Optic Nerve/ Neuro-ophthalmic Pathways/Blood Flow Flashcards

1
Q

Classic triad of Horner’s

A

PAM!!! PAM!!!
1. Ptosis (small, affects Muller’s muscle)
2. Anhidrosis (lack of sweat on one side)
3. Miosis (pupil constriction)

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2
Q

Argyll Robertson pupil associated with what infectious disease?

A

Late-stage syphilis

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3
Q

Physiological anisocoria

A
  • Anisocoria equal under dim and bright conditions
  • no ptosis
  • confirm stability by referring to previous photos of patient
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4
Q

Signs of pupil involving 3rd nerve palsy

A

Eye is down and out with dilated (blown out) pupil

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5
Q

Patient presents with diplopia, headache, eye is down and out with a blown out pupil, what is your A&P?

A

A. Pupil involving cranial nerve 3 palsy caused by aneurysm of the posterior communicating artery
P. Send to emergency room ASAP (EMERGENT!!!)

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6
Q

Congenital Horner’s syndrome signs

A

Iris heterochromia (affected eye will have lighter iris)

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7
Q

Characteristics of tilted disc syndrome

A
  • Bilateral
  • optic nerve enters at an oblique angle superiorly
  • situs inversus
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8
Q

Signs of tilted disc syndrome

A
  • myopic
  • fundus ectasia
  • superior temporal VF defects that do not respect the midline
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9
Q

A&P for Horner’s

A

A. Horner syndrome
1. isolated damage of 3rd order neuron
2. pre-ganglionic lesion

Plan
1. No further investigation
2. Refer for MRI of head and neck and a CT scan of thorax or chest x-ray (pancoast tumor)

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10
Q

Right homonymous hemianopia is associated with stroke on which side of the brain? And can cause hemiparesis on which side of the body?

A

Cerebrovascular accident on left side of brain and patient likely has hemiparesis on right side of their body

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11
Q

Pulfrich phenomenon

A

Pendulum is perceived as moving in a circular motion rather than laterally
* symptom of optic neuritis

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12
Q

Ocular manifestation of multiple sclerosis

A

Optic neuritis

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13
Q

Optic neuritis age demographic

A

18 to 45 years old

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14
Q

Uhthoff sign

A

Associated with MS

Symptoms worsen with increase in body temperature

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15
Q

True or false
Horner’s syndrome can be caused by internal carotid artery dissection

A

TRUE
* 3rd order neuron damage from internal carotid artery dissection can cause Horner’s syndrome

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16
Q

Patients suspected with Horner’s due to a pre-ganglionic lesion should be referred for what further testing?

A
  • MRI of head and neck
  • CT scan of thorax
  • chest x-ray (check for pancoast tumor)
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17
Q

Parietal lobe lesion will produce what VF loss?

A

Inferior incongruous or congruous VF loss (quadrantanopia)
* pie on the floor (parents put you down lesion in parietal lobe)

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18
Q

Lesion in temporal lobe produces what VF loss?

A

Superior quadrant VF defect, incongruous and wedge shaped, can also be complete
* superior quadrantanopia = pie in the sky

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19
Q

Optic radiations traveling through ____ lobe carry visual information from the superior retina

A

Parietal lobe
* VF loss will be opposite therefore superior retina damage will cause inferior VF loss

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20
Q

3rd order neuron irregularities can be caused by?

A

Cluster headaches
Otitis media
Masses in cavernous sinus
Internal artery dissections
Nasopharyngeal tumors

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21
Q

Pancoast tumor can cause which order neuron irregularity in Horner’s?

A

2nd order neuron lesion

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22
Q

What is the most common cause of pupil sparing isolated 3rd nerve palsy?

A

Microvascular disease secondary to HTN &/or diabetes

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23
Q

Blood supply to oculomotor nerve

A

Surface and pupillary fibers are supplied by pial blood vessels; internal fibers are supplied by the vasa nervorum

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24
Q

What are the common triggers of a classic migraine?

A
  • stress
  • coffee
  • chocolate
  • cheese
  • prolonged periods without food
  • bright lights
  • alcohol
  • severe fatigue
  • birth control
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25
Q

Visual aura of a classic migraine would produce what type of visual field defect?

A

Homonymous hemianopsia
* start in center and enlarge in homonymous portions of the visual field
* HA located on contralateral side of field defect

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26
Q

Leber hereditary optic neuropathy is more common in males or females?

A

males

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27
Q

What is Tilted Disc Syndrome?

A

A condition where the optic nerve enters the eye at an oblique angle, causing elevation of superior nerve tissue and ectasia of inferior/infero-nasal tissue

Typically observed bilaterally.

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28
Q

What visual field defects are often associated with Tilted Disc Syndrome?

A

Superotemporal defects

These defects may diminish or disappear with myopic astigmatism correction.

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29
Q

What are common symptoms of Tilted Disc Syndrome?

A

Majority are asymptomatic; some may report visual field defects or blurred vision

Symptoms can be caused by uncorrected astigmatism.

