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 (name at least 3)

A

1) Optic nerve oblique insertion
2) fundus ectasia
3) Situs inverses
4) Myopic
5) superior temporal VF defects that do not respect the midline

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9
Q

A&P for isolated damage to 3rd order neuron causing Horner’s

A

A. Horner syndrome
1. isolated damage of 3rd order neuron

Plan
1. No further investigation

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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 the _________ 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? (Name at least 3)

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? (Name at least 4)

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

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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35
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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36
Q

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

A

brain

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37
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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38
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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39
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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40
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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41
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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42
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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43
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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44
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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45
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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46
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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47
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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48
Q

What is the typical health status of patients with papillophlebitis?

A

Generally healthy.

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49
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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50
Q

What age group is most commonly affected by papillophlebitis?

A

Patients under 50 years of age.

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51
Q

What is the prognosis of papillophlebitis without treatment?

A

Typically good, unless chronic macular edema remains.

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52
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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53
Q

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

A

False.
* common in younger pts

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54
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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55
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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56
Q

What causes aberrant regeneration of the oculomotor nerve?

A

Damage from trauma or compression.

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57
Q

What is the pseudo-Graefe sign?

A

Elevation of the involved eyelid on downgaze or adduction.

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58
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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59
Q

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

A

True.

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60
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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61
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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62
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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63
Q

What major artery runs through each cavernous sinus?

A

The internal carotid artery

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64
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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65
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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66
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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67
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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68
Q

Where does CN V2 exit the cavernous sinus?

A

Through the foramen rotundum

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69
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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70
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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71
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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72
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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73
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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74
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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75
Q

What does sympathetic input cause in the pupillary pathway?

A

Mydriasis

Mydriasis refers to the dilation of the pupil.

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76
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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77
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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78
Q

Which retinal photoreceptors mediate the response to light?

A

Retinal photoreceptors

These receptors conduct signals to the pretectal nucleus.

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79
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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80
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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81
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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82
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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83
Q

What is the effect to the pupil when there’s damage to the parasympathetic pathway?

A

Mydriasis of the pupil

Damage affects pupil constriction capabilities.

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84
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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85
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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86
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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87
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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88
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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89
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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90
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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91
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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92
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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93
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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94
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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95
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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96
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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97
Q

Can serous detachment associated with optic pits resolve spontaneously?

A

Yes, rarely

Spontaneous resolution is uncommon but possible.

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98
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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99
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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100
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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101
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

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102
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)
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103
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

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104
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.

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105
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.

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106
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.

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107
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.

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108
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)

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109
Q

What are optic disc drusen composed of?

A

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

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110
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

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111
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

JUSTIN BEIBER HAS THIS CONDITION!

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112
Q

Argyll-Robertson pupils

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

*caused by late stage syphilis

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113
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
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114
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

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115
Q

Pathophysiology of Adie’s tonic pupil

A

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

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116
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.

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117
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.

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118
Q

What are common conditions that are associated 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.

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119
Q

What causes Argyll-Robertson pupils?

A

Spirochete syphilis

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

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120
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.

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121
Q

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

A

Spirochete syphilis

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122
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

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123
Q

What should be considered before diagnosing Bell’s palsy?

A

Other causes of acquired peripheral facial weakness

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124
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
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125
Q

What type of mass can cause peripheral facial weakness?

A

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

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126
Q

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

A

Diagnosis of exclusion

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127
Q

What symptoms may patients with Bell’s palsy experience?

A
  • Viral prodrome
  • Ear pain
  • Decreased tearing
  • Decreased taste
  • Facial numbness
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128
Q

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

A

Usually progresses over a period of 10 days

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129
Q

Is Bell’s palsy life-threatening?

A

No, it is non life-threatening

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130
Q

What is the incidence of Bell’s palsy?

A

20-30 cases per 100,000 people per year

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131
Q

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

A

60-75%

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132
Q

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

A

40 years

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133
Q

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

A

People older than 70

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134
Q

Does Bell’s palsy affect both sexes equally?

A

Yes

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135
Q

Do most patients with Bell’s palsy recover completely?

136
Q

True or False: Bell’s palsy rarely recurs.

137
Q

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

A

lower facial musculature only

138
Q

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

A

lower motor neuron (peripheral)

139
Q

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

A

With equal frequency

140
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.

141
Q

What muscles are spared in an upper motor neuron lesion?

A

Frontalis muscle.

