jisakuha's version from 2015-12-14 22:43


Question Answer
What is the first synapse in the mid brain for the pupillary light reflex?retinal ganglion cells to pretectal nuclei via optic nerves
Do the pretectal nuclei receive information from ipsilateral source, contralateral, or bilaterally from the eyes?bilaterally
There are interneurons from both pretectal nuclei to each Edinger Westphal nuclei. What is the result of this double innervation when light is shined into one eye?get consensual response where both pupils constrict
From the Edinger Westphal nucleus, the parasympathetics travel with what nerve and in what space before synapsing where?travel along CN3 in both the brainstem and in the subarachnoid space. The last synapse is in the eye socket at the ciliary ganglion.
From where do we believe the Near Reflex pathway is mediated?higher cortical centers at the parieto-occipital-temporal junction.


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In the near Reflex pathway, where do the inputs from the higher cortical centers synapse?directly down to Edinger Westphal nucleus
What is the localization of the light near dissociation?dorsal midbrain where pupils don’t react to light but they react to near (affect only the pretectal nuclei)
What s the innervatino of the pupillary constriction to near objects?parasympathetics, the same as pupillary light reflex
From the hypothalamus, the sympathetics go through the brainstem. Where do the synapse first?C8-T2.
After the first synapse, the sympathetics travel through the brachial plexus to synapse where?synapse at the angle of the jaw where the plexus of the carotid holds 3rd order neurons within its wall


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If you cut the optic nerve and the person is blind, will there be anisocoria?no, only APD
Can you have APD with media opacities such as cataracts?no
If you perform the swinging flashlight test, what happens to pupils in APD?BOTH pupils will dilate after swinging into the bad eye. Get both eyes because pretectal nucleus is intact but not getting as much light info from L eye to midbrain pathways.
How can you tell if there is an APD if the patient has L 3rd nerve palsy and pupil is paralyzed due to efferent problem?If shine light into good Right eye, it will constrict, but then when shine light into L eye, the R eye will dilate.
Can you have an APD with optic tract lesion and if so, typically, which side is it?yes, typically the side with the temporal field loss.


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In evaluating anisocoria, a physiologic anisocoria would be the same difference in light and dark. However, if there is pathology, which pupil is the problem in the dark?if more anisocoria in the dark, then it is the small pupil ie horner’s syndrome
Which pupil is the problem if there is worsening of anisocoria in the light?large pupil
What are 3 examples of pathologic causes of anisocoria in the light?3rd nerve palsy (aneurysm), tonic pupil (ciliary ganglion lesion in orbit), pharmacologic pupil (scopolamine patch on boat).
How does cocaine work in regards to the pupil? It blocks Norepinephrine reuptake, so at the Iris dilator muscle you get dilation
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In a Horner’s syndrome, what happens if patient given cocaine eye drops?since not a lot of NE, there isn’t much NE to block the reuptake, so there isn’t any dilation of pupil. Doesn’t help localize, just shows that Horner’s is present


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What findings would you see if the patient had a Horner’s localizing to the 1st order neuron?see crossed sensory findings as in a spinal cord lesion or Wallenberg brainstem stroke.
What localization of a Horners would you see if there are lower motor neuron signs (dropped reflex, atrophy) on same side of lesion on the arm?2nd order, think apical lung tumor
If a patient has 3rd order neuron affected in a Horner’s syndrome due to carotid dissection, what would you see clinically?sweating preserved on same side of face bc the sudomotor fibers come off at the angle of the jaw at external carotid. The neurons for pupil and lid are in the carotid plexus
How does hydroxyamphetamine work in order to localize a Horner’s syndrome?It localizes a third order neuron lesion bc it will stimulate the release of NE at 3rd order terminal if functioning properly. If that area is compromised, then it will not dilate
What is the most feared cause of a worseninig anisocoria in the light?aneurysm compressing CN 3 until proven otherwise