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30
Q

What clinical signs indicate Tilted Disc Syndrome?

A
  • Obliquely inserted disc
  • Myopic astigmatism
  • Tilted optic disc with inferior ectasia
  • Superior elevation of nerve tissue
  • Situs inversus
  • Fundus ectasia
  • Superotemporal visual field defects

Visual field defects generally do not respect the midline.

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31
Q

What is the treatment for Tilted Disc Syndrome?

A

Visual correction to neutralize the associated refractive component

No additional treatment is required.

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32
Q

How often should patients with Tilted Disc Syndrome be evaluated?

A

Annually

Regular follow-up helps monitor any changes.

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33
Q

Fill in the blank: Tilted Disc Syndrome is caused by an optic nerve that enters the eye _______.

A

[superiorly at an oblique angle]

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34
Q

VF defects of tilted disc syndrome similar to what type of tumor VF defect?

A

Pituitary gland tumor —> bitemporal field defect
* neuroimaging required to establish concrete diagnosis

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35
Q

What is the primary function of the Circle of Willis in relation to the eyes?

A

The Circle of Willis provides collateral circulation to the brain, including areas that supply blood to the eyes.

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36
Q

True or False: The ophthalmic artery is a branch of the internal carotid artery, which is part of the Circle of Willis.

A

True

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37
Q

Fill in the blank: The Circle of Willis is located at the base of the ______.

A

brain

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38
Q

Multiple Choice: Which of the following arteries is NOT part of the Circle of Willis? A) Anterior cerebral artery B) Middle cerebral artery C) Posterior tibial artery D) Posterior cerebral artery

A

C) Posterior tibial artery

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39
Q

What are the main arteries supplying blood to the iris and ciliary body?

A

Long posterior ciliary arteries and anterior ciliary arteries

These arteries are branches of the ophthalmic artery.

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40
Q

What is formed by the terminal branches of the long posterior ciliary arteries and anterior ciliary arteries?

A

The major arterial circle of the iris

This circle lies behind the root of the iris in the ciliary body.

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41
Q

Where does the major arterial circle of the iris lie?

A

Behind the root of the iris in the ciliary body

It is formed by anastomoses of the long posterior and anterior ciliary arteries.

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42
Q

What is the path of blood vessels from the major arterial circle?

A

They course around the circumference of the iris, from the periphery toward the pupil

This arrangement supports blood flow to the iris.

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43
Q

What forms the minor arterial circle of the iris?

A

Centripetal branches of the major arterial circle

Minor circle is incomplete and lies just inside the pupillary border.

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44
Q

What is the location of the minor arterial circle of the iris?

A

Just inside the pupillary border

It is involved in the initial signs of neovascularization of the iris.

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45
Q

True or False: The minor arterial circle of the iris is responsible for the complete blood supply to the iris.

A

False

The minor circle is incomplete and primarily indicates neovascularization.

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46
Q

Fill in the blank: The _______ arteries anastomose with the anterior ciliary arteries to form the major arterial circle of the iris.

A

long posterior ciliary

These arteries are crucial for the vascular supply to the iris.

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47
Q

Initial signs of neovascularization of the iris is located where?

A

The minor arterial circle of the iris at the pupillary margin

Initial signs of neovascularization are observed in this area.

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48
Q

What is papillophlebitis?

A

A rare condition observed in younger patients, usually under 50 years of age.
* inflammation of the optic disc venous drainage

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49
Q

What is the typical health status of patients with papillophlebitis?

A

Generally healthy.

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50
Q

What are the clinical signs of papillophlebitis?

A

Sudden unilateral blurring of vision, disc edema, cotton wool spots, dilation and tortuosity of veins, and retinal hemorrhages restricted to the posterior pole.

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51
Q

What age group is most commonly affected by papillophlebitis?

A

Patients under 50 years of age.

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52
Q

What is the prognosis of papillophlebitis without treatment?

A

Typically good, unless chronic macular edema remains.

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53
Q

Fill in the blank: Clinical signs of papillophlebitis include _______.

A
  • sudden unilateral blur
  • disc edema
  • cotton wool spots
  • dilation and tortuosity of veins
  • retinal hemorrhages.
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54
Q

True or False: Papillophlebitis is more common in older patients.

A

False.
* common in younger pts

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55
Q

What is aberrant regeneration in the context of cranial nerve palsy?

A

It occurs when third cranial nerve fibers misdirect to alternate muscles innervated by the same nerve.
* does not occur with ischemic 3rd nerve palsies

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56
Q

What muscles does the oculomotor nerve control?

A
  • Medial rectus
  • Superior rectus
  • Inferior rectus
  • Inferior oblique
  • Iris dilator muscle
  • levator
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57
Q

What causes aberrant regeneration of the oculomotor nerve?

A

Damage from trauma or compression.

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58
Q

What is the pseudo-Graefe sign?

A

Elevation of the involved eyelid on downgaze or adduction.

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59
Q

List the most common signs of aberrant third nerve regeneration.