142
Q

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

A

Normal furrowing of the brow. (Upper facial feature)

143
Q

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

144
Q

What are common causes of upper motor neuron lesions?

A

Space occupying lesions or cerebrovascular accidents.

145
Q

How does an upper motor neuron lesion affect facial innervation?

A

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

146
Q

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

A

Contralateral lower face.

147
Q

What characterizes lower motor neuron lesions?

A

Weakness of all muscles of facial expression.

148
Q

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

149
Q

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

150
Q

How is eye closure affected in lower motor neuron lesions?

A

Eye closure is weak.

151
Q

What condition is commonly associated with lower motor neuron lesions?

A

Bell’s palsy.

152
Q

Which facial areas are affected by lower motor neuron lesions?

A

Ipsilateral upper and lower face.

153
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

154
Q

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

155
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

156
Q

Are optic nerve drusen typically unilateral or bilateral?

A

Generally bilateral, but may present unilaterally

Seen almost exclusively in Caucasians

157
Q

What are the symptoms of optic nerve drusen?

A

Most patients are asymptomatic; visual field defect may cause symptoms

158
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

159
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

160
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

161
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

162
Q

What characteristic do drusen exhibit during ultrasonography?

A

Possess high acoustic reflectivity

Drusen will autofluoresce

163
Q

Is treatment typically required for optic nerve drusen?

A

No, treatment is typically not required

164
Q

What are optic nerve drusen?

A

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

165
Q

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

A

Patients may experience elevated intraocular pressure.

166
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.

167
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.

168
Q

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

A

Discs with drusen will typically not develop cupping.

169
Q

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

A

Cupping is observed with glaucomatous damage.

170
Q

What are the typical causes of Visual Pathway Lesions?

A

Vascular disorders or tumors

171
Q

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

A

They become more homonymous and congruent

172
Q

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

A

Bitemporal Hemianopsia

173
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

174
Q

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

175
Q

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

A

Inferior quadrantanopia

176
Q

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

A

Superior quadrantanopia

177
Q

What typically causes a Contralateral Homonymous Hemianopia?

A

Stroke or tumor

178
Q

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

A

Posterior Cerebral Artery Occlusion

179
Q

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

A

Macular sparing

180
Q

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

A

There will be no macular sparing

181
Q

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

182
Q

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

183
Q

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

A

Visual fields

184
Q

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

A

PCP or neurologist

185
Q

How do Acute Cranial Nerve Palsies present on MRI?

A

Evidence of acute trauma

186
Q

What is a characteristic feature of Chronic Cranial Nerve Palsies?

A

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

187
Q

What is Warfarin commonly used for?

A

Oral anticoagulant

188
Q

What does Warfarin inhibit?

A

Activation of clotting factors that depend on vitamin K for synthesis

189
Q

What process does Heparin inhibit?

A

Conversion of prothrombin to thrombin

190
Q

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

A

Irreversible inhibition of platelet cyclooxygenase

191
Q

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

A

Wernicke’s = wordy speech (hard to understand spoken or written language, but speaking appears fluent but lacks meaning, jargon)

Broca’s = broken speech (hard to speak, but can understand speech)

192
Q

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

A

Contralateral upper quadrantanopia
* pie in the sky

193
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)

194
Q

Pre-chiasmal lesion leads to what VF defect?

A

Total blindness of ipsilateral eye

195
Q

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

A

Junctional scotoma

196
Q

What is Cortical Blindness?

A

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

197
Q

What are the possible causes of Cortical Blindness?

A

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

198
Q

What symptoms do patients with Cortical Blindness typically report?

A

Complete, sudden, bilateral blindness with possible visual hallucinations.

199
Q

What is Anton’s Syndrome?

A

A condition where patients deny vision loss despite being blind.

200
Q

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

A

Normal eye exam and normal pupillary response
BUT
Vision will be no light perception in both eyes

*functional visual loss

No treatment, poor prognosis
*refer for CT or MRI
*refer to neurology

201
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.

202
Q

What is the Riddoch phenomenon?

A

The ability to perceive moving but not stationary objects.

203
Q

What is blindsight?

A

The ability to navigate around objects despite being blind.

204
Q

Is there a treatment available for Cortical Blindness?

A

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

205
Q

What is Vertebrobasilar Insufficiency?

A

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

206
Q

What can cause Vertebrobasilar Insufficiency?

