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179 Cards in this Set
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what is the input, output, and function of the basolateral nuclear complex of the amygdala?
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input: high order association sensory cortex
output: association cortex, central neurons of amygdala function: modifies sensory input (especially if an input is unpleasant) |
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what is the input, output, and function of the corticomedial nuclear complex of the amygdala/
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input: olfactory
output: hypothalamus and brainstem via stria terminalis function: modifying olfactory stimuli? |
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what is the input, output, and function of the central nuclear complex of the amygdala?
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input: basal amygdala
output: brainstem CPGs and autonomics function: affect whole body reaction to unpleasant stimuli |
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what is the specific histological characteristic of sensory cortex?
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is has granular layers
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how is limbic cortex histologically unique?
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it is agranular
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what constitutes the limbic striatum?
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the ventral caudate and nucleus accumbens
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what are the 4 biogenic amines?
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serotonin, dopamine, histamine, norepinephrine
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what brain nuclei produce serotonin?
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raphe nuclei
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what brain nuclei produce norepinephrine
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locus ceruleus
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what is the precursor for serotonin?
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tryptophan
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what is the precursor for norepinephrine?
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tyrosine
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what is the precursor for dopamine
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tyrosine
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what is the precursor for histamine
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histadine
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what is another name for serotonin?
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5-hydroxytryptamine (5-HT)
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serotonin has output to what structures?
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cortex, amygdala, hippocampus, striatum, thalamus, and hypothalamus
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what drug increases serotonin levels and how does it do it?
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MAO inhibitors
MAO breaks serotonin down to 5-HIAA |
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what types of receptors are 5-HT receptors?
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serotonin receptors that are GPCRs
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what is the one 5-HT receptor that is not a GPCR and what is its significance?
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5-HT3 is a ligand gated cation channel
blocking the 5-HT3 stops nausea during chemo |
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what kind of diet can predispose a person towards depression?
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tryptophan depleted diet
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how do Prozac, zoloft, and paxil work?
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they inhibit SERT (SErotonin Reuptake Tranpsorter)
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how do SSRI's work and how long do they need to be taken before effects are seen?
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fx unknown
need to be taken for 2 weeks |
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what is serotonin syndrome?
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hyperserotonergic state
COGNITIVE confusion, mania, agitation, headache AUTONOMIC: fever, HTN, tachycardia, diarrhea SOMATIC: myoclonus (twitching), hyperreflexia, tremor, insomnia |
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what is the function of the locus ceruleus?
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default: little/no activity
attention to stimuli: moderate activity dangerous intense stimuli: lots of output, activates SNA |
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what structures receive NE input from locus ceruleus?
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cortex, amygdala, hippocampus, striatum, thalamus, hypothalamus
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what is a way to release NE besides locus ceruleus?
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hypothalamus-pituitary-adrenal axis
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what is the rate limiting enzyme in making NE from tyrosine?
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tyrosine hdroxylase
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what is the sequence of synthesis of tyrosine to biogenic amines?
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tyrosine
L-DOPA dopamine NE E |
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what is the effect of taking alpha1 antagonists (prazosin)
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lowers BP
decreases PTSD |
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what is the effect of taking alpha2 agonists (clonidine)
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feedback suppression of NE release
lowers BP ADHD trx |
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what is the effect of taking beta1/2 antagonists (propanalol)
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reduces tremor, agitation, aggression
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what is the mechanisms of action of tricyclic antidepressants and ritalin
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inhibits norepinephrine reuptake transporter (NET)
increases attention |
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what what MAO break down?
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serotonin and NE
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what two enzymes break down NE
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MAO and COMT
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what does COMT break down
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NE and dopamine
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what is tardive dyskinesia
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movement abnormalities due to antipsychotic meds decreasing dopamine
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what is the function of the nucleus accumbens and which biogenic amine affects it?
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pleasure and addiction
dopamine mediates these effects |
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what two structures produce dopamine
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ventral tegmental area of the midbrain and substantia nigra
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what is the mesolimbic pathway?
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dopamine from ventral tegmental area of midbrain to nucleus accumbens and amygdala (pleasure and addiction)
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what is the mesocortical pathway?
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dopamine from ventral tegmental area to prefrontal and cingulate cortices (
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what are the two pathways responsible for positive and negative symptoms of schizophrenia?