A
  • Eyelid-gaze dyskinesis
  • Pupil-gaze dyskinesis
  • Constriction of the pupil on downgaze or adduction
  • Elevation of involved eyelid on downgaze or adduction
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60
Q

True or False: Aberrant regeneration can lead to limitation of elevation or depression of the eye.

A

True.

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61
Q

Fill in the blank: Aberrant regeneration may lead to _____ on attempted elevation or depression.

A

adduction

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62
Q

What is a less common sign of aberrant third nerve regeneration?

A

Absent optokinetic nystagmus response.

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63
Q

What is the cavernous sinus?

A

A large collection of thin-walled veins that create a cavity within the human head, bordered by the temporal and sphenoid bones

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64
Q

How does the cavernous sinus receive blood?

A

Via the superior and inferior ophthalmic veins and the superficial cortical veins

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65
Q

What channels drain the cavernous sinus?

A

The superior and inferior petrosal sinuses and into the jugular vein via the sigmoid sinus

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66
Q

What major artery runs through each cavernous sinus?

A

The internal carotid artery

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67
Q

Which cranial nerves are contained within the cavernous sinus?

A
  • Oculomotor nerve (CN III)
  • Trochlear nerve (CN IV)
  • Ophthalmic nerve (V1 branch of CN V)
  • Maxillary nerve (V2 division of CN V)
  • Abducens nerve (CN VI)
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68
Q

How do the cranial nerves run within the cavernous sinus?

A

From superior to inferior within the lateral wall of the cavernous sinus

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69
Q

Where does the abducens nerve (CN VI) run in relation to the cavernous sinus?

A

Through the middle of the sinus alongside the internal carotid artery

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70
Q

Which cranial nerves pass through the cavernous sinus and enter the orbital apex via the superior orbital fissure?

A
  • CN III
  • CN IV
  • CN VI
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71
Q

Where does CN V2 exit the cavernous sinus?

A

Through the foramen rotundum

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72
Q

Where is the optic nerve located in relation to the cavernous sinus?

A

Just outside and superior to the cavernous sinus on each side, entering the orbital apex via the optic canal

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73
Q

What is the typical result of lesions involving the cavernous sinus?

A

Dysfunction of several nerves due to their close proximity

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74
Q

Which CN pass through the cavernous sinus and enter the orbital apex through the superior orbital fissure?

A
  • CN 3
  • CN 4
  • V1 of CN 5
  • CN 6
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75
Q

Pt with pupil involving CN 3 palsy and has medical history of congenital heart defect and has a pace maker should NOT get what type of imaging done?

A

MRI
* pt should get CT and CTA instead to confirm diagnosis of intracranial arterial aneurysm

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76
Q

If neuroimaging is negative for pt with pupil involving third nerve palsy what additional test should be considered next?

A

Lumbar puncture

  • to evaluate possible presence of blood in CSF, an inflammatory reaction, neoplastic infiltration or infection
  • blood in CSF = rupture of posterior communicating artery aneurysm
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77
Q

What is the pupillary pathway responsible for?

A

The light reflex and the near reflex

The pupillary pathway involves several neurons responding to stimuli.

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78
Q

What does sympathetic input cause in the pupillary pathway?

A

Mydriasis

Mydriasis refers to the dilation of the pupil.

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79
Q

What does parasympathetic innervation cause in the pupillary pathway?

A

Pupil miosis

Miosis refers to the constriction of the pupil.

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80
Q

What does the absence of a light reflex typically indicate?

A

Severe unilateral nerve damage

This absence suggests significant issues with the neural pathways.

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81
Q

Which retinal photoreceptors mediate the response to light?

A

Retinal photoreceptors

These receptors conduct signals to the pretectal nucleus.

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82
Q

Where do fibers from the nasal retina cross over?

A

In the chiasm

This allows signals to enter the contralateral pretectal nucleus.

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83
Q

What happens to fibers from the temporal retina?

A

They do not decussate and send information to the ipsilateral pretectal nucleus

This contributes to the light reflex mechanism.

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84
Q

What is the role of the Edinger-Westphal (EW) nuclei in the pupillary pathway?

A

They receive input from the pretectal nuclei and relay information

This process results in symmetrical pupil constriction when light stimulates one eye.

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85
Q

What occurs after neurons leave the EW nucleus?

A

They synapse onto the ipsilateral ciliary ganglion

This is crucial for innervating the pupil sphincter.

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86
Q

What is the effect of damage to the parasympathetic pathway?

A

Mydriasis of the pupil

Damage affects pupil constriction capabilities.

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87
Q

Where does the first order neuron of the sympathetic pathway originate?

A

In the hypothalamus

This neuron travels down the spine to synapse onto the ciliospinal center of Budge.

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88
Q

What is the pathway of the second order neuron in the sympathetic pathway?

A

Projects from the ciliospinal center of Budge upwards to the superior cervical ganglion

This ganglion is located in the neck.

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89
Q

What does the third order neuron do in the sympathetic pathway?

A

Sends projections from the superior cervical ganglion along the internal carotid artery

This neuron ultimately reaches the ciliary body and dilator muscle of the pupil.

