• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/102

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

102 Cards in this Set

  • Front
  • Back
what are abnormalities of pupils and eye movements warning signs for
signs of pathology in brainstem or CNs
eye movement disorders and pathways are separated into what two levels
1) nuclear and infranuclear pathways 2) supranuclear pathways
nuclear and infranuclear pathways
involve brainstem nuclei of CN III, IV, and VI; peripheral nerves arising from these nuclei; eye movement muscles
supranuclear pathways
involve brainstem and forebrain circuits that control eye movements through connections with nuclei of CN III, IV, and VI
what eye muscles originate on a tendinous ring at the orbital apex and insert onto the sclera
lateral, medial, superior, and inferior rectus muscles
where does the superior oblique originate
sphenoid bone in posterior medial orbit and passes anteriorly through trochlea; inserts on superior surface of eye (intorsion-upper pole inward)
where does the inferior oblique originate
along the anterior medial orbital wall and inserts on the inferior surface of the eye (extorsion-upper pole outward)
what eye CNs pass through cavernous sinus and enter orbit via superior orbital fissure
III (oculomotor), IV (trochlear), and VI (abducens)
what muscles does CN III innervate
all extraocular except lateral rectus and superior oblique; levator palpebrae superioris; preganglionic parasympathetic fibers to pupillary constrictor muscles and ciliary muscles of lens
trochlear innervates
superior oblique
abducens innervates
lateral rectus
what constitute the somatic motor column of CN nuclei
III, IV, VI, along with XII (hypoglossal); all near midline adjacent ventricular system and fibers exit brainstem ventrally near midline (except IV which exits dorsally)
where are oculomotor nuclei
upper midbrain at level of superior collliculi and red nuclei, just ventral to the periaqueductal gray matter
where does CN III exit brainstem
in interpeduncular fossa btwn posterior cerebral and superior cerebellar arteries
what does the Edinger-Westphal nucleus contain
preganglionic parasympathetic fibers
what are parasympathetics controlling pupil constriction in CN III susceptable to
run in superficial portion of nerve as travels in subarachnoid space - susceptible to compression from aneurysms (especially via posterior communicating artery)
location of trochlear nuclei
lower midbrain at level of inferior colliculi and decussation of superior cerebellar peduncle
abducens nuclei location
floor of 4th ventricle under facial colliculi in mid-to-lower pons; exit at pontomedullary jxn
Dorello's canal
abducens nerve travels in-outside dura running btwn dura and skull under petroclinoid ligament
diplopia causes
1) mechanical (fracture) 2) disorders of extraocular muscles (thyroid disease, orbital myositis) 3) disorders of neuromuscular jxn (myasthenia) 4) disorders of CN III, IV, VI and central pathways
what can cause monocular diplopia or polyopia
opthalmological disease, disorders of visual cortex, or psychiatric conditions
extropia
abnormal lateral deviation of one eye
estropia
abnormal medial deviation of one eye
hypertropia
vertical deviation of one eye with respect to other eye
phoria
mild weakness present only with an eye covered (instead of tropia)
remaining movements of eye with complete disruption of CN III and resting position
some abduction (abducens) and some depression and intorsion (superior oblique); eye down and out at rest with complete ptosis and dilated pupil unresponsive to light
red glass testing with 3rd-nerve palsy
diagonal diplopia most severe when looking up and medially with affected eye
common causes of oculomotor nerve palsy
diabetic neuropathy and head trauma (shear forces); compression by intracranial aneurysms; infection, tumor, venous thrombosis, herniation of medial temporal lobe
what aneurysms tend to affect CN III
jxn of Pcomm with internal carotid; less common = jxn Pcomm and PCA, basilar & PCA jxn, or basilar & SCA jxn
what do aneurysms classically cause
painful oculomotor palsy that involves the pupil; may be subtle or complete
what is complete oculomotor palsy that spares the pupil usually caused by
diabetes
trochlear nerve palsy
vertical diplopia (normally causes depression and intorsion of eye)
how do ppl with trochlear nerve palsy compensate
