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BOARDS > Neuroscience > Flashcards

Neuroscience Flashcards

1
Q

Neurons have a resting potential of

A

-60 to -70mV

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2
Q

Intracellular concentration of K

A

140mM

Highest in the cell

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3
Q

Charge of the cell

A

The inside of the cell is relatively negatively charged compared to the exterior environment. In addition, K+ is more abundant inside the cell

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4
Q

Stage of action potential

A

1, Na+ condinctance increases in repsosne to a local depolarization of the membrane, leading to an inward flux of Na

  1. The membrane potential rises steeply, resulting in a self reinforcing cascade whereby more Na channels open
  2. Vm, the membrane potential, peaks at approximately 40mV
  3. At this stage, K+ conductance increases, meaning that K+ readily exits the cell. This resutls in the inactivation of Na+ channels
  4. Membrane potential now falls quickly and briefly overshoots the original. That is, the membrane becomes mroe negative than at its resting stage; hyperpolarization
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5
Q

Cascade of a synapse

A
  • AP occurs at cell A
  • Ca2+ permeability of the membrane increases and Ca enters into call A
  • cell A releases small vesicles filled with NT
  • NT diffuses across synaptic cleft
  • NT binds to receptors on the surface of cell B
  • the binding results in a post synaptic current (called EPSP or IPSP, depending on whether the current is excitatory or inhibitory) in cell B. Such a current will lead to a change in Vm in cell B
  • multiple PSPs falling within small time periods and over small areas are combined. That is, the effects from many PSPs at different locations and times are added together into an aggregate response
  • as a result, a new local membrane potential is reached
  • if this new Vm exceeds threshold, a new AP will happen in cell B
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6
Q

GABA

A

Inhibitory

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7
Q

Glycine

A

Inhibitory

-brainstem, spinal cord, retina

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8
Q

At an electrical synapse, communication occurs via direct electrical contact between cells. This is called

A

Gap junction

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9
Q

Nuclei

A

Collections of neurons

The CNS analog of ganglia

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10
Q

Cortex

A

Sheet like layers of cells

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11
Q

Frontal lobe

A

Premotor cortex
Personality
Broca’s area (speech production)

Personality
Planning
Production of speech

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12
Q

Parietal lobe

A

Sensory activity and recognition

Purists

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13
Q

Temporal lobe

A

Hippocampus-memory

Wernickes=speech recognition (wordy speech)

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14
Q

Gray matter

A

Butterfly shape region of the spinal cord. Cell bodies and unmyelainted axons, dorsal root (sensory) and ventral root neurons (motor)

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15
Q

White matter

A

Bundles of myelinated ax’s on (called fasciculi or tracts)

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16
Q

White matter sections into three fiber divisions

A

Posterior funiculis
Lateral funiculis
Anterior funiculis

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17
Q

Ascending pathway

A

1st order: soma to DRG
2nd order: connects 1st and 3rd neuron
3rd order: cell body in thalamus, projects to the cortex

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18
Q

Descending pathways

A

Carry motor impulses from the brain to the muscles

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19
Q

Hoe many pairs of spinal nerves

A

31

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20
Q

Cervical spine

A

C1-C8
1-4: neck
5-8: upper extremities

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21
Q

Thoracic spine

A

T1-T12

Upper extremities

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22
Q

Lumbar spine

A

L1-L5
1-4: thigh
4-5: thigh, leg, foot

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23
Q

Sacral spine

A

S1-S5
1-3: thigh, leg, foot
2-4: pelvis

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24
Q

Coccygeal spine

A

One nerve

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25
Q

Brainstem

A

Medulla
Pons
Midbrain

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26
Q

Medulla

A

Autonomic functions (HR, digestion, breathing0

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27
Q

Pons

A

Coordinates movement related information transfer between the central hemisphere and the cerebellum

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28
Q

Midbrain

A

Array ofsenaroy and motor functions including coordination of eye movements and visual reflexes

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29
Q

Upper medulla

A

Pyramids and medial lemniscus
Medial lemnisucs made up of gracilis and cuneate fasciculi, which carry info about lower body and trunk respectively
MLF relays vestibular info to exterior eye muscles and coordinates the VOR

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30
Q

Lower/middle medulla

A

Denotes the location of the vestibular nuclei as well as the olivary nucleus, which are assocaited with learning and memory in cerebellar functions. Finally, we see the large motor tracts of the pyramids

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31
Q

Pons

A

Relays info between the midbrain and the medulla. It is the location of the pontine nuclei, which serve as relay stations for motion related information transferred between cortex and the cerebellum. The pons is also involved in the control of respiration and sleep, and is the location of the nuclie for CN V-VIII

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32
Q

Upper midbrain

A

Superior colliculus
-motor neurons controlling orientation of the head/eyes.
Red nucleus
-movement of the arms and the oculomotor nuclei
EW nucleus contribute to the parasympathetic innervation of the iris

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33
Q

Lesion to the oculomotor or EW nucleus

A

Results in a loss of innervation to all EOMs except for the SO and LR

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34
Q

Lower midbrain

A 
Inferior colliculus 
-reflex responses of head and neck to sound
CN IV nucleus
-info to the contralateral SO
Cerebellar peduncle
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35
Q

Forebrain gives rise to

A

Diencephalon and the cerebral hemisphere

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36
Q

Diecenphalon

A

Epithalamus
Thalamus
Subthalamuc
Hypothalamus

Eyes

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37
Q

Epithalamus

A

Pineal gland

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38
Q

Thalamus

A

Relays sensory input to the cortex and includes nucliei for voluntary motor root

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39
Q

Subthalamus

A

Communicates with the basal ganglia to help control muscle movement

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40
Q

Hypothalamus

A

Regulates body temperature, eating, and sleeping behavior

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41
Q

Cerebral hemispheres

A

High level processing related to sensory input, motor control, intelligence, emotion. The dominant hemisphere is more in control of understanding and processing language, intermediate and long term memory, word retrieval, and emotional stability. The non dominant hemisphere is more responsible for recognizing facial expression and vocal intonation, and for music and visual learning

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42
Q

Cerebellum

A

Fine motor movements, posture, and balance

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43
Q

What two sets of arteries is the brain primarily supplied through

A

Internal carotids and the vertebral arteries

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44
Q

Vertebral arteries

A

Arise from the subclavian Artie’s and provide blood supply to the spinal cord. The right and left vertebral join together to form the basilar artery at the brainstem. The basal artery then joined the ICA to form the circle of Willis

