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Neuro 1 > High yield test 2 > Flashcards

High yield test 2 Flashcards

1
Q

In shaken baby syndrome what vein is torn that causes hemorrhaging?

A

bridging vein which creates a subdural space in between the arachnoid and the dural mater and can enter subarachnoid space

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2
Q

If there is a blockage of the internal jugular vein at the base of the school how does blood of the skull drain?

A

Blood would then drain through superficial veins of the school such as the opthalmic vein to the facial vein to common facial then back into internal jug, or through the vertebral venous plexus

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3
Q

what cranial nerves are associated with the cavernous sinus?

A

CN’s III, IV, V1, V2, sit on the edge of the sinus but CN VI sits inside the sinus directly behind the internal carotid artery

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4
Q

A patient presents with an infection or thrombis of the internal carotid artery inside the cavernous sinus. Which CN will be the first to be effected and the most effected? what muscle will be affected?

A

CN VI sits directly posterior to the internal carotid artery inside the sinus
LR which causes abduction of eyeball

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5
Q

where is the skull the thinnest and is most prone to injury?

A

Pterion which blunt injury can cause an epidural hemotoma.

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6
Q

what is the supratentorial fossa innervated by and primary blood supply?

A

V1 V2 V3 middle meningeal artery form maxillary artery

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7
Q

what innervates the underside of the tentorium in the posterior cranial fossa? (Dura of the posterior cranial fossa)

A

X, and C1 C2 via XII

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8
Q

where will large diameter neurons ascend the spinal column?

A

Within the posterior funiculus in the fasiculus cuneatus or fasiculus gracilis aka dorsal column

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9
Q

where will small diametre neurons ascend the spinal column?

A

within the spinothalamic tract

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10
Q

what type of neuron is the first neuron in any ascending pathway?

A

psuedounipolar

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11
Q

merkles discs respond to?

A

pressure pcml pathaway

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12
Q

ruffuni corpuscles respond to?

A

skin stretch pcml pathway

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13
Q

meissner’s corpuslce respond to?

A

fine touch pcml pathway

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14
Q

pacinian corpuscle respond to?

A

vibration pcml pathway

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15
Q

free nerve endings respond to what?

A

pain temperature and itch participate in spinothalamic pathway

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16
Q

what receptors respond to muscle stretch vs muscle tension?

A

golgi tendon organs respond to tension, muscle spindle respond to length

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17
Q

what kinds of somatic sensation does the PCML pathway include?

A
  • discriminative touch (two point discrimination)
  • vibration
  • 3D form
  • proprioception, conscious limb and joint position
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18
Q

What kinds of somatic sensation does the spinothalamic tract include (ALS)?

A
  • non-discriminative touch (crude touch)
  • thermal sensation
  • nociception
  • itch
  • unconscious proprioception
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19
Q

where are the primary cell bodies, 1st synapse, location it enters spinal cord, decussates, 2nd synapse, and final destination for PCML pathway?

A

primary cell bodies are in the dorsal root ganglion then 1st synapse is in nucleus gracilis or nucleus cuneatus in the caudal medula, then enters spinal cord medial aspect of dorsal root in FC and FG, decussates internal arcuate fibers ventral to cuneatus and gracilis (becomes medial lemniscus), 2nd synapse on VPL of thalamus, final destination in primary somatosensory cortex via internal capsule and corona radiata

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20
Q

what receives information from lower body?

A

nucleus gracilis

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21
Q

what receives information from upper body?

A

nucleus cuneatus

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22
Q

Loss of the posterior spinal artery would result in disruption of the PCML pathway at what point?

A

loss of 2nd order cell bodies in the nucleus gracilis and nucleus cuneatus

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23
Q

Loss of the anterior spinal artery would disrupt the PCML pathway at what point?

A

lead to loss of internal arcuate fibers that form the medial lemniscus

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24
Q

what level of information does the gracile fasiculus carry?

A

medial below t6

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25
Q

what level of info does the cuneatus fasciculs carry?