looking up (chin tuck) and tilting head away from affected eye (compensate for hypertropia and extorsion)
when is depressing action of superior oblique most pronounced
when eye is adducted
head movement and eye abnormalities
moves in same direction normally served by the affected muscle
causes of vertical diplopia
trochlear nerve palsy, myasthenia gravis, lesions of superior division of CN III (superior rectus), and skew deviation
skew deviation
vertical disparity in the position of the eyes of supranuclear origin; relatively constant in all positions of gaze (unlike trochlear palsy)
what can cause skew deviation
lesions of cerebellum, brainstem, or inner ear
causes of head tilt
trochlear palsy, cerebellar lesions, meningitis, incipient tonsillar herniation, and torticollis
diplopia in abducens nerve lesions
horizontal diplopia; sometimes estropia present
what is abducens palsy an important early sign of and why
supratentorial or infratentorial tumors, pseudotumor cerebri, hydrocephalus, and other intracranial lesions; due to susceptibility of injury from downward traction caused by elevated ICP
gaze palsy
movements of both eyes in one direction are decreased
causes of horizontal diplopia
abducens palsy, myasthenia gravis, disorders of extraocular muscles
location of edinger-westphal nuclei
just dorsal and anterior to the oculomotor nuclei near midline
where do preganglionic parasympathetic fibers travel bilaterally from the edinger-westphal nuclei to
go via oculomotor nerves to reach ciliary ganglia in orbit
3 components of accomodation response
pupillary constriction, accomodation of lens ciliary muscle, and convergence of the eyes
what occurs when the ciliary muscle contracts
causes suspensory ligament to relax producing a rounder, more convex lens shape
where does the descending sympathetic pathway activate preganglionic sympathetic neurons involved with pupil dilation
intermediolateral cell column of upper thoracic cord
how do preganglionic sympathetic neurons of pupil dilation get to pupil
exit spinal cord via ventral roots of T1-2 and join paravetebral sympathetic vhain via white rami communicantes; synapse in superior cervical ganglion and ascend through carotid plexus along wals of internal carotid artery
anisocoria
pupillary asymmetry
classic horner's syndrome
ptosis, miosis, and anhidrosis along with several other minor abnormalities; due to disruption of sympathetic pathways
anisocoria in oculomotor vs horner's
horner's more obvious in dark, oculomotor more in ambient light
horners and light reflexes
still has direct and consensual response to light; dilation lag relative to normal pupil when light removed
ciliospinal reflex
painful pinch to neck activates sympathetic outflow, causing pupillary dilation on normal side but not on side with Horner's syndrome
anhidrosis
decreased sweating of ipsilateral face and neck in horner's; skin feels smoother due to decreased moisture
posible locations for Horner's syndrome lesions
1) lateral brainstem 2) spinal cord 3) T1-2 roots 4) sympathetic chain 5) carotid plexus 6) cavernous sinus 7) orbit
pontine pupils
both pupils and small but reactive to light; probably caused by bilateral disruption of descending sympathetic pathways
Afferent Pupillary Defect (Marcus Gunn Pupil)
direct response to light in affected eye is decreased or absent while consensual response of affected eye in opposite eye is normal
where are lesions located in Marcus Gunn pupil
lesions in front of optic chiasm
hippus
normal brief oscillation of pupil size that sometimes occurs in response to light
opiates and pupils
bilateral pinpoint pupils
barbituate OD pupils
bilateral small pupils, mimickng pontine lesions
anticholinergic agents affecting muscarinic receptors (atropine or scopolamine) and pupils
dilated pupils
pilocarpine eyedrops are useful when what is suspected
anticholinergic agents; cause pupillary constriction in parasympathetic lesions, but can't overcome pharm muscarinic blockade
light-near dissociation
pupils constrict much less in response to light than to accomodation
example of light-near dissociation
Argyll Robertson pupil associated with neurosyphilis (pupils small and irregular as well); diabetes, Adie's myotonic pupil, Parinaud's syndrome
Adie's myotonic pupil
degeneration of the ciliary ganglion or postganglionic parasympathetic neurons resulting in mid-dilated pupil that reacts poorly to light