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90
Q

What are the effects of damage to the sympathetic division of the pupillary pathway?

A

Pupillary miosis, ptosis of the upper lid, and elevation of the lower lid

Both Mueller’s muscle and lower lid retractors are innervated by the sympathetic system.

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91
Q

What is the chance of developing maculopathy in patients with non-central optic pits?

A

Up to 45%

This statistic highlights the significant risk associated with non-central optic pits.

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92
Q

What are the suggested origins of the subretinal fluid in optic pits?

A

Subarachnoid space or vitreous

Research indicates that the fluid causing issues in optic pits likely originates from these two areas.

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93
Q

What has been observed in eyes that have suffered a retinal detachment associated with optic pits?

A

A small opening in the membrane covering the pit

This observation may indicate a pathway for fluid accumulation and retinal issues.

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94
Q

What factor might contribute to the formation of a retinal detachment in cases of optic pits?

A

Intravitreal traction on the pit by an atypical Cloquet’s canal

This traction can lead to complications such as detachment.

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95
Q

Which types of optic pits are more at risk for developing detachments?

A

Temporal pits and larger pits

The location and size of the optic pit play a critical role in the risk of detachment.

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96
Q

Is there an agreed upon method of treatment for patients with optic pits?

A

No agreed upon method exists

Treatment approaches vary, indicating a lack of consensus in the medical community.

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97
Q

What treatment may be warranted if visual acuity is reduced in patients with optic pits?

A

Laser treatment applied to the peripapillary area

This treatment aims to re-establish the connection between the RPE and retina.

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98
Q

What is the success rate of laser treatment for optic pits?

A

Roughly 30%

This low success rate indicates the challenges in treating conditions associated with optic pits.

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99
Q

What are alternative treatment options for optic pits aside from laser treatment?

A
  • Pars-plana vitrectomy
  • Injection of a gas tamponade without vitrectomy

These options can be considered depending on the specific case.

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100
Q

Can serous detachment associated with optic pits resolve spontaneously?

A

Yes, rarely

Spontaneous resolution is uncommon but possible.

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101
Q

What is the prognosis for maculopathy associated with optic pits?

A

Poor prognosis

The associated risks and complications lead to a generally unfavorable outlook.

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102
Q

What should patients be given to monitor for changes related to optic pits?

A

An Amsler grid

This tool helps patients detect visual changes promptly.

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103
Q

What percentage of cases may also develop macular holes?

A

Up to 25%

This statistic further emphasizes the complications related to optic pits.

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104
Q

RTC for optic pit

A

Annually but should be given amsler grid because risk of serous macular detachment
Pt educated to RTC ASAP if any changes on amsler

105
Q

Foster-Kennedy syndrome

A
  • Optic disc edema in one eye (papilledema on contralateral side of lesion)
  • optic atrophy in other eye (ipsilateral to side of lesion) will have central scotoma
  • caused by frontal lobe tumor and olfactory groove meningiomas (pt complain of decreased sense of smell)
106
Q

What is the correct sequence for the circulation of cerebrospinal fluid (CSF) in the brain?

A

Lateral ventricle → interventricular foramen → third ventricle → cerebral aqueduct → fourth ventricle → subarachnoid space

107
Q

What is the most commonly affected cranial nerve in cases of elevated intracranial pressure?

A

Abducens (6th cranial nerve)

This is often due to space-occupying intracranial tumors.

108
Q

What are the initial manifestations of tumors in around 50% of patients with an abducens nerve palsy?

A

Headaches and/or diplopia

These symptoms can indicate the presence of a tumor affecting the abducens nerve.

109
Q

What causes an abducens nerve palsy?

A

Increase in intracranial pressure leading to stretching and compression of the 6th cranial nerve

This typically occurs as the nerve courses over the bony petrous tip of the skull.

110
Q

What percentage of patients with an abducens nerve palsy experience headaches and/or diplopia?

A

Around 50%

This statistic highlights the commonality of these symptoms in relation to tumors.

111
Q

RTC for optic nerve melanocytoma

A

Monitor with fundus photography every 6 months
* progressive growth, loss of visual acuity, VF loss, or APD suggests malignant transformation (in that case enucleation may be best treatment)

112
Q

What are optic disc drusen composed of?

A

Hyaline-like calcific material
* best visible with B-scan

113
Q

Oral corticosteroids can help with signs and symptoms of Bell’s palsy if initiated within ___ hours of onset

A

72 hours
* acute phase of bell’s, inflammation and edema of facial nerve are causing facial muscle weakness, anti-inflammatory minimizes nerve damage

114
Q

Pt presents with acute peripheral facial nerve palsy + vesicular eruptions on ear, tongue, face or neck

A

Ramsay-hunt syndrome
* + viral prodrome and severe ear pain
* vestibulocochlear dysfunction, nausea, vomiting, tinnitus, and hearing loss

115
Q

Argyll-Robertson pupils

A
  • Small irregular shape pupils
  • light-near dissociation
  • dilate poorly in darkness
  • bilateral, asymmetrical
116
Q

Parinaud syndrome s/s

A
  • bilateral mid-dilated pupils
  • react poorly to light
  • normal constriction at near
  • eyelid refraction
  • supra-nuclear upgaze paralysis
  • convergence retraction nystagmus
117
Q

Pt sus for Adie’s tonic pupil, what pharmacological agent confirms diagnosis?

