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Brain and Behavior > Exam 2 (week 1) > Flashcards

Exam 2 (week 1) Flashcards

1
Q

what nerves are in posterior triangle of neck

A
  1. spinal accessory
  2. nerves of cervical plexus
  3. brachial plexus
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2
Q

what are the little trianges within anterior triangle

A
  1. submental (right under chin)
  2. submandibular
  3. muscular triangle
  4. carotid triangle
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3
Q

what structures are in submandibular triangle (nerve, vasculature, glands)

A
  1. submandibular gland
  2. hypoglossal nerve
  3. facial artery and vein
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4
Q

what structures are in the muscular triangle

A
  1. thyroid and parathyroid

2. laryngeal prominence

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5
Q

what are the suprahyoid muscles (4)

A
  1. digastric (anterior relates to mylohyoid, posterior relates to stylohyoid)
  2. sylohyoid
  3. mylohyoid
  4. geniohyoid
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6
Q

what are the infrahyoid muscles (4)

A
  1. omohyoid (shoulder-hyoid)
  2. sternohyoid
  3. sternothyroid
  4. thyrohyoid
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7
Q

deep muscles of neck

A
  1. scalenes - fix the ribs (1st and 2nd-posterior)

2.

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8
Q

what musches do brachial plexus pass between in neck

A

anterior and middle scalenes

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9
Q

what muscles does phrenic pass through in neck

A

anterior and middle scalenes

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10
Q

what muscles do subclavian artery pass through in neck

A

anterior and middle scalenes

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11
Q

watch the opening of eustacian tube in pharynx called

A

torus tubarius

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12
Q

where is tonsilar fossa located

A

between palatopharyngeal and palatoglossal arch - where the palatine tonsils are

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13
Q

where does food get stuck in throat (not when choking)

A

piriform recess

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14
Q

what is Waldeyer’s tonsilar ring made of? (4)

A
  1. pharyngeal tonsil
  2. tubal tonsils
  3. palatine tonsils
  4. lingual tonsil
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15
Q

what does tensor veli palatini do and what is it innervated by

A

innervated by V3

widens soft palate and opens auditory tube

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16
Q

what does levator veli palatini do and what is it innervated by

A

elevates soft palate, innervated by 10

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17
Q

what does musculus uvulae do and what is it innervated by

A

innervated by 10

shortens and elevates uvula

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18
Q

what does palatoglossus do and what is it innervated by

A

innervated by 10

elevates posterior tongue to soft palate

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19
Q

what does palatopharyngeus do and what is it innervated by

A

innervated by 10

tightens and elevates pharynx

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20
Q

what are the inner pharyngeal muscles and what are they innervated by (3)

A
  1. stylopharyngeus (glossopharyngeal)
  2. salpingopharyngeus (vagus)
  3. palatopharyngeus (vagus)
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21
Q

definition of clouding of consciousness

A

minimally reduced wakefulness/awareness, incomplete orientation, inattentive, agitated OR drowsy

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22
Q

lesions in midbrain cause (in terms of sleep disorder)

A

sleepiness

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23
Q

patients with lesions in hypothalamus cause (in terms of sleep disorder)

A

insomnia

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24
Q

patients with lesions between hypothalamus and midbrain cause (in terms of sleep disorder)

A

narcolepsy

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25
Q

older woman who doesn’t know what year it is, poorly attentive, hyperaroused, purposeless activity, just started a new med. what kind of med might it be

A

anticholinergic - interferes with ascending arousal system - decrease ability to maintain arousal

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26
Q

how does hypoglycemia cause delerium

A

regional impairment of ACh metabolism

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27
Q

older woman, profound memory loss, confabulation (making things up), indifference to noxious stimuli, nystagmus and gait ataxia, vitals are unstable. what could it be

A

thiamine deficiency (also see with severe alcoholism)

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28
Q

path findings for alcohol related thiamine deficiency

A

hemorrhage in shrunken mamillary bodies, whitening on CT in midbrain (most sensitive to thiamine deficiency)

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29
Q

woman with pneumonia, lethargy, confusion, clinical deydration, what could it be

A

hyperglycemia - causes cerebral edema

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30
Q

ammonia in blood causes confusion - how?

