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Clinical Neuro > OPTH Lec06 > Flashcards

OPTH Lec06 Flashcards

1
Q

What is diplopia?

A

Seeing two of the same object

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2
Q

What is the key thing to distinguish with a diplopic patient?

A

Whether the diplopia is monocular or binocular

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3
Q

When would a patient who have diplopia have monocular diplopia?

A

When you cover an eye and the double vision remains

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4
Q

Is monocular or binocular diplopia a neurologic problem?

A

Binocular

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5
Q

What causes monocular diplopia?

A

Refractive problem in the front part of the eye (not in the retina or further back in the neuron pathway)

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6
Q

What is the most common cause of monocular diplopia?

A

Astigmatism - abnormal curvature of the corneal surface (can be caused by corneal deformation or tight corneal stitches after surgery)

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7
Q

What are other causes of monocular diplopia?

A

cataract irregularities, lens displacement, primary problems with corneal curvature such as keratoconus

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8
Q

Why does binocular diplopia occur?

A

Because the eyes don’t move in sync with each other (CN lesion of CNIII, CNIV, CNVI), extraocular muscle abnormalities(muscle fibrosis that occurs with Grave’s disease) derangements at the neuromuscular junction (myasthenia gravis)

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9
Q

What can cause an individual nerve palsy?

A

Microvascular disease, stroke, tumor, aneurysm

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10
Q

What happens when you knock out CNIII?

A

Most eye muscles are innv by CNII so the eye will deviate DOWN AND OUT (because the abducens and superior oblique will pull on it). PTOSIS (due to levator palpaebrae) and BLOWN PUPIL (parasymp from Edinger Westphal)

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11
Q

Paralysis of what muscle causes ptosis?

A

levator palpebrae (innv by CNIII)

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12
Q

What causes most CNIII palsies?

A

Ischemia secondary to DIABETES or HTN

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13
Q

Where will aneurysms causing CNIII palsies occur?

A

Junction of the posterior communicating artery and the internal carotid artery

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14
Q

Compressive lesions of CNIII will affect which component of the nerve?

A

The parasympathetic and cause a blown pupil = EMERGENCY

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15
Q

What do you do when you have pupillary involvement?

A

MRI and ANGIO

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16
Q

What are the common sites of Cerebral Aneurysms?

A

Anterior communicating artery, anterior cerebral, internal carotid, posterior cerebellar, superior cerebellar, basilar, vertebral, posterior communicating, middle cerebral

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17
Q

Why do oculomotor palsies involve the pupil?

A

Because the parasym never innervating the iris travel with the third nerve

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18
Q

What does pupillary involvement suggest?

A

compressive lesion (vascular lesion will spare the pupil); parasymp nerves course the surface of CNIII; damaged by compression from outside (aneurysm from PCA, boney structure, uncal portion of the temporal lobe)

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19
Q

What can cause an ischemic lesion?

A

HTN

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20
Q

Which part of CNIII will an ischemic lesion affect?

A

Inside; affect the motor component, spare the parasymp

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21
Q

If your patient is presenting with CNIII loss and pupillary involvement, what do you do?

A

order MRI and angiogram

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22
Q

If there is a CNIII palsy and there isn’t pupillary involvement; what would you suspect?

A

Vaso-occlusive problems; check glucose and bp

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23
Q

What does the abducens nerve control?

A

The lateral rectus muscle

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24
Q

What would a CNVI lesion look like?

A

eye will not be able to abduct; patients will be cross-eyed; will turn their head to avoid double vision

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25
Q

What is the pathway of the abducens?

A

Starts in the pons; exits the brainstem at the Ponto-medullary junction; runs up the floor of the skull through cavernous sinus into the orbit.

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26
Q

Where is CNVI most susceptible to high intracranial pressure?

A

When it enters the cavernous sinus; makes a 90 degree bend; patients with high ICP from a tumor have a CNVI knocked out

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27
Q

Why do you cry when you see food?

A

Because if you have an aberrant regeneration of CNVII, the nerves that would normally control salivation will go to the lacrimal gland

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28
Q

What would happen if you had aberrant regeneration after CNIII palsy?

A

Nerve regeneration can get mixed up, looking medial may cause eyelid to shoot up (inappropriate contraction of levator palpebrae)

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29
Q

In what situations do you get aberrant regeneration?