A

lateral above t6

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26
Q

walk through the entire ALS (spinothalamic pathway)

A

transmits pain, temp, poorly localized touch, point o forigin is free nerve endings (TRP channels) with primary cell bodies in DRG 1st synapse in lamina 1 and 2, enters spinal cord in dorsal horn (lissaauers fassiculus to ascend at least 1 segment) then ascend through ALS tract, decussates in spinal cord after 1st synapse, 2nd synaps on vpl of thalamus then on to primary somatosensory cortex

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27
Q

where do 2nd order neurons of the spinothalimc pathway decussate?

A

at the vertebral level they enter (or one above) decussate in VENTRAL WHITE COMMISURE

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28
Q

loss of the middle portion of the somatosensory cortex could be from what artery and would result in loss of sensation to what areas of the body?

A

genitals foot lower limb loss of anterior cerebral artery

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29
Q

loss of the lateral portion of the somatosensory cortex could be from what artery and would result in loss of sensation to what areas of the body?

A

face tongue middle cerebral artery

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30
Q

The anterior spinocerebellar tract carries what kind of information?

A

Unconscious proprioceptive info from ipsilateral trunk and lower limb
-carry broad integrated information on entire limb

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31
Q

what kind of information does the rostral cerebellar tract carry?

A

unconscious proprioception from ipsilateral upper limb

-carry broad integrated information on entire limb

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32
Q

what kind of information does the posterior spinocerebellar tract carry?

A

Unconscious proprioceptive from ipsilateral trunk and lower limb

  • fine detailed proprioceptive
  • single muscle cells, muscle tendon complex
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33
Q

are cerebellar ataxia symptoms ipsilateral or contralateral?

A

always ipsilateral

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34
Q

describe the posterior spinocerebellar patheway and cuneocerebellar pathway?

A

point origin is muscle spindle fibers and golgi tendon organs, then primary cell bodies in DRG, 1st synapse in clarkes nucleus lamina VII (nucleus dorslalis) of thoracic cord if dorsal spinal cerebellar or accessory cuneate nucleus if caudal medulla if cuneocerebellar, enters spinal cord posterior funiculi hikes up dorsal columns (cuneocerebellar tract only does not decussate, 2nd synapse is in the vermis/paravermis of the cerebellum via inferior cerebellar peduncle final destination is deep cerebellar nuclei (via purkinji cells)

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35
Q

What kind of information does the cuneocerebellar tract carry?

A

unconscious proprioception from ipsilateral upper limb

  • fine detailed proprioceptive
  • single muscle cells, muscle tendon complex
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36
Q

what level determines if information travels with the cuneocerebellar tract vs the posterior cerebellar tract?

A

C8 below dorsal cerebellar above cuneate nucleus

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37
Q

describe the pathway of the anterior spinal cerebellar tract?

A

origin: muscle spindals, golgi tendon organs in muscles and joints primary cell bodies in DRG 1st synapse in Laminae VII enters spinal cord posterior funiculi decussates immediately in spinal cord second synaps in vermis/paravermis of cerebellum via superior cerebellar peduncle will then decussate again final destination deep cerebellar nuclei via perkinji cells

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38
Q

how can an infection spread from the scalp into the brain?

A

the emissary veins drain through the skull and enters the brain through dural sinuses, emissary veins function to cool the brain

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39
Q

a hematoma seen above the aponeurosis of the scalp is called what?

A

caput succedneum

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40
Q

a hematoma seen just below the aponeurosis of the scalp is called what?

A

subgaleal hematoma not limited by sutures gets worse after birth

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41
Q

a hematoma seen just below the pericardium of the skull is called what?

A

cephalohematoma limited to one bone due to tight adherence of sutures

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42
Q

what two muscles raise the upper eyelid and one muscle that depresses lower eyelid and innervations?

A

levator palpebrae superioris (voluntary striated)
and superior tarsal muscle (involuntary SMC sympathetic)
inferior tarsal muscle depresses lower eyelid

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43
Q

what muscle elevates the eybrow?

A

occipital frontalis

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44
Q

what is sjorgren syndrome?

A

autoimmune disease effecting primarily salivary and lacrimal glands

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45
Q

what foramen does the facial nerve exit?

A

stylomastoid foramen

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46
Q

describe the venous drainage of the skull?

A

superficially the supraorbital and supratrochlear veins form the angular vein with forms the facial vein which drains into common facial to i jug

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47
Q

where does lymph drainage from the lips/ chin drain?

