Behavioral Exam 4

anskorczewski12's version from 2016-05-12 03:21

Sleep (chap 9)

Question Answer
ways to measure sleep1.subjective measurement (asking about sleep) 2. objective (polysomnography or actigraphy)
polysomnographymany sleep measurements: EEG, EKG, respirations, EMG (muscle activity), Temperature
actigraphywearing a watch-like movement measuring device
sleep stages1,2,3,4,3,2,REM (90 minute cycle)
pre-sleepbeta waves (awake aroused) and alpha waves (brain slowing/awake relaxed)
stage 1 sleeptransition between sleep and wake, start of theta waves, 5-10 minutes (hypnic jerk or hypnogogic hallucinations)
stage 2 sleep(shallow sleep) theta waves more regular, clearly asleep, sleep spindles (momentary strong brain activity), K complexes (brain slows way down momentarily), about 20 minutes
stage 3 sleep(transition between shallow and deep), theta and delta waves, 5-10 minutes
stage 4 sleep(deep sleep), delta waves, about 30 minutes, difficult to wake (bed wetting, sleep walking/talking)
REM sleep(paradoxical sleep, brain waves similar to wakefulness, dreaming), eyes move, skeletal muscles paralyzed, sexual arousal
insomniadifficulty initiating/maintaining sleep (most prevalent)
sleep apneastopped breathing during sleep (either obstructive or central)
narcolepsyoverpowering urge to fall asleep/misfired REM sleep (right into REM, sleep attacks, cataplexy-total body paralysis when awake, sleep paralysis-paralysis when waking up, hypnogogic hallucination-dreaming while 1/2 awake)
REM disordersnightmare disorder (repetitive nightmares), REM behavior disorder (similar to sleep walking, except acting out dream)
stage 4 sleep concernssleepwalking (somnambulism), sleeptalking (somniloquy), enurisis (bed wetting), night terrors
rebound phenomenawe make up REM (go to REM faster when we are deprived)
why sleeprest and recovery, development, memory consolidation (declarative requires slow waves, nondeclarative requires REM)
arousal system1.acetylcholine (cortical activation, more active, from pons and basal forebrain) 2.norepinephrine (vigilance, from locus coeruleus) 3.serotonin (species specific behavior, raphe nuclei) 4.histamine (wafefulness, from tuberomamillary) 5.orexin (control hormones, from lateral hypothalamus)
orexin impacted byhunger (more hungry means more tired) safety (less safe means less tired) biological clock (circadian rhythms) homeostasis (high energy expenditure means need to sleep), allostatic/emotions (large emotions make us tired)
sleep promoting system1.ventrolateral preoptic area controls GABA 2.adenosine released by glial cells when low nutrients (promotes sleep)
REM controlsublaterodorsal nucleus (pons-turns on and to paralyze muscles), ventrolateral periaquaductal gray matter (turns it off)
circadian rhythmslight acts as zeitgeber (time keeper), 25 hour cycle, ticking involves protein production and breakdown, controlled by suprachiasmatic nucleus (of hypothalamus)
circadian rhythm mechanismsuprachiasmatic nucleus (of hypothalamus) gets direct input from eye and sends signal to pineal gland to either secrete/stop secreting melatonin (promotes sleep)
circadian rhythm issuesadvanced/delayed sleep phase syndrome, jet lag, shift work

Neurological Disorders (chap 15)