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45
Q

Internal cartoons

A

Arise from the common carotid arteries in the neck. The left common carotid branches off of the aortic arch while the right common carotid artery branches off the brachiocephalic trunk. They branch into the anterior and middle cerebral arteries and supply blood to the forebrain

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46
Q

Circle of Willis

A

The meeting loop for the basilar artery, the internal carotids, and the anteiror and posterior communicating arteries, which are small arteries bridging the basilar and ICAs. The circle of Willis forms an arterial circle beneath the brain stem and distributes blood supply to many parts of the brain

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47
Q

Arteries that form the circle of Willis

A 
Posterior cerebral arteries 
Posterior communicating arteries 
ICAs
Anterior cerebral arteries
Anterior communicating arteries
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48
Q

Health ONH

A

Distinct disc margins
Health rim tissue (coloration and structure)
Absence of hemorrhages and RNFL elevation

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49
Q

Pressure gradient in health optic nerve

A

Pressure gradient between the eye and brain; pressure is higher in the eye compared to the brain, allowing axoplasmic flow to occur in an orthograde (towards the brain) direction

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50
Q

If the pressure gradient is reversed in the eye and brain: anterior the optic chiasm

A

Pressure towards the brain is higher than the eye

Retrograde axoplasmic flow occurs causing unilateral disc edema

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51
Q

If the pressure gradient is reversed posterior to the optic chiasm (due to increased ICP)

A

Retrograde axoplasmic flow will occur in both eyes, resulting in papilledema

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52
Q

Pupil testing and the ONH

A

Can determine whether optic nerve damage is present
The brightness comparison test and red cap desaturation test can also be used ro confirm optic nerve damage. Recall that the photostress test is used to evaluate the macula for damage

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53
Q

What are the different appearances of an unhealthy ONH

A

Edematous
Atrophic
Normal

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54
Q

In what ways can the ONH be atrophic

A

Excavated

Pallid: primary optic atrophy (not previously edematous) and secondary optic atrophy (previously edematous)

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55
Q

A normal looking ONH that is unhealthy

A

Retrobulbar optic neuritis, posterior ischemic optic neuritis

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56
Q

What will be abnornal in someone with a normal looking unhealthy ONH

A

Pupil testing

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57
Q

What is unilateral disc edema caused by

A

Pre-chiasmal disruption in axoplamic flow

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58
Q

Patient presentation of unilateral disc edema

A

Decreased VA
APD
VF defect
Rim tissue and RNFL elevation

Optic nerve edema may also be accompanied by hemorrhages and CWS on the rim tissue or near the disc margin

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59
Q

What helps to rule out optic disc edema

A

Presence of a SVP

  • an absent SVP does not help to diagnose optic nerve edema
  • 10-15% of the population does not have an SVP
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60
Q

The most common causes of unilateral optic disc edema include

A

Anterior ischemic optic neuropathy (AAION/NAION)
Ophthalmic causes (CRVO, hypotony, disc drusen, uveitis)
Inflammtory causes
Optic neuritis
Compressive lesion anterior to the chiasm

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61
Q

What are the anterior ischemic optic neuropathy assoc with unilateral optic disc edema

A

AAION (secondary to GCA)

NAION (includes diabetic papillopathy)

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62
Q

What are the ophthalmic causes of unilateral disc edema

A

CRVO
Hypotony
Optic disc drusen
Uveitis

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63
Q

What are the non-infectious inflammatory causes of unilateral optic disc edema

A

Sarcoidosis
Collagen-vascular disease
Papilophlebitis

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64
Q

What are the infectious inflammatory causes of unilateral optic disc edema

A

Syphilis
TB
Neuroretinitis

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65
Q

What are the compressive lesions anterior the optic chiasm that can cause unilateral optic nerve edema

A

Thyroid eye disease
Optic nerve glioma
Optic nerve sheath meningioma
Orbital cavernous hemangioma

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66
Q

Epidemiology/Hx of AAION

A

Usually >55 years

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67
Q

Pathophysiology of AAION

A

Secondary to occlusion of the SPCA, resulting in decreased perfusion to the anterior optic nerve; the most common cause if GCA, a systemic vasculitis of the medium and large blood vessels

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68
Q

Less common causes of AAION (besides GCA)

A

Polyarteritis nodosa, SLE, herpes zoster

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69
Q

Ocular Symptoms of AAION

A

History of amaurosis fugax and sudden loss of vision in the affected eye

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70
Q

Systemic symptoms os AAION

A

If assocaited with GCA

  • temporal headaches
  • jaw claudication
  • neck pain
  • anorexia
  • tender or nodular temporal artery
  • fever, myalgia, and scalp tenderness
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71
Q

GCA patients and frequency of symptoms

A

1 out of 5 will not have systemic symptoms. A Dx of GCA cannot be ruled out based on the absence of systemic symptoms

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72
Q

Signs of AAION

A

Unilateral disc edema with an associated APD and decreased vision in the affected eye

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73
Q

Diagnosis of AAION

A

Evaluate STAT for elevated platelets, ESR, and CRP

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74
Q

What is considered an elevated ESR

A

> age/2 in men, >(age+10)/2 in women

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75
Q

Elevated CRP

A

> 2.45mg/dL

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76
Q

Elevated platelets

A

> 400,000

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77
Q

What is the most specific test for GCA

A

elevated ESR and CRP

97%

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78
Q

Temporal artery biopsy and GCA

A

May be indicated to confirm the presence of granulomatous inflammation within the blood vessel if blood tests are equivocal or the clinical picture is unclear. Skip lesions on temporal artery biopsies may lead to false negative results, although the incidence is low as long as an adequate length of the artery is biopsies

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79
Q

AAION due to GCA is considered

A

An ocular emergency due to risk of sudden vision loss in the fellow eye within 2 weeks

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80
Q

Epidemiology/Hx of NAION

A

Patients over 50
History of HTN, DM, and/or HLD
90% of patients with NAION have a small, crowded optic nerve with a CD ratio of <0.3 (disk at risk)

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81
Q

What is a disc at risk

A

In NAION if a patient has a small, crowded optic nerve with a CD ratio of <0.3

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82
Q

Pathophysiology of NAION

A

Secondary to irreversible ischemia of the anterior optic nerve due to an unknown etiology, nocturnal hypotension resulting in poor perfusion to the optic nerve may contribute to the development of NAION

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83
Q

NAION and possible associations

A

Sleep apnea, and possibly viagra, although not definitive

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84
Q

Symptoms of NAION

A

Sudden, painless, typically nonprogressive unilateral vision loss that most often occurs upon awakening. Vision rarely improves after the initial onset of NAION

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85
Q

Signs of NAION

A

Decreased vision, APD, unilateral optic disc edema, and VF loss (inferior altitudinal defect is most common)

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86
Q

Diagnosis of NAION

A

Is NOT associated with systemic symptoms that are seen in patients with AAION secondary to GCA. Patients will have a normal CRP, ESR, and platelet count.

