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166 Cards in this Set

  • Front
  • Back
where in the brain is language primarily
left cerebral cortex
which hemisphere is capable of speech
left hemisphere
does right brain have some understanding of language
major language regions in the left brain
broca's area, motor cotex, angular gyrus, wernicke's area, auditory cortex
what is aphasia
loss of ability to produce and/or to comprehend language
what is wernicke's aphasia
fluent aphasia=patients easily generate words, but the statements have little meaning
what are paraphasic errors
when patients substitute incorrect sounds or words.
what is broca's aphasia
motor or nonfluent aphasia= patients have difficulty generating words
what is aggramatism
patients don't use function words (articles, pronouns, conjuctions)
what is the first stage of language processing
frequency and temporal analysis carried out bilaterally in auditory cortex followed by phonological processing (extracting phonemes)
two streams in language processing
1. ventral stream
2. dorsal stream
ventral stream
maps sensory information onto "lexical conceptual representations"
dorsal stream
maps sensory information onto "articulatory motor representations"
what is one problem associated with learning to speak a language
spoken language doesn't reliably indicate breaks between words with a pause
which properties of syllables do humans identify and use
statistical properties
what is attention
a neural process by which you enhance your perception of certain stimuli relative to other stimuli in the environment
what is bottom-up attention
when the object “grabs” your attention without conscious knowledge of the stimulus. The stimulus is more salient than the background.
what is top-down attention
you consciously look for a specific object
steps in change blindness
1. visual transients produced by changes in color, shape,orientation that draw your attention to the location of the change
2. visual memory of what was at the site of the change so that you can identify what changed
what does attention enhance
detection of stimuli at site of attention
what does attention reduce
detection of stimuli away from site of attention
what might the parietal lobe be involved in
disengaging visual attention
4 steps of shifting attention
1. disengage from present location
2. move your attention to the new location
3. engage your attention at the new location
4. inhibit the previous site of attention
neglect syndrome
damage to the right parietal lobe disrupts visual attention to the left side of the visual space
what does the parietal lobe participate in
visual attention, in particular shifting visual attention
Darwin's analysis regarding emotion
1. cross-species similarities in the expression of emotion
2. there were a limited set of fundamental emotions
james lange's theory of emotion
ANS changes precede and produce emotions. We experience emotion as a consequence of autonomic activity
cannon-bard theory of emotion
the stimulus activates the thalamus which distributed the inputs to the cortex to create emotion and autonomic changes simultaneously. the autonomic changes are independent of emotion.
problems with james-lange theory
-emotions can be experienced even if no sense of physiological response is present
-fearful & angry states have similar autonomic responses, how do different emotions arise from similar physiological states?
problems with canon-bard theory
-emotions are less intense with the brain disconnected from the viscera
-artificial manipulations of autonomic activity can induce emotions
zajonc theory of emotion and facial efference
changes in venous blood flow created by patterns of facial muscle contractions produces small changes in brain temperature that alters mood
describe the two stream circuit of emotion starting with the "thought stream" thalamus
->sensory cortex ->cingulate gyrus produced perception, thought, and memory
describe the two stream circuit of emotion starting with the "feeling stream" thalamus
->mammillary bodies (hypothalamus)-> anterior thalamus -> cingulate cortex evoked the body's physiological response.
what do emotions result from
cingulate cortex activity
what can emotions be evoked from
sensory stimuli (thought stream) or physiological responses (feeling stream)
what neural system did MacLean outline
the limbic system= emotion arises by integrating external sensations with information from the body.
