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Brain and Behavior > Exam 1 (week2) > Flashcards

Exam 1 (week2) Flashcards

1
Q

which transmitters are dysregulated in schizoprhenia (2)

A

serotonin

dopamine

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2
Q

which dopamine receptor is blocked in drugs that work for antipsychotics

A

D2

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3
Q

how could amphetamies cause psychotic symptoms

A

amphetamines come in to presynaptic neuron via trasmporter, kicks out dopamine, dopamine in synaptic cleft is increased - stimulates D2 channel causing symptoms

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4
Q

why do you need to wait 4-6 weeks for antispychotics (D2 blockers) to work

A

“depolarization inactivation” - initially the presynaptic nerve fires harder because of autoreceptors - some are inhibited so the neuron thinks there’s less dopamine and wants to release more
eventually it wears out and will stop firing (chronic treatment)

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5
Q

what happens to dopamine pathways during schizoprenia

A

for some reason, the connections between ventral tegmental to cortex die off, but the connections between ventral tegmental to limbic (nucleus accumbens) remain. there is a positive feedback loop from cortex to limbic because the cortex doesn’t sense enough stimulation. ramps up dopa firing to limbic system (nucleus accumbens)

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6
Q

when do you see tardive dyskinesia (iatrogenic)

A

too much dopanie block - prolonged treatment with D2 receptor blockers – causes D2 receptor supersensitivity

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7
Q

endocrine side effects of dopaine block

A

if you block D2, you increase PRL release, causing gynecomastia

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8
Q

dopamine blockade and eating/weight

A

motor neurons around ventricles involved in eating behavior, D2 blockade around ventriles cause weight gain

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9
Q

dopamine blockade and nausea

A

antiemetic because it blocks chemotrigger zone

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10
Q

first gen antipsychotic drug types and prototype for each (2)

A
  1. phenothiazines (chlorpromazine)

2. butyrophenones (haloperidol)

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11
Q

phenothiazine mech of action

A

like tricyclic - binds to a bunch of receptors, not just D2

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12
Q

butyrophenones mech of action

A

way more potent D2 block than alpha 1

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13
Q

second gen antipsychitic drugs - how did they change from first gen with respect to receptor blockade

A

increased the ratio of serotonin (5-HT2):D2 receptor blockade (less chance for tardive dyskinesia)

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14
Q

clozapine mech of action

A

caused selective depolarization inactivation in limbic system
blocks 5-HT2 receptors

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15
Q

adverse for clozzapine

A
  1. have to check blood because of risk for agranulocytosis - can’t give in patients with dyscrasia
  2. diabetes risk
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16
Q

what are the atypicals/second gen antipsychotics (6)

A
  1. clozapine
  2. risperidone
  3. olanzepine
  4. quetiapine
  5. ziprasidone
  6. aripiprazole
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17
Q

side effect ofs risperidone

A

dose-dependent - will cause extrapyramidal symptoms like first gen if dose is too high
NO risk of agranulocytosis or diabetes

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18
Q

side effect of olanzepine (2)

A
  1. risk for diabetes and weight gain

2. increased serum prolactin

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19
Q

side effect of quetiapine

A

diabetes risk

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20
Q

side effect of ziprasidone

A

widens QT interval

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21
Q

mech of action of aripiprazole

A

partial agonist at D2

damp down nucleus accumbens, incrase frontal cortex

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22
Q

whats the super bad early side effect of antipsychotic drugs that could be fatal

A

neuroleptic malignant syndrome - causes catatonia, stupor, fever, HTN, myoglobinemia

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23
Q

what’s the deal with antipsychotics and epilepsy

A

can lower seizure threshold

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24
Q

what’s rabbit syndrome

A

perioral “chewing” syndrome - late neurological side effect of antipsychotic drug

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25
Q

what do you absolutely not give someone with tardive dyskinesia due to antipsychotics

A

anticholinergic, will suppress GABA activity even more by removing Ach tone

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26
Q

which antipsychotics have increased risk for diabetes, weight gain and hyperlipidemia 92)

A

olanzepine

clozapine

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27
Q

alpha block is bad for which patient population

A

elderly (anatihypertensive - falls)

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28
Q

when can you give an anticholinergic to HELP side effects

A

with EPS symptoms from haliperidol, let’s say

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29
Q

glutamate and dopamine relationship

A

glutamate directly increases dopa

and indirectly regulates dopa via regulation of GABA which inhibits dopa

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30
Q

NMDA and schizophrenia

A

hypofunction in glutamate receptor is responsible for neurocognitive symptoms of schizophrenia - same process for PCP

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31
Q

what is timecourse for diagnosis of schizophrenia

A

1 month of active symptoms - 2 or more symptoms (one has to be positive)

and 6months of social dysfunction

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32
Q

what percentage of patients with schizophrenia commit suicide

A

10%

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33
Q

what chromosome might have relevance in schizophrenia

A

C4 component of 6

C4A causes synaptic pruning in prefrontal areas

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34
Q

what are the extrapyramidal side effects of D2 blockade (4)

