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)
2
Q
Argyll Robertson pupil associated with what infectious disease?
A
Late-stage syphilis
3
Q
Physiological anisocoria
A
- Anisocoria equal under dim and bright conditions
- no ptosis
- confirm stability by referring to previous photos of patient
4
Q
Signs of pupil involving 3rd nerve palsy
A
Eye is down and out with dilated (blown out) pupil
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!!!)
6
Q
Congenital Horner’s syndrome signs
A
Iris heterochromia (affected eye will have lighter iris)
7
Q
Characteristics of tilted disc syndrome
A
- Bilateral
- optic nerve enters at an oblique angle superiorly
- situs inversus
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
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
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
11
Q
Pulfrich phenomenon
A
Pendulum is perceived as moving in a circular motion rather than laterally
* symptom of optic neuritis
12
Q
Ocular manifestation of multiple sclerosis
A
Optic neuritis
13
Q
Optic neuritis age demographic
A
18 to 45 years old
14
Q
Uhthoff sign
A
Associated with MS
Symptoms worsen with increase in body temperature
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
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)
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)
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
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
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
21
Q
Pancoast tumor can cause which order neuron irregularity in Horner’s?
A
2nd order neuron lesion
22
Q
What is the most common cause of pupil sparing isolated 3rd nerve palsy?
A
Microvascular disease secondary to HTN &/or diabetes
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
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
25
Visual aura of a classic migraine would produce what type of visual field defect?
Homonymous hemianopsia
* start in center and enlarge in homonymous portions of the visual field
* HA located on contralateral side of field defect
26
Leber hereditary optic neuropathy is more common in males or females?
males
27
What is Tilted Disc Syndrome?
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
## Footnote
Typically observed bilaterally.
28
What visual field defects are often associated with Tilted Disc Syndrome?
Superotemporal defects
## Footnote
These defects may diminish or disappear with myopic astigmatism correction.
29
What are common symptoms of Tilted Disc Syndrome?
Majority are asymptomatic; some may report visual field defects or blurred vision
## Footnote
Symptoms can be caused by uncorrected astigmatism.
30
What clinical signs indicate Tilted Disc Syndrome? (Name at least 4)
* Obliquely inserted disc
* Myopic astigmatism
* Tilted optic disc with inferior ectasia
* Superior elevation of nerve tissue
* Situs inversus
* Fundus ectasia
* Superotemporal visual field defects
## Footnote
Visual field defects generally do not respect the midline.
31
What is the treatment for Tilted Disc Syndrome?
Visual correction to neutralize the associated refractive component
## Footnote
No additional treatment is required.
32
How often should patients with Tilted Disc Syndrome be evaluated?
Annually
## Footnote
Regular follow-up helps monitor any changes.
33
Fill in the blank: Tilted Disc Syndrome is caused by an optic nerve that enters the eye _______.
[superiorly at an oblique angle]
34
What is the primary function of the Circle of Willis in relation to the eyes?
The Circle of Willis provides collateral circulation to the brain, including areas that supply blood to the eyes.
35
True or False: The ophthalmic artery is a branch of the internal carotid artery, which is part of the Circle of Willis.
True
36
Fill in the blank: The Circle of Willis is located at the base of the ______.
brain
37
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
C) Posterior tibial artery
38
What are the main arteries supplying blood to the iris and ciliary body?
Long posterior ciliary arteries and anterior ciliary arteries
## Footnote
These arteries are branches of the ophthalmic artery.
39
What is formed by the terminal branches of the long posterior ciliary arteries and anterior ciliary arteries?
The major arterial circle of the iris
## Footnote
This circle lies behind the root of the iris in the ciliary body.
40
Where does the major arterial circle of the iris lie?
Behind the root of the iris in the ciliary body
## Footnote
It is formed by anastomoses of the long posterior and anterior ciliary arteries.
41
What is the path of blood vessels from the major arterial circle?
They course around the circumference of the iris, from the periphery toward the pupil
## Footnote
This arrangement supports blood flow to the iris.
42
What forms the minor arterial circle of the iris?
Centripetal branches of the major arterial circle
## Footnote
Minor circle is incomplete and lies just inside the pupillary border.
43
What is the location of the minor arterial circle of the iris?
Just inside the pupillary border
## Footnote
It is involved in the initial signs of neovascularization of the iris.
44
True or False: The minor arterial circle of the iris is responsible for the complete blood supply to the iris.
False
## Footnote
The minor circle is incomplete and primarily indicates neovascularization.
45
Fill in the blank: The _______ arteries anastomose with the anterior ciliary arteries to form the major arterial circle of the iris.
long posterior ciliary
## Footnote
These arteries are crucial for the vascular supply to the iris.
46
Initial signs of neovascularization of the iris is located where?
The minor arterial circle of the iris at the pupillary margin
## Footnote
Initial signs of neovascularization are observed in this area.
47
What is papillophlebitis?
A rare condition observed in younger patients, usually under 50 years of age.
* inflammation of the optic disc venous drainage
48
What is the typical health status of patients with papillophlebitis?
Generally healthy.
49
What are the clinical signs of papillophlebitis?
Sudden unilateral blurring of vision, disc edema, cotton wool spots, dilation and tortuosity of veins, and retinal hemorrhages restricted to the posterior pole.
50
What age group is most commonly affected by papillophlebitis?
Patients under 50 years of age.
51
What is the prognosis of papillophlebitis without treatment?
Typically good, unless chronic macular edema remains.
52
Fill in the blank: Clinical signs of papillophlebitis include _______.
- sudden unilateral blur
- disc edema
- cotton wool spots
- dilation and tortuosity of veins
- retinal hemorrhages.