A

submental nodes

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48
Q

where is the first neuron for visceral sensory information for CN VII?

A

geniculate ganglion

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49
Q

where is the second neuron for visceral sensory information in CN VII

A

solitary nucleus

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50
Q

where are the GVE-P’s for CN VII?

A

first neuron is superior salivary nucleus 2nd nueron is pterygopalatine ganglia or otic

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51
Q

where are the somatic sensory neurons for CN IX located?

A

1st neuron: Superior ganglion of IX

2nd neuron: Spinal trigeminal nucleus

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52
Q

where are the visceral sensory neurons for CN IX located

A

1st neuron: Inferior ganglion of IX

2nd neuron: Solitary nucleus

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53
Q

where are the GVE-P for CN IX located?

A

1st neuron: Inferior salivary nucleus

2nd neuron: Otic ganglion

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54
Q

where are the LMN’s for somatic motor of CN IX located?

A

nucleus ambiguus

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55
Q

where are the somatosensory neurons for X?

A

Somatic sensory
1st neuron: Superior ganglion of X
2nd neuron: Spinal trigeminal nucleus

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56
Q

where are the visceral neurons for X?

A

Visceral sensory:
1st neuron: Inferior ganglion of X
2nd neuron: Solitary nucleus

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57
Q

where are the somatic motor neurons for X?

A

nucleus ambiguus

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58
Q

where are the GVE-P for X?

A

Parasympathetic
1st neuron: Dorsal motor nucleus of X (VISCERAL MOTOR)
2nd neuron: Various ganglia

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59
Q

where do the psuedounipolar cell bodies sit for proprioceptive info of the face?

A

they are in the mesencephalic nucleus

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60
Q

the ventral trigeminothalamic tract contain what information

A

Spinal nucleus
crude touch
Pain, temperature
Contralateral

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61
Q

the dorsal trigeminothalamic tract contains what information?

A

Principal (Main, Chief) nucleus
Fine touch
Bilateral

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62
Q

talk me through the ventral trigeminothalamic tract

A

type info: pain temp, origin free nerve endings (TRP channels) primary cell bodies in trigeminal/semilunar/gasserian ganglion 1st synapse in spinotrigeminal nucleus in medulla, enters brainstem in Pons, descends to spinal trigeminal nucleus in medulla, decussates: Internal arcuate fibers in medulla, second synapse is: Ventral posterior medial nucleus (VPM) of the Thalamus, Final destination: Primary somatosensory cortex (via internal capsule and corona radiata)

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63
Q

explain the dorsal trigeminothalamic tract

A

info: tactile discrimination
origin: meissners corpuscle, pacinian corpuslce, ruffunis ending, merkels disc,
primary cell bodies in: trigeminal/semilunar/gassrian nucleus
1st synaps is in main sensory nucleus
enters brainstem: pons ascends contralaterally and ipsilateraly is mainly oral cavity
decussates: in pons ascends with medial lemniscus
second synapse: VPM of thalamus
final destination: somatosensory cortex

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64
Q

what causes wallenberg syndrome (lateral medullary syndorme) and how does is present?

A

stroke to PICA artery leads to ipsilateral pain and temp loss to face and contralateral pain and temp loss in body
horners syndrome

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65
Q

explain the paleospinothalamic tract pathway?

A

info: poorly localized pain, origin: free nerve endings, primary cell bodies in DRG, 1st synapse in lamina I-VI enters dorsal horn (lissaueres fassciuculus ascends 1 segent then travels bilaterally and ascends through anterolateral spinal thalamic tract, decussates in spinal cord after 1st synapse, 2nd synapse is intralaminar nuclei of the thalamus, final destination is bilateral cortex poorly localalized (includes cingulate gyrus and insula)

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66
Q

pathway for spinoreticular and spinomesencephalic tracts

A

info: Pain
origin: free nerve endings, primary cell bodies DRG,
1st synaps lamina 1-2, enters dorsal horn lissauers fassiculus ascend 1 segement, travel b/l through ALST
decussates in spinal cord after 1st synaspe
2nd synapse in medullary/pontine reticular formation/parabrachial nucleus (spinoreticular); periaquedcucatal grey matter ( spinomesencephalic) descend in DLF, 3rd synapse ipsilateral dorsal horn of spinal cord

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67
Q

what compounds can inhibit painful stimuli coming into the spinal cord?