A
  1. acute dystonia (forceful muscle contractions)
  2. akathisia (motor restlessness)
  3. drug-induced parkinsonism (bradykensia, rigidity, tremors)
  4. tardive dyskinesia (hyperkineic movement of head, limbs, tongue)
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35
Q

when do the EPS symptoms occur

A

hours to days - acute dystonia
days to weeks - akasthisa
weeks to months - parkinsonism
months to years - tardive dyskinesia

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36
Q

timecourse for brief psychotic disorder

A

1 day to 1 month

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37
Q

timecourse for schizophreniform disorder

A

1 month to 6 months

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38
Q

what symptoms are NOT present in delusional disorder

A

disorganized thought and behavior

functionality is not generally affected too much

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39
Q

diagnostic criteria for schizoaffective disorder (2)

A
  1. features of schizophrenia AND mood disorder

2. psychotic symptoms for at least 2 weeks WITHOUT mood symptoms (to differentiate between MDD with psychosis etc.)

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40
Q

whats the beginning of the retina (near the lens) called

A

ora serrata

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41
Q

developmental stages of eye (5)

A

from forebrain:

  1. optic sulcus
  2. optic vesicle
  3. lens placode
  4. optic cup
  5. neural epitheilum of retina (in contact with layer behind - pigment epithelium of retina)
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42
Q

function of retinal pigment epihtelium cells (4)

A
  1. support rots and cones
  2. phagocytose 7,500 rod and cone outer segment discs
  3. reconvert trans retinal to 11-cis retinal
  4. make melanin
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43
Q

what disease occurs when there are mutations in genes that control reconversion of trans retinal to 11-cis retinal

A

retinitis pigmentosum - results in blindness

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44
Q

what do you see in fundus for RP

A

pigment deposition in patches

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45
Q

what do patients see with retinitis pigmentosum

A

lose peripheral vision

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46
Q

what do you see with retinal detachment

A

see sudden increase in floaters

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47
Q

what do you see in fundus for retinal detachment

A

“horseshoe tear”

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48
Q

what are the 3 layers of retina from inner to outer

A

ganglion cells, bipoarl cells, phtoreceptors

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49
Q

what nuclear layer are the rods and cones

A

outer nuclear layer

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50
Q

what are the synapse layers between nuclear layers in retina called (2)

A

plexiform layers
(outer is between inner and outer nuclear layers)
(inner is beween gancglion and inner nuclear layer)

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51
Q

what layers do mueller cells make

A

inner limiting and outer limiting membranes

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52
Q

what is nerve fiber layer made of

A

axons of ganglion cells

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53
Q

where are the nuclei of the mueller cells

A

in inner nuclear layer

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54
Q

which cells (rods or cones) contain color vision

A

cone

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55
Q

where are most of your cones

A

macula

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56
Q

difference between macula, fovea and foveola

A

foveola ONLY has cones - tiny central area (200 microns)
fovea more cones than macula (1.5mm)
macula (5.5mm - can appreciate on photo)

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57
Q

what do people see if they have macular degeneration

A

loss of central vision

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58
Q

what do you see on fundus for macular degeneration

A

destruction at macula - difference between wet (blood) and dry

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59
Q

what layer does uveitis affect

A

middle/choroid layer

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60
Q

what are 4 parts of middle layer

A
  1. choroid (under retina)
  2. ciliary body
  3. ciliary processes
  4. iris
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61
Q

what are layers of chroid beneath retina (2)

A
  1. Bruch’s membrane - small capillaries

2. choriocapillaris - larger vessels

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62
Q

what part of ciliary body actually pulls on lens

A

the zonule fibers produced by ciliary body and processes

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63
Q

functions of ciliary body and processes (3)

A
  1. produce aqueous humor
    2 produce zonules to attach to lens
  2. ciliary muscles contract during accommodation
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64
Q

layers of outer eye (4)

A
  1. mostly sclera (posterior to ora serrata)
  2. lamina cribosa (where white meets clear)
  3. corneoslceral junction/limbus
  4. cornea
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65
Q

function of lamina cribosa

A

supports the optic nerve

if pressure is too high, axons of optic nerve get pinched, those retinal gangion cells will die, and you lose vision from hundreds of photoreceptors

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66
Q

what ratio do you measure in glaucoma

A

disc:cup ratio

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67
Q

what is special about corneoscleral jucntion

A
  1. contain canals of schlemm
  2. contain trabecular meshwork that can close vessels when sclerosed
  3. contain corneal epithelial stem cells
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68
Q

layers of cornea from out to in (5)

A
  1. stratefied squamous non-keratinizing epithelium
  2. bowman’s layer (specialized BM)
  3. stroma
  4. descemet’s membrane (specialized BM)
  5. endothelium
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69
Q

functions of cornea(3)

A
  1. smooth surface over which tears can spread for vision
  2. barrier to microbes
  3. glial support for intraepithelial corneal sensory nerves (when you feel like something is in your eye)
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70
Q

what do fibroblasts in corneal stroma do (2)

A
  1. synthesize collagen and proteoglycans that provide strength to cornea
  2. pump out excess water to maintain clarity in cornea
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71
Q

what cells HAVE to be present in corneal transplant

A

endothelial cells

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72
Q

where in lens does proliferation occur

A

in anterior lens epithelial cells (they move posteriroly and differentiate into lens fibers)

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73
Q

when lens is flat, do you see close or far

A

far

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74
Q

when ciliary muscles contract, what happen to lens

A

rounds up

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75
Q

what are the layers of tears (3)

A

lipid outer, then acqueous, then mucin

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76
Q

after optic chiasm, where do optic tracts synapse

A

lateral geniculate nucleus (LGN) of thalamus

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77
Q

do you get convergence/binocular vision from thalamus?

