Visual System - Albustani

8/18/2019 Visual System - Albustani

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Najwa Al-BustaniNajwa Al-Bustani

Neurology AHDNeurology AHD

February 9-2011February 9-2011


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EYES & RETINA:

Light >> lens >> retina

(inverted and reversed

image).

Right part of visual

space >> project to left

hemiretina of each eye,vice versa.


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EYES & RETINA:

Fovea:central

fixation point of each

eye// region of the

retina with highest

visual acuity.

Macula:oval region

approximately 3-5 mm

that surrounds the

fovea, also has high

visual acuity.


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EYES & RETINA:

Optic disc:region

where axons leaving

the retina gather to

form theOptic nerve.

There are no

photoreceptors over the

optic disc >> creates

small blind spot located

15° lateral and inferior

to central fixation point

of each eye.


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PHOTORECEPTORS:

Rods:more numerous thancons-20:1, have poor spatial& temporal resolution ofvisual stimuli, do not detectcolors >> vision in low level

lighting conditions.

Cons:less numerous, muchmore highly represented in

the fovea >> have highspatial & temporalresolution >> they detectcolors.


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OPTIC NERVE, CHIASM AND TRACT:


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VISUAL PATHWAY:

Meyer’s Loop: fibers of inferior optic radiation arc

into the temporal lobe >>> lesion >>> ‘’Pie in the

sky ‘’.

Upper optic radiation fibers pass into the parietal

lobe >>> lesion >>> ‘’Pie in the floor’’.

Primary visual cortex lies on the bank of thecalcarine fissure:

Upper bank >> fibers from upper O.R.

Lower bank >> fibers from lower O.R.


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VISUAL PROCESSING PATHWAYS:Dorsal Pathway:

Project to parieto-

occipital ass.Cortex.

Ventral Pathway:

Project to occipito-

temporal ass.

Cortex.


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VISUAL DISTURBANCE –

LOCALIZATION:

Nature of visual disturbance: time course,

positive/negative phenomenon.

Description of regions of visual field for each eye.

Visual acuity.


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TERMINOLOGY:

Binocular/monocular.

Negative Phenomenon:

Scotoma:a circumscribed region of visual loss.

Homonymous defect: visual field defect in the

same region for both eyes.

Positive Phenomenon:simple or formed.Simple visual phenomenon:light, colors,

geometric shapes >> disturbance anywhere from

the eye to primary visual cortex.


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POSITIVE PHENOMENON:

Light flashes >> retinal detachment.

Rainbow-colored halos around objects >> acute

glaucoma.

Migraine: visual blurring, scotoma that have

scintillating appearance or consist of jagged

alternating light and dark zigzag lines

(fortification scotoma).

Pulsating colored lights/moving geometric shapes

>> occipital seizures.


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POSITIVE PHENOMENON:

Formed visual hallucination:people, animals orcomplex scenes >> arise from inferior temporo-occipital visual association cortex.

Causes:

1.Toxic or metabolic disturbance.

2.Withdrawal from alcohol or sedatives.

3.Focal seizures.

4.Complex migraine.

5.Neurodegenerative diseases: CJD, LB disease.6.Narcolepsy.

7.Midbrain ischemia >> peduncular hallucinosis.

8.Psychiatric disorders: less common than auditory.


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Different field defect:

starting from optic

nerve >>> visual cortex.


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Describe the visual field defect ?


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OPTIC NERVE-TYPE FIELD

DEFECTS:

Retinal fibers enteroptic discs in aspecific manner.

Nerve fiberbundle (NFB)defects are of thefollowing:

1. Papillomacularbundle.

2. Sup. & Inf. Arcuatebundle.

3. Nasal bundle.

http://pn.bmj.com/content/9/6/324/F2.large.jpg


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PAPILLOMACULAR BUNDLE:

Macular fibers that enter the temporal aspectof the disc.

Defect, result in the following:

1. Central scotoma:defect covering centralfixation.

2. Centrocecal scotoma:a central scotomaconneted to the blind spot.

3. Paracentral scotoma: defect of some of thefibers of the papillomacular bundle lying nextto, but not involving central fixation.


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PAPILLOMACULAR BUNDLE-

DEFECTS:


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ARCUATE NFB:

Fibers from the retina temporal to the discenter the superior and inferior poles of thedisc.

Defects, result in the following:

1. Arcuate scotoma:due to involvement ofarcuate NFB (extend from blind-spot).

2. Seidel scotoma:defect in the proximalportion of the NFB >> comma-shapedextension of the blind spot.

3. Nasal step:defect in distal portion of thearcuate NFB (respect the horizontal meridian).

4. Isolated scotoma within arcuate area:defect of the intermediate portion of thearcuate NFB.


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NASAL NFB:

Fibers that enter the nasal aspect of the

disc, course in a straight ‘nonarcuate’

fashion.

Defect:results in a wedge-shaped temporal

scotoma arising from the blind spot and

does not necessarily respect the temporal

horizontal meridian.


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KEY Q.: IN A PATIENT WITH

QUADRANTIC FIELD DEFECT:DOES THE FIELD DEFECT GO

TO FIXATION OR TO THE

BLIND SPOT ?


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Junctional scotoma: lesion at junction of

optic nerve and chiasm


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Bitemporal Homonymous Hemianopia


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RULES OF THE ROAD FOR THE

OPTIC CHIASM:

1. Nasal retinal fibers (including the

nasal half of the macula) of each eye

cross in the chiasm to the

contralateral optic tract, temporalfibers remain uncrossed.