A

seretonin, norepi

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68
Q

what kind of pain fibers carry visceral pain?

A

C-fibers

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69
Q

what bones in the skull come from NC cells?

A

all bones in front of ear/ frontal/ mandible, maxilla, zygomatic, hyoid

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70
Q

what bones in the skull come form paraxial mesoderm?

A

all bones behind ear, parital occipital

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71
Q

what time frame does the anterior frontanelle close?

A

around 18 months

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72
Q

what time frame does the anterolateral and posteriolateral frontanelle, and posterior frontanelle close?

A

around 6 months

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73
Q

what is craniosynostosis?

A

premature fusion of sutures

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74
Q

what can result from premature fusion of saggital sutures

A

can cause scaphocephaly protrusions on sides of head

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75
Q

what causes brachiocephaly?

A

premature fusion of coronal suture

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76
Q

achondroplasia primariyly effects what kind of bone growth?

A

long bone formation through premature closure of growth plates, has little effect on intermembranous bone formation like flat bones of skull however can narrow cervicl canal and foramen magnum

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77
Q

what makes up the fused medial nasal prominences?

A

nose ridge, tip, philtrum, and primary palate

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78
Q

what forms the uvula

A

created by fusion at caudal end of palatine shelves.

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79
Q

what is the cause of an oblique cleft?

A
  • failure of maxillary prominence to fuse with lateral nasal prominence.
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80
Q

what is the cause of a primary cleft lip/pallet?

A

failure of maxillary prominence to fuse with medial nasal prominence (or intermaxillary segment).

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81
Q

what is the cause of a secondary cleft pallet/lip?

A

failure of maxillary prominences (lateral palatine plates) to fuse in midline.

82
Q

where does the superior constrictor attach?

A

posteromedially from the occipital bone

83
Q

what is the significance of the pharyngeal raphe?

A

point where the left and right halfs of the pharyngeal muscles meet in essesnce all pharyngeal muscles suspended from the pharyngeal tubercle

84
Q

what is the role of the superior constrictor in swallowing?

A

initiates peristaltic like movements to push food to esophogus
-seals off nasopharynx

85
Q

what is the pathology associated with zenker’s diverticulum?

A

mucosa pushes out in between thyropharygeus and cricopharyngeaus created a pocket for food to get stuck

86
Q

what structure does the auditory tube pierce in order to access the nasopharynx?

A

the pharngobasilar fascia

87
Q

what goes through gap 1 of the pharynx and where is it located?

A

gap 1: above the superior constrictor Gap 1 transmits the auditory tube and levator veli palentini muscle (elevates soft palet)

88
Q

what goes through gap 2 of the pharynx and where is it?

A

between the superior and middle constrictor: transmits the stylopharyngeaus muscle and the stylohyoid ligament, and glossopharygeal nerve

89
Q

what defines gap 3 of the pharynx and what does it transmit?

A

in between middle constrictor and lower constrictor internal branch of superior laryngeal nerve and superior laryngeal artery (thru the thyrohyoid membraine)

90
Q

what defines gap 4 of the pharynx and what does it transmit?

A

below the inferior constrictor transmits inferior laryngeal N and inferior laryngeal A.

91
Q

what muscle is primarily responsible for opening the auditory tube when swallowing?

A

tensor levi palaltini

92
Q

CN X provides motor efferents to all the muscles of the pharynx except?

A

tensor veli palentini which is CN V and stylopharygeus which is CN IX

93
Q

what nerve carries sensory information to the piriform recesses?

A

CN X via superior laryngeal nerve

94
Q

what nerves contribute to the gag reflex?

A

motor is CN X sensory is CN IX

95
Q

what artery provide the blood supply to the pharynx?

A

sup inf thyroid and ascending pharyngeal a

96
Q

what are extrinsic laryngeal muscles?

A

Many attach to the hyoid bone, function to elevate, depress, or constrict the larynx as a whole (supra/infra hyoid strap muscles, pharyngeal constrictors)

97
Q

what are intrinsic laryngeal muscles?