A

no - the inputs from R and L eye are separated

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78
Q

after lateral geniculate nucleus, where do they go

A

optic radiations/ geniculocalcarine tract project to visual/calcarine cortex via EITHER retrolenticular internal capsule through parietal lobe
OR sublenticular internal capsule through temporal lobe

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79
Q

what’s the difference between sublenticular and retrolenticular

A

(meyer’s loop) sublenticular detect upper part of visual field (detects bottom of retina)

retrolenticular detect lower part of visual field (detects upper part of retina)

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80
Q

what are the lenticular nuclei

A

putamen and globus pallidus

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81
Q

what are the Brodmann’s area numbers for vision

A

area 17 = primary visual cortex

areas 18 and 19 are visual association cortex (above and below calcarine sulcus

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82
Q

homonymous visual field defect

A

means corresponding halves of visual field for both eyes (L for both, R for both)

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83
Q

what is hemionospia

A

half of vision lost

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84
Q

blood supply to visual cortex, and what kind of vision losses do you have with issues with this vessel

A

posterior cerebral artery, get macular sparing because of collateral blood supply from middle cerebral artery

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85
Q

what are the components of the “ventral stream” of image processing and what kinds of vision processing does it do

A

V1 is light, detects a lot of things, projects to V2, which detects fewer, but more specific things, V3 which detects even fewer and more specific things

pathway used for object recognition

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86
Q

what are components of the “dorsal stream” of image processing and what kinds of vision processing doe sit do

A

V1 to V2 to MT (which detects movement)

pathway used for spatial vision

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87
Q

when are photoreceptors hyper or depolarized

A

in the dark, cGMP is constituately produced, which causes Na+ influx and K+ efflux, DEPOLARIZING the cell

in the light, decreased cGMP is hydrolyzed (due to opsin coupled to cis retinal) causes closing sodium channel, reducing Na+ influx and K+ efflux, causing HYPERPOLARIZATION

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88
Q

how long do manic symptoms have to last for a diagnosis

A

at least 1 week (OR requiring hospitalization)

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89
Q

how many symptoms do people need to express for diagnosis of mania

A

3 (or 4 if irritable)

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90
Q

time course for hypomania

A

4 days (could be less)

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91
Q

diagnostic criteria for bipolar 1 (in terms of episodes)

A

one manic episode

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92
Q

diagnostic criteria for bipolar 2 (in terms of episodes)

A

one hypomanic plus one major depressive episode

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93
Q

in bipolar 1 and 2, which episodes are more common, manic or depressive

A

depressive by a lot

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94
Q

definition of rapid cycling in bipolar disorder

A

4 or more episodes in a y ear

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95
Q

which cranial nerves have parasympathetic function

A

3
7
9
10

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96
Q

what does gag reflex test

A

CN9 (sensation/afferent)

CN10 (motor/efferent)

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97
Q

what does “open and say ah” test

A

CN10

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98
Q

what does sticking out your tongue test

A

CN12

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99
Q

what 3 things does dysfunction of CNX cause

A
  1. loss of gag/swallow reflex
  2. loss of carotid sinus (heart rate control)
  3. loss of oculocardiac reflex causing dysphagia
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100
Q

what are the nuclei of CNX (4)

A
  1. dorsal motor nucleus (parasymp output)
  2. nucleus ambiguus (skeletal motor output)
  3. nucleus solitaris (visceral sensory input and taste input)
  4. spinal trigeminal nucleus (general sensory input)
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101
Q

what does visceral sensory function of CN10 control (2)

A
  1. cough reflex

2. nausea and vomitting reflex

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102
Q

what is skeletal motor nucleus of CN10 called

A

nucleus ambiguus

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103
Q

what specific nerve branch is responsible for cough reflex

A

internal laryngeal nerve (branch of vagus nerve)

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104
Q

what’s the medical term for hoarseness

A

dysphonia

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105
Q

what’s the medical term for “losing your voice”

A

dysarthria

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106
Q

which branch of which nerve can cause dysfunction of vocal cords

A

recurrent laryngeal branch of vagus

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107
Q

where is the general sensory location (on skin) of vagus

A

small area of skin of external ear canal

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108
Q

where is taste location of vagus

A

epiglottis and pharynx

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109
Q

patient with bilateral loss of smell and taste for 7mo and headache for 5mo

A

meningioma

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110
Q

patient with unilateral painful loss of vision and otpic neuritis

A

MS

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111
Q

patient with papilledema and horizontal diplopia

A

brain tumor causing increased ICP

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112
Q

patient with syncope, shaking, confusion, numbness over left jaw for past 2 years

A

lesion impacting CN5 as it exits cerebellar/pontine angle in medial temporal lobe (epileptic location)