53
True or False: Papillophlebitis is more common in older patients.
False.
* common in younger pts
54
What is aberrant regeneration in the context of cranial nerve palsy?
It occurs when third cranial nerve fibers misdirect to alternate muscles innervated by the same nerve.
* does not occur with ischemic 3rd nerve palsies
55
What muscles does the oculomotor nerve control?
* Medial rectus
* Superior rectus
* Inferior rectus
* Inferior oblique
* Iris dilator muscle
* levator
56
What causes aberrant regeneration of the oculomotor nerve?
Damage from trauma or compression.
57
What is the pseudo-Graefe sign?
Elevation of the involved eyelid on downgaze or adduction.
58
List the most common signs of aberrant third nerve regeneration.
* Eyelid-gaze dyskinesis
* Pupil-gaze dyskinesis
* Constriction of the pupil on downgaze or adduction
* Elevation of involved eyelid on downgaze or adduction
59
True or False: Aberrant regeneration can lead to limitation of elevation or depression of the eye.
True.
60
What is the cavernous sinus?
A large collection of thin-walled veins that create a cavity within the human head, bordered by the temporal and sphenoid bones
61
How does the cavernous sinus receive blood?
Via the superior and inferior ophthalmic veins and the superficial cortical veins
62
What channels drain the cavernous sinus?
The superior and inferior petrosal sinuses and into the jugular vein via the sigmoid sinus
63
What major artery runs through each cavernous sinus?
The internal carotid artery
64
Which cranial nerves are contained within the cavernous sinus?
* 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)
65
How do the cranial nerves run within the cavernous sinus?
From superior to inferior within the lateral wall of the cavernous sinus
66
Where does the abducens nerve (CN VI) run in relation to the cavernous sinus?
Through the middle of the sinus alongside the internal carotid artery
67
Which cranial nerves pass through the cavernous sinus and enter the orbital apex via the superior orbital fissure?
* CN III
* CN IV
* CN VI
68
Where does CN V2 exit the cavernous sinus?
Through the foramen rotundum
69
Where is the optic nerve located in relation to the cavernous sinus?
Just outside and superior to the cavernous sinus on each side, entering the orbital apex via the optic canal
70
What is the typical result of lesions involving the cavernous sinus?
Dysfunction of several nerves due to their close proximity
71
Which CN pass through the cavernous sinus and enter the orbital apex through the superior orbital fissure?
- CN 3
- CN 4
- V1 of CN 5
- CN 6
72
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?
MRI
* pt should get CT and CTA instead to confirm diagnosis of intracranial arterial aneurysm
73
If neuroimaging is negative for pt with pupil involving third nerve palsy what additional test should be considered next?
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
74
What is the pupillary pathway responsible for?
The light reflex and the near reflex
## Footnote
The pupillary pathway involves several neurons responding to stimuli.
75
What does sympathetic input cause in the pupillary pathway?
Mydriasis
## Footnote
Mydriasis refers to the dilation of the pupil.
76
What does parasympathetic innervation cause in the pupillary pathway?
Pupil miosis
## Footnote
Miosis refers to the constriction of the pupil.
77
What does the absence of a light reflex typically indicate?
Severe unilateral nerve damage
## Footnote
This absence suggests significant issues with the neural pathways.
78
Which retinal photoreceptors mediate the response to light?
Retinal photoreceptors
## Footnote
These receptors conduct signals to the pretectal nucleus.
79
Where do fibers from the nasal retina cross over?
In the chiasm
## Footnote
This allows signals to enter the contralateral pretectal nucleus.
80
What happens to fibers from the temporal retina?
They do not decussate and send information to the ipsilateral pretectal nucleus
## Footnote
This contributes to the light reflex mechanism.
81
What is the role of the Edinger-Westphal (EW) nuclei in the pupillary pathway?
They receive input from the pretectal nuclei and relay information
## Footnote
This process results in symmetrical pupil constriction when light stimulates one eye.
82
What occurs after neurons leave the EW nucleus?
They synapse onto the ipsilateral ciliary ganglion
## Footnote
This is crucial for innervating the pupil sphincter.
83
What is the effect to the pupil when there’s damage to the parasympathetic pathway?
Mydriasis of the pupil
## Footnote
Damage affects pupil constriction capabilities.
84
Where does the first order neuron of the sympathetic pathway originate?
In the hypothalamus
## Footnote
This neuron travels down the spine to synapse onto the ciliospinal center of Budge.
85
What is the pathway of the second order neuron in the sympathetic pathway?
Projects from the ciliospinal center of Budge upwards to the superior cervical ganglion
## Footnote
This ganglion is located in the neck.
86
What does the third order neuron do in the sympathetic pathway?
Sends projections from the superior cervical ganglion along the internal carotid artery
## Footnote
This neuron ultimately reaches the ciliary body and dilator muscle of the pupil.
87
What are the effects of damage to the sympathetic division of the pupillary pathway?
Pupillary miosis, ptosis of the upper lid, and elevation of the lower lid
## Footnote
Both Mueller's muscle and lower lid retractors are innervated by the sympathetic system.
88
What is the chance of developing maculopathy in patients with non-central optic pits?
Up to 45%
## Footnote
This statistic highlights the significant risk associated with non-central optic pits.
89
What are the suggested origins of the subretinal fluid in optic pits?
Subarachnoid space or vitreous
## Footnote
Research indicates that the fluid causing issues in optic pits likely originates from these two areas.
90
What has been observed in eyes that have suffered a retinal detachment associated with optic pits?
A small opening in the membrane covering the pit
## Footnote
This observation may indicate a pathway for fluid accumulation and retinal issues.
