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NBB Test 2 > Extra-Ocular Movements and Pupillary Reflexes > Flashcards

Extra-Ocular Movements and Pupillary Reflexes Flashcards

1
Q

In bright environments, constricts the pupil

A

Pupillary sphincter muscle

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2
Q

In dim environments, dilates the pupil

A

Pupillary dilator muscle

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3
Q

The lense is thinner and flatter when objects are

A

Further away (unaccomidation)

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4
Q

The lense thickens to focus light on retina when objects are closer. This is called

A

Accomodation

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5
Q

Which 4 extraocular muscles does CN III control?

A

Medial, inferior, and superior rectus and inferior oblique

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6
Q

The biggest complaint of people with extraoccular muscle weakness is

A

Diplopia (double vision)

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7
Q

Caused by the inability to position the image on the macula of both eyes

A

Diplopia

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8
Q

Provides somatic motor (GSE) to 4 extraocular muscles and the levtor palpebrae superioris

A

Oculomotor nucleus and nerve

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9
Q

Provides parasympthetic (GVR) innervation from Edinger-Westphal and preganglionic to pupillary constrictoy and ciliary muscles of lens

A

Occulomotor nucleus and nerve

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10
Q

What are the 4 eye movements that result from CN III innervation?

A

Move eye up and down, towards the nose, and rotate externally

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11
Q

Drooping of the upper eyelid (ptosis) occurs with

A

CN III Palsy, Horner’s syndrome, and Myasthenia gravis

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12
Q

When the ipsilateral eye deviates down and out when patient looks straight ahead

-Due to CN III lesion

A

Exotropia

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13
Q

With a CN III lesion, patient will complain of

A

Diplopia

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14
Q

The most dorsal and medial part of the oculomotor nucleus

A

Edinger-Westphal nucleus

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15
Q

The pupillary dilator muscle receives

A

Sympathetic innervation

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16
Q

Lesions to the sympathetic fibers controlling the dilator muscle cause

A

Miosis (constricted pupil) with Horner’s syndrome

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17
Q

Innervates the ciliart and constrictor muscles

-parasympathetic

A

Edinger-Westphal (GVE) nucleus

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18
Q

Lesions to the Edinger-Westphal nucleus cause

A

Mydriasis (dilated pupil) and loss of pupillary constriction and accommodation

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19
Q

Pupil constricts to light in normal eye, but when light is moved quickly to defective eye, it will dilate in response to it (because the input is “less”). This is called the

A

Swinging flashlight test for afferent pupillary defec

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20
Q

It is best to diagnose Horner’s syndrome in

A

Dark light

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21
Q

It is best to diagnose CN III damage in

A

Light

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22
Q

Characterized by ptosis, miosis, and anhidrosis (decreased sweating)

A

Horner’s Syndrome

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23
Q

Lesions may be in brainstem, hypothalamus, spinal cord (cervical and upper thoracic),T1-T2 spinal nerves, carotid plexus, or orbit for

A

Horner’s syndrome

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24
Q

What is the near response triad in response to an object coming closer to the face?

A
  1. ) Convergence (CN III)
  2. ) Accomodation (Ciliary muscle CN III)
  3. ) Pupillary constriction (Constrictor, CN III)
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25
Q

Increases depth of field

A

Pupillary constriction

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26
Q

Convergence and divergence are controlled by neurons in the midbrain near the oculomotor n.called the

A

Vergence center

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27
Q

During accomodation, the ciliary muscle contracts. This releases zonule fibers allowing the lense to

A

Thicken

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28
Q

For blurred images, we use

A

Accomodation

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29
Q

For retinal disparity, we use

A

Vergence

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30
Q

Causes mydriasis, loss of pupillary constriction (ipsilateral), and loss of accomodation

A

CN III E-W damage

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31
Q

Ipsilateral lens will not change curve to adjust to view near objects with a deficit due to

A

E-W (CN III) damage

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32
Q

The deficits seen in E-W damage of CN III are all

A

Ipsilateral

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33
Q

Pupils are small bilaterally and irregular with

A

Light-near dissociation (Argyll-Robertson Pupil)

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34
Q

Pupils constrict to accommodation,but are not reactive to light

A

Argyll-Robertson Pupil

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35
Q

The Argyll-Robertson pupil is associated with

A

Syphilis and diabetes

36
Q

Caused by midbrain lesions affecting light reflex pathway

A

Argyll-Robertson Pupil

37
Q

Often, pupil changes will be the first symptoms of CN III lesions due to

38
Q

An Uncal hernia (transtentorial herniation) causes a clinical triad of “blown” pupil, hemiplegia, and coma. The three signs are

A

Ipsilateral CN III signs, Hemiplegia (cerebral peduncles), and decreased consciousness or coma (Reticular formation)

39
Q

Innervates the superior oblique muscle

A

Trochlear nerve (IV)

40
Q

The primary action is intorsion, but also depresses (in adducted position) and abducts

A

Superior oblique

41
Q

Innervates the lateral rectus muscle

A

Abducens Nerve (VI)