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87
Q

How do you diagnose NAION

A

Diagnosis of exclusion
-patients should be thoroughly investigated for possible GCA by a careful case history, fundoscopic exam (disk at risk), and blood work before making the diagnosis of NAION

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88
Q

Why is it important to correctly diagnose AAION due to GCA

A

Prompt treatment is necessary to prevent vision loss in the fellow eye. It is equally important to correctly diagnose NAION to avoid overtreatment with high doses of oral steroids that may cause complications in elderly patients (esp if they have HTN or DM)

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89
Q

Epidemiology/Hx of diabetic papillopathy

A

Most commonly occurs in young (<50) patients with type I DM; however the condition may also occur in the elderly patients and patients with type II DM

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90
Q

Pathophysiology of Diabetic papillopathy

A

Mild form of NAION with REVERSIBLE ISCHEMIA of the anterior optic nerve from an unknown etiology

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91
Q

What is the difference between NAOIN and diabetic papillopathy

A

Diabetic is REVERSIBLE ISCHEMIA

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92
Q

Symptoms of diabetic papillopathy

A

Rarely present with loss of visual function; the most common reported symptoms include blurry vision or distorted vision

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93
Q

Signs of diabetic papillopathy

A

Mild to no decrease in vision, only a mild APD, optic disc edema, and only mild depression on VF. DR is present at the time of diagnosis in more than 80%. Similar to NAION, the fellow optic nerve is small and crowded (disc at risk)

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94
Q

Diagnosis of diabetic papillopathy

A

Similar to NAION, diabetic papillopathy is a diagnosis of exclusion; patients should be investigated for possible AAION (in cases of unilateral disc edema), or for causes of papilledema (in cases of bilateral disc edema), including malignant HTN

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95
Q

Disc edema and CRVO

A

May present with unilateral disc edema due to ischemia and decreased perfusion of the anterior optic nerve, most commonly due to thrombus just posterior it the optic nerve head. Patients will also present with intraretinal hemorrhages in all 4 quadrants, CWS, and dilated and tortuous retinal veins

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96
Q

Epidemiology/HX of hypotony

A

History of trabeculectomy, blunt ocular trauma, cyclodestruction procedures, and/or intraocular inflammation

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97
Q

Pathophysiology of hypotony

A

Defined as an IOP at which the eye anatomically and pjhysiologically changes

  • usually occurs IOP < 6mmHg (varies with each patient though depending on scleral rigidity)
  • elderly patients with more rigid scleras are often able to tolerate lower IOPs compared to younger patients with less rigid scleras
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98
Q

Hypotony causes

A

May occur due to an over filtering bleb dollying trabeculectomy, wound leak, cyclodialysis cleft, iridocyclitis, CB detachement, RD, or ocular hypoperfusion

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99
Q

Which is worse for visually significant hypotony, trabeculectomy with or without MMC

A

With MMC

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100
Q

Symptoms and signs of hypotony

A

Decreased vision and pain, especially in the presence of ocular inflammation. Signs include folds within descemets membrane, corneal edema, a shallow AC, cataract formation, hypotony maculopathy, chorioretinal folds, and optic disc edema in the presence of low IOP

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101
Q

Epidemiology/Hx of optic disc drusen

A

Present in appx 3.4-24 persons per 1000 people

102
Q

Pathophysiology/Dx of optic disc drusen

A

They are hyaline bodies located within the optic disc; they can be hereditary (mostly AD). Will appear hyperrefelctive on a B scan even at reduced gain levels. FA photos and an OCT raster through the optic nerve may also help confirm the presence of optic disc drusen

103
Q

Signs and symptoms of optic disc drusen

A

Rarely causes symptoms; they tend to be buried when patients are young, and then become more evidence with age as they move towards the surface. Extensive optic disc drusen can compress the retinal ganglion cell fibers in the optic nerve, resulting in VF defects that mimic glaucoma. May cause pseudo-disc edema (rim tissue and RNFL appears elevated due to “bumps” of optic nerve drusen) or true disc edema (unilateral or bilateral) due to compression of the RNF and obstruction of axoplasmic flow. Optic disc drusen are also associated with CNVM

104
Q

Disc edema and uveitis

A

Unilateral disc edema may develop in patients with posterior uveitis, although it is rare

105
Q

Sarcoidosis and disc edema

A

Inflammatory, noninfectious caused of unilateral disc edema
-idiopathic condition that mostly affects middle aged AA females. Characterized by granulomatous inflammation throughout the body, with 90% of patients having lung invovlemt. Appx 1-5% of patients with sarcoidosis will also develop optic nerve disease

106
Q

Collagen vascular disorders and disc edema

A

Inflammatory, noninfectious cause of unilateral disc edema

  • includes RA, SLE, polyarteritis nodosa, and Wegner’s granulomatosis
  • SLE is an AI disorder that affects multiple organ systems, including the skin, kidneys, joints, and heart; it affects females more often than males and occurs in the 2nd and 3rd decade of life. Neuro ophthalmic compilations include unilateral disc edema and papilledema
107
Q

Syphilis and disc edema

A
  • inflammtory, infectious cause of unilateral disc edema
  • STD caused by spirochete treponema pallium. Clinical findings are grouped into three phases (primary, secondary, and tertiary); tertiary syphilis is characterized by nervous system and ophthalmic involvement, including optic disc edema, CN neuropathies, and an Argyll Robertson pupil.
108
Q

TB and disc edema

A
  • inflammatory, infectious cause of unilateral disc edema
  • infectious disease of the lungs caused by airborne droplets of mycobacterium tuberculosis. Patients will present with a fever, chronic cough, and night sweats. TB may cause a variety of ocular complications including bilateral anterior granulomatous uveitits and CME. Optic disc edema is a less common finding
109
Q

Neuroretinitis and disc edema

A
  • inflammatory, infectious caused of unilateral disc edema
  • Type of anterior optic neuritis characterized by optic disc edema, macualr edema with hard exudates in a star pattern (macular star). It is due to leakage of the superficial vasculature on the optic disc; retinal vessels located near the macula are normal with no leakage on FA
110
Q