91
What factor might contribute to the formation of a retinal detachment in cases of optic pits?
Intravitreal traction on the pit by an atypical Cloquet's canal
## Footnote
This traction can lead to complications such as detachment.
92
Which types of optic pits are more at risk for developing detachments?
Temporal pits and larger pits
## Footnote
The location and size of the optic pit play a critical role in the risk of detachment.
93
Is there an agreed upon method of treatment for patients with optic pits?
No agreed upon method exists
## Footnote
Treatment approaches vary, indicating a lack of consensus in the medical community.
94
What treatment may be warranted if visual acuity is reduced in patients with optic pits?
Laser treatment applied to the peripapillary area
## Footnote
This treatment aims to re-establish the connection between the RPE and retina.
95
What is the success rate of laser treatment for optic pits?
Roughly 30%
## Footnote
This low success rate indicates the challenges in treating conditions associated with optic pits.
96
What are alternative treatment options for optic pits aside from laser treatment?
* Pars-plana vitrectomy
* Injection of a gas tamponade without vitrectomy
## Footnote
These options can be considered depending on the specific case.
97
Can serous detachment associated with optic pits resolve spontaneously?
Yes, rarely
## Footnote
Spontaneous resolution is uncommon but possible.
98
What is the prognosis for maculopathy associated with optic pits?
Poor prognosis
## Footnote
The associated risks and complications lead to a generally unfavorable outlook.
99
What should patients be given to monitor for changes related to optic pits?
An Amsler grid
## Footnote
This tool helps patients detect visual changes promptly.
100
What percentage of cases may also develop macular holes?
Up to 25%
## Footnote
This statistic further emphasizes the complications related to optic pits.
101
RTC for optic pit
Annually but should be given amsler grid because risk of serous macular detachment
Pt educated to RTC ASAP if any changes on amsler
102
Foster-Kennedy syndrome
- 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)
103
What is the correct sequence for the circulation of cerebrospinal fluid (CSF) in the brain?
Lateral ventricle → interventricular foramen → third ventricle → cerebral aqueduct → fourth ventricle → subarachnoid space
104
What is the most commonly affected cranial nerve in cases of elevated intracranial pressure?
Abducens (6th cranial nerve)
## Footnote
This is often due to space-occupying intracranial tumors.
105
What are the initial manifestations of tumors in around 50% of patients with an abducens nerve palsy?
Headaches and/or diplopia
## Footnote
These symptoms can indicate the presence of a tumor affecting the abducens nerve.
106
What causes an abducens nerve palsy?
Increase in intracranial pressure leading to stretching and compression of the 6th cranial nerve
## Footnote
This typically occurs as the nerve courses over the bony petrous tip of the skull.
107
What percentage of patients with an abducens nerve palsy experience headaches and/or diplopia?
Around 50%
## Footnote
This statistic highlights the commonality of these symptoms in relation to tumors.
108
RTC for optic nerve melanocytoma
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)
109
What are optic disc drusen composed of?
Hyaline-like calcific material
* best visible with B-scan
110
Oral corticosteroids can help with signs and symptoms of Bell’s palsy if initiated within ___ hours of onset
72 hours
* acute phase of bell’s, inflammation and edema of facial nerve are causing facial muscle weakness, anti-inflammatory minimizes nerve damage
111
Pt presents with acute peripheral facial nerve palsy + vesicular eruptions on ear, tongue, face or neck
Ramsay-hunt syndrome
* + viral prodrome and severe ear pain
* vestibulocochlear dysfunction, nausea, vomiting, tinnitus, and hearing loss
JUSTIN BEIBER HAS THIS CONDITION!
112
Argyll-Robertson pupils
- Small irregular shape pupils
- light-near dissociation
- dilate poorly in darkness
- bilateral, asymmetrical
*caused by late stage syphilis
113
Parinaud syndrome s/s
- bilateral mid-dilated pupils
- react poorly to light
- normal constriction at near
- eyelid refraction
- supra-nuclear upgaze paralysis
- convergence retraction nystagmus
114
Pt sus for Adie’s tonic pupil, what pharmacological agent confirms diagnosis?
0.125% pilocarpine
* diluted pilocarpine would constrict abnormal pupil with minimal constriction in normal pupil
115
Pathophysiology of Adie’s tonic pupil
Damage to postganglionic nerve fibers of the iris sphincter and ciliary muscle
116
What is the cause of an Adie tonic pupil?
Damage to the ciliary ganglion
## Footnote
This damage results in dysfunction of the postganglionic nerve fibers to the iris sphincter and ciliary muscle.
117
What is the typical pupil appearance in Adie tonic pupil?
Large pupil on the affected side
## Footnote
This occurs due to the initial insult to the ciliary ganglion.
118
What are common conditions that are associated with Adie pupil?
* Orbital trauma
* Surgery
* Viral infections
* Chronic tonsillitis
* Sinusitis
* Upper respiratory infections
* Dental anesthesia and tooth extractions
## Footnote
While many cases are idiopathic, some patients can link their Adie pupil to these factors.
119
What causes Argyll-Robertson pupils?
Spirochete syphilis
## Footnote
This infection damages the intercalated neurons between the pretectal and Edinger-Westphal nuclei.
120
What type of anisocoria is caused by Horner syndrome?
Anisocoria due to a paresis or palsy
## Footnote
This paresis or palsy is located in the oculosympathetic pathway.
121
Damage to intercalated neurons between the pretectal and E-W nuclei in Argyll Robertson pupil is caused by what organism?
Spirochete syphilis
122
What is Bell's palsy characterized by?
Acute onset of unilateral weakness of the upper and lower muscles of the face with no apparent cause
123
What should be considered before diagnosing Bell's palsy?