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113
Q

facial weakness in upper vs lower motor neuron lesion

A

lower motor - can’t more upper or lower facial muscles (whole face)

upper motor - deficits in lower facial ONLY

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114
Q

if someone complains of things being really loud, what CN are you thinking about

A

CN7 (stapedius in innervated by CN7 - doesn’t dampen stapes)

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115
Q

Rinne and Weber testing - how to do it, and what does it test

A

tuning fork (512 Hz)

Weber: place fork in middle of center head on top (should hear on both sides equally, conducive (blockage) louder on affected ear)

Rinne: compare air and bone (normally air is louder than bone, conducive bone is louder than bone, sensorineural air is louder than bone)

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116
Q

someone with unilateral sensorineural hearing loss, vertigo, and tinnitis

A

Meniere’s (increased endolymph production)

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117
Q

when neurons need to regenerate, what structural components are upregulated and downregulated

A

upregulate microfilaments and microtubules (which are more dynamic), downregulate intermediate filaments, neurofilaments (which are more stable)

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118
Q

what is the most common way to damage neurons

A

upregulation of glutamate that triggers caspase elevation and apoptosis

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119
Q

functional recovery vs regeneration

A

functional recovery = getting function back via recruitment of OTHER neurons, versus repairing the damaged neurons themselves

120
Q

what are neurotrophins

A

growth factors that bind to neurons to promote growth

121
Q

3 things that happen in CNS in response to neuronal injury

A
  1. astrocyte proliferation and expression of GFAP, resulting in “glial scar”
  2. proliferation of oligodendroglial precursors and oligodendrocytes
  3. microglial recruitment and activation
122
Q

what do olfactory unsheathing cells do

A

cells like Schwann cells that can be transplanted into CNS to promote recovery

123
Q

animal examples of neuronal stem cells (2)

A

1) fish retinas that get bigger as fish grows

2) song birds learning new songs each year

124
Q

2 areas of human brain where stem cell populations reside

A
  1. subventricular zone (SVZ) that give rise to olfactory bulb
  2. dentate gyrus in hippocampus (memory and learning?)
125
Q

symptoms of lateral medullary syndrome and what areas are affected (4)

A
  1. dizziness (vestibular)
  2. hoarseness, difficulty swallowing (nucleus ambiguus of CN9,10,11)
  3. loss of pain and temp ipsilaterally in face (CNV)
  4. loss of pain and temp contralaterllly in body (spinothalamic)
126
Q

lateral medullary syndrome caused by issue in what blood vessel

A

PICA

127
Q

symptoms and areas affected by medial medullary syndrome

A
  1. deviation of tongue, tongue atrophy, speech problems (hypoglossal nerve)
  2. contralateral hemiplegia in body (corticospinal tract)
  3. loss of discriminative touch contralaterally in body (medial lemniscus)
128
Q

what blood vessel causes medial medullary syndrome

A

anterior spinal artery from vertebral artery

129
Q

oculocardiac reflex

A

pressure on orbit due to sx or tumor, travels along opthalmic V1 through trigeminal ganglion to sensory nucleus in pons, where INTERNUCLIAL FIBERS in RETICUALAR FORMATION connect to DORSAL MOTOR nucleus of 10 which SLOWS HEART

130
Q

what CN does special sensory to posterior 1/3 of tongue

A

CN9 - glossopharyngeal

131
Q

what is parasymp nucleus of glossopharyngeal nerve and what does it control?

A

inferior salivatory nucleus - controls parotid gland function

132
Q

middle ear sensory i smediated by what nerve

A

glossopharyngeal 9

133
Q

visceral sensory of CN9 - what nucleus and what function

A

into nucleus solitaris, sensory from carotid body and sinus

134
Q

which part of carotid body/sinus senses what (chemo/baro)

A 
body = chemo
sinus = baro
135
Q

skeletal motor component and nucleus for CN9

A

nucleus ambiguus - stylopharyngeal muscle for swallowing

136
Q

what is general sensation for CN9 - what nucleus and what sensation (4)

A

through spinal trigeminal nucleus

sensation for:

  1. soft palate
  2. pharynx
  3. posterior 1/3 of tongue
  4. middle ear cavity
137
Q

what does CN11 do

A

motor only- innervates trapezius and sternocleidomastoid

138
Q

where is CN12 nucleus

A

most ventral and medial

139
Q

what does CN12 do

A

innervates muscle of tongue - protrusion

140
Q

what side does tongue deviate to with CN12 injury

A

lower motor neuron - flaccid paralysis, deviates to the side of injury

141
Q

what muscle attaches to coronoid process of mandible

A

temporalis

142
Q

what bones articulate to form TMJ

A

condyloid process of mandible with zygomatic arch - articular tubercle prevents anterior dislocation

143
Q

what ligament stabilizes TMJ

A

lateral ligament to prevent posterior dislocation

144
Q

what movement does superior compartment of TMJ allow for

A

gliding/translation - jutting chin out when you open very wide

145
Q

what movements does inferior compartment of TMJ allow for

A

elevation

depression

146
Q

what is the blood supply to the infratemporal fossa and what is it a branch from

A

superficial temporal artery - branch of external carotid

147
Q

what is the sensory innervation of the infratemporal fossa and what is it a branch of

