures lead to increased dopamine activity </li></ul><ul><li>Recent research has dopamine & nucleus accumbens playing role in attention-getting or arousal rather than pleasure </li></ul>
  3. 3. Common Drugs & Their Synaptic Effects <ul><li>Stimulants </li></ul><ul><li>Produce excitement, alertness, elevated mood, decreased fatigue, & sometimes motor activity </li></ul><ul><li>Highly addictive </li></ul><ul><li>Amphetamines </li></ul><ul><li>Increases dopamine release from presynaptic terminals by reversing the direction of dopamine transfer </li></ul><ul><li>Cocaine </li></ul><ul><li>Blocks the reuptake of catechola-mines & serotonin at the synapse </li></ul><ul><li>Behavioral effects are believed to be mediated primarily by dopamine & secondarily by serotonin </li></ul>Normal Brain Cocaine Brain
  4. 4. Common Drugs & Their Synaptic Effects <ul><li>Effects of Amphetamine & Cocaine </li></ul><ul><li>Short-lived because of the depletion of dopamine stores & tolerance </li></ul><ul><li>Methylphenidate </li></ul><ul><li>Ritalin </li></ul><ul><li>Prescribed for ADHD </li></ul><ul><li>Works like cocaine by blocking reuptake of dopamine at presynaptic terminals </li></ul><ul><li>Repeated use of stimulants can have permanent effects on brain functioning </li></ul>
  5. 5. Common Drugs & Their Synaptic Effects <ul><li>Nicotine </li></ul><ul><li>Stimulates the nicotinic receptor (a type of acetylcholine receptor) in the CNS & neuromuscular junction of skeletal muscles </li></ul><ul><li>Also increased dopamine release by attaching to neurons that release dopamine in the nucleus accumbens </li></ul><ul><li>The nicotine in tobacco is 4 ½ times more addicting than heroin </li></ul>
  6. 6. Common Drugs & Their Synaptic Effects <ul><li>Opiate Drugs </li></ul><ul><li>Morphine, heroin & methadone </li></ul><ul><li>The net effect is of increasing the release of dopamine by stimulating endorphin receptors </li></ul><ul><li>They decrease the activity in the locus coeruleus resulting in a decreased response to stress & decreased memory storage </li></ul>
  7. 7. Common Drugs & Their Synaptic Effects <ul><li>Marijuana </li></ul><ul><li>Contains  9 -THC which works by attaching to canabinoid receptors </li></ul><ul><li>Hallucinogenic Drugs </li></ul><ul><li>Drugs that distort perception </li></ul><ul><li>Many hallucinogenic drugs resemble serotonin & bind to serotonin type 2A receptors </li></ul>
  8. 8. Alcohol & Alcoholism <ul><li>Alcoholism & Alcohol Dependence </li></ul><ul><li>A common type of substance abuse that produces significant harm to the lives of others & the drinker </li></ul><ul><li>Alcohol inhibits the Na + ion flow across the neuron membrane </li></ul><ul><li>It decreases serotonin activity, facilitates the transmission of GABA A receptor & blocks glutamate receptors & increases dopamine activity </li></ul><ul><li>Types of Alcoholism </li></ul><ul><li>Type I alcoholism: less dependent on genetic factors, develops gradually over years, affects men & women equally & is less severe </li></ul><ul><li>Type II alcoholism: has a strong genetic basis, is rapid & has an early onset, primarily affects men, is more severe & is associated with criminality </li></ul>
  9. 9. Alcohol & Alcoholism <ul><li>Risk Factors for Alcohol Abuse </li></ul><ul><li>1. Less than average intoxication after drinking a small to moderate amount of alcohol </li></ul><ul><li>2. Experiencing more than average relief from tension after drinking alcohol </li></ul><ul><li>3. Having a smaller than normal amygdala in the right hemisphere </li></ul>Alcohol's Addictive Cycle 2. Alcohol High (Stimulating Opioid Receptors) 4. Motivated to Consume More Alcohol (Increased craving & Loss of Control) 1. Alcohol Consumption 3. Alcohol High Diminishes (Desire to stimulate The Opioid Receptors)
  10. 10. Major Depression <ul><li>Characteristics: </li></ul><ul><li>Feeling sad, helpless, lacking energy & pleasure for weeks at a time, feelings of worthlessness, trouble sleeping, can’t concentrate, little pleasure from food or sex, contemplating suicide & can’t imagine being happy </li></ul>
  11. 11. Major Depression More Shortness Of Breath Increased Anxiety Less Energy Tiredness More Shortness Of Breath Muscle Tension Shallow Breathing Anxiety Deprsssion