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A young female has unequal pupils and difficulty reading near. When shining light in L pupil, it is large and irregular and doesn’t react, however, if testing for near, both her pupils constrict. Where is the lesion?has a tonic pupil due to ciliary ganglion in the eye socket. This is Light near dissociation. The ratio of fibers for the ciliary muscle (involved in light response) to the number for the constrictor pupillae (involved in accommodation) is high, as well as the ciliary muscle is much bigger than constrictor. If 70% of the ciliary ganglion cells are injured, then more likely that enough strength in accommodation. Esp after regeneration, more likely to have abberant growth of the constrictor pupillae fibers
An important cause of light near dissociation is deafferented pupils in b/l optic neuropathy. What will you see if they try to focus on a thumb in front of them?constriction of pupils
What is the localization of Argyll Robertson pupils and what clinically do you see in this?light near dissociation and it affects interneurons from pretectal nuclei to edinger westphal nuclei
What is the localization of Parinaud’s syndrome?dorsal mibrain
A patient has midposition/large pupils with light-near dissociation; upgaze paresis; convergence retraction nystagmus (convergence retraction saccades); eyelid retraction (eyelids don’t follow eyes down when looking down). What is dx?dorsal midbrain syndrome (Parinauds)


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What is the difference in pupils between Argyll Robertson and parinaud’s?Argyll Robertson will be small and fixed instead of midposition/large and fixed that Parinaud’s has
Where would the lesion be in a comatose patient that has pupils with mid or fixed position?mibrain process
Where would the lesion be in a pt with pinpoint pupils in coma?pontine
Where would the lesion be with a unilateral, dilated, fixed pupil in a comatose patient?uncal herniation causing 3rd nerve impingement
If a patient has diplopia due to refractive error or cataracts, would he have monocular or binocular diplopia?monocular


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If a patient has worsening of diplopia at a distance, which CN is affected?6th
What direction of gaze does the superior oblique depress in?adduction
What does the superior oblique do in primary gaze?intorts
What direction of gaze does inferior oblique elevate in?adduction
What direction of gaze does inferior rectus best depress in?abduction


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What direction of gaze does superior rectus best elevate in?abduction
What are the 5 potential places for CN 3,4,6 nerve localization?brainstem nucleus, brainstem fascicle, subarachnoid space, cavernous sinus, orbital apex
If a pt presents with efferent visual lesion and optic neuropathy, where would this likely localize to?orbital apex
If a patient presents with headache and binocular vertical/horizontal diplopia, what CN nerve is likely involved?3rd nerve, also would have ptosis
Would a patient with CN3 palsy have light near dissociation?no, would have pupillary dilation in both because it is proximal to brainstem so no afferent is going through


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What division of CN3 innervates levator and superior rectus?superior division
What division of CN3 innervates pupil, inferior and medial recti, and inferior oblique?inferior division
What is the localization of CN3 if pt has bilateral ptosis, contralateral superior rectus weakness, and unilateral 3rd nerve signs?nuclear 3rd
What is the syndrome of 3rd nerve palsy with contralateral movement disorder/tremor?Benedikt’s,
What is the syndrome of 3rd nerve with contralateral hemiparesis?Weber’s, cerebral peduncle invovlement


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What is the syndrome of 3rd nerve with contralateral ataxia?Claude’s
What are the 2 most common causes of lid/gaze dyskinesis (eyelid pops up when looking down and adducting) and pupil/gaze dyskinesis (pupil constrction on downgaze and convergence/adduction) which are aberrant regeneration of 3rd nerve?trauma and compressive (aneurysm) etiology, never diabetic/vascular
What is the cause of ophthalmoplegic migraines where children get recurrent CN3 palsies?inflammation in midbrain or of the nerve
What nerve is affected if upon looking down, pt gets increased vertical separation but may see a tilt of one of the images?CN4 palsy
Why in a CN4 palsy the patient will have worsening of ipsilateral hypertropia (eye on side of CN4 is higher)when looking to the contralateral side?the sup oblique has more of a depressor effect in adduction


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In what direction will a head tilt improve symptoms for a pt with CN4 palsy?head tilt away from the side with the problem. Because the superior rectus is trying to intort but it is not good at that. It is good at elevating, however.
Where would the localization of a CN4 palsy with ipsilateral Horner’s take place?nuclear/fasicular 4th.
What are the causes of nuclear/fascicular 4th (3)trauma, demyelination, trauma
What would the clinical picture look like in a pt with nuclear CN6 palsy or PPRF?ipsilateral horizontal gaze palsy (either eye)
Where would the localization of CN6 lesion be if patient has ipsilateral horizontal gaze palsy with intact oculocephalics?PPRF