A

small muscles directly on or inside the laryngeal cartilages, act on the glottis or move laryngeal cartilages

98
Q

what is the only intrinsic muscle of the larynx that can abduct the glotis?

A

posterior cricoarytenoid muscle

99
Q

what is the action of the cricothyroid muscle?

A

lengthens the vocal ligament/ adds tension increase in frequency

100
Q

what muscles adduct the glotis?

A

oblique pull them close together and transverse arytenoid pull together but leave a gap

101
Q

what is the function of the thyroarytenoid vocalis?

A

tenses VL

102
Q

which intrisnsic laryngeal muscle is not innervated by the RLN? and what is its innervation

A

cricothyroid external branch of SLN

103
Q

what is the venturi effect?

A

the narrower a tube the lower the pressure in that tube

104
Q

what is bernoulis principle?

A

as you increase speed in a pipe pressure decrreases

105
Q

where do the superior and inferior laryngeal veins drain?

A

both drain into superior thyroid vein/ superior laryngeal vein comes out of whole in cricothyroid membrane

106
Q

what happens to the thyroid cartilage in a male during puberty?

A

entire cartilage lengthens due to sensitivity to testosterone which lengthens the vl causing a deeper voice.

107
Q

what regulates UMN’s?

A

modulated by basal ganglia and cerebellum

108
Q

what is areflexia?

A

loss of muscle tone

109
Q

what are fasiculations?

A

local small twitch due to alpha motor neuron damage

110
Q

where are the LMN cell bodies located?

A

ventral horn lamina IX

111
Q

descending pathways for voluntary movement is located where in the spinal cord?

A

lateral corticospinal pathways

112
Q

descending pathways for maintenance of posture and balance is located where in the spinal cord?

A

ventromedial cortical spinal

113
Q

where is the supplemental and premotor cortexes located?

A

medial to premotor is sup

and anterior to primary motor cortex is premotor

114
Q

where do you find the cell bodies of all UMN?

A

in the primary motor cortex

115
Q

what layer of the cortex do UMN’s (betze/pyramidal reside)

A

layer V

116
Q

UPN’s of the corticospinal tract that innervate axial musculature through thoracic spinal cord (trunk and spine muscles) travels what route?

A

they travel from layer V of cortex down posterior limb of internal capsule but do not decussate in the pyramids instead travel down anterior and ventral spinal tracts ipsilaterally

117
Q

what is the pathology associated with cerebral palsy?

A

Hypertonia is most pronounced symptom
+ developmental delay, visual & auditory impairments
causes: prenatal hypoxia, perinatal asphyxia, infection
 damage to white matter lateral/dorsal to lateral ventricles
= UMN lesion
= Cortex, Internal capsule, CST

118
Q

what is a babinski sign?

A

toes go upwards associated with UMN damage

119
Q

what is the role of the lateral vestibulospinal tract and where are their UMN located?

A

maintains posture to compensate for body movement/ DESCENDS IPSILATERAL UMN located in brainstem specifically lateral vestibular nucleus in rostral medulla not in cortex mostly goes to lower spinal cord through anterior funiculus
-Projects ipsilaterally the full length of the spinal cord

120
Q

What is the role of the medial vestibulospinal tract and where are there UMN located?

A

coordinates head and eye movement/ stabilizes head/ DESCENDS BILATERALY head stability mostly goes to cervical cord/ UMN located in medial vestibular nucleus of rostral medulla in brainstem
-Projects to medial longitudinal fasiculus (MLF) on both sides
Travels bilaterally in cervical spinal cord

121
Q

trauma to the anterior spinal artery would effect which portion of the vestibulospinal tract pathway?

A

the tracts

122
Q

trauma to the posterior inferior cerebellar artery would effect which portion of the vestibulospinal parthway?

A

nuclei or cerebellum

123
Q

trauma to the posterior medulla would effect what tracts the most?

A

most likely knock out lateral and medial vestibulospinal tracts because there nuclei sit on posterior medulla (rostral)

124
Q

initial flaccid paralysis that leads to atrophy /hypotonia/ weak lost stretch reflex/fasciculations/damage along one myotome are indicative of what kind of damage

A

damage to LMN’s

125
Q

initial flaccid paralysis that leads to spasticity /hypertonia/ hyperflexia/ clonus/ babinski sign/ damge to groups of muscles is usually a sign of what kind of damage?