A

ammonia is typically converted to urea in liver for excretion. if liver stops working, brain and muscle get the ammonia, and up-regulate enzymes (glutamate from astrocytes). glutamine is a waste product, which causes astrocyte swelling - focal brain dysfunction in midbrain

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31
Q

older woman with known alcoholic liver disease, asterixis, acting strangly

A

hepatic encephalopathy

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32
Q

what do you see with hepatic encephalopathy on histo of brain

A

astrocyte swelling - alzheimer’s type two

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33
Q

woman is confused, apathetic, dull, tremor, known renal failure

A

uremic encephalopathy

  • won’t see any classic path or imaging findings
  • dialysis improves symptoms
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34
Q

what are the basal ganglia/nuclei of cerebral hemispheres

A

grey matter deep to cerebral hemispheres:

  • caudate nucleus
  • putamen
  • globus pallidus
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35
Q

where do association fibers run

A

within the same hemisphere

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36
Q

where do commissural fibers run

A

cross over to other cerebral hemisphere

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37
Q

where do projection fibers run

A

descend to connect cerebral cortex with subcortical structures

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38
Q

where does arcuate fasciculus go

A

from frontal down through parietal, occipital and temporal

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39
Q

where does uncinate faciculus go

A

from parietal through temporal

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40
Q

what kind of fibers make up corpus callosum

A

commissural fibers from L to R and vis versa (for hand movement coordination etc)

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41
Q

what does anterior commissure connect

A

temporal gyri on both sides

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42
Q

internal capsule contains what (2)

A

descending projection fibers

thalamocortical axons

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43
Q

what is contained within corona radiata

A

corticospinal fibers from cortex before it hits internal capsule (then as it descends, it’s called crus cerebri, the pyramids, and then corticospinal tracts)

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44
Q

where do corticopontine fibers start and end

A

start from widespread cortex areas to pontine grey - for controlling motor activity with cerebellum (middle cerebellar peduncle)

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45
Q

which fibers in corona radiata are the most numerous

A

corticopontine fibers

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46
Q

what part of brain is subthalamic nucleus located

A

diencephalon

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47
Q

what part of brain is substantia nigra located

A

midbrain

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48
Q

what is phrenology

A

lumps on surface of head - determine features or personality traits of individual - hopeful, constructive etc.

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49
Q

primary brodman’s area for somatosensory

A

3, 1, 2

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50
Q

primary brodman’s area for visual

A

17

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51
Q

primary brodman’s area for auditory

A

41

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52
Q

what is the secondary sensory area for somatosensory

A

area S2

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53
Q

what is secondary sensory area for auditory

A

area 42

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54
Q

what is association area for somatosensory

A

5, 7 in superior parietal lobule

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55
Q

what is association area for visual system

A

18, 19 above and below primary visual cortex

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56
Q

what is assocation area for auditory

A

22, in superior temporal gyrus

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57
Q

difference between unibodal and multimodal areas

A

unimodal (somato, visual, auditory) concerned with processing signals from one primary area

multimodal - involved in higher processing

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58
Q

major thalamic input to somatosensory cortex

A

VPM from face

VPL from body

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59
Q

what sensory deficit will someone have if you have lesion in superior parietal lobule

A

lesion in somatosensory areas 5 and 7 - results in astereognosis

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60
Q

what sensory deficit will someone have if you have lesion in inferior parietal lobule

A

results in contralateral neglect - ignores opposite side of body

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61
Q

what brodmans areas are within wernickes

A

areas 22, 39, and 40

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62
Q

what does a lesion to superior temporal gyrus, supramarginal gyrus, or angular gyrus

A

difficulty understanding speech

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63
Q

speech and handed-ness

A

R handed person has speech areas on L side of brain

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64
Q

where is brocas area

A

inferior frontal gyrus

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65
Q

what does the temporal/parietal area on opposite side of wernicke’s/broca control

A

prosody - emotional content of speech

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66
Q

what site of brain is involved in agraphia

A

dominant angular gyrus (angular 39)