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POSITIVE symptoms: mesolimbic pathway (pleasure and addiction)
NEGATIVE symptoms: mesocortical pathway (avolition, apathy, flat affect) |
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what is the function and biogenic amine of the tuberoinfundibular pathway?
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arcuate nucleus to medial eminence of pituitary
stimulates prolactin secretion |
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antipsychotic medications are...
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D2 receptor antagonists
the stronger the receptor antagonist the better the drug |
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Dopamine receptors are...
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GPCRs
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what is the effect and action of clozapine?
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D3 and D4 antagonist
also 5-HT2 antagonist antipsychotic |
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how do cocaine and amphetamines cause paranoia and delusions
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they inhibit dopamine reuptake transporter (DAT)
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dopamine increases/decreases are psychotogenic
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increase: psychotogenic
decrease: antipsychotic |
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what are the two types of explicit (declarative) memory?
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semantic (facts)
episodic |
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what is the difference between anterograde and retrograde memory loss?
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anterograde: can't remember episodes after the injury
retrograde: can't remember events before the injury |
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what is the target and symptoms of herpes simplex encephalitis?
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it targets medial temporal lobe and causes severe anterograde amnesia
graded retrograde amnesia |
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what structures are targeted by herpes simplex encephalitis and what are the symptoms?
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medial temporal lobe
sx: complete anterograde mem loss graded retrograde mem loss procedural memory intact! |
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what is the consequence of a anterior thalamic nucleus lesion?
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moderate anterograde mem loss (papez circuit)
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what is the consequence of basal forebrain lesions?
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basal forebrain amnesia
moderate anterograde memory loss (can't remember if something happened yesterday or a year ago) |
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what is almost always the cause of graded retrograde amnesia?
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hippocampal lesions
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hippocampal lesions affect what part of memory?
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complete anterograde
graded retrograde very distant memory INTACT hippocampus has no role in very distant memory |
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what type of lesions are associated with semantic memory deficits?
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lateral temporal lobe (or whole temporal lobe)
parts of occipital and parietal lobes these are polymodal association cortices |
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what is perceptual priming?
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increased ability to perceive stimuli based on recent exposure to similar objects
how a sailor can see a gust of wind coming |
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what are the 3 important things to know if a patient has memory loss?
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1. cognitive context: are there cognitive deficits as well?
2. content or domain: what is being forgotten? 3. onset and course: sudden? gradual? resolving? progressing? |
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visual memory loss can be caused by what type of lesion?
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lesion to Right temporal lobe
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what are the symptoms and lesion of a person in Frontal dysexecutive amnesia?
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lesion in frontal lobe (hippocampus fine)
fails to ENGAGE the memory forgets to turn off the car "forgets to remember" |
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what is the cause of "acute amnesic syndrome"?
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hippocampus is vulnerable to hypoxia
post MI or CO poisoning |
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what are the symptoms of transient global amnesia?
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complete anterograde and retrograde amnesia lasting less than 24 hours
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what would you see on the EEG of an epileptic patient between seizures?
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huge focal INTERICTAL spikes that are controlled (pt doesn't realize)
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what are the two hypotheses for epilepsy pathophys?
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hippocampus: loss of inhibitory basket cells
mossy fiber sprouting: increase in positive feedback |
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what is the cause and symptoms of an absence seizure?
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hyperexcitability in thalamocortico loop
slow wave unconsciousness no postictal symptoms no convulsions |
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what is the pathophysiology of absence seizures?
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hyperexcitability in the loop between cortex and thalamic relay neuron
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what is the pathophysiology of complex partial seizures?
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arise in hippocampus
excessive self-excitatory sprouting of dendrites |
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which seizure has no post-ictal symptoms? absence or complex partial?
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absence has no post-ictal confusion
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which seizure lasts longer, absence or complex partial?
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complex partial lasts longer (about a minute)
absence lasts around 15 seconds |
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what is the main strategy for treating generalized seizures?
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give a calcium antagonist (decreases excitability)
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which cortical neurons are the source of projection fiberse?
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pyramidal neurons
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pyramidal neurons are primarily located in which layers of cortex?
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III and V
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what cortical layer has absolutely no pyramidal neurons?
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layer I
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pyramidal neurons produce what NT?
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glutamine
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granule neurons produce mostly what type of NT?