Question Answer
tumormass of cells with no function and uncontrolled growth
types of tumorsmalignant (not encapsulated, may metastasize, cancer), benign (encapsulated); 1.glioma (tumors of glial cells) 2.meningioma (tumors of the meninges)
tumor dangers1.compression (either direct or indirect-tumor blocked blood flow) 2.infiltration (specific to malignant tumor-wraps/moves into healthy tissue)
treatments for tumorstumorectomy, radiation, chemotherapy (targets cell proliferation)
seizurea period of sudden, excessive activity of cerebral neurons
causes of seizuresinjury, tumor, drugs, fever, genetic conditions (scarring in brain, withdrawal from alcohol, epilepsy)
types of seizures1.partial (common-remain localized around a focus area such as motor, sensory, autonomic, or psychic) 2.generalized (involves most of the brain)
subtypes of partial seizuresimple (no change in consciousness) complex (lose/change in consciousness)
subtypes of generalized seizurestonic clonic (convulsions/pass out of floor), absence (starring spells, lose awareness of surroundings), atonic (go completely limp)
status epilipticusseizures that don't stop, keep happening rapidly and before you can recover
aurassensory experiences before seizures
treatments for seizuresanticonvulsant medications, surgery
types of cerebrovascular accidentshemorrhagic stroke (bleeding into brain) or ischemic stroke (blockage; either thrombus-blood clot that creates blockage or embolus-bit of blockage breaks off and clogs elsewhere)
ischemic stoke mechanismcell excites itself to death (in absence of oxygen and glucose), not starved
cerebrovascular accident treatments/preventionsurgery to stop hemorrhagic bleeding, anticoagulant meds (tPA) to break up clots in ischemic; prevent by breaking up atherosclerotic plaque (with surgery or stents)
recovery of strokesrelearning fxn or adaptation, stimulate sensory/motor neurons, mirror neurons
Traumatic brain injuryeither open head (meninges penetrated) or closed head
coup and countercoupinitial blow and when brain bounces and hits again
diffuse axonal injuryaxons rip away from cell bodies (happens in shaken baby syndrome) -tramatic brain injury
locked in syndromemotor cortex is damaged beyond point of ability to interact with you (eyes usually still work, could still be able to think); may come from traumatic brain injury

(chap. 15) More disorders

Question Answer
teratogenstoxins introduced prenatally that cross through the placenta and impact child development
alcoholcommon teratogen that interferes with neural adhesion proteins, causes cognitive problems, alters neuronal progenitor and stem cells, interferes with LTP (fetal alcohol syndrome)
Inherited Metabolic Disordersmissing enzymes to breakdown critical proteins, so they build up (all genetically based) Phenylketonuria (PKU), phyridoxine dependency, galactosemia, maple syrup urine disease
PKU (phenylketonuria)missing enzyme that converts the phenylalanine to tyrosine (build of leads to cognitive impairment)
Down Syndrometrisomy 21 (have 2 21st chromosomes on ova-3 overall), mild-moderate mental retardation (language skills develop late), physical malformations, brain degenerates in adulthood
transmissible spongiform encephalopathies(degenerative disorder) contagious brain disease that leaves the brain with a spongelike appearance (holes), caused by accumulation of misfolded proteins leading to cellular apoptosis (ex- Mad Cow disease, Creutzfeldt-Jakob disease, Kuru)
Alzheimer's diseasedegenerative brain disorder of unknown origin (progressive memory loss -usually of most recent memories, motor deficits- slowed and slight tremor, eventual death), amyloid plaques, or neurofibrillary tangle
amyloid plaquesextracellular deposit containing protein, degenerating axons/dendrites, microglia, and astrocytes (take place of dead cells)
neurofibrillary tangledying neuron containing intracellular accumulations of filaments that formerly served as the cell's internal skeleton (skeleton gets in way of normal cell processing)
Alzheimer's disease degenerateshippocampus, entorhinal cortex (olfactory/some memory), association cortex (frontal/temporal), locus coeruleus, raphe nuclei (norepinephrine and serotonin system)
alzheimers treatmentsmedications- acetylcholinesterase inhibitors (stops breakdown of ACh, keeps brain active), NMDA antagonist/glutamate antagonist (slows down LTP process, may stop degeneration)
Parkinson's diseasedisruption of dopamine basal ganglia (and information from substantia nigra); muscular rigidity, slow movements, resting tremor, postural instability
Huntington's diseasedegeneration of neurons in caudate nucleus and putamen of basal ganglia; uncontrollable jerking movements, writhing movements, dementia, fatal (very generic)
Amyotrophic lateral sclerosis (ALS)attacks spinal cord and cranial nerve motor neurons; spasticity/exaggerated stretch reflexes, progressive weakness and atrophy, paralysis, death, preserved eye movements and cognitive functioning
multiple sclerosisan autoimmune demyelinating disease, immune system attacks myelin sheaths in CNS leaving behind sclerotic plaques, transmission is interrupted, impact depends on brain area (remitting-relapsing vs. progressive)
encephalitisinflammation of the brain (bacterial, viral, parasitic)
meningitisinflammation of the meninges (bacterial-severe, viral)