Who gets neuroretinitis

A

Most common in the 3rd and 4th decades of life. Preceded by a viral illness in up to 50% of cases, although there is limited evidence that supports a viral etiolgoy

111
Q

Associations with neuroretinitis

A

May be assocaited with non-viral infections, most commonly cat scratch fever. Additional associated infections include spirochete infections, histoplasmosis, and toxoplasmosis

112
Q

Common symptoms of neuroretinitis

A

Mild to severe vision loss and occasionally an aching sensation behind the affected eye that may slightly worsen on eye movement. Patients may present with cells in the vitreous and AC in addition to the unilateral macular star and disc edema. Any type of VF possible, but most commonly cecocentral defects are most common

113
Q

Epidemiology/Hx of optic neuritis

A

Most common in young patients, between the ages of 20-45; affects females more than males

114
Q

Pathophtysiology/Dx of optic neuritis

A

Caused by primary inflammation of the optic nerve, demyelinating optic neuritis is the most commonly associated with MS

115
Q

The 15 year risk of developing MS after an isolated episode of optic neuritis is

A

50%

72% if one or more white matter lesions are present on an MRI, and 25% if there are no white matter lesions on an MRI

116
Q

MRI and optic neuritis

A

An MRI is not necessary to diagnose an optic neuritis, however, the optic neuritis treatment trial recommends an MRI at the time of diangosises of acute optic neuritis in order to determin the patient’s risk of development of MS based on the number of white matter lesions characteristic of demyelinating disease

117
Q

MS patietns chances of optic neuritis

A

Up to 2/3 of MS patients will have an episode of optic neuritis at some potion during the disease course; 15-20% of patients with MS will have optic neuritis as the initial presenting symptom

118
Q

Symptoms of optic neuritis

A

Sudden onset, unilateral vision loss and pain on eye movement. Vision gradually begins to improve over the course of 2-4 weeks

119
Q

Signs of optic neuritis

A

May present with or without disc edema, depending on the location of inflammation within the optic nerve

  • papillitis is secondary to inflammation of the anterior optic nerve and will present with disc edema; it occurs in 1/3 of cases of optic neuritis
  • retrobulbar optic neuritis is secondary to inflammation of the posterior optic nerve and will not present with disc edema; the ONH will appear normal
  • regardless of location, patient will repent with APD, decreased VA, decreased contrast sensitivity, decreased corri vision, and a variable VF defect
  • contrast will remain decreased even after regained vision
  • ON becomes pallid appx 4-6 weeks after the acute episodes of optic neuritis
120
Q

Symptoms suggestive of optic nueritis assocaited with MS

A

Uthoff’s phenomenon
Lhermitte’s phenomenon
Internuclear Ophthalmoplgia (INO)

121
Q

Uhtoff’s phenomenon

A

Transient vision loss due to an increase in body temperature (after exercise); although it occurs in only 6% of patients, it is considered highly suggestive of MS

122
Q

Lhermitte’s Phenomenon

A

The sensation of an “electric shock” that quickly travels down the back and into the limbs with flexure of the neck; occurs in 30-40% of patients

123
Q

Internuclear Ophthalmoplegia

A

Characterized by a lack of adduction on the affected side with contralteral nystagmus on abduction; due to a white matter lesion in the MLF that results in poor conduction from the contralateral CN6 nucleus to the ipsilateral 3 nucleus

124
Q

Bilateral INO

A

Highly suggestive of MS and occurs in about 15-30% of patients with MS; patients will present with an ADduction deficit on both sides, and convergence may or may not remain intact

125
Q

Thyroid eye related eye disease and optic disc edema

A

AI disorder characterized by TSH receptor Abs directed against the EOMs and orbital tissue; it resutls in significant inflammation and thickening of the EOMs and orbital adipose tissue, resulting in optic nerve compression in 5% of patients

126
Q

Presentation of thyroid related ophthalmopathy (TRO) and optic disc edema

A
  • unilateral disc edema, an APD, reduced color vision, and variable VF loss
  • unilateral or bilateral proptosis, upper eyelid retraction, eyelid erythema and edema, and conjunctiva; injection and edema; IOP may be elevated in primary upgaze
127
Q

Symptoms of thyroid related ophthalmopathy (TRO)

A

Decreased vision, prominent eyes, FB sensation, tearing, diplopia; diplopia is often worse in the AM due to excess fluid retention within the EOMs overnight when laying down

128
Q

Which EOMs are usually effected first in thyroid related ophthalmopathy

A

IR

MR

129
Q

Diagnosis of thyroid related ophthalmopathy

A

Exophthalmometry, VF, and forced duction testing, an orbital CR or MRI scan will confirm diagnosis by showing enlargement of EOMs (with sparing of tendons)

130
Q

Optic nerve sheath meningioma

A

A benign tumor that arises from the optic nerve sheath (meninges); most often affects young to middle aged women, and makes up 1/3 of cases of optic nerve neoplasms. Most often unilateral

131
Q

Optic nerve glioma

A

The most common intrinsic tumor of the optic nerve; it most commonly causes symptoms within the first decade of life (2-6 years of age). Appx 30-50% of cases of optic nerve glioma in infants are assocaited with NF1
-typically benign if they present during childhood, and malignant of they present in adulthood

132
Q

Most common intrinsic tumor of the optic nerve

A

Optic nerve glioma

133
Q

Optic nerve glioma in kids

A

Benign

134
Q

Optic nerve glioma in adults

A

Malignant

135
Q

Most benign orbital neoplasm in adults

A

Orbital cavernous hemangioma

136
Q

Orbital cavernous hemangioma and optic disc edema

A

The most common benign orbital neoplasm in adutls. More common in females and most often occurs in the 4th to 6th decade if life

  • collection of vascular channels and fibrous tissue. Orbital cavernous hemangiomas most commonly occur within the muscle cone posterior to the globe, resulting in compression of the optic nerve and resulting in unilateral disc edema
  • patients may also present with diplopia due to EOM restriction
137
Q

Optic nerve tumors or orbital tumors that compress the optic nerve are characterized by

A

Painless, slowly progressive vision loss and proptosis, with unilateral disc edema that is eventually followed by secondary optic atrophy

138
Q

Melanocytoma

A

Darkly pigmented neoplasm that lies adjacent to or on the ONH, and is most common in AA. It has no effect on vision and does NOT result in disc edema

139
Q

Papilledema

A

Bialteral disc edema due to increased ICP. Elevated cerebrospinal fluid within the subarachnoid space of the intraorbital (post chiasmal) portion of the ON results in axoplasmic stasis, with resulting bilateral disc edema. Patients will present with elevated optic nerve rim tissue and an elevated and opaque RNFL due to edema. May also present with Paton’s folds, hyperemia of the optic disc, CWS, exudates, venous dissension, splinter hemorrhages, and an absent SVP