Other causes of acquired peripheral facial weakness
124
List some associated conditions with Bell's palsy.
* Diabetes
* Hypertension
* HIV
* Lyme disease
* Ramsay-Hunt syndrome
* Sarcoidosis
* Sjogren syndrome
* Parotid-nerve tumors
* Temporal bone fracture
* Guillain-Barre syndrome
125
What type of mass can cause peripheral facial weakness?
Cerebellopontine angle mass (e.g., acoustic neuroma, facial neuroma, meningioma, cholesteatoma)
126
How is Bell's palsy classified in terms of diagnosis?
Diagnosis of exclusion
127
What symptoms may patients with Bell's palsy experience?
* Viral prodrome
* Ear pain
* Decreased tearing
* Decreased taste
* Facial numbness
128
What is the typical progression time for facial palsy in Bell's palsy?
Usually progresses over a period of 10 days
129
Is Bell's palsy life-threatening?
No, it is non life-threatening
130
What is the incidence of Bell's palsy?
20-30 cases per 100,000 people per year
131
What percentage of unilateral facial paralysis does Bell's palsy account for?
60-75%
132
At what median age does Bell's palsy typically onset?
40 years
133
Which age group has the highest incidence of Bell's palsy?
People older than 70
134
Does Bell's palsy affect both sexes equally?
Yes
135
Do most patients with Bell's palsy recover completely?
Yes
136
True or False: Bell's palsy rarely recurs.
True
137
Fill in the blank: Facial paralysis due to an upper motor neuron lesion will cause weakness of the _______.
lower facial musculature only
138
Fill in the blank: Bell's palsy is due to a _______ lesion.
lower motor neuron (peripheral)
139
How often do both sides of the face get affected in Bell's palsy?
With equal frequency
140
What is the significance of determining whether facial weakness is due to an upper or lower motor neuron lesion?
It helps to determine the etiology of the disorder.
141
What muscles are spared in an upper motor neuron lesion?
Frontalis muscle.
142
In upper motor neuron lesions, what facial feature is preserved?
Normal furrowing of the brow. (Upper facial feature)
143
Are eye closure and blinking affected in upper motor neuron lesions?
No.
144
What are common causes of upper motor neuron lesions?
Space occupying lesions or cerebrovascular accidents.
145
How does an upper motor neuron lesion affect facial innervation?
Innervation of the contralateral upper and lower face, and ipsilateral upper face.
146
What part of the face is usually affected by an upper motor neuron lesion?
Contralateral lower face.
147
What characterizes lower motor neuron lesions?
Weakness of all muscles of facial expression.
148
What happens to the angle of the mouth in lower motor neuron lesions?
It falls.
149
Is weakness of the frontalis muscle present in lower motor neuron lesions?
Yes.
150
How is eye closure affected in lower motor neuron lesions?
Eye closure is weak.
151
What condition is commonly associated with lower motor neuron lesions?
Bell's palsy.
152
Which facial areas are affected by lower motor neuron lesions?
Ipsilateral upper and lower face.
153
What is the most prevalent form of color discrimination deficiency among males and females?
Deuteranomaly
* have all 3 photo pigments but there is a shift of maximum sensitivity of chlorolabe towards longer wavelengths
* red-green color blindness
154
Optic nerve disease may cause what kind of acquired color vision deficiency?
Red-green
155
What are optic nerve drusen?
Hyaline-like calcific material deposition in the optic nerve
## Footnote
Present in roughly 0.3% of the general population
156
Are optic nerve drusen typically unilateral or bilateral?
Generally bilateral, but may present unilaterally
## Footnote
Seen almost exclusively in Caucasians
157
What are the symptoms of optic nerve drusen?
Most patients are asymptomatic; visual field defect may cause symptoms
158
What clinical signs are observed in the early stages of optic nerve drusen?
Drusen may be located deep beneath the optic disc surface, causing elevation with clear margins
## Footnote
The disc will not appear hyperemic and surface vessels remain visible
159
What happens to optic nerve drusen with age?
Drusen become more prominent and move anteriorly, exposing irregular nerve margins
## Footnote
The disc may appear elevated with no physiological cup
160
What associated condition may occur with optic nerve drusen?
Associated field loss can occur
## Footnote
Rarely, a choroidal neovascular membrane may develop adjacent to the optic nerve
161
How is a diagnosis of buried drusen best confirmed?
Via B-scan ultrasonography or optical coherence tomography (OCT)
## Footnote
Turning down the gain while performing B-scan ultrasonography allows for visualization of the drusen
162
What characteristic do drusen exhibit during ultrasonography?
Possess high acoustic reflectivity
## Footnote
Drusen will autofluoresce
163
Is treatment typically required for optic nerve drusen?
No, treatment is typically not required
164
What are optic nerve drusen?
Optic nerve drusen are calcified deposits that form on the optic nerve head.
165
What condition may patients with optic nerve drusen experience in addition to drusen?
Patients may experience elevated intraocular pressure.
166
Why may treatment be required for patients with both optic nerve drusen and elevated intraocular pressure?
Field loss may be due to the elevated intraocular pressure rather than the drusen.
167
What challenge arises when both elevated intraocular pressure and optic nerve drusen are present?
It is difficult to attribute field loss to either elevated intraocular pressure or drusen.
168
What is typically observed in discs with drusen in terms of cupping?
Discs with drusen will typically not develop cupping.
169
What type of damage is associated with cupping in the optic nerve?
Cupping is observed with glaucomatous damage.
170
What are the typical causes of Visual Pathway Lesions?
Vascular disorders or tumors
171
As the lesion moves posteriorly in the visual pathway, how do the visual field defects change?