A

0.125% pilocarpine
* diluted pilocarpine would constrict abnormal pupil with minimal constriction in normal pupil

118
Q

Pathophysiology of Adie’s tonic pupil

A

Damage to postganglionic nerve fibers of the iris sphincter and ciliary muscle

119
Q

What is the cause of an Adie tonic pupil?

A

Damage to the ciliary ganglion

This damage results in dysfunction of the postganglionic nerve fibers to the iris sphincter and ciliary muscle.

120
Q

What is the typical pupil appearance in Adie tonic pupil?

A

Large pupil on the affected side

This occurs due to the initial insult to the ciliary ganglion.

121
Q

What are common associations with Adie pupil?

A
  • Orbital trauma
  • Surgery
  • Viral infections
  • Chronic tonsillitis
  • Sinusitis
  • Upper respiratory infections
  • Dental anesthesia and tooth extractions

While many cases are idiopathic, some patients can link their Adie pupil to these factors.

122
Q

What causes Argyll-Robertson pupils?

A

Spirochete syphilis

This infection damages the intercalated neurons between the pretectal and Edinger-Westphal nuclei.

123
Q

What type of anisocoria is caused by Horner syndrome?

A

Anisocoria due to a paresis or palsy

This paresis or palsy is located in the oculosympathetic pathway.

124
Q

Damage to intercalated neurons between the pretectal and E-W nuclei in Argyll Robertson pupil is caused by what organism?

A

Spirochete syphilis

125
Q

What is Bell’s palsy characterized by?

A

Acute onset of unilateral weakness of the upper and lower muscles of the face with no apparent cause

126
Q

What should be considered before diagnosing Bell’s palsy?

A

Other causes of acquired peripheral facial weakness

127
Q

List some associated conditions with Bell’s palsy.

A
  • Diabetes
  • Hypertension
  • HIV
  • Lyme disease
  • Ramsay-Hunt syndrome
  • Sarcoidosis
  • Sjogren syndrome
  • Parotid-nerve tumors
  • Temporal bone fracture
  • Guillain-Barre syndrome
128
Q

What type of mass can cause peripheral facial weakness?

A

Cerebellopontine angle mass (e.g., acoustic neuroma, facial neuroma, meningioma, cholesteatoma)

129
Q

How is Bell’s palsy classified in terms of diagnosis?

A

Diagnosis of exclusion

130
Q

What symptoms may patients with Bell’s palsy experience?

A
  • Viral prodrome
  • Ear pain
  • Decreased tearing
  • Decreased taste
  • Facial numbness
131
Q

What is the typical progression time for facial palsy in Bell’s palsy?

A

Usually progresses over a period of 10 days

132
Q

Is Bell’s palsy life-threatening?

A

No, it is non life-threatening

133
Q

What is the incidence of Bell’s palsy?

A

20-30 cases per 100,000 people per year

134
Q

What percentage of unilateral facial paralysis does Bell’s palsy account for?

A

60-75%

135
Q

At what median age does Bell’s palsy typically onset?

A

40 years

136
Q

Which age group has the highest incidence of Bell’s palsy?

A

People older than 70

137
Q

Does Bell’s palsy affect both sexes equally?

A

Yes

138
Q

Do most patients with Bell’s palsy recover completely?

A

Yes

139
Q

True or False: Bell’s palsy rarely recurs.

A

True

140
Q

Fill in the blank: Facial paralysis due to an upper motor neuron lesion will cause weakness of the _______.

A

lower facial musculature only

141
Q

Fill in the blank: Bell’s palsy is due to a _______ lesion.

A

lower motor neuron (peripheral)

142
Q

How often do both sides of the face get affected in Bell’s palsy?

A

With equal frequency

143
Q

What is the significance of determining whether facial weakness is due to an upper or lower motor neuron lesion?

A

It helps to determine the etiology of the disorder.

144
Q

What muscles are spared in an upper motor neuron lesion?

A

Frontalis muscle.

145
Q

In upper motor neuron lesions, what facial feature is preserved?

A

Normal furrowing of the brow.

146
Q

Are eye closure and blinking affected in upper motor neuron lesions?

A

No.

147
Q

What are common causes of upper motor neuron lesions?

A

Space occupying lesions or cerebrovascular accidents.

148
Q

How does an upper motor neuron lesion affect facial innervation?

A

Innervation of the contralateral upper and lower face, and ipsilateral upper face.

149
Q

What part of the face is usually affected by an upper motor neuron lesion?

A

Contralateral lower face.

150
Q

What characterizes lower motor neuron lesions?

A

Weakness of all muscles of facial expression.

151
Q

What happens to the angle of the mouth in lower motor neuron lesions?