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67
Q

what site of brain is involved in alexia

A

dominant parietal lobe

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68
Q

if patient has PCA stroke on eft side, what deficits would he hve

A

can see, can write but can’t read

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69
Q

what area thalamus is involved iwth primary auditory cortex

A

MGN

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70
Q

what areas of thalamus are involved im notor activity

A

VA and VL thalamus

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71
Q

what area of thalamus is involved in prefrontal cortex

A

MDN

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72
Q

what are absence seizures

A

petit mal - 10-45s start in childhood

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73
Q

what ions are involved in seizures

A

increase in extracellular potassium depolarizes neirghboring neurons, this causes accumulation of calcium in presynaptic terminals which increases transmitter release and increased glutamate (NMDA) activation

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74
Q

what area of brain is involved in termporal lobe epilepsy, and how could this cause problems

A

hippocampus- severe memory issues

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75
Q

what cells have glutamate

A

pyramidal

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76
Q

what kind of molecule is glutamate

A

amino acid

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77
Q

what cells have GABA

A

interneurons

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78
Q

3 types of glutamate receptors

A

NMDA
AMPA
kainate

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79
Q

what kind of seizures do you use benzos for

A

status epilepticus

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80
Q

vigabatrin mech of action

A

inhibits GABA-transaminase (GABA-T)

reduces GABA breakdown

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81
Q

vigabatrin side effect

A

concentric field deficit retina dies - lose peripheral vision

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82
Q

benzo mech of action

A

increases affinity of GABA for GABA a receptor

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83
Q

carbamazepine mech of action

A

increase inactivation of sodium channels by keeping sodium gate in closed position for longer.

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84
Q

what kind of seizures do you use carbamazepine for

A

focal seizures or tonic clonic seizures

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85
Q

side effects of carbamazepine (2)

A

stevens johnosn symdrome

blood dyscrasias

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86
Q

pheytoin used for what seizures

A

status epilepticus and focal seizures and GTCS

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87
Q

phenytoin mech of action

A

increases sodium channel inactivation, reducing neurotansmitter release

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88
Q

dosing of phenytoin

A

non-linear relationship between dose and plasma level, have to monitor

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89
Q

adverse effects of phenytoin

A
  1. cardiac arrythmias
  2. SJS, TEN
  3. gingival hyperplasia

HLA-B 1502 in Han Chinese can be at higher risk (also for carbamazepine)

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90
Q

primidone mech of action

A

increases sodium channel inactivation

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91
Q

topiramate mech of action (3)

A
  1. increases sodium channel inactivation
  2. inhibits kainate and/or AMPA receptors
  3. enhances actions of GABA
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92
Q

uses for topiramate 92)

A

focal seizures, GTCS

also anti migraine and migraine prophylaxis

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93
Q

lamotrigine mech of action (2)

A
  1. increases sodium channel inactivation

2. inhibits release of excitatory amino acids by acting on presynaptic voltage gated Ca2+ channels

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94
Q

lamotrigine adverse

A

rash - SJS

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95
Q

zonisamide use

A

adjuct therapy

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96
Q

zonisamide mech of action (2)

A

primary sit of action on sodium channel, also on T-type voltage gated calcium channels

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97
Q

benefit of zonisamide

A

does not interact with other AEDs

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98
Q

gabapentin use

A

adjuct therapy for focal seizures and chronic pain management

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99
Q

gabapentin mech of action (2)

A

binds to voltage gated Ca2+ subunit to decrease glutamate release

also inhibits GABA-T

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100
Q

gabapentin benefit

A

no drug reactions

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101
Q

levetiracetam mech of action

A

synaptic vesicle protein 2A protein ligand, inhibits excitatory amino acid transmitter release by interfering with fusion of vesicles

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102
Q

adverse effect of levetiracetam

A

behavioral changes, espectially in patients with psychiatric conditions

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103
Q

ethosuximide mech of action

A

inhibits T-type Ca2+ channel activity in thalamic neurons

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104
Q

side effect of ethosuximide

A

gastric distress

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105
Q

valproic acid side effects (2)

A
  1. GI distress

2. hepatotox

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106
Q

mech of action of valproic acid (3)

A
  1. like phenytoin increases Na channel inactivation
  2. reduces T-type Ca2+ activity
  3. increases GABA levels by inhibiting breakdown
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107
Q

uses of valpoic acid

A

GTCS, absence, myoclonic

108
Q

TIA time definition

A

less than 24 hours

109
Q

if you have a young person with stroke, what do you think it could be a result of

A

drug use (cocaine, heroin, amphetamines)

110
Q

what is the limiting factor in cerebral meatbolism - glucose or oxygen?