They become more homonymous and congruent
172
What visual field defect is typically caused by a Pituitary Gland Tumor?
Bitemporal Hemianopsia
173
In a Junctional Scotoma, where is the lesion located in relation to the visual field defect?
Ipsilateral to the central visual field defect; superior temporal quadrant defect on the contralateral side
174
What mnemonic can be used to remember the visual field defect locations caused by Parietal and Temporal lobe lesions?
PITS
175
What visual field defect is caused by a Parietal lobe lesion?
Inferior quadrantanopia
176
What visual field defect is caused by a Temporal lobe lesion?
Superior quadrantanopia
177
What typically causes a Contralateral Homonymous Hemianopia?
Stroke or tumor
178
What type of stroke is commonly associated with Contralateral Homonymous Hemianopia?
Posterior Cerebral Artery Occlusion
179
What phenomenon often occurs with Contralateral Homonymous Hemianopia due to dual blood supply?
Macular sparing
180
What happens to macular sparing if a tumor compresses both sides of the Posterior Cerebral Artery?
There will be no macular sparing
181
What is the onset of symptoms for visual field loss caused by a tumor?
Gradual
182
What is the onset of symptoms for visual field loss caused by a stroke?
Acute
183
What should be checked first in the treatment/management of visual pathway lesions?
Visual fields
184
What type of medical specialists should patients be referred to for further evaluation?
PCP or neurologist
185
How do Acute Cranial Nerve Palsies present on MRI?
Evidence of acute trauma
186
What is a characteristic feature of Chronic Cranial Nerve Palsies?
Spread of comitance identified with cover test in 9 positions of gaze
187
What is Warfarin commonly used for?
Oral anticoagulant
188
What does Warfarin inhibit?
Activation of clotting factors that depend on vitamin K for synthesis
189
What process does Heparin inhibit?
Conversion of prothrombin to thrombin
190
What is the mechanism of action of Aspirin in relation to platelets?
Irreversible inhibition of platelet cyclooxygenase
191
Symptoms associated with lesions in Wernicke’s and Broca’s areas
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
What VF defect is caused by lesion at the temporal lobe?
Contralateral upper quadrantanopia
* pie in the sky
193
Contralateral homonymous hemianopia with macular sparing has a lesion in which part of the visual pathway?
Primary visual cortex of the occipital lobe
* caused from stoke
* macular sparing because has dual blood supply (posterior and middle cerebral arteries)
194
Pre-chiasmal lesion leads to what VF defect?
Total blindness of ipsilateral eye
195
Compression of Willenbran’s knee leads to what VF defect?
Junctional scotoma
196
What is Cortical Blindness?
Sudden, bilateral, complete blindness due to extensive damage to the occipital lobe.
197
What are the possible causes of Cortical Blindness?
Congenital, cerebrovascular accident (stroke with bilateral cerebral artery blockage), cardiac surgery.
198
What symptoms do patients with Cortical Blindness typically report?
Complete, sudden, bilateral blindness with possible visual hallucinations.
199
What is Anton's Syndrome?
A condition where patients deny vision loss despite being blind.
200
What findings are expected during an eye exam for Cortical Blindness?
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
What is the pupillary light reflex in patients with Cortical Blindness?
Present, because the occipital lobe is not responsible for the pupillary response.
202
What is the Riddoch phenomenon?
The ability to perceive moving but not stationary objects.
203
What is blindsight?
The ability to navigate around objects despite being blind.
204
Is there a treatment available for Cortical Blindness?
No treatment is available; loss of vision is usually permanent.
205
What is Vertebrobasilar Insufficiency?
Occurs when the Vertebrobasilar arterial blood supply to the brain becomes blocked.
206
What can cause Vertebrobasilar Insufficiency?
Thrombus, emboli, hypertension, or anything causing a hypercoagulable state.
207
What are common symptoms of Vertebrobasilar Insufficiency?
Flashes of light (photopsia), bilateral transient visual loss (amaurosis fugax), diplopia, nystagmus.
208
What systemic symptoms are associated with Vertebrobasilar Insufficiency?
Vertigo, unilateral weakness and sensory loss, history of syncope (drop attacks).
209
What signs might be present in a patient with Vertebrobasilar Insufficiency?
Homonymous visual field defects.
210
What is the treatment focus for Vertebrobasilar Insufficiency?
Controlling the hypercoagulable state with prophylactic use of daily aspirin.
211
What is Cortical Blindness?
Sudden, bilateral, complete blindness due to extensive damage to the occipital lobe.
212
What are the possible causes of Cortical Blindness?
Congenital, cerebrovascular accident (stroke with bilateral cerebral artery blockage), cardiac surgery.
213
What symptoms do patients with Cortical Blindness typically report?
Complete, sudden, bilateral blindness with possible visual hallucinations.
214
What is Anton's Syndrome?
A condition where patients deny vision loss despite being blind.
215
What findings are expected during an eye exam for Cortical Blindness?
Normal eye exam aside from bilateral no light perception.
216
What is the status of the pupillary light reflex in patients with Cortical Blindness?
Present, because the occipital lobe is not responsible for the pupillary response.
217
What is the Riddoch phenomenon?
The ability to perceive moving but not stationary objects.
218
What is blindsight?
The ability to navigate around objects despite being blind.
219
Is there a treatment available for Cortical Blindness?
No treatment is available; loss of vision is usually permanent.
220
What is Vertebrobasilar Insufficiency?
Occurs when the Vertebrobasilar arterial blood supply to the brain becomes blocked.
221
What can cause Vertebrobasilar Insufficiency?
Thrombus, emboli, hypertension, or anything causing a hypercoagulable state.