A

trauma or mass lesions - not with microvascular events

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30
Q

What does the trochlear nerve (CNVI) innervate?

A

Superior oblique muscle

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31
Q

How will a patient with a CNIV lesion present?

A

upward deviation of the affected eye and twisting of their eye which will make them TILT THEIR HEAD AWAY FROM THE LESION

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32
Q

What can cause a CNIV lesion?

A

trauma, ischemic event, congenital

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33
Q

Why is CNIV more susceptible to injury than the other one?

A

Be it is the skinniest and RUNS THE LONGEST DISTANCE inside the cranial vault and EXITS FROM THE BACK of the brainstem so can be pulled from the root.

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34
Q

What are caused of a CNIV palsy?

A

Trauma, tumor, congenital, ischemia

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35
Q

How do you determine whether a CNIV is congenital?

A

Ask for history and look at old photos for head tilt; neck pain

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36
Q

What does the trochlear muscle do?

A

From the back of the orbit forward through the trochlear pulley; inserts AT THE BACK OF THE EYE.

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37
Q

What does the superior oblique muscle do?

A

pulls the eye down; intorsional component (rotates toward the nose)

38
Q

What should you think if a single nerve is affected?

A

Problem is along the nerve’s tract

39
Q

What should you think if all three nerves are damaged?

A

The lesion is near cavernous sinus or orbital apex (where 3 nerves bunched together)

40
Q

What is the number one reason that cranial nerve is knocked out?

A

vasculitic event from diabetes

41
Q

What is myasthenia gravis?

A

autoimmune disease with antibodies attacking the NICOTINIC ACETYLCHOLINE RECEPTORS in the NEUROMUSCULAR JUNCTION of striated muscle = decreased number of Ach receptors (>30% receptors = symptoms and fatigue)

42
Q

What are the effects of myasthenia gravis on the eye?

A

DIPLOPIA and PTOSIS - diplopia not associated with any specific CN; diplopia and ptosis WORSE ON PROLONGED GAZE

43
Q

Which type of muscle is affected by myasthenia gravis?

A

Striated (smooth and cardiac muscle is not)

44
Q

How do you diagnosis myasthenia gravis?

A

TENSILON TEST - give edrophonium chloride (ANTICHOLINESTERASE) and look for improvement of symptoms. ICE-PACK TEST, EMG

45
Q

What are toxic reactions to the TENSILON test?

A

salivation, BRONCHOSPASM, BRADYCARDIA (treatment with atropine)

46
Q

What is an ice-test used to diagnose?

A

myasthenia gravis - hold ice pack over eye and look for improvement

47
Q

What problems do patients with myasthenia gravis have?

A

Problems with mastication, talking, drinking, swallowing

48
Q

What do you check a patient with myasthenia gravis for?

A

thymoma and check thyroid levels!!!!! IMPORTANT!

49
Q

What is optic neuritis?

A

Demyelinating, inflammation of nerve

50
Q

What are the signs of optic neuritis?

A

decreased vision (COLOR VISION), PAIN WITH EYE MOVEMENT, enhancement or the optic nerve on MRI, potential association with MULTIPLE SCLEROSIS. Occurs in YOUNGER PATIENTS, WOMEN! INCREASED RISK OF DEVELOPING MS.

51
Q

What is this a picture of?

A

Optic Nerve Swelling

52
Q

What is Ischemic optic neuropathy?

A

AKA NAION; localized ischemic event where the optic nerve joins when it enters the back of the eyeball. Not very stretchy here and insult here= swelling and vision loss.

53
Q

What is altitudinal visual defect?

A

damage to the hemispheric vascular supply to the optic nerve head can cause loss of vision above or below the horizontal

54
Q

What is MS?

A

DEMYELINATING disease of the CNS; LESIONS OCCURRING AT DIFFERENT TIME AND DIFFERENT PLACES; common in YOUNG, WHITE, WOMEN, in NORTHERN CLIMATES. Most will develop optic neuritis

55
Q

What are the signs and symptoms of optic neuritis?

A

sudden vision loss; decreased contrast and color sensitivity; PAIN WITH EYE MOVEMENT, OPTIC NERVE HEAD EDEMA, AFFERENT PUPILLARY DEFECT

56
Q

What is this?