111
Q

at what time point does irreversible brain damage occur with hypoxia

A

~6 minutes

112
Q

difference between hypoxia and ischemia

A

ischemia is not enough blood volume (oxygen content is normal)

hypoxia is not enough oxygen content (blood flow is normal)

113
Q

what neuronal sites are the most vulnerable to hypoxia (3)

A
  1. hippocampal pyramida nuerons in sommer sector (CA1)
  2. pyramidal nuerons of cerebral cortex (layers 3+5)
  3. purkinje cells of cerebellum
114
Q

what neurotransmiter predominates in neurons that are highly susceptible to hypoxia

A

glutamate

decreased ATP leads to increased excitatory transmitter receptor activation, this causes calcium influx increases, damages mitochondria, stimulates NO and free radical production, leading to apoptosis and inflammatory mediators

115
Q

what areas in the brain are the most damaged in global hypoxia

A

zones at outer limit of vascualr territories

“watershed infarcts” - between ACA and MCA areas

116
Q

what areas in brain are affected by ACA issue

A

middle cerebral

117
Q

what areas in brain are affected by MCA issue

A

lateral cerebral, along lateral fissure

118
Q

what areas of brain are affected by central artery issue

A

around 3rd ventrical

119
Q

what areas are affected by PCA issue

A

occipital and inferior temporal

120
Q

anemic infarct characteristics and cause

A

pale, bland, non-hemorrhagic

no reperfusion to necrotic area, characteristic of thrombotic (in situ) infarct

121
Q

hemorrhagic infacrt characteristics and cause

A

red

reperfusion of necrotic area, characteristic of embolic (travelled) infarcts

122
Q

stages of infarct gross (and timing) (3)

A
  1. acute; 0-2 days (dusky blurring)
  2. subacute; 2-4 days (edema, soft)
  3. chronic; 4 days on (liquefactive necrosis first, cystic cavitation later)
123
Q

stages of infarct microscopic (histo)

A
  1. acute (red neurons, neutrophil migration to edge)
  2. subacute (red neurons break up - liquefactive necrosis, and neutrophils replaced by foamy macrophages and lymphocutes)
  3. chronic (necrotic cavity with edge of reactive astrocytes and new capillary formation and hemosiderin deposition on rim)
124
Q

major causes of subarachnoid hemorrhage (4)

A
  1. trauma
  2. saccular aneurysm rupture
  3. AVM rupture
  4. spread of intracerebral or intraventricular hemorrhage)
125
Q

major causes of intracerebral (parenchymal) hemorrhages (4)

A
  1. trauma
  2. chroninc HTN
  3. hemorrhagic infacrt
  4. cerebral amyloid angiopathy
126
Q

what are charcot-bouchard aneurysms

A

microaneurysms caused by hyaline arteriolosclerosis in deep perforating central branches

127
Q

what kind of hemorrhages do you see with chronici HTN

A

Intracerebral/ganglionic

128
Q

what kind of hemorrhages do you see with amyloid

A

intracerebral/lobar - peripheral. not in region of basal ganglia

129
Q

where are the sites of hemorrhage with chronic HTN

A

in area of basal ganglia

130
Q

what does epithalamus contain

A

pineal gland and habenular nucleus (limbic)

131
Q

what does subthalamus control

A

somatic motor control

132
Q

what part of thalamus is pineal gland near

A

posterior pole

133
Q

what are the divisions made by internal medullary lamina

A

anterior thalamic nuclei, medial thalamic nuclei, lateral and ventral thalamic nuclei

134
Q

what are nuclei within intralamina called and where do they project

A

midline nuclei

project to basal nuclei and diffuse areas of cerebral cortex

135
Q

what does reticular thalamic nucleus do

A

projects to different thalamic nuclei

136
Q

what are the lateral thalamic nuclei (what info do they recieve)

A 
lateral posterior (association of cortex)
lateral dorsal (limbic)
137
Q

pulvinar does what

A

connect with association areas of cortex (parietal, temporal and occipital)

138
Q

what are the ventral thalamic nuclei (what info do they recieve)