222
What are common symptoms of Vertebrobasilar Insufficiency?
Flashes of light (photopsia), bilateral transient visual loss (amaurosis fugax), diplopia, nystagmus.
223
What systemic symptoms are associated with Vertebrobasilar Insufficiency?
Vertigo, unilateral weakness and sensory loss, history of syncope (drop attacks).
224
What signs might be present in a patient with Vertebrobasilar Insufficiency?
Homonymous visual field defects.
225
What is the treatment focus for Vertebrobasilar Insufficiency?
Controlling the hypercoagulable state with prophylactic use of daily aspirin.
226
What is idiopathic intracranial hypertension also known as?
Pseudotumor cerebri
227
What causes papilledema in idiopathic intracranial hypertension?
Elevated intracranial pressure in the absence of an intracranial space-occupying lesion
228
In which demographic is idiopathic intracranial hypertension most commonly observed?
Females of child-bearing age who are overweight
229
Name medications associated with idiopathic intracranial hypertension. (Name at least 4)
CATS!!
1. Contraceptives
2. Accutane (isotretinoin)
3. Tetracyclines
4. Synthroid
And also:
naladixic acid
steroids
vitamin A
growth hormones
sulfa drugs
tamoxifen
phenytoin
230
Fill in the blank: Idiopathic intracranial hypertension is characterized by _______.
Papilledema caused by elevated intracranial pressure
231
True or False: Idiopathic intracranial hypertension can occur with enlargement of the ventricles due to hydrocephalus.
False
232
What are the two main suggested origins of subretinal fluid in optic pits?
* Subarachnoid space
* Vitreous
## Footnote
This indicates ongoing debate and research regarding the source of the fluid.
233
What has been observed in eyes with retinal detachment related to optic pits?
A small opening in the membrane covering the pit
## Footnote
This finding suggests a structural change associated with retinal detachments.
234
What anatomical feature might contribute to retinal detachment in cases of optic pits?
Atypical Cloquet's canal traction
## Footnote
This indicates a potential mechanical factor in detachment formation.
235
Which types of optic pits are more at risk for developing detachments?
* Temporally located pits
* Larger pits
## Footnote
This suggests that location and size are important risk factors.
236
What is the success rate of laser treatment applied to the peripapillary area for reduced visual acuity?
Approximately 30%
## Footnote
This low success rate indicates the challenges in treating maculopathy associated with optic pits.
237
What are alternative treatment options for patients with optic pits experiencing maculopathy?
* Pars-plana vitrectomy
* Injection of gas tamponade without vitrectomy
## Footnote
These options reflect the limited approaches available for management.
238
What is the prognosis for maculopathy associated with optic pits?
Poor prognosis
## Footnote
This emphasizes the seriousness of the condition and its complications.
239
What should patients be given to monitor changes in their vision associated with optic pits?
An Amsler grid
## Footnote
This tool helps in detecting vision changes that may indicate complications.
240
Ocular complications of optic pit
Serious macular detachment
* maculopathy associated with optic put does not have good prognosis
* patient should be given amsler and RTC ASAP if changes
241
What type of migraine has visual aura followed by a headache
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
Common migraine
- last several hours to days
- nausea/vomitting
- photophobia
*no visual aura preceeding headache
243
What is an ocular migraine?
A type of migraine characterized by visual disturbances, such as flashing lights, zigzag patterns, or temporary loss of vision, usually in one eye.
244
How long do the symptoms of an ocular migraine typically last?
About 20 to 30 minutes.
245
Do ocular migraines always occur with a headache?
No, they can occur with or without a headache.
246
What is the understood cause of ocular migraines?
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
Fill in the blank: Ocular migraine is characterized by _______.
visual disturbances.
248
True or False: Ocular migraines can affect both eyes.
False.
*its unilateral
249
Leber hereditary optic neuropathy signs on fundus photos
Optic nerve head pallor, both eyes
*genetic testing for dx, mutation in maternal mitochondrial DNA
* M>F
250
Pseudotumor cerebri symptoms
Symptoms: blurry vision, headache, nausea, color vision abnormalities (dyschromatopsia), transient vision disturbances, and reduced affect
251
Idiopathic intracranial hypertension signs
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
Tx for pseudotumor cerebri?
1. Discontinue associated medications (ex: birth control, Accutane)
2. Lose weight
3. Oral acetazolamide (Diamox 1000mg po QD)
253
With OIS, the carotid artery is blocked by ___%
90% blocked
254
What are migraines defined as?
Unilateral headaches that may involve the entire cranium with variable intensity and duration
## Footnote
Migraines are a common genetic condition observed more frequently in females.
255
What neurological symptoms may be present during migraine episodes?
Neurological deficits and visual disturbances
## Footnote
These symptoms can vary among individuals.
256
What characterizes a classic migraine?
Occurs with a visual aura that precedes the headache
## Footnote
A classic migraine is less frequently encountered but easier to diagnose.
257
What is a visual aura in classic migraines?
A small paracentral scotoma appearing as a light or bright area with zigzag borders
## Footnote
The visual disturbance grows larger over time.
258
What may develop during a visual aura episode?
Homonymous hemianopsia
## Footnote
This is a condition that affects the visual field on the same side in both eyes.
259
How long do visual auras typically last?
Around 20 minutes
## Footnote
They are followed by a headache, often with nausea and light sensitivity.
260
What are common symptoms of a common migraine?
Nausea, vomiting, photophobia, and sensitivity to noise
## Footnote
These migraines last several hours to days.
261
What is a notable characteristic of a common migraine compared to a classic migraine?
No visual aura precedes the headache
## Footnote
However, mood alterations and other prodromal indicators may occur.