A

It falls.

152
Q

Is weakness of the frontalis muscle present in lower motor neuron lesions?

A

Yes.

153
Q

How is eye closure affected in lower motor neuron lesions?

A

Eye closure is weak.

154
Q

What condition is commonly associated with lower motor neuron lesions?

A

Bell’s palsy.

155
Q

Which facial areas are affected by lower motor neuron lesions?

A

Ipsilateral upper and lower face.

156
Q

What is the most prevalent form of color discrimination deficiency among males and females?

A

Deuteranomaly
* have all 3 photo pigments but there is a shift of maximum sensitivity of chlorolabe towards longer wavelengths
* red-green color blindness

157
Q

Optic nerve disease may cause what kind of acquired color vision deficiency?

A

Red-green

158
Q

What are optic nerve drusen?

A

Hyaline-like calcific material deposition in the optic nerve

Present in roughly 0.3% of the general population

159
Q

Are optic nerve drusen typically unilateral or bilateral?

A

Generally bilateral, but may present unilaterally

Seen almost exclusively in Caucasians

160
Q

What is thought to contribute to the condition of optic nerve drusen?

A

A genetic component

The exact inheritance mode remains unclear

161
Q

What are the symptoms of optic nerve drusen?

A

Most patients are asymptomatic; visual field defect may cause symptoms

162
Q

What clinical signs are observed in the early stages of optic nerve drusen?

A

Drusen may be located deep beneath the optic disc surface, causing elevation with clear margins

The disc will not appear hyperemic and surface vessels remain visible

163
Q

What happens to optic nerve drusen with age?

A

Drusen become more prominent and move anteriorly, exposing irregular nerve margins

The disc may appear elevated with no physiological cup

164
Q

What associated condition may occur with optic nerve drusen?

A

Associated field loss can occur

Rarely, a choroidal neovascular membrane may develop adjacent to the optic nerve

165
Q

How is a diagnosis of buried drusen best confirmed?

A

Via B-scan ultrasonography or optical coherence tomography (OCT)

Turning down the gain while performing B-scan ultrasonography allows for visualization of the drusen

166
Q

What characteristic do drusen exhibit during ultrasonography?

A

Possess high acoustic reflectivity

Drusen will autofluoresce

167
Q

Is treatment typically required for optic nerve drusen?

A

No, treatment is typically not required

168
Q

What are optic nerve drusen?

A

Optic nerve drusen are calcified deposits that form on the optic nerve head.

169
Q

What condition may patients with optic nerve drusen experience in addition to drusen?

A

Patients may experience elevated intraocular pressure.

170
Q

Why may treatment be required for patients with both optic nerve drusen and elevated intraocular pressure?

A

Field loss may be due to the elevated intraocular pressure rather than the drusen.

171
Q

What challenge arises when both elevated intraocular pressure and optic nerve drusen are present?

A

It is difficult to attribute field loss to either elevated intraocular pressure or drusen.

172
Q

What is typically observed in discs with drusen in terms of cupping?

A

Discs with drusen will typically not develop cupping.

173
Q

What type of damage is associated with cupping in the optic nerve?

A

Cupping is observed with glaucomatous damage.

174
Q

What are the typical causes of Visual Pathway Lesions?

A

Vascular disorders or tumors

175
Q

As the lesion moves posteriorly in the visual pathway, how do the visual field defects change?

A

They become more homonymous and congruent

176
Q

What visual field defect is typically caused by a Pituitary Gland Tumor?

A

Bitemporal Hemianopsia

177
Q

In a Junctional Scotoma, where is the lesion located in relation to the visual field defect?

A

Ipsilateral to the central visual field defect; superior temporal quadrant defect on the contralateral side

178
Q

What mnemonic can be used to remember the visual field defect locations caused by Parietal and Temporal lobe lesions?

A

PITS

179
Q

What visual field defect is caused by a Parietal lobe lesion?

A

Inferior quadrantanopia

180
Q

What visual field defect is caused by a Temporal lobe lesion?

A

Superior quadrantanopia

181
Q

What typically causes a Contralateral Homonymous Hemianopia?

A

Stroke or tumor

182
Q

What type of stroke is commonly associated with Contralateral Homonymous Hemianopia?

A

Posterior Cerebral Artery Occlusion

183
Q

What phenomenon often occurs with Contralateral Homonymous Hemianopia due to dual blood supply?

A

Macular sparing

184
Q

What happens to macular sparing if a tumor compresses both sides of the Posterior Cerebral Artery?

A

There will be no macular sparing

185
Q

What is the onset of symptoms for visual field loss caused by a tumor?

A

Gradual

186
Q

What is the onset of symptoms for visual field loss caused by a stroke?

A

Acute

187
Q

What should be checked first in the treatment/management of visual pathway lesions?

A

Visual fields

188
Q

What type of medical specialists should patients be referred to for further evaluation?

A

PCP or neurologist

189
Q

How do Acute Cranial Nerve Palsies present on MRI?

A

Evidence of acute trauma

190
Q

What is a characteristic feature of Chronic Cranial Nerve Palsies?