Schizophrenia, Affect, Anxiety (chap. 15)

Question Answer
Schizophrenia symptomspositive (hallucinations, delusions), negative (anhedonia, avolition, alogia, affective flattening, social withdrawal), cognitive (disorganization, attention difficulties, physchomotor slowing)
hallucinations vs. delusionssensory experience in absence of stimuli vs. beliefs with no basis in reality
anhedonialoss of pleasure in things you used to like
avolitionlack of desire/motivation
alogialack of expressive communication
course of Schizophreniapremorbid (not specific symptoms, before onset), prodromal (1-2 years, beginning of onset), active (full symptoms)
neurology of positive symptomsdopamine hypothesis (excess dopamine)-dopamine antagonists reduce pos. symptoms, and agonists produce in normal people; visual hallucinations (from visual association cortex), auditory hallucinations (from auditory association cortex and broca's area)
neurology of neg/cognitive symptomsenlarged lateral ventricles, decreased gray matter, pre-frontal hypoactivity( (dorsalateral prefrontal cortex problems, so bad at inhibiting and zoning out excess info)
diathesis stressneed interaction between genetic vulnerability and environmental stress
schizophrenia risk factorspolygenic susceptibility (diathesis stress), prenatal (teratogens, winter/spring births, malnutrition, abnormal fetal development), perinatal (labor-related complications), advanced paternal age, urban setting, childhood malnutrition
schizophrenia medsfirst generation antipsychotics like thorazine and haldol (pretty effective for positive symptoms, motor-related side effects from dopamine being blocked), atypical antipsychotics like risperdol, olanzopine, abilify is dopamine modulator(some side effects)
major depressive disorderhas episodes of depressive symptoms (sad mood, anhedonia, lack of energy, feeling worthless)
bipolar disorderrequires a manic episode, may also have depressive episodes
neurology of depressionmonoamine hypothesis (low levels of monamines-serotonin agonists decrease symptoms and opposite), prefrontal cortex (decreased activity, slow psychomotor), subgenual ACC (increased), neurogenesis (decreased in hippocampus)
depression risk factors(polygenic and diathesis stress), increased REM, winter/spring birth, limited sunlight (seasonal affective disorder)
affective disorders treatmentsmeds for depression increase serotonin (monoamine oxidase inhibitors, tricyclics, SSRI and SNRI-reuptake inhibitors), meds for bipolar (lithium-unknown mechanism); ECT (shock), deep brain stimulation, transcranial magnetic stimulation, sleep deprivation (REM and slow wave deprivation or total deprivation), phototherapy (increase light exposure)
anxietyapprehension regarding a future outcome
fearreaction to an immediate threat/fight or flight response
anxiety disordersspecific phobia (irrational fear plus impairment), panic disorder (out of the blue fear reaction), social anxiety disorder (fear of judgment), generalized anxiety disorder(uncontrolled worry) (also kind of obsessive/compulsive spectrum)
neurology of anxiety disordersamygdala (increased activity), pre-frontal cortex (decreased-not keeping amygdala from going too much), cingulate cortex (decreased/emotion center), insular cortex (increased, disgust reaction, specific for blood/injection phobia)
risk of anxiety disorderspolygenic (except GAD not heritable), conditioned emotional response (with objects, judgment situations, interoceptive cues, not worry)
anxiety disorder treatmentsbenzodiazapines, SSRIs (antidepressants), D-cycloserine and exposure (exposure to fear plus these intensify learning in vmPFC for faster extinction)
Obsessive-compulsive disorderhave thoughts you can't stop thinking/distressing, and behaviors to neutralize the thought (polygenic)
OCD neurologybasal ganglia (increased, motor compulsions), prefrontal cortex (increased, rule based obsession), insular cortex (increased, disgust)
OCD treatmentscingulotomy (removal of some of cingulate gyrus to decrease obsessions), deep brain stimulation (some success), SSRIs and tricyclic antidepressants, benzodiazepines (help in midst of panic, don't treat)
Other OC Spectrum DisordersTrichotillomania (pull out hair), excoriation (skin picking), body dysmorphic disorder (fascination with a defect of body), (also nail biting and tic disorder)

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