A

ventral anterior (motor)
ventral lateral (motor)
ventral posterior lateral (sensory body)
ventral posterior medial (sensory face)

139
Q

where are LGN and MGN located

A

under pulvinar in posterior thalamus

140
Q

anterior nucleus of thalamus does what

141
Q

medial dorsal thalamus does what

A

connects to association areas of cortex

142
Q

relay nuclei of thalamus in general go where (specific or broad areas)

A

to specific areas,

143
Q

anterior and lateral dorsal pathway to where

A

project to cingulate gyrus of limbic system

144
Q

medial dorsal projects to where and controls what functions

A

reciprocal to prefrontal cortex for executive function (ambition, drive, planning and personality)

145
Q

ventral anterior and ventral lateral input and output

A

input from globus pallidus and cerebellum

output to primary and premotor cortex

146
Q

what lesions cause thalamic pain

A

lesion in VPL or VPM

147
Q

PICA is brach off of what

A

vertebral artery

148
Q

anterior spinal artery is branch off of what

A

vertebral artery

149
Q

major branches of ICA (interal carotid) (4)

A
  1. ophthalmic
  2. anterior cerebral
  3. middle cerebral
  4. lenticulostriate and penetrating arteries
150
Q

what do lenticulostriate and penetrating artieries supply and what is stroke of these arteries called

A

internal capsule

stroke causes lacunar stroke

151
Q

branches of vertebral artery (2)

A
  1. spinal arteries

2. posterior inferior cerebellar artery (PICA)

152
Q

PICA infarct causes what

A

lateral medullary syndrome (wallenberg)

153
Q

what are the spinal arteries and where do they come out

A

1 anterior spinal artery
2 posterior spinal arteries

come out sporadically down the spinal cord - not regular

154
Q

branches of basilar artery (4)

A
  1. anterior inferior cerebellar artery (AICA)
  2. pontine branches
  3. superior cerebellar artery (SCA)
  4. posterior cerebral artery (PCA)
155
Q

“FAST” pneumonic is for what kind of stroke

A

MCA

face, arm, speech, time

156
Q

imipramine characteristics and use

A

very lipid soluble - TCA antidepressant

157
Q

problem with giving large amount of L-Dopa

A

body will change transport mech to make it harder to take up dopa

158
Q

how many of CSF is produced daily

159
Q

how many times is CSF turned over daily

A

3x (drugs will be washed away within 8 hrs)

160
Q

how much protein should you have in CSF

A

basically 0 – 0.004

161
Q

how much glucose should you have in csf

162
Q

CSF:plasma protein level increases in CSF, what does that mean

A

neurodegenerative disorder

163
Q

what causes aura in migraine

A

cortical spreading depression (CSD) - firing then not firing, changing blood flow

164
Q

what causes pain in migraine

A

activation of trigeminal system - vasodilated and inflammed vessels, relayed up through trigeminal system

165
Q

relation between aura and pain in migraine

A

CSD triggers neurons to release inflammatory mediatiors, which dilate meningial vellsel, causing activation of trigmeinal system and pain

166
Q

what nuclei give inputs/modulation into trigeminal system in migrains and what neurotransmitters are invovled

A

raphe and locus coeruelues (NE and serotonin)

167
Q

serotonin and migraine connection

A

serotonin constricts cerebral vessels, and effective migraine drugs have serotonin receptor effects

168
Q

what are the 5HT receptor subtype targets for migraine

A

5-HT1B, 5-HT1Da,b

169
Q

migraine prophylaxis and CSD relationship

A

migraine prophylactic meds elevate CSD threshold and suppress CSD (implicated in aura)

170
Q

beta blocker used for migraine and mech

A

propranolol

- mech unknown

171
Q

anticonvulsants used for migraine and mech (2)

A

valproate:

  • increases GABA
  • side effects not great

topiramate:

  • blocks Na and Ca channels, inhibits glutamate, enhances GABA, inhibits trigeminal system
  • weight loss, fuzziness, taste abmormalities
172
Q

how does botox work for migraine

A

cleaves SNARES in release of CGRP

173
Q

erenumab use and mech

A

migraine prophyaxis

monoclonal ab to CGRP receptor

174
Q

what antidepressants are used in migraine prophylaxis (2)