A

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

207
Q

What are common symptoms of Vertebrobasilar Insufficiency?

A

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

208
Q

What systemic symptoms are associated with Vertebrobasilar Insufficiency?

A

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

209
Q

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

A

Homonymous visual field defects.

210
Q

What is the treatment focus for Vertebrobasilar Insufficiency?

A

Controlling the hypercoagulable state with prophylactic use of daily aspirin.

211
Q

What is Cortical Blindness?

A

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

212
Q

What are the possible causes of Cortical Blindness?

A

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

213
Q

What symptoms do patients with Cortical Blindness typically report?

A

Complete, sudden, bilateral blindness with possible visual hallucinations.

214
Q

What is Anton’s Syndrome?

A

A condition where patients deny vision loss despite being blind.

215
Q

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

A

Normal eye exam aside from bilateral no light perception.

216
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.

217
Q

What is the Riddoch phenomenon?

A

The ability to perceive moving but not stationary objects.

218
Q

What is blindsight?

A

The ability to navigate around objects despite being blind.

219
Q

Is there a treatment available for Cortical Blindness?

A

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

220
Q

What is Vertebrobasilar Insufficiency?

A

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

221
Q

What can cause Vertebrobasilar Insufficiency?

A

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

222
Q

What are common symptoms of Vertebrobasilar Insufficiency?

A

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

223
Q

What systemic symptoms are associated with Vertebrobasilar Insufficiency?

A

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

224
Q

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

A

Homonymous visual field defects.

225
Q

What is the treatment focus for Vertebrobasilar Insufficiency?

A

Controlling the hypercoagulable state with prophylactic use of daily aspirin.

226
Q

What is idiopathic intracranial hypertension also known as?

A

Pseudotumor cerebri

227
Q

What causes papilledema in idiopathic intracranial hypertension?

A

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

228
Q

In which demographic is idiopathic intracranial hypertension most commonly observed?

A

Females of child-bearing age who are overweight

229
Q

Name medications associated with idiopathic intracranial hypertension. (Name at least 4)

A

CATS!!
1. Contraceptives
2. Accutane (isotretinoin)
3. Tetracyclines
4. Synthroid

And also:
naladixic acid
steroids
vitamin A
growth hormones
sulfa drugs
tamoxifen
phenytoin

230
Q

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

A

Papilledema caused by elevated intracranial pressure

231
Q

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

232
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.

233
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.

234
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.

235
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.

236
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.

237
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.

238
Q

What is the prognosis for maculopathy associated with optic pits?

A

Poor prognosis

This emphasizes the seriousness of the condition and its complications.

239
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.

240
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

241
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

242
Q

Common migraine

A
  • last several hours to days
  • nausea/vomitting
  • photophobia
    *no visual aura preceeding headache
243
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.

244
Q

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

A

About 20 to 30 minutes.

245
Q

Do ocular migraines always occur with a headache?

A

No, they can occur with or without a headache.

246
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.

247
Q

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

A

visual disturbances.

248
Q

True or False: Ocular migraines can affect both eyes.

A

False.

*its unilateral

249
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

250
Q

Pseudotumor cerebri symptoms

A

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

251
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

252
Q

Tx for pseudotumor cerebri?

A
  1. Discontinue associated medications (ex: birth control, Accutane)
  2. Lose weight
  3. Oral acetazolamide (Diamox 1000mg po QD)
253
Q

With OIS, the carotid artery is blocked by ___%

A

90% blocked

254
Q

What are migraines defined as?

A

Unilateral headaches that may involve the entire cranium with variable intensity and duration

Migraines are a common genetic condition observed more frequently in females.

255
Q

What neurological symptoms may be present during migraine episodes?

A

Neurological deficits and visual disturbances

These symptoms can vary among individuals.

256
Q

What characterizes a classic migraine?

A

Occurs with a visual aura that precedes the headache

A classic migraine is less frequently encountered but easier to diagnose.

257
Q

What is a visual aura in classic migraines?

A

A small paracentral scotoma appearing as a light or bright area with zigzag borders

The visual disturbance grows larger over time.

258
Q

What may develop during a visual aura episode?

A

Homonymous hemianopsia

This is a condition that affects the visual field on the same side in both eyes.

259
Q

How long do visual auras typically last?

A

Around 20 minutes

They are followed by a headache, often with nausea and light sensitivity.

260
Q

What are common symptoms of a common migraine?