140
Q

Va and papilledema

A

Usually normal, but VF will show an enlarged blind spit in the early stages of papiledema. An APD is often absent due to relatively symmetric invovlemtn of the optic nerves

141
Q

The most common causes of papilledema include

A
  1. Malignant HTN
  2. IIH (pseudotumor cerebri)
  3. Space occupying lesion (post chiasmal)
  4. Inflammatory causes (same ones as for optic neuritis)
  5. Compromised or obstructed venous outflow
  6. Systemic medications
142
Q

How can you distinguish papilledema from bilateral disc edema if a patient presents with an acute finding of two swollen optic nerves

A

In general, papilledema is assocaited with normal VA and bialteral disc edema is associated with a decreased in VA. Remember, papilledema cannot be definitively diagnosed until a lumbar puncture confirms elevated CSF pressure

143
Q

Pathophysiology.Dx of malignant HTN

A

Defined as dangerously high BP > 200mmHg systolic and/or 120mmHg diastolic; at this level of blood pressure, CSF produced in the ventricles cannot drain into the venous system, resulting in an increased ICP and papilledema

144
Q

What should be the first thing you check in someone with papilledema

A

IMMEDIATELY check BP in patients with papilledema in order to rule out malignant HTN. Patients must be hospitalized immediately to have BP slowly lowered due to high risk of stroke

145
Q

Symptoms of malignant HTN

A

Decreased vision, HA, nausea/vomiting, chest pain, shortness of breath, and neurological defects (numbness of the face, legs, etc)

146
Q

Signs of malignant HTN

A

Arteriolar attenuation, AV crossing changes, CWS, exudates, intracranial hemorrhages, and papilledema

147
Q

Epidemiology/Hx of idiopathic intracranial HTN

A

Classically presents in over weight females of child bearing age

148
Q

Pathophysiology/Dx of IIH

A

An increase in ICP from an unknown etiology; IIH is a diagnosis of exclusion, i.e., the following normal findings must be present

  • MRI and MRV reveal no space occupying lesion or venous obstruction
  • CSF has a normal composition
  • BP not extremely elevated
  • Norma CBC with no clotting issues
  • patient must be awake and alert with no other neuro findings (except CN 6 palsy)
  • an elevated CSF opening pressure > 200mm of water (or >250mm in patients who are obese) with lumbar puncture
149
Q

In what order do you do diagnostic testing for pseudotumor cerebri

A

MRI first then lumbar puncture. If a space occupying lesion is present on MRI, a lumbar puncture may result in herniation of the brain through the foramen magnum

150
Q

Systemic medications that can cause papilledema

A

CANT

  • contraceptives
  • vitamin A
  • accutane
  • Naladinic acid (quinolone)
  • tetracyclines
151
Q

Symptoms of IIHTN

A

Transient visual obscurations and HA

152
Q

Signs of IIH

A

Enlarged blind spot on VF, diplopia due to CN 6 palsy, and papilledema. Late signs include variable (and sometimes permanent) VF defects and bilateral optic nerve atrophy

153
Q

CN 6 and elevated ICP

A

Intracranial portion of the CN 6 travels along the petrous ridge of the temporal bone. Elevated ICP compresses CN 6 along the bony petrous ridge, resulting in damage to CN 6 and impaired innervation to the LR, with a resulting eso deviation

154
Q

Optic atrophy is due to

A

Destruction and degeneration of the retinal ganglion cell axons (RNFL)

155
Q

What are the two types of optic atrophy

A

Excavation and pallor

156
Q

Optic atrophy: excavation

A

Loss of the neuroretinal rim due to glaucoma

157
Q

Optic atrophy: pallor

A

Characterized by whitening of the neuroretinal rim tissue. Pallor may develop in two ways:

  • primary optic atrophy: optic nerve was NOT previously edematous (trauma, toxic/nutrition, orthograde degeneration, retrograde degeneration, hereditary)
  • secondary optic atrophy: ON was previously edematous before becoming pallid. All of the causes of unilateral disc edema and papilledema may lead to secondary optic atrophy
158
Q

Examples of primary optic atrophy

A 
Truama 
Toxic/nutritional
Orthograde degeneration 
Retrograde degeneration 
Hereditary (Lebers optic neuropathy, dominant optic atrophy)
159
Q

Toxic/nutritional optic atrophy

A

Results from alcoholism, tobacco abuse, toxicity from medications (ethambutol, isoniazid, amiodarone) and/or malnutrition (vitamin B12 or B1 deficiencies)

  • classically temporal pallor of the ONH
  • complain of bilateral, painless, progressive vision loss and will have a central or cecocentral VF defect due to damage of the papillomacular bundle at the temporal rim of the optic nerve
160
Q

Things that can cause toxic/nutritional optic atrophy

A 
Alcohol 
Tobacco
Ethambutol 
Isoniazid 
Amiodarone 
Malnutrition
161
Q

Orthograde degeneration: optic atrophy

A
  • extensive damage to the retinal ganglion cells may lead to degeneration fo the RNFL, with corresponding atrophy of the neuroretinal rim tissue of the ONH. The following may cause it:
  • PRP
  • CRAO
  • RP
  • extensive geographic atrophy
162
Q

Retrograde degeneration and optic atrophy

A

Damage to the retrobulbar optic nerve may resutls in descending degeneration of the optic nerve axons within the ONH, resulting in pallor. The classic example of optic nerve pallor due to retrograde degeneration is a pituitary tumor
-pituitary gland is located inferior to the optic chiasm in the sella turcica; a tumor resutls in compression of the nasal optic nerve fibers within the optic chiasm, commonly causing a horizontal band of pallor across the optic nerve (bow-tie atrophy)

163
Q

What are the two types of VF caused by a pituitary tumor

A

Bitemporal hemianopsia

Junctional scotoma

164
Q

Bitemporal hemianopsia and pituitary tumor

A

Due to compression of the nasal fibers that cross that optic chiasm

165
Q

Junctional scotoma and pituitary tumor

A

Characterized by temporal field loss in one eye, and central or diffuse field loss in the fellow eye due to a chiasmal lesion that compresses an odjacent optic nerve

166
Q

Pituitary adenomas

A

Account for an estimated 10% of intracranial neoplasms and may be functional or non functional. The smog common functional pituitary macroadenoma is a prolactin secreting tumor, and is assocaited with amenorrhea, galactorrhea, infertility, and loss of libido. Patietns with a pre existing asympatomic pituitaty adenoma may become symptaotmic during pregnancy

167
Q

Lebers optic neuropathy

A

Secondary to mutations in mitochondrial DNA that are inherited from the mother; 85% of affected patients are males, with an onset of the contion in the late teens or early 20s. Patients will present with a sudden onset of decreased central vision. Early signs include optic disc hyperemia that eventually progresses to optic disc pallor in the late stages. The condition spontaneously improves in 35% of cases

168
Q

Dominant optic atrophy

A

The most common hereditary optic atrophy; it develops early childhood and is characterized by insidious onset of mild to moderate vision loss; patietns will present with temporal optic nerve pallor and excavation.