A

Spread of comitance identified with cover test in 9 positions of gaze

191
Q

What is Warfarin commonly used for?

A

Oral anticoagulant

192
Q

What does Warfarin inhibit?

A

Activation of clotting factors that depend on vitamin K for synthesis

193
Q

What process does Heparin inhibit?

A

Conversion of prothrombin to thrombin

194
Q

What is the mechanism of action of Aspirin in relation to platelets?

A

Irreversible inhibition of platelet cyclooxygenase

195
Q

Symptoms associated with lesions in Wernicke’s and Broca’s areas

A

Wernicke’s = wordy speech
Broca’s = broken speech (aphasia)

196
Q

What VF defect is caused by lesion at the temporal lobe?

A

Contralateral upper quadrantanopia
* pie in the sky

197
Q

Contralateral homonymous hemianopia with macular sparing has a lesion in which part of the visual pathway?

A

Primary visual cortex of the occipital lobe
* caused from stoke
* macular sparing because has dual blood supply (posterior and middle cerebral arteries)

198
Q

Pre-chiasmal lesion leads to what VF defect?

A

Total blindness of ipsilateral eye

199
Q

Compression of Willenbran’s knee leads to what VF defect?

A

Junctional scotoma

200
Q

What is Cortical Blindness?

A

Sudden, bilateral, complete blindness due to extensive damage to the occipital lobe.

201
Q

What are the possible causes of Cortical Blindness?

A

Congenital, cerebrovascular accident (stroke with bilateral cerebral artery blockage), cardiac surgery.

202
Q

What symptoms do patients with Cortical Blindness typically report?

A

Complete, sudden, bilateral blindness with possible visual hallucinations.

203
Q

What is Anton’s Syndrome?

A

A condition where patients deny vision loss despite being blind.

204
Q

What findings are expected during an eye exam for Cortical Blindness?

A

Normal eye exam aside from bilateral no light perception.

205
Q

What is the pupillary light reflex in patients with Cortical Blindness?

A

Present, because the occipital lobe is not responsible for the pupillary response.

206
Q

What is the Riddoch phenomenon?

A

The ability to perceive moving but not stationary objects.

207
Q

What is blindsight?

A

The ability to navigate around objects despite being blind.

208
Q

Is there a treatment available for Cortical Blindness?

A

No treatment is available; loss of vision is usually permanent.

209
Q

What is Vertebrobasilar Insufficiency?

A

Occurs when the Vertebrobasilar arterial blood supply to the brain becomes blocked.

210
Q

What can cause Vertebrobasilar Insufficiency?

A

Thrombus, emboli, hypertension, or anything causing a hypercoagulable state.

211
Q

What are common symptoms of Vertebrobasilar Insufficiency?

A

Flashes of light (photopsia), bilateral transient visual loss (amaurosis fugax), diplopia, nystagmus.

212
Q

What systemic symptoms are associated with Vertebrobasilar Insufficiency?

A

Vertigo, unilateral weakness and sensory loss, history of syncope (drop attacks).

213
Q

What signs might be present in a patient with Vertebrobasilar Insufficiency?

A

Homonymous visual field defects.

214
Q

What is the treatment focus for Vertebrobasilar Insufficiency?

A

Controlling the hypercoagulable state with prophylactic use of daily aspirin.

215
Q

What is Cortical Blindness?

A

Sudden, bilateral, complete blindness due to extensive damage to the occipital lobe.

216
Q

What are the possible causes of Cortical Blindness?

A

Congenital, cerebrovascular accident (stroke with bilateral cerebral artery blockage), cardiac surgery.

217
Q

What symptoms do patients with Cortical Blindness typically report?

A

Complete, sudden, bilateral blindness with possible visual hallucinations.

218
Q

What is Anton’s Syndrome?

A

A condition where patients deny vision loss despite being blind.

219
Q

What findings are expected during an eye exam for Cortical Blindness?

A

Normal eye exam aside from bilateral no light perception.

220
Q

What is the status of the pupillary light reflex in patients with Cortical Blindness?

A

Present, because the occipital lobe is not responsible for the pupillary response.

221
Q

What is the Riddoch phenomenon?

A

The ability to perceive moving but not stationary objects.

222
Q

What is blindsight?

A

The ability to navigate around objects despite being blind.

223
Q

Is there a treatment available for Cortical Blindness?

A

No treatment is available; loss of vision is usually permanent.

224
Q

What is Vertebrobasilar Insufficiency?

A

Occurs when the Vertebrobasilar arterial blood supply to the brain becomes blocked.

225
Q

What can cause Vertebrobasilar Insufficiency?

A

Thrombus, emboli, hypertension, or anything causing a hypercoagulable state.

226
Q

What are common symptoms of Vertebrobasilar Insufficiency?

A

Flashes of light (photopsia), bilateral transient visual loss (amaurosis fugax), diplopia, nystagmus.

227
Q

What systemic symptoms are associated with Vertebrobasilar Insufficiency?