A

damage to UMN’s

126
Q

what is the function of the tectospinal tract?

A

originates in superior colliculus: Decussates (posterior tegmentum) goes to cervical spinal cord
Affect musculature of neck, eyes
Postural reflexes to alarming visual stimuli, some auditory stimuli
found very anterior medial in spinal cord

127
Q

following primary damage to your corticospinal tract what tract may be able to take over function?

A

Rubrospinal tract: Decussates
(anterior tegmentum)
To cervical spinal cord
Laterally-based tract, involved with flexor muscles…arm?

128
Q

what kind of neurons control neurons coming out of the reticuospinal tracts?

A 
controlled by cortical motor centers
-from reticular formation
Decussates 
To axial and postural muscles
Stabilizes movement on uneven surfaces
Can provide secondary control when CST is dysfunctional
129
Q

what tract can provide secondary control if your corticospinal tract is damaged?

A

reticuospinal tract

130
Q

a lesion in the cortex would cause what kind of symptoms for Bronchiomeric muscles, facial expression above above the eyes?

A

bilateral but minor usually/ a lesion of then nucleus causes ipsilateral deficiency

131
Q

a lesion in the cortex would cause what kind of symptoms for Muscles of facial expression below the eyes, tongue?

A

contralateral/ Lesion of nucleus causes ipsilateral deficiency.

132
Q

the nucleus ambiguus includes the motor components of what nerves?

A

9,10

133
Q

If a patient can raise eyebrows and wrinkle forehead but has hemiparalysis left side of face where might there be an issue?

A

most likely in the right cortex

134
Q

if an entire side of facial muscles are not working where might you suspect damage?

A

could be lower motor neuron or lesion of nucleus causing ipsilateral symptoms

135
Q

If a patient sticks their tongue out and the tongue points to the left where might there be a lesion?

A

left lesion of CN XII nerve or nucleus (or right motor cortex) motor fibers for the tongue all go contralaterally

136
Q

what structures are part of basal ganglia?

A 
Striatum
    caudate nucleus
    nucleus accumbens
    putamen
Globus pallidus (pallidum)
    Globus pallidus external
    Globus pallidus internal
137
Q

In the direct basal ganglia pathway what types of nuerotransmitters are released where?

A

motor cortex sends off GLU which activates muscles and striatum caudate and putamen which then sends gaba to globus pallidis internal- which inhibits it from dending its gaba to thalamus which allows thalumus (VA/VL nuclei) to send more glu to motor cortex. The substancia nigra pars campacta also sends dopamine which acts on d1 of “striatum caudate putamen to tell it to pump out more gaba

138
Q

what is the overall effect of the indirect basal ganglia pathway and all the steps?

A

overall effect is to decrease motor output. motor cortex (M1)-sned Glu to muscles and to striatum (caudate &putamen) which sends GABA to globus palludis external which blocks it from sending gaba to subthalamic nucleus allowing it to send more glu to Globus palludis interus (GPI) which sends more gaba to thalamus blocking it from sending glu to motor cortex

**still have substancia nigra but this time sends dopa to D2 receptors which inhibits Striatum from sending out gaba

139
Q

what is the root cause behind parkinsons disease?

A 
loss of DOPA neurons
Resting tremor
Rigidity (lead pipe)
Bradykinesia (akinesia)
damages the direct basal ganglia pathway causing a hypokinesia type disease (loss of motor movement)
140
Q

What is the pathology associated with huntingtons disease?

A

CAG repeats cause damage to indirect basal ganglia pathway neurons leading to Targets the striatum
Chorea (random, involuntary, flicking mvmt.)
Considered a disorder of “hyperkinesia”
-often begins with depression

141
Q

how does a lens placode form?

A

optic vesicles come into contact with surface ectoderm which causes them to form lens placodes

142
Q

what allows the hyloid artery to enter into the eye?

A

Optic vesicles invaginate forming a double-walled optic cup. Inferior surface of optic cup invaginates to create choroid fissure, which allows hyaloid a. to reach inner chamber of eye.