A

Nausea, vomiting, photophobia, and sensitivity to noise

These migraines last several hours to days.

261
Q

What is a notable characteristic of a common migraine compared to a classic migraine?

A

No visual aura precedes the headache

However, mood alterations and other prodromal indicators may occur.

262
Q

In which demographic are cluster headaches more frequently observed?

A

Males in their 40s or 50s

Cluster headaches are known for excruciating pain.

263
Q

What symptoms accompany cluster headaches?

A

Ipsilateral sweating, lacrimation, ptosis, rhinorrhea, and conjunctival injection

Pain typically occurs over the temporal or frontal area.

264
Q

What age group typically experiences ophthalmoplegic migraines?

A

Children younger than 10 years of age

These migraines involve transient extraocular muscle palsy.

265
Q

What are the characteristics of basilar artery migraines?

A

Migraines with numbness and tingling of the extremities, speech and gait disturbances, and vertigo

They also primarily affect children.

266
Q

Fill in the blank: A classic migraine is less frequently encountered than a _______.

A

common migraine

Classic migraines are easier to diagnose due to their distinct features.

267
Q

During a classic migraine attack, what medication can be taken to alleviate it?

A

Aspirin
Oral NSAIDs
* take as early as possible

268
Q

If initial therapy of aspirin or oral NSAIDs does not work for alleviating classic migraine symptoms, stronger medications need to be used. Such as?

A

Ergotamine or Sumatriptan

Amitriptyline, topamax, calcium channel blockers, propranolol, anti-nausea (for prophylactic purposes)

269
Q

Tilted disc syndrome may be associated with what systemic syndromes?

A

Crouzon and Apert syndromes
* crouzon is AD, causes proptosis due to shallow ocular orbits, maxillary hyperplasia, abnormal craniofacial formation , hypertelorism and strabismus

270
Q

What is AAION?

A

AAION is caused by an infarction of the pre-laminar and laminar segment of the optic nerve, characterized by an acute, unilateral, painless loss of vision.

AAION is associated with giant cell arteritis and typically occurs in individuals over the age of 50.

271
Q

What are common symptoms of AAION?

A

Common symptoms include:
* Neck pain
* Jaw pain with chewing (jaw claudication)
* Scalp tenderness over the temporal artery
* New onset headaches
* Polymyalgia rheumatica
* Weight loss due to anorexia
* Fever
* Malaise

These symptoms are often related to vasculitis affecting the blood vessels of the head.

272
Q

What visual symptoms may patients with AAION report?

A

Patients may report:
* Amaurosis fugax (transient loss of vision)
* Profound loss of vision
* Diplopia

Amaurosis fugax can last for several minutes to hours.

273
Q

What findings are observed during ocular examination in AAION?

A

Ocular examination may reveal:
* Afferent pupillary defect
* Swollen, pale optic disc
* Splinter hemorrhages in new onset cases
* Optic atrophy in long standing cases

These findings are critical for diagnosis.

274
Q

What is NAION?

A

NAION is caused by an infarction of the optic nerve head, resulting in a sudden, unilateral, painless decrease in vision and acuity loss.

NAION generally occurs in patients with a ‘crowded’ disc and is typically seen in slightly younger patients than those with AAION.

275
Q

What are the common predisposing factors for NAION?

A

Common predisposing factors include:
* High cholesterol
* Diabetes mellitus
* Acute hypotensive events
* Cataract surgery
* Collagen vascular disease
* Hypertension

These factors contribute to the risk of developing NAION.

276
Q

What is papilledema and how is it characterized?

A

Papilledema is characterized by increased intracranial pressure and is almost always bilateral.

It can lead to various visual disturbances.

277
Q

What symptoms may patients with papilledema experience?

A

Patients may experience:
* Headaches
* Visual disturbances (especially with body position changes)
* Decreased acuity
* Diplopia

Some patients may be free of symptoms despite having papilledema.

278
Q

Is an afferent pupillary defect typically observed in papilledema?

A

No, an afferent pupillary defect is not typically observed because it is a bilateral condition.

Patients generally do not note pain upon eye movement.

279
Q

What is the typical age demographic for patients presenting with optic neuritis?

A

Patients younger than 50

Optic neuritis frequently occurs in younger patients.

280
Q

How does the initial vision loss in optic neuritis typically compare to that in temporal arteritis?

A

Not as severe

Initial vision loss in optic neuritis is usually less severe than in temporal arteritis.