what parts of brain play important roles in emotion
-ventromedial prefrontal cortex/orbital frontal
-anterior cingulate cortex
-nucleus acumbens
-vental pallidum (basal ganglia)
-hypothalamus/basal forebrain
what did Domasio and colleagues hypothesize
that PFC creates "somatic markers" that link ANS activity to emotionally significant previous events, the somatic marker hypothesis
what cant PFC lesion patients do
identify long-term negative or positive consequences
effect of frontal lobotomies
disconnect the frontal and cingulate cortex in individuals with severe psychosis, blocking "too much" emotion
"almond shaped" nucleus in the anterior end of the temporal lobe with several subdivisions- involved in fear
evidence required to show that amygdala is involved in fear conditioning
1. lesion of the amygdala b4 learning should prevent acquisition of fear conditioning
2. blocking cellular changes in the amygdala necessary to convert short-term to a long term memories should prevent long-term conditioned fear
3. the amygdala should alter its activity with fear conditioning
does memory for emotional stimuli differ between sexes
explain women's superior memory for emotional pictures
better integration of brain processes associated with emotional experience into memory
what is the insula
neural center for disgust
what receives emotional info for further evaluation
1. rostral anterior cingulate cortex
2. dorsal anterior cingulate cortex
3. dorsomedial prefrontal cortex
4. ventromedial prefrontal cortex
what do raCC and vmPFC do
-gate info flow into conscious awareness
-provide excitatory and inhibitory feedback to core limbic structures
what is arousal a measure of
excitement level
what is valence a measure of
part of brain associated with positive arousal
nucleus accumbens
part of brain associated with negative arousal
where does nucleus accumbens receive dopamine input from
ventral tegmental area (VTA)
in who does activation of nucleus accumbens occur
ppl who report experiencing pleasure
what do humorous stimuli inc
blood flow in many brain regions including nucleus accumbens
what does amphetamine cause
release of dopamine from dopamine terminals
what is nucleus accumbens
rostral striatum region in humans where the caudate and putamen and not divided by the internal capsule
how much do the primary sensory and primary motor area account for
20% of the neocortex
association cortex
remaining 80% of neocortex which is involved in further perceptual processing of sensory info, in motor planning, and in cognition
collective term for the complex functions of the brain having to do with language, thought, and the construction perceptions
what does the neurochemical basis of mental illness typically involve
norepinephrine, dopamine, serotonin
cartesian dualism
body and mind were considered separate entities- disorders of the body has a physical cause and were province of medicine but disorders of the mind had a spiritual or moral basis and were the province of religion
Freud's influence on mental illness views
mental illness arose from conflict between conscious and unconscious aspects of the psyche (mind)
Freud's treatment for mental illness
helping patients uncover incidents, usually from childhood that were suppressed from consciousness and hidden in the unconscious mind.
how did psychopharmacology treatment of mental illness start
with the chance discovery of antipsychotic action of chloropromazine (1952)
what does biological psychiatry attempt to do
establish the underlying neurochemical basis for mental illness
anxiety disorders
inappropriate expression of fear that is disabling
threatening stimulus
what is the stress response characterized by
-avoidance behaviors
-elevated arousal and vigilance
-activation of sympathetic division of the ANS
-release of cortisol (a glucocorticoid hormone) from the adrenal glands
normal response to stress
hypothalamic-pituitary-adrenal (HPA) axis:
-release of cortisol from adrenal glands is triggered by ACTH
-ACTH is released by the anterior pituitary gland under control of parvocellular neurosecretory neurons located in the paraventricular nucleus of the hypothalamus
-parvocellular hypothalamic neurons release CRH into the blood of the portal circulation
what causes CRH (corticotropin releasing hormone) release
neocortex & thalamus send sensory info that increases activity in the amygdala, which in turn activates the hypothalamus and stimulates CRH release
where has inappropriate activation of the amygdala by non-threatening stimuli been implicated
anxiety disorders
effect of cortisol binding to glucocorticoid receptors on hippocampal neurons
enhances their activity, inhibits CRH release from hypothalamic neurosecretory neurons. (hypothalamus provides neg feedback regulation of HPA)
effect of continuous exposure of hippocampus to cortisol during chronic stress
-reduces the number of dendrites of hippocampal neurons
-neuronal death in hippocampus
-loss of inhibitory control of HPA axis by the hippocampus, inducing a vicious cycle of runaway activation
what have anxiety disorders been linked to
-hyperactivity of the amygdala
-reduced activity in the hippocampus
describe the regulation of HPA axis by the hippocampus
prolonged elevation of cortisol -> loss of neurons in the hippocampus -> dec. inhibition of HPA axis by the hippocampus
-> enhanced release of cortisol from adrenal glands ->cycle restarts
treatments for anxiety disorders
-anxiolytic drugs
psychotherapy mechanism
may use the ability of the brain to alter synaptic efficacy based on experience to reduce the ability of non-threatening stimuli to activate the stress response
anxiolytic drugs
-selective serotonin reuptake inhibitors
-serotonin norepinephrine reuptake inhibitors
benzodiazepine action
bind to GABA_A receptors and make them more responsive to GABA.