169
Q

Foster Kennedy syndrome

A

Rare condition caused by a frontal lobe tumor; characterized by simultaneous optic disc edema in one eye and optic disc atrophy in the fellow eye

170
Q

Optic nerve pit

A

Unilateral depression of the optic disc that is usually located inf/temp; may develop a serous retinal detachment that extends from the optic pit towards the macula. Patients are asymptomatic unless the macula isinvolved

171
Q

Morning glory syndrome

A

Unilateral condition characterized by an enlarged, funnel-shape, excavated nerve with resulting poor VA

172
Q

Optic nerve hypoplasia

A

Incomplete development of optic nerve that may be unilateral or bilateral; characterized by a hypoplastic disc surrounded by a ring of sclera and a ring of hypopigmentation (double ring sign), with mild to severe vision loss. Patients may have additional associated systemic defects. This condition is associated with fetal alcohol syndrome and maternal drug abuse

173
Q

Optic nerve coloboma

A

Large, abnormally shaped optic disc due to incomplete closure of the fetal fissure; the coloboma is typically located infer/nasal. Patients may also present with systemic defects

174
Q

Functions of the pupil

A
  • pupil movement optimizes retinal illumination: pupil size can be adjusted depending on light levels to enhance visual performance
  • depth of focus: near work induces miosis and allows for an increased depth of focus
  • reduces optical aberrations: smaller pupils decrease chromatic and spherical aberrations. The amount of SA scales with the square of the diameter of the entrance pupil
175
Q

Swinging flashlight test

A

Allows for comparison of the afferent pupillary pathway between the two eyes. If one eye has damage or if there is asymmetric bilateral damage, an APD will be present

176
Q

Causes of an APD

A
  • dense vitreous heme
  • extensive retinal damage (RD)
  • ON damage (glaucoma)
  • optic chiasm damage that involves the adjacent optic nerve

Damage to the remaining areas of the visual pathway (cornea, iris, crystalline lens, optic tract, optic radiations, occipital lobe) will not result in an APD

177
Q

Testing for an APD

A
  • after confirming the direct response in each eye, the transilluminator light is shown in one eye for appx 3s while the clinician views the pupil size of the fellow eye
  • the transilluminator is quickly moved to the fellow eye while the clinician continues to observe the pupil response; the transilluminator is held for 3s while the clinician switches his gaze to the pupil of the inital eye to observe the pupil size
  • the transilluminator is then quickly moved back to the initial eye as the clinician continues to oversee the pupil response
178
Q

What does the swinging flashlight test allow

A

Comparison of the direct and consensual response in the same eye. These responses should be equal, and no net movement of the pupil should occur in either eye with bilateral health optic nerves

179
Q

Abnormal efferent pathway OS

A
  • the direct response OD will be brisk, but the direct response OS will be slow
  • when the transilluminator light is initially shown in the right eye, the left pupil will constrict to the consensual response
  • when the transilluminator light is quickly switched to the left eye, the left pupil will dilate due to damage to the afferent pathway (direct response is weaker than consensual)
  • when the transilluminator light is quickly switched back to the right eye, the right pupil will constrict due to the APD in the fellow eye (direct response is stronger than the consensual response)
180
Q

Constriction of the “good eye” during the swinging flashlight test when the fellow eye has an APD

A

Is known as a reverse APD. This is helpful to note when pupil movement in the “bad eye” cannot be observed or when there is no iris movement in the “bad eye” due to efferent pathway damage

181
Q

Abnormal efferent pathway OS

A
  • the direct repsonse OD will be brisk, but the direct response OS will be slow
  • when the TI light is initially shown in the OD the left pupil will be dilated due to damage to the efferent pathway
  • when the TI light is quickly switched to the left eye, the left pupil will stay dilated
  • when the TI light is quickly switched back to the right eye, the right pupil will stay constricted because the afferent pathway OS is intact (equal director and consensual response OD)
182
Q

Abnormal afferent and efferent pathways OS

A
  • the direct response OD will be brisk, but the direct repsonse OS will be slow
  • when the TI is initially shown in the OD, the left pupil will be dilated due to damage to the efferent pathway
  • when the TI light is quickly switched to the OS, the left pupil will stay dilated
  • when the TI is quickly switched back. To the right eye, the right pupil will constrict due to the APD i nthe fellow eye
183
Q

The swinging flashlight tests helps differentiated

A

Whenever an abnormal repsosne is due to an afferent or efferent issue

184
Q

Anisocoria is a CN ____ problem

A

III

185
Q

CN ____ is responsible for efferent innervation and CN ____ is responsible for afferent respsone in pupils

A

2
3
Anisocoria will always be caused by an efferent issue

186
Q

physiologic Anisocoria

A

In 20% of cases, it is physiologic, and therefore should be of no concentration. This can be determined simply by measuring the pupil size in light and dark conditions; if the difference remains constant between the two eyes, and both pupils are equally reactive to light, then it is physiologic anisocoria

187
Q

Things that cause an abnormal miotic pupil

A

Horners
Argyll Robertson
Uveitis with PS

188
Q

Things that cause an abnormal dilated pupil

A

CN 3 palsy
ADie’s tonic pupil
Iris sphincter trauma
Pharmacological dilation

189
Q

Internal ophthalmoplegia

A

Paralysis of the pupil; external ophthalmoplegia refers to paralysis of the EOMs

190
Q

Pathophysiology of horners syndrome

A

Due to a lesion in the sympathetic nervous system pathway from the hypothalamus to the eye. It may be due to a pre-ganglionic or a post-ganglionic lesion

191
Q

preganglionic Etiologies of horners syndrome

A

Pre ganglionic central lesion (between the hypothalamus and the ciliospinal center of budge (C8-T2)): cerebravoascular accident, neck trauma, demyelinating disease, tumor

