exam 4 Flashcards
according to the DSM, what are the hallmark symptoms of schizophrenia?
positive symptoms (hallucinations, delusions)
negative symptoms (depression, reduced emotional expression)
cognitive impairment (changes in memory, attention, social perception)
compare and contrast delusions and hallucinations
delusion - a false belief that is strongly held in spite of contrary evidence
hallucination - a false perception of objects or events involving senses (smell, taste, sound, touch, sight)
what do family, twin, and adoption studies tell us about the heritability of schizophrenia
family studies - In general, risk tends to increase along with degree of relatedness
twin studies - Identical twins share identical genes; fraternal (dizygotic) have half of their genes in common
Often, diagnosed twin has developmental history of low birth weight, early life stressors, some neurological markers
adoption studies - Tend to confirm a strong genetic component, with birth parents of children with schizophrenia more likely to have had the disorder than adoptive parents
DISC1; paternal age; no one gene “determines” schizophrenia
DISC1 - a mutant, disabled version of a gene that is found in several members of one family diagnosed with schizophrenia
paternal age - a well known epigenetic factor involved; older men are more likely to have children with schizophrenia
no one gene - It is difficult to determine any one gene as most important to developing the disorder; the genes that influence schizophrenia are scattered across many chromosomes
integrative model of schizophrenia & stressors
An integrative model of schizophrenia emphasizes the interaction of genetic factors and stress
Stressors include: Prenatal stress, maternal stress
Transition from childhood to adulthood
Ex: City Living - possibly due to pollutants, exposure to other diseases, crowded conditions, tense social interactions
brain changes from schizophrenia
-Accelerated cortical thinning of gray matter
-Enlarged lateral ventricles
Also found in mice with DISC 1 mutation
-Differences in the structure and function of the corpus callosum
-Hypofrontality hypothesis: underactive frontal lobe
prevalence of schizophrenia & risk factors
-Schizophrenia affects approximately 24 million people or 1 in 300 people (0.32%) worldwide. This rate is 1 in 222 people (0.45%) among adults
-risk factors: both environmental and genetic influences
history of treatment approaches for schizophrenia
lobotomy - the surgical separation of the frontal lobes from the rest of the brain (made patients easier to handle but made them reliant on institutional care)
first generation antipsychotics - used in the 1950’s, neuroleptics (antipsychotic medications) revolutionized the treatment of schizophrenia; most blocked dopamine receptors (ex: chlorpromazine, haldol)
the dopamine hypothesis & the problem with it
-The dopamine hypothesis proposed that schizophrenia is caused by an excess of either dopamine release or dopamine receptors
-Problems with dopamine hypothesis:
Drugs block D2 receptors much faster than symptoms are reduced
Some other symptoms of schizophrenia respond to manipulations of other NT systems
Second generation antipsychotics (atypical antipsychotics) only moderately act upon D receptors but instead have the biggest impact blocking serotonin receptors (especially 5-HT2A)
the glutamate hypothesis & risk for seizures
-Observations of the effects of phencyclidine (PCP) and the ketamine prompted the hypothesis that schizophrenia is caused by an underactivity of glutamate receptors
-PCP is an NMDA receptor antagonist
-Prevents glutamate from acting normally
-Produces schizophrenia-like syndrome
-glutamate agonists are not a viable treatment due to increased risk for seizures
characteristics of depression
-Unhappy mood
-Loss of interests, reduced energy
-Changes in appetite and sleep patterns
-Difficulty in concentration
-Restless agitation or mental/motor inactivity
-Pessimism and thoughts of death
-Depression may last for several months
-Inheritance is a determinant in depression
brain changes from depression
-Brain changes with depression found from fMRI/PET studies
-Increased activation in:
Frontal lobes, during cognitive tasks
Amygdala, during emotional processing
Decreased blood flow to areas implicated in attention processes
Reduced hippocampal volume and activity during memory tasks
-Descendants of people with severe depression have a thinner cortex in the right hemisphere
treatment of depression - ECT and rTMS
ECT - Electroconvulsive shock therapy: a strong electrical current is passed through the brain, causing a seizure
rTMS - Repetitive transcranial magnetic stimulation: alters cortical electrical activity through magnetic stimulation
-both of these treatments alter cortical electrical activity
treatments for depression - medications (for monoamine levels)
MAO inhibitors - raise the level of monoamines at the synapse (first antidepressants developed)
tricyclics - 2nd generation of antidepressants which inhibit reuptake of monoamines which similarly boosts synaptic activity
both of these medications increase monoamine levels
treatments for depression - SSRIs & problems with them
selective serotonin reuptake inhibitors - block the reuptake of serotonin in the brain
problem - Long lag-time (often weeks) between treatment and reduction of symptoms, Not everyone responds to SSRIs, Some SSRI benefits are attributable to placebo effect
treatment for depression - CBT
cognitive behavioral therapy - can be as effective as SSRIs, and when used together are more effective than either alone
CBT aims to correct negative, self-defeating thinking and to improve interpersonal relationships
treatment for depression - DBS
deep brain stimulation (DBS) - through a surgically implanted electrode
gender differences in depression
-More females compared to males report suffering from major depression
-May reflect: Patterns of help seeking, Gender differences in endocrine physiology, related to the reproductive cycle, & Postpartum depression, which immediately precedes or follows childbirth
what is mania?
periods of expansive mood that include sustained overactivity, talkativeness, strange grandiosity, and increased energy
bipolar 1, bipolar 2, and cyclothymia
bipolar disorder is characterized by periods of depression alternating with periods of mania
-bipolar 1: experience more severe highs (mania) and may not have depressive episodes
-bipolar 2: experience a less severe high, their diagnosis includes depressive episodes
-cyclothymia: emotional ups and downs, but they’re not as extreme as those in bipolar I or II disorder
brain changes in bipolar disorder
not very well understood, changes are similar to those seen in schizophrenia
-enlarged ventricles and reduced gray matter
treatment for bipolar disorder - lithium
an effective treatment that has been reported to increase gray matter in patients’ brains, but its use must be carefully monitored for toxic side effects of overdose
-many patients also will stop taking lithium to experience the mania
treatment for bipolar -TMS
used for depressive swings, transcranial magnetic stimulation may provide a nonpharmacological treatment alternative in difficult cases of bipolar disorder
treatment for bipolar - CBT
evidence suggests that some forms of CBT for mild cases of bipolar disorder can be as effective as drug treatments and perhaps can be beneficially combined with other forms of treatment.
generalized anxiety disorder
persistent, excessive anxiety and worry
phobic disorders
intense irrational fears centric on an object, activity, or situation that a person avoids