A

auriculotemporal nerve - branch of V3

148
Q

movements of temporalis muscle (2)

A
  1. elevation of mandible

2. retraction of mandible

149
Q

movements of masseter

A
  1. elevation of mandible

2. protrusion

150
Q

movements of lateral pterygoid muscle

A

bilateral:

  1. protrusion
  2. depression

unilateral
1. contralateral excursion

151
Q

medial pterygoid muscle movements

A

bilateral

  1. protrusion
  2. elevation

unilateral
1. contralateral excursion

152
Q

which pterygoid muscle is superior

A

lateral

153
Q

what are the 2 terminal branches of external carotid

A

maxillary artery

superficial temporal artery

154
Q

what are the sections of the maxillary artery

A
  1. deep to neck of mandible
  2. laterl pterygoid (anterior)
  3. pterygopalatine fossa
155
Q

branches of maxillary artery first portion (what is supplied)

A
  1. middle meningeal (goes up to dura)

2. inferior alveolar (dives down, supplies teeth exits mental foramen)

156
Q

branches of maxillary artery second portion (what is supplied)

A
  1. deep temporal (goes up to muscles of mastication)

2. buccal artery (down to buccinator)

157
Q

branches of maxillary artery third part (what is supplied)

A

infra orbital artery (floor of orbit)

158
Q

venous drainage of infratemporal fossa (3)

A
  1. retromandibular vein (side of face/neck)
  2. facial (front of face)
  3. inferior ophthalmic vein (to cavernous sinus)
159
Q

what foramen does V3 exit from skull

A

foramen ovale

160
Q

what is special about auriculotemporal nerve

A

acts as a highway for postganglionic parasympathetic (from otic ganglion) to parotid gland

161
Q

sensory info to anterior 2/3 of tongue supplied by what

A

lingual nerve of V3

162
Q

what is special about lingual nerve

A

highway for chorda tympani (branch of facial) that carries BOTH taste and preganglionic parasympthatetic fibers of submandibular and sublingual glands

163
Q

what does parasymp of CN7 do

A

innervates submandibular and sublingual glands

164
Q

what does parasymp of CN9 do

A

innervates parotid gland

165
Q

what is the ganglion that parasymp of CN7 go to

A

submandibular ganglion

166
Q

what are the SENSORY nuclei of trigeminal from superior to inferior

A

mesencephalic
main
spinal trigeminal

167
Q

where are first order neurons of sensory trigeminal nerve

A

in trigeminal ganglion (analagous to dorsal root ganglion)

168
Q

where are the second order neurons of sensory trigeminal nerve

A

EITHER main sensory or spinal trigeminal nuclei

169
Q

where are the 3rd order neurons of sensory trigeminal nerve

A

ventral posteroMEDIAL nucleus (VPM) of thalamus

170
Q

when do sensory trigeminal nerves deccusate

A

between 2nd and 3rd order neurons

171
Q

what info is carried in main sensory nucleus

A

discriminative touch and pressure - like dorsal column, meets up with medial lemniscus

172
Q

where is main sensory nucleus

A

PONS

173
Q

where does info go after main sensory nucleus

A

ascends in medial lemniscus - most contralaterally, but some from ORAL CAVITY are ipsilateral as trigeminothalamic tract

174
Q

where is face on homunculous

A

laterally, right above lateral fissure

175
Q

what info is carried in spinal trigeminal nucleus (2)

A
  1. pain and temp from face

2. sensory info from CN 7, 9, 10

176
Q

where is spinal trigeminal nucleus located

A

pons, medulla and spinal cord C1-C3

177
Q

what is the pathway of trigeminal trigeminal tract neurons

A

enter from trigeminal ganglion and DESCEND in spinal trigeminal tract (lateral) to reach spinal trigeminal nculeus

178
Q

what info does mesencephalic nucleus contain?

A

prprioception from head (how to regulate force of bite)

179
Q

what is different about mesencephalic nucleus compared to the other trigeminal sensory nuclei

A

it contains first order neurons (the other first order neurons are in the trigeminal ganglion)

180
Q

what is path of neurons in mesencephalic nucleus

A

from mesencephalic to trigeminal motor nucleus (below and medial) and then back out through V3

181
Q

what is input to motor trigeminal nucleus

A
  1. mesencephalic for force of bite

2. bilateral corticobulbar

182
Q

how to test motor of CN5

A

jaw jerk test - USUALLY DOES NOT CAUSE RESPONSE. if there’s an upper motor neuron lesion, there will be a reflex

183
Q

what can cause someone to have violent bursts of pain sensation coming from all 3 branches of CN5

A

trigeminal neuralgia caused by arterial compression from superior cerebellar artery (SCA)

184
Q

nuclei of CN7 and location in mid-pons

A
  1. motor nucleus (middle and medial, tract loops up and around abducens nucleus)
  2. spinal trigeminal (middle and lateral)
  3. nucleus solitarus (up/dorsal, between abducens and spinal trigeminal)
  4. superior salivatory nucleus (medial and up to motor nucleus)
185
Q

where are 1st order neurons for CN7

A

geniculate ganglion

186
Q

what info does nucleus solitaris carry for CN7

A

taste from anterior 2/3rd of tongue

187
Q

what info does spinal trigeminal nucleus carry for CN7

A

somatic sensory from external ear

188
Q

what info does superior salivatory nucleus carry

A

parasymp neurons to lacrimal, nasal, palatal, submandibular and sublingual glands