A

Vertigo, unilateral weakness and sensory loss, history of syncope (drop attacks).

228
Q

What signs might be present in a patient with Vertebrobasilar Insufficiency?

A

Homonymous visual field defects.

229
Q

What is the treatment focus for Vertebrobasilar Insufficiency?

A

Controlling the hypercoagulable state with prophylactic use of daily aspirin.

230
Q

What is idiopathic intracranial hypertension also known as?

A

Pseudotumor cerebri

231
Q

What causes papilledema in idiopathic intracranial hypertension?

A

Elevated intracranial pressure in the absence of an intracranial space-occupying lesion

232
Q

In which demographic is idiopathic intracranial hypertension most commonly observed?

A

Females of child-bearing age who are overweight

233
Q

Name a medication associated with idiopathic intracranial hypertension.

A

Tetracyclines, naladixic acid, oral contraceptives, steroids, vitamin A, isotretinoin, growth hormones, sulfa drugs, tamoxifen, thyroid replacement therapy, phenytoin

234
Q

Fill in the blank: Idiopathic intracranial hypertension is characterized by _______.

A

Papilledema caused by elevated intracranial pressure

235
Q

True or False: Idiopathic intracranial hypertension can occur with enlargement of the ventricles due to hydrocephalus.

A

False

236
Q

What is the chance of developing maculopathy in patients with non-central optic pits?

A

Up to 45%

This statistic highlights the significant risk associated with non-central optic pits.

237
Q

What are the two main suggested origins of subretinal fluid in optic pits?

A
  • Subarachnoid space
  • Vitreous

This indicates ongoing debate and research regarding the source of the fluid.

238
Q

What has been observed in eyes with retinal detachment related to optic pits?

A

A small opening in the membrane covering the pit

This finding suggests a structural change associated with retinal detachments.

239
Q

What anatomical feature might contribute to retinal detachment in cases of optic pits?

A

Atypical Cloquet’s canal traction

This indicates a potential mechanical factor in detachment formation.

240
Q

Which types of optic pits are more at risk for developing detachments?

A
  • Temporally located pits
  • Larger pits

This suggests that location and size are important risk factors.

241
Q

What is the success rate of laser treatment applied to the peripapillary area for reduced visual acuity?

A

Approximately 30%

This low success rate indicates the challenges in treating maculopathy associated with optic pits.

242
Q

What are alternative treatment options for patients with optic pits experiencing maculopathy?

A
  • Pars-plana vitrectomy
  • Injection of gas tamponade without vitrectomy

These options reflect the limited approaches available for management.

243
Q

What is the prognosis for maculopathy associated with optic pits?

A

Poor prognosis

This emphasizes the seriousness of the condition and its complications.

244
Q

What should patients be given to monitor changes in their vision associated with optic pits?

A

An Amsler grid

This tool helps in detecting vision changes that may indicate complications.

245
Q

Ocular complications of optic pit

A

Serious macular detachment
* maculopathy associated with optic put does not have good prognosis
* patient should be given amsler and RTC ASAP if changes

246
Q

What type of migraine has visual aura followed by a headache

A

Classic migraine
* zig zag light that grows larger with time
*aura lasts for 20 minutes
*then followed by headache with nausea and light sensitivity

247
Q

Common migraine

A
  • last several hours to days
  • nausea/vomitting
  • photophobia
    *no visual aura preceeding headache
248
Q

What is an ocular migraine?

A

A type of migraine characterized by visual disturbances, such as flashing lights, zigzag patterns, or temporary loss of vision, usually in one eye.

249
Q

How long do the symptoms of an ocular migraine typically last?

A

About 20 to 30 minutes.

250
Q

Do ocular migraines always occur with a headache?

A

No, they can occur with or without a headache.

251
Q

What is the understood cause of ocular migraines?

A

The exact cause isn’t fully understood, but it is thought to be related to changes in blood flow in the eye or brain.

252
Q

Fill in the blank: Ocular migraine is characterized by _______.

A

visual disturbances.

253
Q

True or False: Ocular migraines can affect both eyes.

A

False.

254
Q

Leber hereditary optic neuropathy signs on fundus photos

A

Optic nerve head pallor, both eyes
*genetic testing for dx, mutation in maternal mitochondrial DNA
* M>F

255
Q

Pseudotumor cerebri symptoms

A

Symptoms: blurry vision, headache, nausea, color vision abnormalities (dyschromatopsia), transient vision disturbances, and reduced affect

256
Q

Idiopathic intracranial hypertension signs

A
  1. Papilledema (increased ICP)
  2. Normal brain MRI/CT
  3. High cerebral spinal fluid on lumbar puncture (>250 mmH2O for obese patients)

IIH mostly seen in young, fertile and fat females

*CSF for non-obese patients >200mmH2O

257
Q

Tx for pseudotumor cerebri?

A
  1. Discontinue associated medications (ex: birth control, Accutane)
  2. Lose weight
  3. Oral acetazolamide (Diamox 1000mg po QD)
258
Q

With OIS, the carotid artery is blocked by ___%

A

90% blocked