262
In which demographic are cluster headaches more frequently observed?
Males in their 40s or 50s
## Footnote
Cluster headaches are known for excruciating pain.
263
What symptoms accompany cluster headaches?
Ipsilateral sweating, lacrimation, ptosis, rhinorrhea, and conjunctival injection
## Footnote
Pain typically occurs over the temporal or frontal area.
264
What age group typically experiences ophthalmoplegic migraines?
Children younger than 10 years of age
## Footnote
These migraines involve transient extraocular muscle palsy.
265
What are the characteristics of basilar artery migraines?
Migraines with numbness and tingling of the extremities, speech and gait disturbances, and vertigo
## Footnote
They also primarily affect children.
266
Fill in the blank: A classic migraine is less frequently encountered than a _______.
common migraine
## Footnote
Classic migraines are easier to diagnose due to their distinct features.
267
During a classic migraine attack, what medication can be taken to alleviate it?
Aspirin
Oral NSAIDs
* take as early as possible
268
If initial therapy of aspirin or oral NSAIDs does not work for alleviating classic migraine symptoms, stronger medications need to be used. Such as?
Ergotamine or Sumatriptan
Amitriptyline, topamax, calcium channel blockers, propranolol, anti-nausea (for prophylactic purposes)
269
Tilted disc syndrome may be associated with what systemic syndromes?
Crouzon and Apert syndromes
* crouzon is AD, causes proptosis due to shallow ocular orbits, maxillary hyperplasia, abnormal craniofacial formation , hypertelorism and strabismus
270
What is AAION?
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.
## Footnote
AAION is associated with giant cell arteritis and typically occurs in individuals over the age of 50.
271
What are common symptoms of AAION?
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
## Footnote
These symptoms are often related to vasculitis affecting the blood vessels of the head.
272
What visual symptoms may patients with AAION report?
Patients may report:
* Amaurosis fugax (transient loss of vision)
* Profound loss of vision
* Diplopia
## Footnote
Amaurosis fugax can last for several minutes to hours.
273
What findings are observed during ocular examination in AAION?
Ocular examination may reveal:
* Afferent pupillary defect
* Swollen, pale optic disc
* Splinter hemorrhages in new onset cases
* Optic atrophy in long standing cases
## Footnote
These findings are critical for diagnosis.
274
What is NAION?
NAION is caused by an infarction of the optic nerve head, resulting in a sudden, unilateral, painless decrease in vision and acuity loss.
## Footnote
NAION generally occurs in patients with a 'crowded' disc and is typically seen in slightly younger patients than those with AAION.
275
What are the common predisposing factors for NAION?
Common predisposing factors include:
* High cholesterol
* Diabetes mellitus
* Acute hypotensive events
* Cataract surgery
* Collagen vascular disease
* Hypertension
## Footnote
These factors contribute to the risk of developing NAION.
276
What is papilledema and how is it characterized?
Papilledema is characterized by increased intracranial pressure and is almost always bilateral.
## Footnote
It can lead to various visual disturbances.
277
What symptoms may patients with papilledema experience?
Patients may experience:
* Headaches
* Visual disturbances (especially with body position changes)
* Decreased acuity
* Diplopia
## Footnote
Some patients may be free of symptoms despite having papilledema.
278
Is an afferent pupillary defect typically observed in papilledema?
No, an afferent pupillary defect is not typically observed because it is a bilateral condition.
## Footnote
Patients generally do not note pain upon eye movement.
279
What is the typical age demographic for patients presenting with optic neuritis?
Patients younger than 50
## Footnote
Optic neuritis frequently occurs in younger patients.
280
How does the initial vision loss in optic neuritis typically compare to that in temporal arteritis?
Not as severe
## Footnote
Initial vision loss in optic neuritis is usually less severe than in temporal arteritis.
281
What symptom do patients with optic neuritis frequently report that is exacerbated with eye movement?
Orbital pain
## Footnote
Orbital pain is due to inflammation of the optic nerve.
282
What may be observed in the optic disc of patients with optic neuritis?
Swelling of the disc with or without flame hemorrhages
## Footnote
Swelling and flame hemorrhages can occur in optic neuritis.
283
What is retrobulbar optic neuritis and in which demographic is it more commonly observed?
A type of optic neuritis observed more commonly in adults
## Footnote
The nerve appears normal in retrobulbar optic neuritis.
284
What type of pupillary defect may testing reveal in unilateral or asymmetrical optic neuritis?
Afferent pupillary defect
## Footnote
This defect is a key finding in optic neuritis.
285
What visual disturbances might patients with optic neuritis report?
Flashes of light (photopsias)
## Footnote
Photopsias are common visual disturbances in optic neuritis.
286
Why is it important to refer a patient with optic neuritis for an MRI?
To evaluate for plaques of demyelination
## Footnote
There is a strong correlation between optic neuritis and multiple sclerosis.
287
What is the typical presentation of a central retinal vein occlusion?
Sudden painless loss of vision
## Footnote
Central retinal vein occlusion can lead to rapid vision loss.
288
What findings on the fundus may indicate a central retinal vein occlusion?
Diffuse retinal hemorrhages extending to all four quadrants
## Footnote
Hemorrhages in central retinal vein occlusion are extensive.
289
What may be observed in the optic disc of patients with central retinal vein occlusion?
Potentially a swollen optic disc
## Footnote
Swelling of the optic disc can occur with central retinal vein occlusion.