189
Q

where does CN7 exit skull

A

with vestibular cochlear through INTERNAL ACOUSTIC MEATUS

190
Q

what does geniculate ganglion contain

A

CN7 taste and sensory neurons

191
Q

what is the “hay fever” ganglion

A

pterygopalatine galgnion (pregang parasymp from CN7)

192
Q

where does CN7 exit face

A

stylomastoid foramen

193
Q

what nerve branch of 7 is parasymp

A

petrosal nerve

194
Q

which part of face recieves bilateral innervation

A

upper face

195
Q

what kind of innervation does lower face recieve

A

ONLY contralateral innervation

196
Q

what kind of facial paralysis will you see with upper motor neuron lesions

A

partial paralysis of upper, full paralysis of lower

197
Q

what kind of facial paralysis will you see with lower motor neuron lesions

A

paralysis to both upper and lower face (bell’s palsy)

198
Q

what carries taste from hard palate

A

greater petrosal

199
Q

what nerve does pterygopalatine postganglionic neruons hitchhike on to get to lacrimal

A

V2

200
Q

componentes of blink reflex

A

afferent via V1 of CN5
motor via CN7 to blink
tearing via parasymp of CN7

201
Q

is high or low cortisol protective against PTSD

A

high (fast cortisol response shuts down the stress response)

202
Q

what areas of brain are hypoactive in PTSD (3)

A

prefrontal cortex
dorsal cingulate cortex
hippocampus (can become damaged/ atrophied)

203
Q

what area of brain is hyperactive in PTSD

A

amygdala

204
Q

medicine in PTSD (3 to use, 1 not to)

A

firstline = SSRIs

Prazosin for nightmares

Topiramate for nightmares

avoid prolonged use of benzos - could cause more risk

205
Q

gender risk for PTSD

A

female:male is 2:1

206
Q

what percentage of PTSD risk is genetic

A

30%

207
Q

how to test CN8 in comatose patient

A

caloric reflex

warm water into ear - eyes deviate toward contralateral ear, fast nystagmus towards ipsilateral

cold water into ear - eyes deviate toward ipsilateral ear and fast phase is in opposite direction

208
Q

dizziness in diabetic patient when standing, what could the cause be

A

orthostatic hypertension due to dysautonomia - disruption of autonomic nervous system
or position sense
or medication

209
Q

definition of orthostatic hypotension

A

drop in systolic BP of 20 or diastolic BP of 10 within 3 min of standing

210
Q

what does pulse do in neurogenic orthostatic hypertension

A

doesn’t change

211
Q

what phase of nystagmus do you define it by

A

fast phase

212
Q

in peripheral vertigo, what direction is fast phase of nystagmus

A

away from the affected ear

213
Q

if you see vertical nystagmus, what could it be

A

Brainstem disease

214
Q

which type of nystagmus is fatiguable

A

peripheral (inner ear)

215
Q

which pole of eye determines direction of nystagmus in rotatory nystagmus

A

upper

216
Q

what is head impulse thrust test

A

move head to left and to right, look at eyes. if eyes are able to stay fixed forward, that’s normal. if you turn the head to the right and it takes some time before the eyes turn back forward, there’s a vestibular lesion on the right

217
Q

3 maini causes of peripheral vertigo

A
  1. benign postural vertigo
  2. meniere’s
  3. vestibular neuronitis
218
Q

what is hallpike maneuver

A

patient sits down, turn head 45 degrees, keep eyes open, tell them to lie down with head over edge - you will see delayed nystagmus that will eventually disappear (if inner ear vertigo)

219
Q

what to do for benign paroxismal postural vertigo

A

ekley maneuver to try to move crystals away

220
Q

tx for meneiers

A

salt and volume reduction

221
Q

kinocilium structure and function

A

nonmotile cilium (no central core)- only one per array of stereocilia in vestibules that bend towards kinocilium to cause calcium flux via pulling on tip-links between stereocilia

222
Q

what is source of endolymp

A

stria vascularis in cochlear duct, drains through endolymphatic sac

223
Q

NCC and ear development

A

NCC stimulate differentiation of hair cells

224
Q

emmetropic means what

A

normal eye

225
Q

normal length from lens to retina

A

17mm

226
Q

diopters of cornea and lens

A

40 and 20

227
Q

myopia - where do rays converge and what kind of lens do you need

A

before the retina - too much converging power - need concave (-) lens

228
Q

hyperopia - where do rays converge and what kind of lens do you need

A

behind the retina - not enough converging power, need convex (+) lens

229
Q

what does lens have to do when you’re trying to read

A

has to get more round - ciliary muscles have to contract so that the zonule fibers relax