Preganglionic lesions (between the ciliospinal center of budge and the SCG): pancoast tumor, thyroid mass, neck trauma, history of thyroid or neck surgery

192
Q

Post ganglionic etiologies of horners syndrome

A

(Between the SGC and the iris dilator muscle): head trauma, cavernous sinus syndrome, carotid dissection, cavernous sinus fistula, and ICA aneurysm

193
Q

Pancoast tumor

A

At the apex of the lung. The most common pre-ganglionic lesion that resutls in horners syndrome

194
Q

Signs/symptoms of horners

A

The classic triad of mild ptosis, miosis, and anhydrosis. Patients with a carotid artery dissection may also present with pain (neck and shoulder) and a history of trauma

195
Q

Horners: anhydrosis is most prominent when

A

In patients with preganglionic lesions. Because most of the sweat fibers diverge away from the sympathetic fibers near the SCG, a postganglionic leison will only result in anhydrosis to the ipsilateral forehead

196
Q

Diagnosis of horners: step 1

A

Cocaine: inhibits the reuptake of NE at the post ganglionic receptor of the sympathtic nervous system

  • normal pupil=dilation
  • horners pupil=will NOT dilate
197
Q

Diagnosis of horners: step 2

A

Wait 24-48 hours between step one and two
Hydroxamphetamine: stimulates the release of NE from healthy post ganglionic neurons. It aids in determination of the location of the lesion in horners syndrome
-pre-ganglionic: pupil WILL dilate
-post ganglionic: no dilation

198
Q

Preganglionic horners lesion and testing

A

No pupil dilation with cocaine, but pupil dialtion with HA

199
Q

Postganglionic horners lesion and testing

A

No dialtion with cocaine or HA

200
Q

Apraclonidine and horners testing

A

Weak alpha receptor agonsit. In the normal pupil, it does not cause dilation
-in horners: lack of sympathetic innervation to the iris dilator muscle results in hypersensitivity of the adrenergic receptors: thus, apraclonidine will cause pupillary dialtion and reversal of anisocoria

201
Q

Pathophysiology of argyll Robertson pupil

A

Due to a lesion of the tectotegmental tract, which carries info from both nuclei to thei respective ipsilateral and contralateral EW nuclei. It is most commonly associated with neurosyphilis (tertiary), DM and alcoholism

202
Q

Signs of argyll Robertson pupil

A

Miotic pupil and light near dissociation (does not constrict to light but will constrict to near work)

  • recall that pupil consitrciont in repsonse to near is mediated by fibers from the FEF that provide input to the EW nuclei
  • typically unilateral but becomes bialteral over time

Argyll Robertson Pupil=Accommodative Response Present

203
Q

Pathophysiology of pupil invovled CN III palsy

A

Due to a lesion within the pathway of CN III, most commonly secondary to an aneurysm of the postieror communicting artery, a tumor, or trauma; microvascular infarcts rarely cause this

204
Q

Pupillary fibers of CN III

A

Travel on the outside of CN 3; thus a pupil invovled CN 3 palsy is much more likely to be caused by a compressive lesion rather than a microvascular infarct. Patients with pupil invovled CN 3 palsies warrant immediate imaging with an MRI/MRA to rule out a compressive tumor or aneurysm

205
Q

Signs of pupil involving CN 3 palsy

A

Pupil will be fixed and dilated, and will not constrict to light or to accommodation. Pupil involved CN 3 palsies rarely affect only the pupil without afffecting the other EOMs innervated by CN 3 (MR, IO, IR, SR), and a significant ipsilateral ptosis (due to impaired levator function)

206
Q

Diagnosis of pupil involving CN III palsy

A

1% pilo may be used to aid in the Dx; it will cause constriction of the pupil in the affected eye

207
Q

What should CN3 palsy patietns do if they do not have an invovled pupil

A

Because the pupil can rarely become invovled after the initial presentation of a pupil invovled CN 3 palsy, patients wil pupil sparing CN 3 palsies should be closely followed for 1 week to ensure that the pupil does not become involved

208
Q

Epidemiology/Hx of ADies tonic pupil

A

Commonly affects young females (20-40)

209
Q

Pathophysiology of ADies tonic pupil

A

Caused by a lesion in the CG or ciliary nerves from an unknown benign etiology. It is not associated with any systemic disease

210
Q

Symptoms of ADIes tonic pupil

A

Pre-presbyopia patietns will complain of blurred vision at near; most patietns rarely complain of photosensitivty

211
Q

Signs of ADies tonic pupil

A

An acute dilated pupil that has slow or minimal constitution in response to light, but will slowly constrict in repsosne to a near object; anisocoria will be greates under bright light due to poor innervation of the iris sphincter muscle. The iris will have a vermiform movement when viewed with a slit lamp. Decreased accommodation due to impaired innervation to the CBM. Typically unilateral, although becomes bilateral at a rate of 4%/ year. Diminished deep tendon reflexes as well

212
Q

Diagnosis of ADies tonic pupil

A

0.125% pilocarpine can be used to confirm the diagnosis of ADies tonic pupil. Normal pupils will not consitrct in response to a weak concentration of pilo, however in ADies, 0.125% pilo will cause pupil constriction due to hypersensitivity of the cholinergic receptros on the iris sphincter muscles

ADies=Acute Dilated pupil caused by a leison in the CG

213
Q

Iris sphincter trauma

A

Blunt or penetrating trauma may result in a tear in the iris sphincter, resulting in traumatic pupil dialtion and anisocoria that is greatest in bright light

214
Q

Signs of iris sphincter trauma

A

Vermiform movement of the iris in slit lamp
Iris atrophy
Notching of the iris at the pupillary margin

Additional signs that may be assocaited with an iris sphincter tear due to trauma include a traumatic hyphema, iridodialysis, traumatic cataract, crystalline lens subluxation, Vossius ring, commotio retinae, and angle recession

215
Q

The most common cause of a fixed and dialted pupil is

A

Pharmacological dialtion secaondry to mydriatics/cycloplegics, overuse of visine, or a scopolamine patch

216
Q

How d owe confirm if a dialted pupil is pharmacological induced or not

A

Put pilo 1% in there and they will not constrict

217
Q

If pupil constricts with 0.125% pilo

A

ADies

218
Q

If pupil does not constrict with 0.125% pilo, but it does with 1%

A

CN3 palsy

219
Q

If the pupil does not constrict with 0.125% or 1% pilo

A

Pharmacological dilation or sphincter tear

220
Q

Coma pupils

A

Hutchinson’s pupil

Miosis

221
Q

Hutchinson’s pupil

A

Dilated pupil in a comatose patietns, commonly as a result of a ipsilateral tumor or subdural hematoma compressing the superficial pupillary fibers of CN 3

222
Q

Miosis in coma

A

The early stages of a coma include miosis due to loss of the inhibitory cortical input to the EW nucleus; however the pupils will retain their respsonvienwess to light

223
Q

Superior division of CNIII innervated

A

Levator and SR

224
Q

Inferior division of CN III innervated

A

IR
MR
IO
Parasympathetic

225
Q

When isa CN3 palsy considered complete

A

If all 4 EOMs and the levator are invovled. An incomplete CN 3 palsy is involvement of anthging less than a complete CN 3 palsy, and may affect an isolated muscle, only the inferior divisions, or only the superior division.