143
Q

what is congenital retinal detachment?

A

separation of internal and external layer of optic cup (separating pigmented epithelium from rods/cones

144
Q

what is the embreological origin of the choroid, muscles in the eye (intraocular muscles), and sclera of eye?

A

comes from undifferenciated mesenchyme from NC cells

145
Q

what causes a persistant Iridopupilary membrane?

A

Cause = failure of iridopupillary membrane degeneration

146
Q

what causes a coloboma?

A

Cause = failure of choroid fissure to close

147
Q

what is the name of the anomoly where lens does not form on eye?

A

Congenital aphakia-

148
Q

what is the cause of Leber’s congenital amaurosis?

A

Abnormal development of photoreceptor cells

149
Q

what is the embreological origin of extraoccular eye muscles?

A

Extraocular eye muscles form directly from paraxial mesoderm (GSE)

150
Q

what fascia layer of the eye is continuous with the dura?

A

periorbita

151
Q

what fascia layer surrounds the globe directly and is attached to the sclera?

A

bulbar fascia

152
Q

what muscle is usually damaged with ptosis of the eyelid and what is its innervation?

A

levator palpebrae superioris GSE CN III

153
Q

define the following: dipopia, enopthalmus, eccymosis

A

diplopia- double vision

enopthalmus: posterior displacement of the eyeball within the orbit
eccymosis: discoloration of the skin resulting from bleeding underneath,

154
Q

what is the site of muscle attaqchments in the eye?

A

sclera

155
Q

how does the cornea receive oxygen?

A

dissolved tears

156
Q

what muscle constricts the pupil and innervation?

A

sphincter pupilae parasympatheitc

157
Q

what muscle dilates the pupil and innervation?

A

dilator pupilae, sympathetics

158
Q

what are the functions of the ciliary body?

A

aqueous humor production and accommodation, paraympatheitically innervated

159
Q

what is the main cause of glaucoma?

A

blockage in the trabecular meshwork called an open angle glaucoma this results from too much aqueous humor putting pressure in ant segment that puts pressure on post segment which compromises blood flow

160
Q

how does closed angle glaucoma result?

A

iris physically blocks iridiocorneal junction; painful and rapid onset.

161
Q

where does the superior opthalmic vein drain?

A

cavernous sinus

162
Q

where does the inferior opthalmic vein drain?

A

pterygoid venous plexus

163
Q

what nerve and specific branch gives you sensation when you touch your eye?

A

V1- nasocilliary branch

164
Q

what nerves are responsible for the corneal reflex (blink reflex)?

A

Afferent nerve – CN V1

Efferent nerve – CN VII

165
Q

what is the vestibulo ocular reflex?

A

Movement of the eyes to compensate for movement of the head

166
Q

what is the Optokinetic reflex?

A

Nystagmus during movement of visual stimuli across the retina

167
Q

If a patient has difficulty moving her left eye where in the midbrain would you expect damage?

A

medial longitudinal fasciculus connects the cranial nerves and integrates movements directed by gaze. travel ipsilaterally

168
Q

what does the superior colliculus use to control eye movements?

A

goes through pprf (paramedian pontine reticular formation) to orient eyes stimulating abducens nuclei and occulomotor of opposite eye

169
Q

for voluntary saccades what is the pathway taken?

A

BA 8 (frontal eye fields) go to contralateral superior colliculus which then follows its normal routs of sc to PPRF to abducens nuclei and contralateral occulumotor nucleu

170
Q

parietal eye fields are at what part of the brain and follow what pathway?

A

angular and supramarginal gyrus contralateral projection to superior colliculus follows that path

171
Q

what part of the brain has an inhibitory effect on parietal eye fields and frontal eye fields?

A

dorsolateral prefrontal cortex

172
Q

what is the function of the RIP (OPN) Raphe Interpositus (Omnipause)?

A

tonic inhibition of the PPRF by secreting glycine

173
Q

exact pathway and neurotransmitters for the superior colliculus disinhibition pathway?

A

contralateral cortex tells for disinhibition sup colliculus sends out GABA which inhibits the inhibitor RIP OPN causing it to send out less glycine to PPRF allowing pprf to activte abducens nucleus and internuerons that connect to occulomotor nucleus

174
Q

what neurotransmiter does substansia nigra pars reticulata release?