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Describe the pathway from L frontal eye fields that drives eyes fast to R side?L FEF goes to R PPRF and CN6 nucleus, and the CN6 nucleus has connections with Left CN3 nucleus which activates L medial rectus
What is the localization if patient has peripheral CN7 deficit, horizontal gaze deficit?facial colliculus syndrome
What eye movements can someone with L 1.5 syndrome perform?can abduct the contralateral eye only.
What is the pathophysiology of a L 1.5 syndrome?IF on the L, would have 6th nuclear lesion or PPRF (have horizontal ipsilateral gaze palsy (unable to look L) from fibers for ipsilateral lateral rectus and contralateral medial rectus via MLF) as well as get fibers going from contralateral MLF (right) after they have crossed. So would have L INO due to contralateral MLF fibers being affected. All pt can do is abduct the contralateral (R) eye.
What would you expect clinically from a patient with PPRF lesion?ipsilateral horizontal gaze palsy


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R INO is problem with connection between R 6th nerve and L CN3. What would you expect if there was a L MLF lesion?ipsilateral INO, so when looking to R, L eye is unable to adduct and when looking L, there will be nystagmus of R eye
What would the localization be in a patient with 6th nerve palsy with contralateral hemiparesis?pyramidal tract
Why can you have isolated EOM palsies in pituitary apoplexy and which CN palsy is most common with pituitary apoplexy?sella is close to cav sinus; CN3 is most commonly affected
In a cav sinus syndrome causing EOM dysfunction, which CN is the most commonly affected and why?CN6 because it floats freely in cav sinus
What structures enter the superior orbital fissure?3,4,6,V1


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If patient is immunocompromised and has acute onset of ophthalmoparesis with orbital infection, what infectious etiology should you think and what is 2nd?mucormycosis, number 2 is aspergillosis
If patient has CN 3,4, or 6 palsy with neck pain, what is diagnosis?carotid dissection
What CN dysfunction would you see in a Wernicke’s patient?bilateral 6th
What AED is associated with ophthalmoparesis?Dilantin
What vascular problem would you think in a patient with orbital disease?carotid cavernous dural fistula


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If given a case history of abnormality in pursuit, then where would you localize the lesion?parietal lesion
If there is abnormality in saccades and gaze, where would the lesion be?frontal eye fields
Skew deviation is the abnormal wiring between the vestibular system (from inner ear or vestibular nuclei) and the 3rd and 4th subnuclei that subserve vertical gaze. There can be lesions anywhere in pathway up to the midbrain. What is localization if in midbrain and if in medulla?ipsilateral if in midbrain (i-high) and contralateral if in medulla (la-low)
What is pendular nystagmusPendular nystagmus has no fast phase
A patient has a brainstem tumor, and 6 months later his wife reports he makes a clicking noise at night when going to sleep. He has pendular nystagmus. What type of nystagmus is this and where is the localization?oculopalatal nystagmus; central tegmental tract


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A pt has GI disease and pendular waveform of nystagmus. What is the disease he has and what is the nystagmus that he has? How would you treat?whipples disease; oculomasticatory myorhythmia; treat with ceftriaxone
What is the most common cause of a see saw nystagmus?parasellar lesion
Where does downbeat nystagmus localize to?cervicomedullary junction
Where is Brun’s nystagmus localize to (gaze evoked)?cerebellopontine angle.
Where does convergence retraction nystagmus localize to?dorsal midbrain


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Where does upbeat nystagmus localize to?cerebellum, pontomesencephalic, pontomedullary
If patient has peripheral vertigo, where would be the most common location?posterior semicircular canals
What kind of nystagmus would you see in benign positional vertigo?torsional upbeat nystagmus
If a patient has upbeat, torsional nystagmus to the right shoulder, where is the dysfunction?right posterior canal.
What is the treatment for R posterior canal problem?epley maneuver with right ear down first


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What features would you expect in a central cause of vertigo while performing dix hallpike?no latency, >1min, no fatigability, and torsional wave form
What are dramatic, involuntary, conjugate multidirectional saccades (saccadomania) and it is different from ocular flutter (which has primarily horizontal movement)?opsoclonus
What paraneoplastic antibodies are associated with opsoclonus?anti-hu and anti-ri
What disease in childhood can cause opsoclonus?neuroblastoma
What do you treat periodic alternating nystagmus?lioresal