A

low doses of amitryptyline and nortriptyline

175
Q

drugs for acute MILD/MODERATE migraine (3)

A
  1. naproxen
  2. caffeine
  3. metoclopramide (good for nausea, not for pain)
176
Q

drugs for acute SEVERE migraine (2)

A
  1. ergots (bad side effects)

2. triptans

177
Q

mech of action of ergotamine

A

non-selective 5HT agonist at trigeminal nerve

178
Q

when to use ergotamine

A

very early in the migraine

179
Q

ergotamine side effects

A

nausea, vomiting, cramps, vertigo, ischemia, gangrene, cold extremities

180
Q

triptans (all) mech of action

A

5-HT1B, 5-HT1D and new ones F

D = peripheral to meningieal vessles, reduce release of inflammatory mediators

B = on blood vessels - direct vasoconscriptions

B, D and F also centrally to inhibit neurotransmission

181
Q

side effect of triptans (2)

A
  1. re-emergent/rebound migraine

2. coronary artery vasoconstriction (Avoid with ischemic heart disease)

182
Q

what is CGRP

A

calcitonin gene-related peptide

183
Q

what does amyloid look like on histo

A

vessel within a vessel, pright pink. or congo red apple green birefringence

184
Q

what is the most common cause of non-traumatic subarachnoid hemorrhage (and what’s a cause of that)

A

berry anueyrsm in branch points in circle of willis due to integrity defects in vessel (autosomal dominant polycystic kidney disease)

185
Q

most common site of berry aneurysim

A

junction between anterior communicating artery and anterior cerebral artery

186
Q

what are complications of berry aneurysm rupture (2)

A
  1. vasospasm due to blood causing infarct

2. arachnoid fibrosis causing communicating hydrocephalus (not in ventricular system)

187
Q

arteriovenous malformation location and description

A

commonly in MCA - artery goes to vein without capillary. “tangle of worms”

188
Q

how might arteriovenous malformation and cavernous hemangiomas present

A

can leak over time and cause seizure disorders

189
Q

histology of cavernous hemangioma

A

benign growth of capillaries, vessels with thin fibrous walls, no SM

190
Q

what is Binswanger’s disease

A

subcortical arteriosclerotic leukoencephalopathy causing vascular dementia (related to HTN, DM and atherosclerosis)

191
Q

diastatic fracture

A

fracture crossing bony suture line

192
Q

what artery is often involved in epidural hematoma

A

middle meningeal

193
Q

why are epidural hematomas emergencies

A

quick buildup of pressure pushes brain down and can herniate into brainstem and be fatal very quickly

194
Q

symptoms of epidermal hematoma

A

might be confused at first, and then can have lucid interval as blood accumulates

195
Q

common cause of subdural hematoma

A

tear in bridging vein between cortical surface and dural sinus

196
Q

why are subdural hematomas less emergent

A

they’re venous blood - don’t go as quickly. only sometimes fatal

197
Q

subarachnoid hemorrhage causes (3)

A

extend from AVM aneurysms
can come from trauma
contusions from parenchymal

198
Q

coup injury site, and contrecoup injury site

A

coup contusion AT impact site

contrecoup contusion on opposite side of skull due to rebound of brain

199
Q

where is damage seen with contusions

A

crowns of gyri

200
Q

diffuse axonal injury (what is it, and when is it seen)

A

stretching and shearing in deep white matter. axonal flow is disrupted - see axonal swellings with silver stain

concussion and shaken baby syndrome

201
Q

where do olfactory info neurons synapse in brain (4)

A

pyriform cortex
orbitofrontal cortex
amygdala
entorhinal cortex

202
Q

which epithelium is thicker, respiratory or olfactory epithelium

A

olfactory is thicker

203
Q

how many genes are in the family of odorant receptors

A

1,000, each receptor only expresses one allele of one gene

204
Q

cells in piriform cortex

A

2 types - finely tuned versus not finely tuned

205
Q

vomeronasal system purpose

A

sensing mates, predators and prey

dimorphism in genders

206
Q

what are olfactory glomeruli

A

single glomeruli are innervated by axons from ORNs that express the same single type of odorant receptor