  12. 12. Major Depression <ul><li>Evidence of Genetic or Other Prior Predispositions </li></ul><ul><li>If there were relatives with depression that manifests before the age of 30 </li></ul><ul><li>It tends to be episodic & there were incoming feelings of depression </li></ul><ul><li>May have normal feelings for weeks, months or years between episodes </li></ul><ul><li>It is more common among women than men but equally common among children </li></ul><ul><li>Most experiencing depression have decreased activity in the left hemisphere & increased activity in the right prefrontal cortex </li></ul>
  13. 13. Major Depression <ul><li>Borna Disease </li></ul><ul><li>A viral infection of the nervous system leading to periods of frantic activity alternating with periods of inactivity </li></ul><ul><li>In 1990 study, 30% of severely depressed persons tested positive for the Borna virus </li></ul><ul><li>Hypoglycemia </li></ul><ul><li>Causes: too little food, too much insulin or diabetes or diabetes medication, or extra activity </li></ul><ul><li>A sudden onset may progress to insulin shock </li></ul>
  14. 14. Treatment for Depression <ul><li>Tricyclics </li></ul><ul><li>Prevent the presynaptic neuron from reuptake of catecholimes or serotonin </li></ul><ul><li>MOA Inhibitors </li></ul><ul><li>Block the enzyme monamine oxydase from metabolizing catecholamines & serotonin into active forms </li></ul><ul><li>SSRIs </li></ul><ul><li>Similar to tricyclics but are specific to serotonin </li></ul><ul><li>Atypical Antidepressants </li></ul><ul><li>A miscellaneous group of drugs with antidepressant actions & mild side effects; they inhibit reuptake of dopamine & to some extent norepinephrine </li></ul>
  15. 15. Treatment for Depression <ul><li>Cognitive Therapy </li></ul><ul><li>Produces effects similar to drugs for many depressed people </li></ul><ul><li>Recovered are less likely to relapse </li></ul><ul><li>Electroconvulsive Therapy </li></ul><ul><li>Inducing seizures with an electric shock to the head </li></ul><ul><li>Application: every other day for about 2 weeks </li></ul><ul><li>About ½ will relapse within 6 mos. </li></ul><ul><li>Most depressed people will enter REM sleep within 45 mins. of going to bed </li></ul>Thoughts Emotions Behavior
  16. 16. Bipolar Disorder <ul><li>Manic-Depressive Disorder </li></ul><ul><li>Alternates between depression & mania </li></ul><ul><li>2 types of bipolar disorder: </li></ul><ul><li>Bipolar I disorder: Has full-blown episodes of mania </li></ul><ul><li>Bipolar II disorder: His milder phases of mania (hypomania) </li></ul><ul><li>Characteristics </li></ul><ul><li>Mean onset is in the late 20s </li></ul><ul><li>Brain activity is higher than normal during mania & lower than normal during depression </li></ul><ul><li>There is a strong hereditary basis but there is no specific gene </li></ul><ul><li>Lithium salts are the most effective therapy but it isn’t known how they work </li></ul><ul><li>Drugs used include valproic acid and carbamazepine </li></ul>
  17. 17. Seasonal Affective Disorder <ul><li>Usually in the Winter </li></ul><ul><li>Most common in regions closest to the poles where the nights are very long and there’s a very short summer </li></ul><ul><li>Treatment is with bright lights in either the morning or evening for about 1 hour </li></ul>
  18. 18. Schizophrenia <ul><li>Characteristics </li></ul><ul><li>Deteriorating ability to function in everyday life, delusions, hallucinations, movement disorders, thought disorders, & inappropriate emotional expression </li></ul><ul><li>Behavioral Symptoms </li></ul><ul><li>Positive Symptoms: (behaviors that should be absent) delusions, hallucinations, inappropriate emotional responding, bizarre behavior, & thought disorders </li></ul><ul><li>Negative Symptoms: (missing behaviors that should be there) deficits in social interaction & emotional expression </li></ul><ul><li>Can be either acute or chronic </li></ul>
  19. 19. Schizophrenia <ul><li>Diagnosing </li></ul><ul><li>Difficult to diagnose </li></ul><ul><li>Conditions with similar symptoms: </li></ul><ul><li>1. mood disorder with psychotic features </li></ul><ul><li>2. substance abuse </li></ul><ul><li>3. brain damage </li></ul><ul><li>4. undetected hearing loss </li></ul><ul><li>5. Huntington’s disease </li></ul><ul><li>6. nutritional abnormalities </li></ul><ul><li>Demographic Data </li></ul><ul><li>Occurs in all ethnic groups & is about equal in men & women </li></ul><ul><li>It tends to develop earlier in men </li></ul><ul><li>Expressed emotions: hostile expressions by a caretaker can aggravate the conditions </li></ul><ul><li>May be the reason for increased number of cases in the U.S. & Europe compared to 3 rd world countries </li></ul><ul><li>The older the father at the time of birth, the greater the risk </li></ul>