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GABA
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what type of cortex has all 6 layers
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neocortex (90% of cortex)
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what type of cortex has only 3 layers?
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archicortex (hippocampus)
paleocortex (olfactory cortex) |
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what is unique about motor cortex?
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it is "agranular"
has very thin layers II and IV pyramidal cells predominate |
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what is unique about primary sensory cortex?
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has very thick layer IV, granule cells predominate
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how many broadman's areas are there?
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51
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what is the concept of columnar cortex organization in visual cortex?
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all the neurons in a "column" will respond to the same stimulus. adjacent columns get input from the same parts of the visual field from separate eyes
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interhemisphereic axons arise from which cortical layer(s)?
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layer III (pyramidal)
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long association fiber axons arise from which cortical layer(s)?
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III and V
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short association fiber axons arise from which cortical layer?
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layer II
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granule cell neurons are what type of neurons?
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GABA-ergic interneurons
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corticobulbar and corticospinal axons arise from which layers?
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III and V
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corticothalamic fibers arise from which layer?
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layer VI (multimodal)
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what is the direction of corticofugal vs. corticopetal fibers?
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fugal: away from cortex
petal: toward cortex |
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when does most neurogenesis occur?
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2nd to 4th gestational month
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what stimulates a "wave" of neuronal migration to form a new layer of cortex?
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noradrenergic input
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what cortical layer is oldest?
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layer I (it was there as an accelular layer but new layers grew into it and it thinned out)
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what is lissencephaly?
what cortical layers are abnormal, which are intact? |
smooth cortex, failure of gyri and sulci formation
NO layer II reduced III and IV normal V and VI |
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what is the problem of cortical dysplasia?
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pyramidal cells are scattered rather than confined to layers III and V
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alzheimer's is responsible for approximately ___% of dementia?
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65
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what is the definition of alzheimer's
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an age related dementia which causes the progressive loss of memory, thinking capabilities, orientation, and normal behavior.
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in what conditions can you expect to see neurofibrillary tangles (NFTs)?
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in alzheimers, down syndrome, and normal aging
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are NFTs cause or consequence of neuronal cell death?
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cause
lead to tombstone cells |
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what are the primary areas affected in alzheimer's?
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hippocampus/parahippocampal gyrus
amygdala nucleus basalis of meynert association cortex |
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where are neuritic plaques most heavily deposited in Alzheimer's?
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frontal lobe
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which is a better predictor of symptoms, neuritic plaque deposition or NFTs?
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NFTs
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in AD, NFTs deposited in what structure prevent memory stamping?
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entorhinal cortex
no entry into papez circuit |
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what is the most significant gene associated with AD?
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APOE4 (really bad if you have 2 copies)
but ~35% do not have even one APOE4 |
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what type of drugs are typically used for AD?
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cholinesterase inhibitors
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what is the new immunological tx strategy for AD?
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gammaguard, IV anti-amyloid Ig
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what are the main diagnostic criteria for AD?
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disturbances in 2 or more cognitive functions
amnesia progression worse than other cognitive deficits associated with age conscious age 40-90 |
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what are saccadic eye mov'ts?
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fast movements to get something on the fovea
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what controls saccadic eye mov'ts?
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frontal eye fields
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what cortical area controls pursuit eye mov'ts?
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posterior parietal lobe
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what is the path for control of pursuit eye mov'ts?
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posterior parietal lobe
descends IPSILATERALLY Paramedian Pontien Reticular Formation (PPRF) |
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what is the path for conjugate R gaze?
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R VI nerve to LR
decussate at level of VI nucleus to travel in contralateral MLF L III nucleus/nerve to L MR |
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what brainstem nuclei control horizontal and vertical gaze?
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horizontal: paramedian pontien reticular formaiton
vertical: rostral interstitial nucleus of MLF |
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how is vestibular conjugate lateral gaze different than FEF mediated conjugate gaze
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vestibular induced does not synapse in the PPRF, it goes straight to VI nucleus
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what are the symptoms of a person with a supranuclear lateral gaze palsy?
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can't quickly look laterally
DOLL's head lateral intact can track moving object to lateral field ?? |
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how can you simply test vestibuloocular reflex?
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have a patient read while walking
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what is the caloric test?
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irrigate ear with cold water, eyes should move toward water
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what is bell's phenomenon?