230
Q

types of blepharatis

A

anterior (ulcerative or sebhorreic)

posterior

231
Q

what is a stye

A

AKA external Hordeolum

staph abcess of lash follicle

232
Q

what is chalazion

A

chronic blockage of meibomian gland - PAINLESS

233
Q

sx for acute lacrymal sac infection/inflammation

A

dacryocystorhinostomy - connect sac with nasal mucosa

234
Q

what is the discharge like in viral conjunctivitis

A

watery

235
Q

what is pingueculum

A

whitish deposit on bulbar conjuctiva (does not involve cornea) usually due to UV exposure - deveneration of conjunctiva. lubricate for tx

236
Q

what is pterygium

A

can extend over cornea - can happen in hot climates

237
Q

how to test between episcleritis or scleritis

A

episcleritis will blanch with phenlephrine and is mobile

238
Q

causes of scleritis

A

usually connected to connective tissue disorders, can also be (rarely) infectious like syphilis. rule out infection betfore treating with immunosuppression or steroids

239
Q

risk factors for infectious keratitis (2)

A 
contact wearing
herpes simplex (see dendritic keratitis)
240
Q

when to check eye with herpes zoster

A

when tip of nose is involved

241
Q

3 components of uvea

A

iris
ciliary body
choroid

242
Q

symptoms of uveitis (4)

A
  1. diffuse injection
  2. keratic percipitates
  3. hypopyon
  4. inflammation of blood vessels if posterior is involved
243
Q

what does traumatic cataract look like

A

rosette shaped

244
Q

sx of choice for catarats

A

phacoemulsification

245
Q

what is dreaded complication of cataract sugery

A

endophthalmitis (1:1,000) - inflamation of cavities caused by infection - 50% of eyes will become blind

246
Q

when you do peripheral iridotomy, where are you maing a hole

A

between anterior and posterior chambers

247
Q

which is worse for the eye, acids or bases

A

bases - can result in liquefaction necrosis - can penetrate tissues faster

248
Q

older one day of vision loss, shadow at bottom of vision, now middle too, flashing lights and floaters, hx of cataract surgery

A 
retinal detachment (shadow)
(retina tear caused floaters/flashers)
249
Q

what kind of retinal detachment do you see in DM

A

tractional

250
Q

older woman, decreased vision for 2 weeks, black spot in center of vision, hx of smoking and HTN

A

macular degeneration (see hemorhage in one eye, drusen in the other)

251
Q

which are better, soft or hard drusen

A

hard. soft will more likely become wet macular degeneration

252
Q

hx of blurriness for a year, getting worse. last week noticed new floaters. decreased red reflex. hx of DM, HTN and smoking

A

diabetic retinopathy - proliferative

253
Q

decreased vision, progressively worse, feels “darker”, hx: HTN, PE, smoking, lots of infarcts and bleeding on fundoscope “blood and thunder”

A

central retinal vein occlusion

254
Q

older man, 1 day of dark vision in R eye, last week, vision became blurry, then black, then normal. hx of HTN, high cholesterol and smoking. see “cherry red spot” on fundoscope

A

central retinal artery occlusion

255
Q

older man, dark vision, blurry then black then normal, headache, jaw claudication, scalp tenderness, joint aches

A

giant cell arteritis

256
Q

tx for GCA

A

steroids

257
Q

older woman, pain redness photophobia and decreased vision. had cataract sx 1 week ago

A

post op endophthalmitis due to staph

258
Q

tx for post op endophthalmitis

A

aspirate vitreous (or sx if really bad vision), inject broad spectrum antibiotics

259
Q

what are the “order” neurons for the vestibular reflexes

A 
1 = vestibular ganglion cells
2 = vestibular nuclei 
3 = motor nucleus
260
Q

which vestibular nuclei are involved in vestibuloocular reflex

A

all 4

261
Q

which vestibular nuclei are involved in vesteibulocolic reflex

A

medial vestibular nucleus

262
Q

which vestibular nuclei are involved in vestibulospinal reflex

A

lasteral vestibular nucleus only

263
Q

what is the range of hearing for intensity/loudness of sound (in decibels)

A

0 dB = threshold of hearing
20 dB = whisper
60 dB = convo
120 dB = thunder

264
Q

which middle ear bones have muscles attached to them and what are they innervated by

A

malleus = tensor tympani muscle innervated by CN5

stapes = stapedius muscle innervated by CN7

265
Q

what ions and neurotransmitters cause transduction at inner hair cells

A

potassium at tip links, calcium at base, glutamate to auditory nerve cell

266
Q

pathway from orgain of corti to auditory cortex

A

auditory ganglion cell to dorsal and ventral cochlear nuclei, then most cross over, synapse in superior olive or just straight ascend to inferior colliculus, then to MGN, then to auditory cortex

267
Q

describe the vetsibuloocular reflex as you turn your head left

A

left vestibular nerve excites neurons in left vestibular nuclei. neurons then cross over and excite the RIGHT ABDUCENS nucleus to excite RIGHT LATERAL RECTUS. the abducens nucleus also contains INTERNUCLEAR NEUROS which cross back over, ascend in MEDIAL LONGITUDINAL FASCULIS and excite LEFT OCULOMOTOR and thus LEFT MEDIAL RECTUS

268
Q

if you have on left sided internuclear opthalmoplegia, what would happen when you move your head to the left

A

right eye lateral rectus would work, but medial rectus on left eye wouldn’t

269
Q

woman with colors looking pink in one eye, with bluriness and dark spot in superior visual field, got worse with hot bath

A

MS - clinically isolated syndrome

papilledema

270
Q

patient with white matter lesions that is NOT MS, what is it?