290
Pathophysiology of vertebrobasilar insufficiency
Vertebrobasilar arterial blood supply to the brain becomes blocked
* blocked from a thrombus, emboli, HYN or anything that can cause hypercoagulable state
291
Symptoms of Vertebrobasilar insufficiency
Photopsia
Bilateral amaurosis fugax
Diplopia
Nystagmus
Systemic symptoms:
Vertigo
Unilateral weakness and sensory loss
History of syncope (drop attacks)
292
Etiology of optic pits
Congenital, occur secondary to deficiency within lamina cribrosa that allows for dysplastic retina to enter defective area
293
What are optic pits?
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
Are optic pits usually unilateral or bilateral?
Unilateral
295
How do optic pits appear on ophthalmoscopy?
Darker or gray
296
Where are optic pits most frequently located?
Temporally
297
What typically remains unaffected in optic pits?
Disc margin
298
What is the typical visual acuity of patients with optic pits?
Normal, unless there is a serous detachment of the macula
299
What may be observed adjacent to an optic pit?
Area of peripapillary atrophy
300
How does the nerve with the optic pit compare to the contralateral eye's nerve?
It is usually larger
301
What is commonly observed in eyes with optic pits?
Cilioretinal arteries
302
What symptoms do patients with optic nerve sheath gliomas typically present?
Decreased visual acuity, proptosis, potential APD, optic disc pallor, swelling, hyperemia
303
In which age group are optic nerve sheath gliomas usually observed?
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
What is the prevalence of optic disc drusen in the general population?
Roughly 0.3%
305
Is optic disc drusen typically bilateral or unilateral?
Bilateral, but may present unilaterally
306
How do early-stage optic disc drusen appear?
Deep beneath the surface of the optic disc, mimicking papilledema
307
What happens to optic disc drusen as time passes?
They become more exposed and cause irregular nerve margins
308
What is a common associated symptom with optic disc drusen?
Visual field loss
309
In which demographic is optic disc drusen almost exclusively seen?
Caucasians
310
What is morning glory anomaly?
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
What does the optic nerve head look like in morning glory anomaly?
Funnel-shaped with a white dot in the center and an elevated ring of pigment
312
What visual appearance may result from reflection within the eye in morning glory anomaly?
White pupil
313
What is the typical vision status in the affected eye with morning glory anomaly?
Severely impaired
314
A&P for 1st or 2nd order lesion causing Horner’s
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
Visual symptoms of AAION
Amaurosis fugax, followed by profound loss of vision or diplopia
Acute, unilateral painless vision loss
316
True or false
+APD in AAION
TRUE
*unilateral swollen and pale optic disc
*caused by infarction of pre-laminar and laminar segment of optic nerve
317
_______ generally occurs in patients with a “crowded” disc
NAION
* infarction of optic nerve head
* risk factors: high cholesterol, diabetes, hypotensive events, CE, collagen vascular disease and HTN
318
NAION vs AAION age demographic
NAION: older population, younger than AAION
AAION: geriatric population (~60 and older)
319
What occurs in patients with malignant hypertension related to the optic nerve?
Optic disc edema occurs
## Footnote
This is a significant finding in patients with malignant hypertension.
320
What causes optic disc edema in malignant hypertension?
Vasoconstriction of the short posterior ciliary arteries
## Footnote
These arteries supply the optic nerve head.
321
What triggers the vasoconstriction of the short posterior ciliary arteries?
Release of certain vasoconstrictive agents such as angiotensin II
## Footnote
Angiotensin II is a key regulator in blood pressure and fluid balance.
322
What is a consequence of the vasoconstriction of the vessels supplying the optic nerve?
Subsequent ischemia of the optic nerve
## Footnote
Ischemia refers to insufficient blood supply to an organ.
323
What condition can result from the ischemia of the optic nerve?
Stasis of axoplasmic flow
## Footnote
This stasis is a form of anterior ischemic optic neuropathy.
324
Fill in the blank: The release of angiotensin II leads to _______ of the short posterior ciliary arteries.
vasoconstriction
325
True or False: Ischemia of the optic nerve can lead to optic disc edema.
True
326
What is functional vision loss?
Visual abnormalities that cannot be attributed to any organic disease process.
## Footnote
It encompasses non-physiologic visual loss types such as malingering and hysteria.
327
What are the two main types of non-physiologic visual loss?
* Malingering
* Hysteria
## Footnote
Both types are characterized by different motivations and behaviors.
328
What is malingering in the context of vision loss?
A condition where patients fabricate the existence of a vision disorder for secondary gain, often associated with legal action or compensation claims.
## Footnote
Malingerers tend to be uncooperative and combative.
329
How do patients with hysteria typically behave?
They are commonly indifferent and cooperative, with a history of emotional distress.
## Footnote
Hysteria is a subconscious manifestation of visual symptoms.
330
What are some tests used to determine the authenticity of claimed vision loss?
* Optokinetic test
* Menace reflex
* Mirror test
* Visual field testing
## Footnote
These tests help assess the level of vision loss claimed by the patient.
331
Describe the optokinetic test.
Patients look straight ahead while an optokinetic drum is rotated in front of their eyes, leading to uncontrollable nystagmus if they have sufficient vision.
## Footnote
The better seeing eye should be patched if the patient claims a visual deficiency in only one eye.
332
What happens if a patient is truly blind during the optokinetic test?
An optokinetic response cannot be elicited.
## Footnote
This test does not differentiate between hysteria and malingering.
333
True or False: Malingering is a willful expression of visual symptoms.
False
## Footnote
Malingering involves fabrication for secondary gain, while hysteria is a subconscious manifestation.
334
Fill in the blank: Hysteria is characterized by a history of _______.
[emotional distress]
335
What is a key behavioral difference between malingering and hysteria patients?
Malingerers are typically uncooperative and combative, while hysteria patients are indifferent and cooperative.
## Footnote
This highlights the psychological differences in their conditions.