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eyes move up and out when you close your eyelids
this is a reflex, sub-cortical |
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what are the symptoms of internuclear ophthalmaplegia?
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if it is a lesion to LEFT MLF
left eye can't adduct on conjugate gaze (R eye CAN abduct) convergence intact |
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what is the nucleus responsible for vertical gaze?
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rostral interstitial nucleus of the MLF
upgaze travel through posterior comissure downgaze goes directly to III and IV nuclei |
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what are the symptoms of parinaud's syndrome?
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posterior comissure lesion
supranuclear loss of upgaze |
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in a lesion to the III nerve nucleus, what other symptom (besides CN III palsy) is common?
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palsy of contralateral SR (these fibers cross right at level of III nucleus
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which EOM is supplied by a CN of the opposite side?
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CN IV innervates the contralateral SO muscle
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what is the eye position of a person with a IV nucleus lesion?
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the contralateral eye is elevated and extorted
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in perimetry, what is an isopter?
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a line around the visual field where you can respond to light of the same intensity
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damage to a region of the optic disc lead to what type of VF deficit?
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arcuate (fibers travel in an arch around the macula)
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what are the signs and symptoms of Optic Nerve Syndrome?
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cecocentral scotoma (most of the fibers are from central)
loss of color loss of VA RAPD |
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what is the difference between lesions to optic tract in the temporal lobe vs. parietal lobe
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temporal lobe: homonomous superior quandrantopsia
parietal lobe: homonomous inferior quandrantopsia both are semi-congruous |
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where is the lesion in complete homonomous hemianopsia?
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retrochiasmatic (you can't specifically say optic tract, LGN, radiations, or visual cortex)
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where are the "what" and "where" systems of visual processing? (R vs. L)
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"what": ventral surface. L side for reading, R side for face recognition, perception of images
"where": dorsal - puts things in space, motion |
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what is the function of the R sided wernicke's area?
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environmental sounds, pitch/harmony, prosody, cadence
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what is the function of the inferior part of the temporal lobes and what is the differential function from posterior to anterior?
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visual decoding
posterior: nonunique (it is a face) anterior: unique (it is KJ!) |
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what is the differential function of inferior/lateral left temporal lobe posterior-anterior?
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finding lexical terms (proper nouns)
posterior: non specific anterior: very specific nouns |
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what is the general function of the amygdala?
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emotional memory
recognizing fear in people's faces |
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what is the function of the R inferior parietal lobule?
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spatial proessing/mapping
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what is the function of L inferior parietal lobule
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repeating verbal phrases, (auditory assn cortex)
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what cortical area is active when you mispronounce a word (error monitoring)
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limbic lobe
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what part of the limbic lobe in high firing frequency in default, "zoned out" state?
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posterior cingulate gyrus of limbic lobe
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what are the constellation of symptoms of a person with damage to the ventral median frontal cortex?
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can't hold employment
doesn't respond to punishment can't express/experience emotions impaired judgement lack of concern for others lack of care for future |
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what are the symptoms of a person with damage to dorsolateral frontal cortex?
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decreased intellectual fx
lack of working memory |
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what are the symptoms of a person with damage to the medial superior frontal cortex?
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akinetic mutism
avolitional: does't even try to speak only body movements associated with survival/daily living are intact this region important for movement induction |
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what is the difference between dysarthria and aphasia?
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dysarthria is a motor difficulty in articulating speech (reading and writing intact)
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what is verbal/semantic paraphasia?
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substitution of words ("hot" for "wet")
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what is phonemic paraphasia?
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mixing up phenomes in a word ("table" because "taber")
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what is jargon aphasia?
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highly fluent paraphasic speech that sounds good but is basically babble
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what is the speech of a person with Broca's aphasia?
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non fluent (agrammatic, "the"s and "of"s drop out)
phonemic paraphasia initiation of speech difficult comprehension preserved |
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what is the speech of a person with wernicke's aphasia?
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semantic, phonemic, neologistic paraphasia
no proper nouns impaired comprehension |
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what are the main symptoms of someone with a conduction aphasia?
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verbatim repetition impaired
cannot write to dictation |
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what is the speech of a person with subcortical damage to left basal ganglia and thalamus?
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dysarthria
comprehension problems (like a wernicke's) |
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how are transcortical motor/sensory aphasias different than broca's and wernicke's aphasias?
