Brain And Behavior 2011- Visual System And Deficits

Front 1

dorsal stream (aka, pathway)

Back 1

"where" or "motion" pathway; M cells retina -> LGN 1/2 -> Layer IVC alpha in V1 -> Layer IVB in V1 -> V2 thick stripes -> MT (V5) -> MST/LP -> PPA

Front 2

ventral stream (aka, pathway)

Back 2

"what" pathway; P cells retina -> LGN 3-6 -> Layer IVC beta in V1 -> Layer II/III in V1 (CO blobs) -> V2 thin stripes and interstripes -> V4 (lingual and fusiform gyri) -> ITC

Front 3

Meyer's loop

Back 3

inferior optic radiations -> supply inferior V1; carry info from inferior retina (superior visual field); often lesioned during epilepsy surgery or in herpes to cause upper quadrantanopsia

Front 4

pituitary tumor

Back 4

compresses optic chiasm -> bitemporal hemianopia (no temporal vision)

Front 5

PCA stroke

Back 5

homonymous hemianopia sparing macula (macula receives dual blood supply from MCA)

Front 6

alexia without agraphia

Back 6

can write but not read; usually associated with right homonymous hemianopia; need two lesions - one affecting corpus collosum (so no info from R V1 can be sent to language centers on L) and one affecting left V1 (either occipital lobe lesion or optic radiations -> this is what gives us right homonymous hemianopia)

Front 7

associative visual agnosia

Back 7

inability to recognize objects because of defect in ventral "what" stream; medial occipital-temporal (often bilateral) affecting the inferior longitudinal fasculus

Front 8

prosopagnosia

Back 8

inability to recognize faces; occipital-temporal (fusiform face area)

Front 9

cerebral hemi-achromatopsia

Back 9

lack of color vision in homonymous hemifield, usually coupled with upper quadrantanopsia; affects V4 (fusiform and lingual gyri in inferior occipital lobe) and probably parts of inferior V1 (thus giving upper quadrantanopsia on the same side as color defect)

Front 10

hemi-neglect

Back 10

ignore objects, usually in left hemispace; localized to right (posterior) parietal lobe usually ("where" pathway)

Front 11

Balint's syndrome

Back 11

simultanagnosia (can't recognize whole scene), ocular apraxia (can't move eyes to target), optic ataxia (can't reach under visual guidance); caused by bilateral parieto-occipital lesions; Alzheimer's can be associated with Balint's

Front 12

Akinetopsia

Back 12

can't detect motion; localized to lateral occipital-temporal-parietal junction (V5)

Front 13

consensual response to light

Back 13

retina -> optic nerve -> optic chiasm -> bilateral optic tracts -> bilateral pretectal nuclei -> bilateral edinger westphal nuclei -> bilateral CN III; two crosses: first at optic chiasm, leading to bilateral pretectal nuclei, second at pretectal nuclei, with each nuclei sending axons to both bilateral EW nuclei

Front 14

near triad

Back 14

convergence, miosis, accomodation

Front 15

light reflex vs near response

Back 15

94% of parasymp fibers are for near response, only 6% for light reflex; thus if near response is affected, light reflex usually is too but not vice-versus (Argyll Robertson pupil accommodates but doesn't react)

Front 16

afferent pupil defect

Back 16

almost always CN II problem - can't be bilateral (it's a relative problem); usually causes dilated pupil when light it shined in affected eye (paradoxical dilation)

Front 17

Horner's anisocoria

Back 17

anisocoria is greater in dark (abnormally constricted eye can't dilate, or has dilation lag), constricted eye has slight ptosis

Front 18

ptosis causes (3)

Back 18

levator dehiscence (mechanical) from contact lens or cataract surgery; mypoathic (i.e. myasthenia gravis); neurogenic (i.e. oculomotor palsy or Horner's)

Front 19

cocaine test

Back 19

cocaine causes NE reputake to be inhibited and thus pupils to dilate (more sympathetic input); if sympathetic neuron is damaged than no NE released so cocaine has no affect (no dilation)

Front 20

sympathetic pathway

Back 20

first neuron: hypothalamus to C8-T1; second neuron: travels under lower branch of brachial plexus, over lung apex, and synapses in superior cervical ganglion; third neuron: travels with ICA, jumps on nasociliary nerve of V3 (pupil dilator), or travels into cavernous sinus with carotid plexus and joins III to reach Muller's muscles of upper and lower eyelids

Front 21

1st order Horner's syndrome

Back 21

affects neuron from hypothalamus to C8-T1 in brainstem and spinal cord -> likely to see other ipsi CN problems or crossed sensory/motor problems if other tracts affected (travels with spinothalamic tract so likely to affect that)

Front 22

2nd order Horner's syndrome

Back 22

affects neuron that travels under lower branch of brachial plexus, over lung apex, and synapses in superior cervical ganglion; may be only sign of apical (Pancoast) lung tumor; likely to see signs of ipsi LMN dysfunction due to brachial plexus involvement

Front 23

3rd order Horner's syndrome

Back 23

affects neuron that travels up ICA to effector muscles; may result with cartoid dissection (painful Horner's)

Front 24

carotid dissection occurs with...

Back 24

3rd order Horner's

Front 25

Pancoast tumor occurs with...

Back 25

2nd order Horner's

Front 26

painful Horner's most likely

Back 26

carotid dissection with 3rd order Horner's

Front 27

pharmocologic pupil

Back 27

doesn't constrict to near, to light, or to pilocarpine

Front 28

ciliary ganglion pupil

Back 28

produces large tonic pupil - no reaction to light, tonic response to near (b/c more fibers dedicated to near than light), and supersensitivity to dilute pilocarpine

Front 29

Adies pupil (8)

Back 29

tonic (large) pupil - no reaction to light, slow response to near (b/c more fibers dedicated to near than light), and supersensitivity to dilute pilocarpine (normal pupil doesn't constrict but Adies does); young females 20-30; follows ciliary ganglion injury; distinguish from pharmacologic because constriction to near is conserved; Adies patients also have absent deep reflexes

Front 30

isolated pupil involving CN III palsy

Back 30

aneurysm until ruled out - us. at junction of PComm and ICA

Front 31

syphilis

Back 31

Argyll Robertson pupil -> accomodates briskly but doesn't react

Front 32

Argyll Robertson pupil

Back 32

associated with syphylis, dorsal midbrain lesion, or diabetes; accommodates briskly but doesn't react; distinguish from Aides bec. Adies responds slower to near response (although it responds eventually) while AR pupil has a brisk near response

Front 33

cataract

Back 33

lens clouding

Front 34

glaucoma

Back 34

10% closed angle - quick and painful (emergency!); 90% open angle - chronic, less likely to be caught before blindness, causes incr. P b/c of reduced flow through trabecular mesh

Front 35

myopia

Back 35

nearsighted, due to light convergence in front of retina

Front 36

hyperopia

Back 36

farsighted, due to light convergence behind retina

Front 37

astigmatism

Back 37

light doesn't converge properly

Front 38

SCN

Back 38

circadian rhythms - 1% RGCs project here

Front 39

binocular overlap zone

Back 39

120 degrees, from 60 degrees left to 60 degrees right

Front 40

LGN layers

Back 40

1,2 M cells; 3-6 P cells; 1,4,6 contra; 2,3,5 ipsi; ON and OFF separated in P layers

Front 41

first binocular cells in visual system

Back 41

IVB M cells -> binocular, stereoscopically selective, direction selective, orientation selective (pinwheels), ocular dominance columns