281
Q

What symptom do patients with optic neuritis frequently report that is exacerbated with eye movement?

A

Orbital pain

Orbital pain is due to inflammation of the optic nerve.

282
Q

What may be observed in the optic disc of patients with optic neuritis?

A

Swelling of the disc with or without flame hemorrhages

Swelling and flame hemorrhages can occur in optic neuritis.

283
Q

What is retrobulbar optic neuritis and in which demographic is it more commonly observed?

A

A type of optic neuritis observed more commonly in adults

The nerve appears normal in retrobulbar optic neuritis.

284
Q

What type of pupillary defect may testing reveal in unilateral or asymmetrical optic neuritis?

A

Afferent pupillary defect

This defect is a key finding in optic neuritis.

285
Q

What visual disturbances might patients with optic neuritis report?

A

Flashes of light (photopsias)

Photopsias are common visual disturbances in optic neuritis.

286
Q

Why is it important to refer a patient with optic neuritis for an MRI?

A

To evaluate for plaques of demyelination

There is a strong correlation between optic neuritis and multiple sclerosis.

287
Q

What is the typical presentation of a central retinal vein occlusion?

A

Sudden painless loss of vision

Central retinal vein occlusion can lead to rapid vision loss.

288
Q

What findings on the fundus may indicate a central retinal vein occlusion?

A

Diffuse retinal hemorrhages extending to all four quadrants

Hemorrhages in central retinal vein occlusion are extensive.

289
Q

What may be observed in the optic disc of patients with central retinal vein occlusion?

A

Potentially a swollen optic disc

Swelling of the optic disc can occur with central retinal vein occlusion.

290
Q

Pathophysiology of vertebrobasilar insufficiency

A

Vertebrobasilar arterial blood supply to the brain becomes blocked

  • blocked from a thrombus, emboli, HYN or anything that can cause hypercoagulable state
291
Q

Symptoms of Vertebrobasilar insufficiency

A

Photopsia
Bilateral amaurosis fugax
Diplopia
Nystagmus

Systemic symptoms:
Vertigo
Unilateral weakness and sensory loss
History of syncope (drop attacks)

292
Q

Etiology of optic pits

A

Congenital, occur secondary to deficiency within lamina cribrosa that allows for dysplastic retina to enter defective area

293
Q

What are optic pits?

A

A congenital condition with a round or oval depression within the optic nerve

*usually located temporally
*associated with peripapillary RPE changes which develop intraretinal fluid with schisis cavities
*can progress to subretinal fluid collection with serous RD looks like a tear drop from pit to macula 💧

294
Q

Are optic pits usually unilateral or bilateral?

A

Unilateral

295
Q

How do optic pits appear on ophthalmoscopy?

A

Darker or gray

296
Q

Where are optic pits most frequently located?

A

Temporally

297
Q

What typically remains unaffected in optic pits?

A

Disc margin

298
Q

What is the typical visual acuity of patients with optic pits?

A

Normal, unless there is a serous detachment of the macula

299
Q

What may be observed adjacent to an optic pit?

A

Area of peripapillary atrophy

300
Q

How does the nerve with the optic pit compare to the contralateral eye’s nerve?

A

It is usually larger

301
Q

What is commonly observed in eyes with optic pits?

A

Cilioretinal arteries

302
Q

What symptoms do patients with optic nerve sheath gliomas typically present?

A

Decreased visual acuity, proptosis, potential APD, optic disc pallor, swelling, hyperemia

303
Q

In which age group are optic nerve sheath gliomas usually observed?

A

First or second decade of life

*slow growing brain tumor that arises around optic nerve
*glioma is a malignant tumor of the glial tissues of the nervous system

304
Q

What is the prevalence of optic disc drusen in the general population?

A

Roughly 0.3%

305
Q

Is optic disc drusen typically bilateral or unilateral?

A

Bilateral, but may present unilaterally

306
Q

How do early-stage optic disc drusen appear?

A

Deep beneath the surface of the optic disc, mimicking papilledema

307
Q

What happens to optic disc drusen as time passes?

A

They become more exposed and cause irregular nerve margins

308
Q

What is a common associated symptom with optic disc drusen?

A

Visual field loss

309
Q

In which demographic is optic disc drusen almost exclusively seen?

A

Caucasians

310
Q

What is morning glory anomaly?