A

Optic neuritis edema

57
Q

What do you do for a patient with optic neuritis?

A

refer for MRI to look for demyelinating lesions

58
Q

What are you looking for on an MRI of a patient with optic neuritis?

A

enhancing (demyelinating) lesions. The more found; the greater the chance of developing MS

59
Q

What is the treatment for optic neuritis?

A

IV steroids ONLY, ORAL STEROIDS MAY INCREASE REOCCURRENCE OF MS

60
Q

What is temporal arteritis?

A

aka Giant Cell arteritis; inflammation affecting MEDIUM-SIZED BLOOD VESSELS; similar to POLYMYALGIA RHEUMATICA (except this affects the blood supply to the head, face and eyes)

61
Q

What causes temporal arteritis?

A

Caused by VASCULITIS WITHIN THE MEDIUM and SMALL ARTERIES around the head. Can occlude the blood to the eye = vision loss. Common in OLDER patients

62
Q

How will temporal arteritis present?

A

Older (60+), sudden, painless, vision loss

63
Q

What are other systems involved in temporal arteritis?

A

SCALP TENDERNESS, headache, JAW CLAUDICATION, POLYMYALGIA of arm and shoulder, fevers, night sweats, WEIGHT LOSS

64
Q

What labs should be ordered if you suspect your patient has temporal arteritis?

A

ESR and CRP; TEMPORAL ARTERY BIOPSY (because more specific than ESR and CRP); can delay biopsy for 2 weeks

65
Q

What is the normal ESR?

A

Men: age/2 Women: (age+10)/2

66
Q

How do you treat temporal arteritis?

A

start on steroids ASAP to decrease inflammation, decrease potential vision loss in remaining eye (prevent blindness)

67
Q

What is this?

A

Giant cell arteritis (Temporal)

68
Q

Pupil is dilated by parasymp or symp?

A

symp

69
Q

Pupil is constricted by parasymp or symp?

A

parasymp

70
Q

What is Horner syndrome?

A

Sympathetic pathway knocked out = pupillary dilator muscles don’t work so PUPIL CONSTRICTS and stays small; decreased Muller’s muscle action = PTOSIS; scalp ANHYDROSIS (decreased sweating) on the affected side

71
Q

How do you localize a lesion in Horner syndrome?

A

using the COCAINE TEST or the PARADRINE TEST

72
Q

What is the Cocaine test and what does it tell you?

A

Decides if the patient really have Horner pupil or not. COCAINE STIMULATES PUPILLARY SYMPATHETHICS (dec NorE uptake) Good eye will dilate, bad eye will not do anything

73
Q

What is the Paradine Test?

A

Done aft the cocaine test. Used to localize the lesion when know that it’s a Horner syndrome. Stimulates the FINAL 3RD ORDER NEURON via hydroxyamphetamine causes the end nerve to fire at the pupil.

74
Q

What will a pupil that will not dilate using the Paradine test tell you?

A

FINAL; “LOWER MOTOR NEURON” is dead

75
Q

What will a pupil that will dilate using the Paradine test tell you?

A

a HIGHER ORDER NEURON IS OUT and request imagining

76
Q

If a patient complains of a painful Horner’s; what should you think about?

A

CAROTID DISSECTION

77
Q

What is Adie’s Tonic Pupil?

A

Parasymp pathway gets knocked (constrictor) so eye REMAINS DILATED and DOESN’T CONSTRICT TO LIGHT (parasymp from Edinger-Westphal nucleus is blocked) PUPIL WILL CONSTRICT WITH NEAR VISION but slowly. Tonic pupil because always slow

78
Q

What can cause Adie’s Tonic Pupil?

A

Benign viral infection

79
Q

You have a patient with diplopia. His left eye is turned down and out and his lid is photic on that side. What nerve do you suspect and what should you check next?

A

CNIII Palsy; check pupillary reflex. Pupillary involvement = lesion from compressive source such as an aneurysm

80
Q

Why do diabetic patients with oculomotor paralysis have “sparing of their pupil?”