226
Q

Pathophysiology of CN 3 palsy

A

Secondary to a lesion along the pathway of CN 3. The most common causes include a microvascular infarct (secondary to DM or HTN), trauma, and an aneurysm (most commonly the posterior communicating artery)

227
Q

Symptoms of a CN 3 palsy

A

Diplopia, depending on the extent of the ptosis.
Most patients with a complete CN 3 palsy do not complain of diplopia because of the significant ipsilateral ptosis blocking the visual axis

228
Q

Signs of a CN3 palsy

A

In a complete CN 3 palsy, the patient will present with the involved eye down and out, with a large ipsilateral ptosis. A compressive lesion that causes a CN 3 palsy will always involve the pupil (will appear fixed and dilated) due to the superficial location of the pupil fibers along CN3. The pupil typically is NOT involved in a CN3 palsy due to a microvascular infarct

229
Q

Imaging and a pupil involving CN3 palsy

A

Any pupil involving or incomplete CN 3 palsy warrants immediate imaging with an MRI or MRA to rule out a compressing tumor or aneurysm (most commonly the posterior communicating artery)

230
Q

CN3 palsy and aberrant regeneration

A

CN 3 palsies can develop aberrant regeneration (abnormal retiring of the damaged nerve), as they heal. Signs inclue lid-gaze dyskinesia (upper eyelid retraction with downgaze) and pupil-gaze dyskinesis (pupil constriction with down gaze or aDDuction). Aberrant regeneration is vary rare in ischemic CN 3 palsies, patients should be evaluated for a possible tumor or trauma in these cases

231
Q

CN 4 innervated

A

SO (contralateral)

232
Q

Which CN is most susceptible to trauma

A

CN 4

It has the longest course in the body of all the CN

233
Q

Things that can cause CN 4 palsy

A

Congenital or acquired

  • trauma
  • undetermined
  • ischemic
  • neoplasm and/or aneurysm
234
Q

CN 4 palsies and vertical vergence ranges

A

Congenital will have large vertical vergence ranges

Acquires will have normal vertical vergence ranges

235
Q

Diagnosis of a CN 4 palsy

A

Parks three step
Double Maddox rod (Dx torsional component in CN 4 palsies)
Versions (overaction of ipsilateral IO)

236
Q

Signs and symptoms of CN 4 palsy

A

Vertical diplopia and may also present with a compensatory head tilt AWAY from the side of the lesion in order to minimize diplopia. Cover test will reveal a hyperdeviation on the affected side

237
Q

What EOM CN is the most common to get a palsy

A

6

238
Q

Pathophysiology of CN 6 palsy

A

Due to damage along the pathway of CN 6. Possible cause

  • pseudotumor cerebri (pressure against the petrous ridge)
  • horners syndrome (tumor in the cavernous sinus)
  • microvascular infarction (DM/HTN)
  • trauma
  • tumor
239
Q

Symptoms and signs of CN6 palsy

A

Horizontal diplopia

Head turn towards affected side

240
Q

DiffDx of CN6 palsy

A

Duane retraction syndrome

Infantile or accommodative ET

241
Q

Immediate imaging (MRI/CT) is warranted for the following cases

A 
Young patietns (<50)
Other neuro symptoms 
Multiple CN are involved 
History of cancer 
Incomplete or pupil-involving CN 3 palsy
Presumed ischemic CN palsy that does not resolve in 3m
242
Q

What two systemic diseases should always be considered when there is an ocular CN palsy

A

TED

MG

243
Q

Epidemiology/Hx of ocular MG

A

4-5 persons per 100,000
May affect any age and race
Tends to present in women when they are younger and in men when they are elderly

244
Q

Pathophysiolgoy of ocular MG

A

AI condition tear is characteristic by autoAbs directed against the ACH receptors within the NMJ, resulting in blockage of NM signals and resulting weakness and fatigue of the skeletal muscles
-ocular MG is a manifestation of systemic MG that affects the muscles of the eyes. 90% of patietns with systemic MG will have ocular MG at some point during the course of the disease; in 70% of cases, ocular findings are the initial sign of systemic MG

245
Q

What is a common additional finding in MG

A

About 10% of MG patients will have a thymoma (tumor of the thymus); a chest CT (or chest X ray) is indicated to confirm whether a thymoma is present in patients with MG

5% of MG patients will also have a concomitant thyroid disease; T3 and T4 and TSH labs are indicated to determine whether thyroid disease is present

246
Q

Symptoms of ocular MG

A

Diplopia and ptosis; the orbicularis oculi may also be affected. Ocualr signs and symptoms are variable and often worse at the end of the day or with exertion of the muscles. Systemic symptoms of MG include dysarthria (difficulty talking), dysphasia, difficulty holding head upright, and respiratory failure (myasthenia crisis)

247
Q

Diagnosis of MG

A

Tension test

  • IV edrophonium
  • ptosis and/or diplopia will improve within 3-4m of the injection in patients with MG
248
Q

Antidote for potentially dangerous side effects caused by the tensilon test

A

IV atropine
Or pralidoxime

Can get bradycardia, bronchospams, and angina

249
Q

Ice pack test for MG

A

Ptosis and/or diplopia improve after application of an ice pack for 5 min in MG patients

250
Q

Cogans lid twitch

A

Pateints with suspected MG and ptosis are asked to look down for appx 15s and then look in primary gaze. A positive test is characterized by an initally absent ptosis when the patietns refixates in primary gaze, followed by the upper eyelid lowering in a twitching fashion to its original position; this finding is considered highly suggestive of MG

251
Q

Other tests for MG

A

Orbicularis oculi strength test
Sleep test
ACH ab test
Repetitive nerve stimulation through electromyography (single fiber EMG is more sensitive and specific for MG)

BOARDS (14 decks)

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