A

A birth defect of the optic nerve with a coloboma of the optic disc
* reflection from within the eye may give appearance of a white pupil
***vision in affected eye is severely impaired **

311
Q

What does the optic nerve head look like in morning glory anomaly?

A

Funnel-shaped with a white dot in the center and an elevated ring of pigment

312
Q

What visual appearance may result from reflection within the eye in morning glory anomaly?

A

White pupil

313
Q

What is the typical vision status in the affected eye with morning glory anomaly?

A

Severely impaired

314
Q

A&P for 1st or 2nd order lesion causing Horner’s

A

Assessment
1. Pre-ganglionic lesion
*must localize lesion by instillation of hydroxyamphetamine, will dilate 1st and 2nd order lesion

Plan
1. Refer for MRI of head and neck and a CT scan of thorax or chest x-ray (pancoast tumor)

315
Q

Visual symptoms of AAION

A

Amaurosis fugax, followed by profound loss of vision or diplopia
Acute, unilateral painless vision loss

316
Q

True or false
+APD in AAION

A

TRUE
*unilateral swollen and pale optic disc
*caused by infarction of pre-laminar and laminar segment of optic nerve

317
Q

_______ generally occurs in patients with a “crowded” disc

A

NAION
* infarction of optic nerve head
* risk factors: high cholesterol, diabetes, hypotensive events, CE, collagen vascular disease and HTN

318
Q

NAION vs AAION age demographic

A

NAION: older population, younger than AAION
AAION: geriatric population (~60 and older)

319
Q

What occurs in patients with malignant hypertension related to the optic nerve?

A

Optic disc edema occurs

This is a significant finding in patients with malignant hypertension.

320
Q

What causes optic disc edema in malignant hypertension?

A

Vasoconstriction of the short posterior ciliary arteries

These arteries supply the optic nerve head.

321
Q

What triggers the vasoconstriction of the short posterior ciliary arteries?

A

Release of certain vasoconstrictive agents such as angiotensin II

Angiotensin II is a key regulator in blood pressure and fluid balance.

322
Q

What is a consequence of the vasoconstriction of the vessels supplying the optic nerve?

A

Subsequent ischemia of the optic nerve

Ischemia refers to insufficient blood supply to an organ.

323
Q

What condition can result from the ischemia of the optic nerve?

A

Stasis of axoplasmic flow

This stasis is a form of anterior ischemic optic neuropathy.

324
Q

Fill in the blank: The release of angiotensin II leads to _______ of the short posterior ciliary arteries.

A

vasoconstriction

325
Q

True or False: Ischemia of the optic nerve can lead to optic disc edema.

326
Q

What is functional vision loss?

A

Visual abnormalities that cannot be attributed to any organic disease process.

It encompasses non-physiologic visual loss types such as malingering and hysteria.

327
Q

What are the two main types of non-physiologic visual loss?

A
  • Malingering
  • Hysteria

Both types are characterized by different motivations and behaviors.

328
Q

What is malingering in the context of vision loss?

A

A condition where patients fabricate the existence of a vision disorder for secondary gain, often associated with legal action or compensation claims.

Malingerers tend to be uncooperative and combative.

329
Q

How do patients with hysteria typically behave?

A

They are commonly indifferent and cooperative, with a history of emotional distress.

Hysteria is a subconscious manifestation of visual symptoms.

330
Q

What are some tests used to determine the authenticity of claimed vision loss?

A
  • Optokinetic test
  • Menace reflex
  • Mirror test
  • Visual field testing

These tests help assess the level of vision loss claimed by the patient.

331
Q

Describe the optokinetic test.

A

Patients look straight ahead while an optokinetic drum is rotated in front of their eyes, leading to uncontrollable nystagmus if they have sufficient vision.

The better seeing eye should be patched if the patient claims a visual deficiency in only one eye.

332
Q

What happens if a patient is truly blind during the optokinetic test?

A

An optokinetic response cannot be elicited.

This test does not differentiate between hysteria and malingering.

333
Q

True or False: Malingering is a willful expression of visual symptoms.

A

False

Malingering involves fabrication for secondary gain, while hysteria is a subconscious manifestation.

334
Q

Fill in the blank: Hysteria is characterized by a history of _______.

A

[emotional distress]

335
Q

What is a key behavioral difference between malingering and hysteria patients?

A

Malingerers are typically uncooperative and combative, while hysteria patients are indifferent and cooperative.

This highlights the psychological differences in their conditions.