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

Extra-Ocular Movements and Pupillary Reflexes Flashcards

(87 cards)

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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
Increases depth of field
Pupillary constriction
26
Convergence and divergence are controlled by neurons in the midbrain near the oculomotor n.called the
Vergence center
27
During accomodation, the ciliary muscle contracts. This releases zonule fibers allowing the lense to
Thicken
28
For blurred images, we use
Accomodation
29
For retinal disparity, we use
Vergence
30
Causes mydriasis, loss of pupillary constriction (ipsilateral), and loss of accomodation
CN III E-W damage
31
Ipsilateral lens will not change curve to adjust to view near objects with a deficit due to
E-W (CN III) damage
32
The deficits seen in E-W damage of CN III are all
Ipsilateral
33
Pupils are small bilaterally and irregular with
Light-near dissociation (Argyll-Robertson Pupil)
34
Pupils constrict to accommodation,but are not reactive to light
Argyll-Robertson Pupil
35
The Argyll-Robertson pupil is associated with
Syphilis and diabetes
36
Caused by midbrain lesions affecting light reflex pathway
Argyll-Robertson Pupil
37
Often, pupil changes will be the first symptoms of CN III lesions due to
Aneurysms
38
An Uncal hernia (transtentorial herniation) causes a clinical triad of "blown" pupil, hemiplegia, and coma. The three signs are
Ipsilateral CN III signs, Hemiplegia (cerebral peduncles), and decreased consciousness or coma (Reticular formation)
39
Innervates the superior oblique muscle
Trochlear nerve (IV)
40
The primary action is intorsion, but also depresses (in adducted position) and abducts
Superior oblique
41
Innervates the lateral rectus muscle
Abducens Nerve (VI)
42
Lesion to the abducens nerve causes
Paralysis of lateral rectus and esotropia
43
Can occur with increased intracranial pressure, because brainstem is pushed downwards
Abducens nerve lesion
44
Can be used to determine the cause of diplopia
Red glass test
45
Most pronounced in the direction that the eye cannot move
Diplopia
46
There are 6 systemsto control eye movements to place an image on thefovea, and enable it to stay there. It is part
Voluntary and part reflexive
47
People with disorders of the visual fixation system have poor
Vision
48
Used to point the eyes to an object
Saccadic System
49
Extremely fast movements that are initiated in response to visual targets, tactile stimuli, verbal commands, remembered locations
Saccades
50
Holds a MOVING image on the fovea, Maximum velocity of 100°/s, and Requires moving target
Smooth-[usuit eye movement (SPEM) system
51
Act together when a target moves
Saccades and SPEMs
52
The vestibulo-ocular reflexes that hold images still on the retina during brief head movements are elicited by
Vestibular inputs
53
Optokinetic movements that hold images still on the retina during translation or sustained rotation are elicited by
Visual field movements
54
Saccades are produced by bursts of activity called
Saccadic Pulse
55
Coordinates eye movements from CNs III, IV, and VI
Medial Longitudinal Fasciculus (MLF)
56
The descending part of the MLF is the medial vestibulospinal tract for
Head position
57
What are the three brianstem gaze centers
Horizol, vertical, and vergence gaze centers
58
Located next to the nucleus of VI. Controls left and right gaze
Paramedian Pontine Reticular Formation (PPRF) Horizontal Gaze Center
59
PPRF ---> VI lower motor neurons and interneurons. Interneurons project to CN III neurons to innervate the
Contralateral medial rectus
60
Used for voluntary movements to the contralateral side
Frontal Eye Fields (FEF)
61
The FEF projects directly to the
1. ) Contralateral PPRF | 2. ) Superior Colliculus
62
Causes transient loss of horizontal gaze to contralateral side
FEF lesion
63
Longer lasting deficits in horizontal gaze to the ipsilateral side
PPRF lesion
64
Transient deficit in accuracy, frequency, and velocity of saccades
Superior Colliculus Lesion
65
We see a permanent loss of reflexive saccades with
Superior Colliculus Lesions
66
Directs movements into the visual space
Superior Colliculus
67
In cortical lesions involving the FEF and UMNs, eyes point
Towards the lesion
68
In Brainstem lesions involving the PPRF and UMNs, the eyes point
Away from the lesion
69
Caused by increased pressure on the dorsal, rostral mid-brain, including posterior commissure
Parinaud's Syndrome
70
Ventral regions of the brainstem controls
Downgaze
71
Dorsal regions of the brainstem control
Upgaze
72
Presents with paralysis of upward gaze, large irregular pupils, and loss of convergence
Parinaud's syndrome
73
When horizontal eye movement is lost - Caused by pontine lesion - Vertical eye movements canbe spared
Locked-in syndrome
74
When midbrain atrophy affects vertical eye movements
Supranuclear palsy
75
What are the two stabilizing reflexes?
1. ) Vestibulo-ocular reflex (VOR) | 2. ) Oculocephalic reflex
76
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.
Vestibulo-ocular reflex
77
Abnormal VOR can be caused by
Vestibular diseae, CNVIII disease, or cerebellar lesions
78
The inability to see clearly while walking/driving is characteristic of
VOR abnormality
79
A sensation that the environment is moving -Common with VOR lesion
Oscillopsia
80
We have the patient focus on a distant object and move the head 5-10 degrees. The eyes should stay stable if
VOR is intact
81
Patient stares at their own hand with outstretched arm in front of their face, while being turned. They should be able to suppress
VOR
82
An unsuppressed VOR means there is a lesion in the
Cerebellum flocculonodular lobe or posterior vermis
83
(“doll’s eye”) tests integrity of brainstem. Vestibular input cause eyes to move in opposite direction
Oculocephalic reflex
84
Impaired oculocephalic reflex indicates
Brainstem dysfunciton
85
Response to retinal slippage of an image, such as when we are moving - Keeps eyes focusedon an image - Works with the VOR
Optokinetic response
86
Tests the visual pathways, cortex, cerebellum, and brainstem centers for horzontal gaze
Optokinetic response
87
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
Optokinetic response

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