A

migraine

271
Q

what will you find more of in CSF in MS

A

IgG

272
Q

what are dawson’s fingers and what are they characteristic of

A

lesions at 90 degree angles to ventricles - characteristic of MS

273
Q

if you find aquaporin 4 in blood, why dont you think it’s MS

A

because it’s Devic’s disease/neuromyelitis optica - also the lesion will travel for multiple spinal cord segments

274
Q

what is a big risk for biologics used for MS (underlying issue)

A

PML (Progressive multifocal leukoencephalopathy) due to JC virus

275
Q

first medication with defined benefit in primary progressive MS

A

ocrelizumab (very similar to rituximab)

276
Q

most common reason for relapse in MS

A

non compliance with meds

277
Q

DSM criteria (2+) for personality disroder

A

deviation from cultural norms in 2+ ways:

  1. cognition
  2. affectivity
  3. interpersonal functioning
  4. impulse control

these traits are inflexibile and maladaptive

278
Q

how old do you have to be to be dx with personality disorders

A

can be less than 18 if you have symptoms for more than a year, however, antisocial personality disorder needs you to be 18y/o for dx

279
Q

what are cluster A personality disorders (3)

A

“odd, eccentric, weird”

  1. paranoid personality disorder (no psychosis)
  2. schizoid personality
  3. schizotypal personality
280
Q

what are cluster B personality disorders (4)

A

“dramatic, emotional, wild”

  1. antisocial personality disroder (need conduct disorder in adolescence)
  2. borderline personality
  3. histrionic personality disorder
  4. narcissistic personality
281
Q

what are the cluster C personality disorders

A

“anxious”

  1. avoidant personality disorder
  2. dependent personality disorder
  3. obsessive compulsive personality disorder
282
Q

schizoid personality traits (and tx)

A

does not enjoy relationships, detachment, emotional coldness, hard to tx with therapy

283
Q

schizotypal personality traits (and tx)

A

odd beliefs, magical thinking, social anxiety, peculiar speech, tx with social skills training

284
Q

antisocial personality traits (and tx)

A

breaks the law, lies, cons people, impulsivity, recklessness, irresponsibility, lack of remorse, violence, use of weapons and drugs, low risk preventional benefit with group parenting training

285
Q

borderline personality disorder traits (and tx)

A

associated with hx of abuse, very sensitive to stress and interpersonal slights, suicidal behavior, or non-suicidal self-harm, impulsivity that are self-damaging, feeling of emtpiness. tx dialectical behavioral therapy, transferance focus, mentalization-based.

286
Q

histrionic personality diroder traits

A

excessive emotionality and attention seeking, provocative, need to be center of attention, rapidly shifting and shallow emotional expression, speech is impressionistic and lacking in detail, is suggestible

287
Q

narcissistic personality disorder traits

A

grandiose sense of self, needs to be liked, lack of empathy, thinks they are special and can only be understood by high-status people, fantasies of power, success, brilliance, is arrogance, interpersonal exploitative.

288
Q

avoidant personality disorder traits

A

avoids interpersonal contact, shows restraint within intimate relationships for fear of being ridiculed, very low self esteem, preoccupied with criticism and rejection, reluctant to take personal risks

289
Q

dependent personality disorder traits

A

needs a lot of reaassurance from others, needs other to assume responsibility, difficulty expressing disagreement with others for fear of loss of support, difficulty initiating project or doing things on their own, will volunteer to do things that are unpleasant to obtain support from others, feels uncomfortable when alone, seeks relationships as source of care

290
Q

obsessive compulsive personality disorder traits

A

preoccupation with orderliness, perfectionism, control, at the expense of efficiency, can’t meet deadlines, excludes leisure activities, can’t delegate, shows rigidity, ego-syntonic (doesn’t see it as an issue),

291
Q

somatic symptom disorder traits

A

excesive thoughts, feelings or behaviors related to symptoms (disproportionate thoughts about severity, energy devoted to symptoms, high anxiety) for 6months

292
Q

illness anxiety diroder traits

A

hypochondria - preoccupation with having or acquiring a serious illness for more than 6 months, with mild or absent somatic symptoms. equally common in men and women (somatic symptom and conversion more common in women)

293
Q

conversion disorder traits

A

symptoms of altered voluntary motor or sensory function incompatible with known conditions - diplopia, blindness, deafness, numbness, dysphasia, seizures, tremor (sometimes with indifference to these symptoms). usually just an acute response to an acute stressor

294
Q

pseudocyesis

A

false belief of pregnancy - amenhhoreah, fat distribution, breast enlargement

295
Q

primary gain

A

something rewarding about being in sick role - i.e. when people were sick in abusive childhood, they were taken care of

296
Q

secondary gain

A

external rewards - bed, drugs, benefits

297
Q

factitious disorder AKA

A

munchausens

Brain and Behavior (6 decks)

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