A

GABA - acts on va/vl nuclei of thamalmus to inhibit

175
Q

what neurotransmitter doe substantia nigra pars compacts release?

A

Dopamine that acts on d1 receptors to activate or d2 receptors to inhibit striatum

176
Q

where do fibers from the temporal aspect of the retina go?

A

these fibers remain ipsilateral after the optic chiasm

177
Q

where do fibers from the nasal aspect of the retina go?

A

contralertally after the optic chiasm

178
Q

where do rod cells project to?

A

magnocellular lamina 1-2 of LGN of thalumus

179
Q

where do cone cells project to?

A

parvocelluar cells of lamina 3-6

180
Q

what layers of the LGN receive contralateral information?

A

1,4,6

181
Q

what layers of the LGN receive ipsilateral info?

A

2,3,5

182
Q

what kind of fibers does meyers loop contain?

A

fibers from superior visual fields

183
Q

what kind of fibers does baums tract contain?

A

fibers from inferior visual fields

184
Q

where would you expect a lesion for bitemporal hemianopia

A

this is loss of lateral field in both eyes usually a problem at the optic chiasm

185
Q

what is the reaction to on bipolar cells in a light environement?

A

since there is light cone or rod will be hyperpolarized meaning no release of glu, on cells hyperpolarize in resposne to glu they will now be active because no glu use MGLUr 6 channel

186
Q

what is the response to off cells in the absense of light?

A

with no light rod or cone cells secrete glu glu causes these cells to depolarize, no light = no glu =active…
use ampa/kaiintae channels
also remember rods have to use extra cell called amacrine instead of direct connection to photoreceptors

187
Q

what tracts enter through the inferior cerebellar peduncle?

A

Ipsilateral info from vestibulocerebllar and spinocerebellar tracts as well as olivocerebellar
ALSO efferents to vestibular nuclei

188
Q

what tracts enter through the middle cerebellar peduncle

A 
Middle: 
(aka brachium pontis)
Contralateral cortical input “cortico-ponto-cerebellar”
-synapse in pontine nuclei
-Part of “basis pontis”
189
Q

what tracts enter through the superior cerebellar peduncle?

A

contralateral info from ventral spinocerebellar tracts
sends efferent info to contralateral red nucleus and thalamus (primarily VL nucleus)
Major output pathway of the
cerebellum

190
Q

what is the effect of perkinji fibers on deep cerebellar nuclei?

A

perkinji fibers send out gaba which inhibits cerebellar nuclei

191
Q

explain the olivocerebellar tract?

A

inferior olive sends tonic input to contralateral cerebellum these are called climbing fibers they are necesary for motor learning

192
Q

which bones failed to fuse for jugular foramen?

A

temporal and occipital failed to fuse lateral to the occipital condyles

193
Q

what is the function anatomical location, principle input, deep nucleus, principle targets, and function of the cebreocerebellum pathway?

A

anatomical region: lateral hemispheres
principle input: motor corticies
deep nucleus: dentate
principle targets: red nucleus motor corticies
function:Initiation, planning, timing of complex motor movements

194
Q

in anterior lobe syndrome of the cerebellum which region of the body is most strongly effected by ataxia?

A

the legs and the vermis of the anterior lobe

195
Q

what region of the body is neocerebellar syndrome associated with?

A

more common in upper limbs, intention tremor

196
Q

where would you expect to see a lesion in the cerebellum for problems with Gait ataxia, inability to do tandem walking

A

anterior lobe cerebellum

197
Q

where would you expect a lesion in the cerebellum if someone had problems with Disturbed equilibrium, truncal ataxia, nystagmus

A

Flocculonodular lobe

198
Q

where would you expect to see damage if someone had problems with Limb ataxia (esp. upper), hypotonia, dysdiadochokinesia

A

lateral lobes

199
Q

which bones failed to fuse for foramen lacerum?

A

lack of fusion of the sphenoid, petrous portion of the temporal, and basilar portion of the occipital bone

200
Q

subarachnoid bleeds are characterized by worst headache of my life

A

know that shit

Neuro 1 (7 decks)

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