207
Q

medial boundary of hypothalamus

A

4rd ventricl e

208
Q

3 regions of hypothalamus

A

anterior, tuberal, posterior

209
Q

what divides lateral and medial area of hypothalamus

210
Q

where is medial forebrain bundle found

A

in lateral hypothalamus

211
Q

what are the nuclei in the anterior medial hypothalamus (5)

A
  1. medial preoptic
  2. supraoptic
  3. paraventricular
  4. anterior
  5. suprachiasmatic
212
Q

what are the nuclei in the tuberal medial region of the hypothalamus (3)

A
  1. dorsomedial
  2. ventromedial
  3. arcuate
213
Q

what are the nuclei in the posterior medial region of the hypothalamus

A
  1. mamilary

2. posterior

214
Q

dorsal longitudinal fasciculus (where does it go to and from, and what info does it convey)

A

From hypothalamus, through periacqueductal grey, to smidbrain where it terminates on reticular formation, dorsal motor nucleus of 10, and salivatory nuclei

conveys visceral, somatic pain and tem, as taste TO hypothalamus

conveys symp and parasymp info FROM hypothalamus to intermediolateral horn and craniosacral parasympathetic neurons

215
Q

medial forebrain bundle (where does it go to and from, and what info does it convey)

A

extends from septal areal and forebrain through hypothalamus, down to spinal cord (parasymp and symp)

plays a role in reward pathway and “higher” function

216
Q

parasymp is mostly controlled by what area of hypothalamus

A

anterior hypothalamus

217
Q

symp is mostly controlled by what area of hypothalamus

A

posterior hypothalamus

218
Q

what is the role of the paraventricular nucleus

A

connects anterior and posterior nuclei of hypothalamus for autonomic control

219
Q

what sends pain and temp info to and motor response from paraventricular nucleus

220
Q

what sends emotional/limbic info to paraventricular for autonomic control

221
Q

how are temperature “set points” set

A

warm sensitive neurons (in preoptic) inhibit cool sensitive neurons (in posterior) when temps increase over 98.6 and increase parasympathetic mechanisms to reduce body temp (slow heart rate, panting)

when body is cooling, warm sensitive neurons reduce inhibition of cool-sensitive neurons, which stimulates sympathetic mechanisms to increase body temp (shivering, vasoconstriction)

222
Q

what controls circadian rhythm, pathway

A

suprachiasmatic nucleus:

blue light to retina to suprachiasmiatic to pineal gland - decreased melatonin secretion

223
Q

pituitary and hypothalamus connections

A

PVN and supraoptic produce ADH/oxytocin down to neurohypohysis (posterior pituitary)

arcuate nucleus produce releasing and inhibiotory factors into portal system (hypothalamophyphyseal portal system) into anterior pituitary

224
Q

what hypothalamic nucleus controls feeding behavior

A

ventromedial nucleus = satiety center

225
Q

eye deviation direction in L MCA stroke

A

toward lesion, away from hemiparesis

226
Q

how might subcortical strokes prsent

A

no eye or speech issues, no behavior change. most likely lacunar

face=arm=leg equally weakened

227
Q

when can you give tpa - what window?

A

up to 4.5 hrs

228
Q

when can you do mechanical clot extraction for large vessel occlusion - what time window?

A

up to 6 hours for anyone, and up to 24 hours if there’s a large enough penumbra

229
Q

what factors contribute to stroke risk after tia

A

ABCDD

  1. age
  2. blood pressure
  3. clinical symptoms (focal weakness or speech impairment)
  4. diabetes
  5. duration of symptoms
230
Q

do you treat HTN after ischemic stroke?

A

not unless BP is over 220/120

231
Q

what kind of saline do you use in stroke patient

A

only normal saline

232
Q

stroke prevention drug for non-cardiogenic recurrent stroke

A

antiplatelet (aspirin)

warfarin (no better than aspirin)

233
Q

stroke prevention drug for cardiogenic recurent stroke

234
Q

examples of cardiogenic causes of stroke (4)

A
  1. afib
  2. mechanical valve replacement
  3. cardiac thrombus
  4. MI
235
Q

most common arteries affected by arterial dissection

A

internal carotid

vertebral artery

236
Q

symptoms with arterial dissection (2 kinds)