42
Q

Lesion to the abducens nerve causes

A

Paralysis of lateral rectus and esotropia

43
Q

Can occur with increased intracranial pressure, because brainstem is pushed downwards

A

Abducens nerve lesion

44
Q

Can be used to determine the cause of diplopia

A

Red glass test

45
Q

Most pronounced in the direction that the eye cannot move

46
Q

There are 6 systemsto control eye movements to place an image on thefovea, and enable it to stay there. It is part

A

Voluntary and part reflexive

47
Q

People with disorders of the visual fixation system have poor

48
Q

Used to point the eyes to an object

A

Saccadic System

49
Q

Extremely fast movements that are initiated in response to visual targets, tactile stimuli, verbal commands, remembered locations

50
Q

Holds a MOVING image on the fovea, Maximum velocity of 100°/s, and Requires moving target

A

Smooth-[usuit eye movement (SPEM) system

51
Q

Act together when a target moves

A

Saccades and SPEMs

52
Q

The vestibulo-ocular reflexes that hold images still on the retina during brief head movements are elicited by

A

Vestibular inputs

53
Q

Optokinetic movements that hold images still on the retina during translation or sustained rotation are elicited by

A

Visual field movements

54
Q

Saccades are produced by bursts of activity called

A

Saccadic Pulse

55
Q

Coordinates eye movements from CNs III, IV, and VI

A

Medial Longitudinal Fasciculus (MLF)

56
Q

The descending part of the MLF is the medial vestibulospinal tract for

A

Head position

57
Q

What are the three brianstem gaze centers

A

Horizol, vertical, and vergence gaze centers

58
Q

Located next to the nucleus of VI. Controls left and right gaze

A

Paramedian Pontine Reticular Formation (PPRF) Horizontal Gaze Center

59
Q

PPRF —> VI lower motor neurons and interneurons. Interneurons project to CN III neurons to innervate the

A

Contralateral medial rectus

60
Q

Used for voluntary movements to the contralateral side

A

Frontal Eye Fields (FEF)

61
Q

The FEF projects directly to the

A
  1. ) Contralateral PPRF

2. ) Superior Colliculus

62
Q

Causes transient loss of horizontal gaze to contralateral side

A

FEF lesion

63
Q

Longer lasting deficits in horizontal gaze to the ipsilateral side

A

PPRF lesion

64
Q

Transient deficit in accuracy, frequency, and velocity of saccades

A

Superior Colliculus Lesion

65
Q

We see a permanent loss of reflexive saccades with

A

Superior Colliculus Lesions

66
Q

Directs movements into the visual space

A

Superior Colliculus

67
Q

In cortical lesions involving the FEF and UMNs, eyes point

A

Towards the lesion

68
Q

In Brainstem lesions involving the PPRF and UMNs, the eyes point

A

Away from the lesion

69
Q

Caused by increased pressure on the dorsal, rostral mid-brain, including posterior commissure

A

Parinaud’s Syndrome

70
Q

Ventral regions of the brainstem controls

71
Q

Dorsal regions of the brainstem control

72
Q

Presents with paralysis of upward gaze, large irregular pupils, and loss of convergence

A

Parinaud’s syndrome

73
Q

When horizontal eye movement is lost

  • Caused by pontine lesion
  • Vertical eye movements canbe spared
A

Locked-in syndrome

74
Q

When midbrain atrophy affects vertical eye movements

A

Supranuclear palsy

75
Q

What are the two stabilizing reflexes?

A
  1. ) Vestibulo-ocular reflex (VOR)

2. ) Oculocephalic reflex

76
Q

A system for gaze stabilization: detects head movements through the vestibular system (heel striking the ground, head turning), and generates eye movements in the opposite direction to stabilize the eyes (prevent image “slippage”.

-For brief movements.

A

Vestibulo-ocular reflex

77
Q

Abnormal VOR can be caused by

A

Vestibular diseae, CNVIII disease, or cerebellar lesions

78
Q

The inability to see clearly while walking/driving is characteristic of

A

VOR abnormality

79
Q

A sensation that the environment is moving

-Common with VOR lesion

A

Oscillopsia

80
Q

We have the patient focus on a distant object and move the head 5-10 degrees. The eyes should stay stable if

A

VOR is intact

81
Q

Patient stares at their own hand with outstretched arm in front of their face, while being turned. They should be able to suppress

82
Q

An unsuppressed VOR means there is a lesion in the

A

Cerebellum flocculonodular lobe or posterior vermis

83
Q

(“doll’s eye”) tests integrity of brainstem. Vestibular input cause eyes to move in opposite direction

A

Oculocephalic reflex

84
Q

Impaired oculocephalic reflex indicates

A

Brainstem dysfunciton

85
Q

Response to retinal slippage of an image, such as when we are moving

  • Keeps eyes focusedon an image
  • Works with the VOR
A

Optokinetic response

86
Q

Tests the visual pathways, cortex, cerebellum, and brainstem centers for horzontal gaze

A

Optokinetic response

87
Q

The pathway is through the vestibular nuclei, which receives projections from the visual system.

-This is why sometimes you feel like you are moving when the visual field moves

A

Optokinetic response

NBB Test 2 (33 decks)

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