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43 Cards in this Set

  • Front
  • Back
mvmt in, toward nose. medial rectus, CN III
elevation w/ adduction
inferior oblique, CN III
depression w/ adduction
superior oblique, CN IV
movement out, away from nose. lateral rectus, CN IV
elevation w/ abduction
superior rectus, CN III
depression w/ abduction
inferior rectus, CN III
deviation of the eye away from the direction of action of the affected eye muscle when the fx of one eye muscle is affected
double vision
optic nerve swelling
light-near dissociation
impaired pupillary rx to light w/ preserved pupillary constriction during accommodation
Argyll Robertson pupils
unequal irregular pupils
tonic pupil
unilateral (most often) dilated pupil
Horner's syndrome
unilateral small pupil and slight ptosis (drooping eyelid)
reactive afferent pupillary defect (Marcus Gunn pupil)
greater constriction in response to illumination of contralateral pupil than to direct illumination of pupil
lid retraction
elevation of eyelid
transient monocular blindness (amaurosis fugax)
maximal for 1-5 min and resolves over 10-20 min; probably due to emboli in retinal arteries
optic neuritis (monocular d/o)
inflammation of the optic nerve. unilateral reduction in visual acuity; many causes, cd be early sign of MS
giant cell arteritis (monocular d/o)
sudden total loss of vision in one eye; usu accompanied by systemic sxs- fever, malaise, night sweats, wt loss, h/a
papilledema (binocular d/o)
optic nerve swelling assoc w/ increased intracranial pressure
chiasmal lesions
bitemporal hemianopia
optic tract and LGN
noncongruous (i.e., defect not the same in both eyes) homonymous hemianopia
optic radiations
congruous and homonymous (bilaterally symmetric). In TL, deficit is superior quadrantanopia. In PL, inferior quadrantanopia or homonymous hemianopia
occipital cortex lesions
contralateral homonymous hemianopia. bilateral lesions - cortical blindness, may have preserved macular fx (tunnel vision).
anton's syndrome
denial of blindness (cortical damage)
visual (associative or true) agnosia
normal visual perception gives evidence of not knowing the meaning of visual stimuli; lack of recognition (give verbal test and visual test, i.e., what is it and copy it)
note- may also have achromatopsia. also- agnosia also implies nonverbal anterograde amnesia and visual learning defects
visual "apperceptive" agnosia
deficit in perception, not just recognition. pts will fail visual perception tests; may or may not have achromatopsia.
intact generic recognition. not just facial recognition, but specific members of a group with visually ambiguous stimuli. interference or destruction of records relevant to the face
usu bilat and symmetrical. inferior and mesial visual association cortices in the lingual and fusiform gyrus or their subadjacent white matter. possible lateralization of fx- R has some recognition of photographs and poor real-time recog. L "deep prosopag" recognize grp but not individual.
prosopagnosia (etiology)
usu CVA posterior cerebral artery occlusion, tumors, esp gliomas that become bilat via splenium of CC. Also ictal phenomenon.
facial expression deficit
bilateral amygdala damage
visual object agnosia
prosopag w/ inability to recognize class to which it belongs, w/ or w/o optic aphasia (visual naming), alexia. S.t. rotating object will lead to recognition, called "static visual agnosia"
visual agnosia (etiology)
dorsal and lateral extension of bilateral lesions in the ventral and mesial occipitotemporal visual areas
category-specific object agnosia
difficulty recognizing objects only w/in a certain category
pure alexia (w/o agraphia)
impaired reading of most words and sentences, st impaired ability to read single letters, can copy what they can't read, commonly assoc w/ right homonymous hemianopsia
pure alexia (etiology)
disconnection b/w T-P language related dominant cortices and both visual cortices. CC lesion prevents interhemispheric connection, L OL lesion prevents info from going from L visual cortex to L lenguage center
d/o of spatial (topographic) orientation
infrequent and involve bilat or R posterior lesions; geographic disorientation is more frequent and can result from unilat or bilat posterior lesions
central achromatopsia
acquired d/o of color perception involving all or part of visual field, w/ relative preservation of form, caused by focal damage of visual assoc cortex or its subadjacent white matter
central achromatopsia (characteristics)
color can be completely or partially lost. differential cone sensitivites (protan =red, deutan = green, tritan = blue/yellow) greatest vulnerability of tritan dimension. may lose color perception below a certain size and may have diminuation of color constancy effect
full field achromatopsia
usu with visual agnosia, esp prosopag, usu with a field impairment, st with pure alexia, always with bilat O-T lesions
hemiachromatopsia (left)
unilat R O-T lesion, in ventral visual assoc cortex, including fusiform and lingual gyri
hemiachromatopsia (right)
unilat L O-T lesion, possible alexia, possible visual field impairment
etiology (color perception deficits)
usu infarct of psoterior cerebral artery; hemianopsia more common than hemiachromatopsia, since primary visual cortex and optic radiations more likely to be damaged than spared in an infarct that affects O-T region.
color naming d/o (manifests as naming and agnosia)
failure to name colors or to point to colors given their name, in the absence of a demonstrable defect of color perception or of aphasia