A

anterior (ICA) = pain, horner’s, hemiparesis, retinal ischemia

posterior (vertebral artery) = pain, cerebellar or lateral medullary syndrome

237
Q

tx for arterial dissection

238
Q

mortality is higher in which kind of stroke - hemorrhagic or ischemic

A

hemorrhagic - 50%

239
Q

biggest risk factor for hemorrhagic stroke

240
Q

what are the areas most commonly involved in HTN intercerebral hemorhage

A

basal ganglia most common

then brainstem or cerebellum

241
Q

if someone has hemorrhagic stroke, what other systemic tests do you do (3)

A
  1. send to ophtho to look for retinopathy
  2. do EKG to look for cardiomyopathy
  3. look at kidney labs to look for renal dysfunction
242
Q

what population do you expect to see amyloid angiopathy in

A

older and with alzheimers

243
Q

what kind of stroke (and where) does amyloid angiopahty cause

A

hemorraghic

recurrent lobar hemorrhage

244
Q

what vessel does an AV malformation commonly affect

245
Q

most common primary brain tumor to cause hemorrhagic stroke

A

glioblastoma multiforme

246
Q

most common mets to brain that cause hehmorrhagic stroke (2)

A

melanoma

carcinoma of lung

247
Q

do you treat HTN after hemorrhagic stroke?

A

yes, if it’s HTN cause. tx with labetalol and nicardipine

248
Q

when do you perform sx after hemorrhagic stroke (2)

A

if there’s a cerebellar hemorrhage greater than 3cm

or intracerebral associated with aneurysm or vascular malformation

249
Q

which way does subarachnoid hemorrhage spread

A

in to out, most common - asosciated with ruptured aneurysm in circle of willis

250
Q

tx for subarachnoid hemorrhage

A

nimodipine to prevent vasospasm to delay ischemic deficit

251
Q

what are the tributaries of internal jugular from top to bottom (7)

A
  1. occipital
  2. retromandibular
  3. lingual
  4. facial
  5. superior thyroid
  6. middle thyroid
  7. inferior thyroid (usually drains into brachiocephalic)
252
Q

branches off of external carotid from bottom to top (8)

A

Some Anatomists Like Freaking Out Poor Medical Students

  1. superior thyroid
  2. ascending pharyngeal (comes off medially)
  3. lingual
  4. facial
  5. occipital (comes of medially)
  6. posterior auricular (comes off medially)
  7. maxillary
  8. superficial temporal
253
Q

carotid sinus innervated by

A

glossopharyngeal

254
Q

after superior cervical ganglion, what to symp fibers travel on into head

A

internal carotid nerve plexus

255
Q

what inputs into superior cervical gnalgion (C_-C_)

256
Q

posterior plexus of cervical plexus carry what info

A

sensory info from scalp, ear, anterior/lateral neck, shelf of shoulder

257
Q

anterior plexus of cervical plexus carry what info

A

motor to muscles of anterior and lateral neck

258
Q

what is punctum nervosum

A

where all 4 sensory nerves exit posterior cervical plexus (where you can put nerve block)

259
Q

what are the posterior plexus nerves and what spinal segment are they from (4)

A
  1. lesser occipital (C2)
  2. great auricular (C2,3)
  3. transverse cervical (C2,3)
  4. supraclavicular (C3,4)
260
Q

what nerve innervates skin on back of head

A

dorsal rami if C2

261
Q

what nerve roots make up ansa cervicalis

262
Q

what are the deep cervical fascial layers (4)

A
  1. investing layer
  2. pretracheal fascia
    includes pretrach infrahyoid investing
    includes pretrach visceral fascia
    includes buccopharyngeal fascia
  3. prevertebral fascia
  4. carotid sheath
263
Q

is ansa cervicalis inside or outside carotid sheath

264
Q

contents of carotid sheath (6)

A
  1. common carotid
  2. internal carotid
  3. internal jugular
  4. vagus
  5. carotid sinus
  6. some sympathetics
265
Q

zones for penetrating neck trauma

A

zone 1 = clativcles to cricoid

zone 2 = cricoid to angles of mandible

zone 3 = angles of mandible

266
Q

which zones of penetrating neck trauma are the greatest risk for morbidity and mortality

A

1 and 3 because they can obstruct airway and the structure are compact and hard to visualize for repair and control bleeding

Brain and Behavior (6 decks)

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