(presumably they act to suppress activity of stress circuits)
ethanol affect on GABA
facilitates GABA actions
where are neurons that release serotonin found, where do they project to
in the raphe nuclei of the brain stem and project diffusely through the brain and spinal cord
how does serotonin act
via G-protein coupled receptors to modulate neuronal activity in many brain regions
what is serotonin's action terminated by
reuptake via serotonin transporters
what is SSRIs therapeutic effect caused by
some unknown adaptive changes in the brain to chronically elevated external serotonin
one adaptive effect of SSRIs
increase the number of glucocorticoid receptors in the hippocampus- this might enhance the feedback inhibition of the HPA axis by the hippocampus
diffuse modulatory system that targets many brain regions
where are the neurons that release norepinephrine found
in the locus coeruleus in the brain stem
what is norepinephrine's action terminated by
reuptake via norepinephrine transporters
effect of SNRIs
inhibit both serotonin and norepinephrine transporters, prolonging the action of both neurotransmitters
affective disorders
disorders of emotional state or mood (affect)
major depression
severe depression lasting >2 weeks, often without obvious external cause and often accompanied by the feeling of losing control of one's emotional state
major depression symptoms
-lowered mood & dec interest
-loss of appetite
-feelings of worthlessness & guilt
-diminished concentration
-recurrent thoughts of death
milder form of depression but is chronic
what is bipolar disorder characterized by
repeated bouts of mania or hypomania, sometimes alternating with depression
manic phase
-abnormally elevated, expansive, or irritable mood (DIGFAST)
Flight of ideas
Activity increase
Sleep deficit
similar to mania but doesn't severely impair social interactions or work performance (in fact creativity & performance can be greatly enhanced)
monoamine hypothesis
depression and mania are disruptions of one or both of these diffuse modulatory systems (catecholamine & serotonin)
clues that led to monoamine hypothesis
1. treatment of high bp with reserpine, which blocks loading of serotonin & catecholamines into synaptic vesicles, caused depression in 30% of patients
2. a drug for treating tuberculosis that inhibited MAO (enzyme that degrades catecholamines & serotonin) produced mood elevation
3. the antidepressant drug, imipramine, was found to block the reuptake of serotonin and norepinephrine
what is the diathesis-stress hypothesis of affective disorders
predisposing factors interact with stress to produce depression
evidence supporting diathesis-stress hypothesis
-anxiety & depression coexist in patients, and anxiety is related to HPA axis
-in depression, pituitary & adrenal gland are enlarged
-in depression, # CRH neurons in hypothalamus and expression of CRH inc.
-blood cortisol & CRH concentration in CSF are elevated in depressed patients
-elevated CRH is reduced by treatments that alleviate depression
-delivery of CRH to the brain in animals produces behavioral effects similar to depression in humans
-rats that receive lots of maternal care as pups have inc glucocorticoid receptors in hippocampus, reduced reduced CRH in hypothalamus, less anxiety
-inc in glucocorticoid receptors in hippocampus is mediated by serotonin release
-effect of experience on adult anxiety is restricted to postnatal critical period
-in humans, childhood abuse & neglect increase risk for developing affective & anxiety disorders
-dec. feedback inhibition of HPA axis may make brain more susceptible to depression & anxiety
treatments for affective disorders
-electroconvulsive therapy
-tricyclic antidepressant drugs (block reuptake of NE & serotonin)
-selective serotonin reuptake inhibitors
-MAO inhibitors (block enzyme degradation of serotonin & norepinephrine)
-lithium (treats bipolar disorder)
loss of contact with reality
disruption of perception, thought, mood, movement, and loss of contact with reality
percent of population schizophrenia affects
1% of population
what are positive symptoms
occurence of abnormal thoughts and behaviors
examples of positive symptoms of schizophrenia
delusions, hallucinations, disorganized speech, catatonic behavior
what are negative symptoms
absence of normal responses
examples of negative symptoms of schizophrenia
reduced expression of emotion, poverty of speech, difficulty initiating goal-directed behavior, memory impairment
describe familial nature of schizophrenia
variations in a number of genes have been linked to increased susceptibility to schizophrenia
can genetic background enhance vulernability to developmental/enrionmental factors that lead to schizo?
gross changes in schizophrenic brains
1. ventricles are enlarged in the brain of schizo identical twin-> consistent with a loss of brain tissue in schizo
2. reduced metabolic activity in frontal lobes of schizo. patient-> consistent with reduced activity or loss of neurons in the frontal lobes of schizo.
what do amphetamine addicts sometimes experience
amphetamine psychosis, with symptoms similar to schizo.
what does amphetamine cause
massive dopamine release
what are drugs that improve positive symptoms of schizo. called?
neuroleptic drugs-> blockers of dopamine D2 receptors
what might be involved in schizo.?