Midbrain Corectopia
pupil assumes irregular, odd-center shape; rare
muscle of eye closure
orbicularis oculi (CN VII)
ptosis vs facial muscle weakness
ptosis upper lid comes down further over iris in affected eye; facial weakness palpebral fissure widened due to sagging of lower lid
what does cavernous sinus drain
eye, superficial cortex
what layer does the cavernous sinus lye
btwn periosteal and dural layers of dura mater-like the other venous sinuses
nerve closest to carotid in cavernous sinus
abducens (III, IV, and V1 also in sinus)
what nerve skirts the lower portion of the cavernous sinus and often runs through it for a short distance
V2-exits via forament rotundum
orbital apex
region where nearly all nerves, arteries, veins or orbit converge b4 communicating with intracranial cavity via optic canal and superior orbital fissure
orbital apex vs cavernous sinus lesions
same deficits, but more likely to involve CN II also
saccades
rapid eye movements reaching velocities up to 700 degrees per second; fxn to bring tagets of interest into field of view
vision during saccade
transiently suppressed
smooth pursuit eye movements
not under voluntary control; reach velocities of 100 degrees/s; allow stable viewing of moving objects
vergence eye movements
maintain fused fixation by both eyes as targets toward or away from viewer; velocity ~20 degrees/s
reflex eye movement examples
optokinetic nystagmus and vestibulo-ocular reflex
nystagmus
rhythmic form of reflex eye movements composed of slow eye movements in one direction interrupted repeatedly by fast saccadelike eye movements in opposite direction
what interconnects the oculomotor, trochlear, abducens, and vestibular nuclei
medial longitudinal fasciculus (MLF)
abducens nucleus fxns as
horizontal gaze center controlling horizontal movement of both eyes in direction ipsilateral to side of nucleus (some fibers project to ipsilateral lateral rectus and some to contralateral oculomotor nucleus)
paramedian pontine reticular formation (PPRF)
horizontal gaze center; provides input from cortex and other pathways to abducens nucleus
lesion of abducens nucleus causes
ipsilateral gaze palsy involving both eyes because of connections through MLF
lesions of MLF and horizontal eye movements
interrupt input to medial rectus; eye ipsilateral to lesion does not fully adduct on attempted horizontal gaze, also nystagmus of opposite eye (unknown reason)
internuclear ophthalmoplegia (INO)
classic neurologic syndrome produced by MLF lesion
where are brainstem centers for vertical eye movements
rostral midbrain reticular formation and pretectal area; ventral portion=downgaze and dorsal = upgaze
nucleus for downgaze
rostral interstitial nucleus of MLF; also Darkschewitsch and interstitial nucleus of Cajal
what controls vergence
descending inputs from visual pathways in occipital and parietal cortex
Parinaud's syndrome cause
constellation of eye abnormalities usually seen with lesions compressing the dorsal midbrain and pretectal area
Parinaud's syndrome 4 components
1) impairment of vertical gaze, especially upgaze 2) large, irregular pupils that don't react to light 3) eyelid abnormalities 4) impaired convergence and sometimes convergence-retraction nystagmus
most common cause of Parinaud's
pineal region tumors and hydrocephalus
hydrocephalus and eyes in kids
bilateral setting-sun sign; eyes deviate inward due to bilateral 6th verve palsies and downward due to Parinaud's syndrome
frontal eye fields
generate saccades in contralateral direction via connections to contralateral PPRF
parieto-occipito-temporal cortex and eye movements
smooth pursuit in ipsilateral direction via connections with vestibular nuclei, cerebellym, and PPRF
optokinetic nystagmus (OKN) is elicited how
moving a thick ribbon with vertical stripes horizontally in front of the eyes; eyes alternate btwn smooth persuit and saccades
slow phase of OKN is mediated by
ipsilateral posterior cortex with connections to vestibular nuclei and flocculonodular lobe of cerebellum projecting to PPRF and abducens nuclei
fast phase of OKN is mediated by
frontal eye fields projecting to contralateral PPRF
vestibulo-ocular reflex (VOR)
stabilizes eyes on the visual image during head and body movements
how is VOR tested
oculocephalic maneuver or cold water calorics