A

Pupil spared with ischemic CNIII palsies (parasym fibers run along the surface of the nerve = susceptible to aneurysm/tumor not infarction)

81
Q

This 32 year old overweight woman complains of several months of headaches, nausea, and now double vision. What cranial nerve lesion do you see in this drawing. What other findings might you expect on fundus exam and what other tests might you get?

A

Bilateral CNVI palsy; patient can’t move eye laterally. Most CNVI palsies occur secondary to ischemic events in diabetics and HTN; unlikely because it’s a young patient with bilateral involvement. Symptoms sounds pseudo tumor. Look for papilledema of optic nerve, get imagining, send to neuro to get lumbar puncture with opening pressure

82
Q

A patient is sent to your neurology clinic with a complaint of double vision. Other than trace cataract changes, the exam seems remarkably normal with good extraocular muscle movement. On covering the left eye with your hand, the doubling remains in the right eye. What do you think is causing this diplopia?

A

Monocular diplopia = refractive problems in film, cornea, lens etc.

83
Q

A patient complains of intermittent double vision that seems to be worse in the evenings. On exam you find a confusing diplopia that doesn’t seem to map out to any particular nerve palsy. What else is on your differential as a cause, and what tests might you perform in the office?

A

Myasthenia Gravis and Orbitopathy cause diplopia. Graves patients = reduced up gaze from inferior rectus muscle restriction; can look like isolated nerve palsy, mixture of nerve involvement, may not be any combination. Check for fatigueable ptosis by prolonged upgaze (hold arm to see who gets tired first). Used old pack test or tensilon test

84
Q

You are giving a tensilon test to a suspected myasthenia gravis patient and he collapses. What do you do?

A

Reaction to anticholinesterase (bradycardia or asystole). Admin atropine

85
Q

A patient with diplopia is finally diagnosed with myasthenia gravis after a positive ice-pack test and a positive acetylcholine receptor antibody test. What else should you work up this patient for?

A

Check for thymoma; highly associated with MG

86
Q

A 26 year old woman presents with decreased vision in her left eye that has gotten progressively worse over the past week. The eye seems to ache and the vision worsens with exercise. On exam she is found to have 20/200 vision, trace APD, and markedly decreased color vision in the affected eye. The optic nerve is mildly swollen on that side. What does this patient most likely have?

A

Classic symptoms of neuritis; Uthoff phenomenon = symptoms worsen when temp increases. Minor pain with eye movement = optic nerve inflamed and tugging on the nerve so eye movement irritates it.

87
Q

A patient develops optic neuritis. Should you treat with steroids? Would you start with IV or oral steroids? Will the MRI findings of numerous demyelinating lesions change your management? Do you tell the patient that she will develop MS?

A

Steroid speed up recovery, little effect on the long term visual outcome; oral steroids increase reoccurrence of optic neuritis - give IV Solu-Medrol. Development of MS depends on number of lesions found in CNS. No lesions = 15% risk. 3+ lesions = 50% risk. involve neuro in higher risk pts

88
Q

An 84-year-old man was out golfing with his buddies and developed sudden vision loss in his right eye. He has no past ocular history, no medical problems. No complaints of flashes or floaters, just that things “look dimmer” in his right eye. What other questions should you ask about his symptoms?

A

Elderly person with vision loss, ask about the symptoms of temporal arteritis; Scalp tenderness, jaw claudication, polymyalgia (muscle aches in shoulders and arms) Sounds like a central retinal artery occlusion; must rule out giant cell arteritis.

89
Q

The patient admits to “not feeling good” and “it hurts my head to brush my hair on the right side” for the past week but denies all other symptoms. Should you order any labs? Start any medications?

A

Suspicion for GCA = over ESR and CRP; start oral prednisone (1mg/kg/day) asap; temporal artery biopsy within a week or so. Steroids won’t help with lost vision but decrease the rick to the other eye

90
Q

A young man complains of complete vision loss (no light perception) in one eye, however, he has no afferent pupil defect. Is this possible? How might you check whether this patient is “faking it?”

A

Should have APD; use test to check for malingering; exciting a reflexive blink by moving fingers near the eye; holding a mirror in front of the eye and eye should fixate on an object. Gentle rocking movements of the mirror will result in synchronous ocular movement as eye unconsciously tracks the objects in the mirror.

Clinical Neuro (6 decks)

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