dopamine projections from VTA to the frontal lobes
effect of "typical" neuroleptics targeting D2 receptors in the striatum and the cortex
common motor problems (extrapyramidal symptoms) in patients taking these neuroleptic drugs->distinct gait that resembles Parkinson's
what is dyskinesia
another common side effect of neuroleptic drugs
what naturally occurring compounds alter perception & cognition, and can induce hallucinations
-psilocybin, found in psilocybin mushrooms
-mescaline, in peyote cactus
what does the similarity of hallucinogens and serotonin suggest
that the diffuse serotonin neuromodulatory system might be involved in some of the symptoms of schizophrenia
what have "Atypical" neuroleptics been found to be more potent blockers of
serotonin receptors
what symptoms do atypical neuroleptics reduce
negative symptoms
what do atypical neuroleptics affect
other neurotransmitter systems like norepinephrine, histamine, and ACh
what is phencylidine
non-competitive antagonist of NMDA receptors, and it blocks by occupying a site within the open pore
what other NMDA receptor blockers that occupy same site on open pore as phencylidine
ketamine and MK-801
what do NMDA hypomorphs exhibit
schizophrenia-like symptoms, such as repetitive movements and altered social interactions
glutamate hypothesis of schizophrenia
reduced NMDA receptor activity plays a role in schizophrenia
what are deficits in cognition caused by brain damage
global cognitive loss
alzheimer's disease
what does damage in perisylvian fissure in dominant hemisphere lead to
severe aphasias
right hemisphere damage
subtle deficits of language, humor or irony
inability to identify objects based on sensory info, even though the primary sensory cortical areas are intact
what do specific types of agnosia typically result from
lesions in parietal or temporal lobe, in areas near the primary sensory cortex for the major sense
what is tactile agnosia where patient has normal sense of touch in hands but cant identify object in hands
what's alexia
-visual agnosia, which results from lesions of angular gyrus
-patients can can't recognize written words
visual agnosia where patients are unable to recognize familiar faces
difficulty in programming complex series of movements, without paralysis, sensory deficits, or problems performing simple tasks
where are lesions responsible for apraxia
in parietal and temporal areas
different forms of apraxia
-ideational apraxia
-ideomotor apraxia
-limb-kinetic apraxia
-orofacial apraxia
-verbal or speech apraxia
what do lesions in supramarginal gyrus produce
conduction aphasia and a form of apraxia in which patients cant follow verbal commands to carry out motor actions (similar to ideomotor apraxia)
loss of cognitive abilities
alzheimers disease
most prevalent form of serious age-related dementia, produced by progressive death of neurons in a wide variety of brain regions including neocortex
gross brain changes in alzheimers brain
-shrinkage of gyri
-sulci expanded
-cortex shrinks
-no hippocampus
what do PET scans of alzheimers patients show
severely depressed metabolic activity cuz of no neurons
why do neurons die in alzheimers disease
two types of abnormal structures accumulate in areas where neurons are dying: neuritic plaques and neurofibrillary tangles
what are neuritic plaques
extracellular accumulations of protein, consisting largely of beta-amyloid protein (A-beta)
what are neurofibrillary tangles
abnormal intracellular aggregates of a microtubule-associated protein called tau
what is tau
normal component of microtubules that helps stabilize the polymers of tubulin molecules
what does dephosphorylated tau do
binds to tubulin and stabilizes microtubules
what does phosphorylated tau do
dissociates from tubulin, destabilizing microtubules
what molecule myperphosphorylates tau in alzheimers disease
cyclin-dependent kinase 5 (cdk5)
what occurs as a result of hyperphosphorylated tau
chronic disruption of microtubules, which may kill neurons
how is A-beta produced
selective proteolytic of a protein called amyloid precursor protein (APP) which is a normal component of neuronal membranes
what is A-beta like normally
soluble, and doesnt accumulate in the extracellular space of the brain. it is cleared into CSF
A-beta in alzheimers disease
insoluble, accumulate into plaques
what are secretases
proteases that release A-beta
what does beta-secretase do
cuts off most of the extracellular part of APP
what does gamma-secretase do
cuts within the membrane to release A-beta
two forms of A-beta produced, which is more toxic and why
40 amino acids or 42 amino acids, the latter is toxic because its more hydrophobic
what has been shown to produce familial alzheimers disease (early onset that progresses rapidly)
variety of mutations in APP
where are mutations for alzheimers
-within A-beta portion of APP or at other sites that inc production of A-beta
-mutations in presenilin, component of gamma-secretase complex responsible for cleavage of A-gamma
when is synthetic Alpha-beta toxic
when applied to cortical and hippocampal neurons in culture or in vivo
why is A-beta toxic
-decreased spontaneous action potential activity
inflammation of A-beta
local inflammation which may damage surrounding neurons
excitotoxicity of A-beta
neuronal death induced exogenous A-beta can be lessened by NMDA receptor blockers. thus, A-beta may cause depolarization which allows Ca in through NMDA receptors
synaptotoxicity of A-beta
exogenous A-beta causes reduced numbers of dendritic spines in hippocampal neurons and loss of excitatory synapses
treatments of alzheimer's disease
-anti inflammatory drugs
-reducing production of beta and gamma-secretase inhibitors; promoting alpha-secretase
-reducing oligomerization of A-beta (prevents formation of dimers)
-up-regulate enzymes that degrade extracellular A-beta
-neuroprotective compounds; try to prevent neuronal death causes by excitotoxicity or prevent loss of synapses