  20. 20. Schizophrenia <ul><li>Genetics </li></ul><ul><li>There is a 50% concordance for schizophrenia for monozygotic twins & a 15% concordance for dizygotic twins </li></ul><ul><li>This does not mean that schizophrenia has a purely genetic cause </li></ul><ul><li>There are no reliable markers for schizophrenia </li></ul>
  21. 21. Schizophrenia Hypotheses <ul><li>Neurodevelopmental Hypothesis </li></ul><ul><li>Caused in large part by abnormalities to the nervous system during the prenatal or neonatal period </li></ul><ul><li>Many schizophrenics had problems before or shortly after birth that could have affected brain development </li></ul><ul><li>Rh incompatibility between mother & offspring is associated with increased probability of schizophrenia </li></ul><ul><li>Season-of-birth effect: tendency for those born in winter months to have a slightly greater probability of schizophrenia </li></ul><ul><li>Mild Brain Abnormalities </li></ul><ul><li>Many schizophrenics have slightly smaller prefrontal cortex, temporal cortex, hippocampus & amygdala </li></ul><ul><li>Have smaller than normal cell bodies & some neurons fail to arrange themselves in a neat, orderly manner </li></ul><ul><li>Have slightly larger right hemisphere & lower than normal activity in the left hemisphere </li></ul><ul><li>It appears late if the damage is done early because the damage is in areas that mature slowly producing minor symptoms in childhood, but impairments increase with maturation </li></ul>
  22. 22. Schizophrenia Hypotheses <ul><li>Dopamine Hypothesis </li></ul><ul><li>Schizophrenia is the result of excess activity at certain dopamine synapses </li></ul><ul><li>Evidence comes from drugs that relieve the symptoms work on dopamine </li></ul><ul><li>Chlorpromazine: Thorazine was the 1 st drug used successfully </li></ul><ul><li>Antipsychotic drugs: Block dopamine receptors </li></ul><ul><li>Phenothaizines: neuroleptic drugs including chlorpromazine </li></ul><ul><li>Butyrophenones: neuroleptic drugs including haloperidol (Haldol) </li></ul><ul><li>Substance-induced Psychotic Disorder </li></ul><ul><li>Characterized by hallucinations & delusions caused by drugs such as cocaine, amphetamine, MDMA & LSD that increase the activity of dopamine synapses </li></ul><ul><li>Stress increased the symptoms & causes release of dopamine from the prefrontal cortex </li></ul><ul><li>Excess dopamine is not the only cause </li></ul><ul><li>Drugs that block dopamine do so almost immediately but behavioral effects over 2 or 3 weeks </li></ul><ul><li>Recent studies show schizophrenics have2 X as many D 2 as normals </li></ul>
  23. 23. Schizophrenia Hypotheses <ul><li>Glutamate Hypothesis </li></ul><ul><li>Schizophrenia is the result of deficient activity at certain glutamate synapses </li></ul><ul><li>The brain releases lower than normal amounts of glutamate in the prefrontal cortex & hippocampus & has fewer glutamate receptors </li></ul><ul><li>Phencyclidine (PCP): blocks glutamate type NDMA receptors & produces a type of psychosis similar to schizophrenia </li></ul><ul><li>No drugs that treat schizophrenia directly stimulate glutamate activity </li></ul>
  24. 24. The Search for Improved Drugs <ul><li>The Mesolimbocortical System </li></ul><ul><li>A set of neurons that project from the midbrain tegmentum to the limbic system </li></ul><ul><li>Believed to be the area where antipsychotic drugs have beneficial effects </li></ul><ul><li>Tardive Dyskinesia </li></ul><ul><li>Characterized by tremors & other involuntary movements </li></ul><ul><li>Probably due to denervation sensitivity caused by prolonged blockade of dopamine receptors </li></ul><ul><li>Atypical Antipsychotic Drugs </li></ul><ul><li>New drugs that alleviate the symptoms of schizophrenia while seldom producing movement problems </li></ul><ul><li>They have less effect on D 2 & stronger effect on D 4 & serotonin 5-HT receptors </li></ul><ul><li>Alleviate both positive & negative symptoms of schizophrenia </li></ul><ul><li>The side effects include increased risk of diabetes & impairment of the immune system </li></ul>