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the lesion is on the periphery of wernicke's/broca's
repetition is INTACT (b/c connecting fibers run from the more central portions |
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what is alpha rhythm?
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when you are awake with eyes closed
8-13 Hz discharge |
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what is the characteristic EEG feature of stage 1 sleep?
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V waves (vertex)
sharp |
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what are the two characteric EEG features of stage 2 sleep?
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sleep spindles
K compelx |
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what is the "wake promoting area"?
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the Lateral Hypothalamus
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what is the "sleep promoting area" or "sleep switch"
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ventrolateral preoptic nucleus (VLPN)
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what are the monaminergic systems that are sleep inhibiting through the reticualr activating system?
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serotonin (dorsal raphe)
norepinephrine (locus ceruleus) histmine (tuberomammilary nucleus) |
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what is the function of the cholinergic pedunculonpontine nucleus (PPN) and laterodorsal tegmental nucleus (LDTN) in sleep fx?
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there are populations of "REM on" active during REM sleep and
"REM off" active during wakefulness |
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what is the most powerful wakefulness center and what does it produce?
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Lateral Hypothalamus - Orexin
it is COMPLETELY off during REM sleep |
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injury to the lateral hypothalamus can lead to what sleep disturbance?
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narcolepsy
insufficient wakefulness promotion |
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activation of the reticular thalamic nucleus leads to....
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N1 sleep
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narcolepsy is primarily due to
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disorder of REM sleep
insufficiency of LH orexin containing neurons |
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what is the cause of REM sleep behavior disorder?
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lesion in descending tract from "REM-on population" of PPN/LDTN to nucleus gigantocellularlis so they are not paralyzed during their dreams
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what is the main treatment strategy for narcolepsy?
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give noradrenergic therapy because of inactivity in Locus ceruleus
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what is the fetal transplantation treatment strategy for narcoleptics?
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implant orexin cells into pontine reticular formation
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what are the symptoms of Neurofibromatosis?
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SKIN:cafe au lait spots, neufibromas
NEURO: nerve sheath tumors, behavior problems |
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what are the symptoms of tuberous sclerosis?
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SKIN: nail fibromas, hypopigmented macules
NEURO: cortical tubers (firm parts of cortex) |
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what are the symptoms of Sturge Weber Syndrome?
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SKIN: port wine stain always on face
NEURO: cortical calcification, epilepsy, MR, paralysis |
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what is Encephalocele?
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protrusion of brian tissue through defect in the skull (usually occiput)
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what is myelomeningocele?
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herniation of the spinal cord through defect in vertebral canal
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what is the difference between encephalocele and meningocele?
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in meningocele, only meninges and CSF herniate out
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what is the malformation and consequence of holoprosencephaly?
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failure of the prosencephalic telencephalon to form into 2 parts, so there is just 1 cerebral hemisphere instead of 2
no corpus callosum MR, epilspey, quadraplegia |
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what is the malformation and consequence of septo-optic dysplasia
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incomplete diverticulation of prosencephalon
one tiny optic nerve, no pituitary, MR |
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what is the cause of microencephaly?
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failure of neuronal proliferation (usually do to teratogen exposure)
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what is the malformation and consequence of hemimegalencephaly?
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one hemisphere underwent excessive neuronal proliferation
big heads, epilspey, MR, hemiparesis opposite elnarged side |
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what are lissencephaly and pachygyria?
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lissencephaly: NO gyri or sulci
pachygyria: lesser degree, big gyri, few sulci |
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what are the symptoms of polymicrogyria?
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if global: seizures and MR
if focal: focal seizures and focal weakness |
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what is schizencephaly?
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a cleft from pia all the way to ventricle lined with GREY matter
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what is cortical heterotopia?
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clusters of neurons that failed to migrate normally. usually asymptomatic unless there are lots of them
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what is the cause and consequence of agenesis of the corpus callosum?
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failure of axon outgrowth
can be normal at least some learning difficulty |
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cocaine exposure to an infant affects what stage of neuronal development?
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neuronal differentiation
can also cause vasospasm leading to prenatal ischemic stroke |
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what is the cause and consequence of metachromatic leukodystrophy?
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failure of myelination
child begins life with normal milestones, then gradually loses them and dies |
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what is the cause and consequence of congenital cytomegalovirus infection?
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calcification of periventricular neurons
MR, epilepsy |