Chiasmal lesion >> bitemporalhemianopia.


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OPTIC CHIASM:2. Lower retinal fibers project

through the optic nerve &

chiasm to lie laterally in the

tracts: upper retinal fibers will

lie medially.

There is a 90- degree rotation offibers from the nerves through

the chiasm into the tract.


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OPTIC CHIASM:

3. Inferonasal retinal fibers

cross into the chiasm & cross

anteriorly ~ 4mm in the

contralateral optic nerve(Wilbrand’s knee) before

turning back to join

uncrossed inferotemporal

temporal fibers in the optic

tract >> junctional

scotoma.


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OPTIC TRACT DEFECTS:

1. All retrochiasmatic lesions result in a contralateralhomonymous hemianopia.

2. Congruity describes incomplete homonymous

hemianopic defects that are identical in allattributes: location, shape, size, depth, slope ofmargins.

3. Remember: the more posterior ‘toward the occipitalcortex’ the lesion in the postchiasmal visualpathways, the more likely the defects will becongruous.


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Left sector sparing homonymous hemianopia

>> lesion at LGN.


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LGN FIELD DEFECTS:

Visual information from

ipsilateral eye synapses in

layers 2,3,5 /// from

contralateral in layers 1,2,6.

Macular vision is subserved

by the hilum and peripheral

field by the medial and

lateral horns.


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LGN FIELD DEFECTS:

1. Incongruous homonymous hemianopia.

2. Unique sector & sector-sparing defectsdue to dual blood supply of LGN from

anterior & posterior choroidal arteries.


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Right superior quadrantanopia >>

temoporal lobe lesion


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Left inferior quadrantanopia >> parietal

lobe lesion


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Left homonymous hemianopia with

macular sparing


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BILATERAL HOMONYMOUS

HEMIANOPIA WITH MACULAR

SPARING: Differential Diagnosis:

1. Non-organic visual field loss.2. Glaucoma.

3. Optic disc drusen.

4. Post-papilledema optic atrophy.

5. Retinitis pigmentosa.


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Optic disc drusen: globules of

mucoproteins and

mucopolysaccharides that

progressively calcify in the optic

disc.

Retinitis Pigmentosa


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Left incongruous homonymous hemianopia


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Right congruous homonymous hemianopia


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CONGRUITY:

It is due to the fact that a lesion affects nerve

fibers from corresponding retinal points that lie

adjacent to one another.

Congruous:when the defect is not complete (does

not occupy the entire half of the field) & the

defect extends to the same angular meridian in

both eyes.

Complete homonymous hemianopiacannot be

categorized as ‘’congruous’’ because it is complete.


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CONGRUITY:

Optic tract lesions tend to produce markedly

incongruous field defect.

The more congruous a homonymous hemianopia,

the nearer the lesion will be to the occipital

cortex (more posterior in the visual pathway).


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Enlarged Blind Spot


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FUNDS EXAM. OF PREVIOUS

PATIENT:

Papilledema


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PAPILLEDEMA-OPHTHALMIC

EXAM.:

V.A:retained because visual loss from papilledemadevelops first in the visual field remote from the pointof fixation, unless optic nerve damage is severe.

VF:enlargement of the blind spots. Visual field loss often occurs in the peripheral nasalvisual field first, eventually encroaching on the centerof the visual field in severe cases.

Pupils: generally normal (there is no afferentpupillary defect).

EOM:normal/CN XI palsy.


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PAPILLEDEMA- FUNDUS:

Early Manifestation:

Disc hyperemia.

Obscuration of the optic disc margins: affecting the

inferior and superior poles of the nerve first, followedby the nasal portion of the nerve and lastly by thetemporal nerve.

Splinter hemorrhage ‘hemorrhage within NFL’.

Absent venous pulsation (if pulsation present >> CSFP. less than 20 cm), 20% of normal patients haveabsent venous pulsation >>> helpful only if present.


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Late Manifestation:

Nerve fiber layer swelling eventually obscures thenormal disc margins and the disc becomes grosslyelevated.

Venous congestion develops, and peripapillaryhemorrhages become more obvious, along withexudates and cotton-wool spots.

The peripapillary sensory retina may developconcentric or, occasionally, radial folds known asPaton lines.

PAPILLEDEMA-FUNDUS:


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Chronic Manifestation:

If the persists for months >>> the disc hyperemia

slowly subsides, giving way to a gray or pale disc

that loses its central cup.

With time, the disc may develop small glistening

crystalline deposits (disc pseudodrusen).

PAPILLEDEMA-FUNDUS:


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25 YR F, C/O LT. EYE BLURRING OF

VISION/COLORS, ? PAIN ON MOVING THEEYE X 3 DAYS ?


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HER FUNDUS EXAM. & VF ?


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OPTIC NEURITIS:

Primary inflammation of optic nerve.

2 clinical forms of optic neuritis:

1. Papillitis:intraocular form in which disc

swelling is present.

2. Retrobulbar neuritis:optic disc appears

normal and inflammatory lesion along course ofoptic nerve is behind globe.


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OPTIC NEURITIS:

Pain:periocular, retrobulbar, tenderness of theglobe, pain especially with eye movement.

Contrast sensitivity is abnormal in nearly 90% of

patients with normal visual acuity.

Afferent pupillary defect.

Visual field defect:usually central scotoma,may be centrocecal or NFB defects.

Cells in vitreous with papillitis.


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OPTIC NEURITIS:

Chronological pattern of visual loss:

Rapid decrease in acuity during the first 2-3

days.

Stable level of decreased vision for 7-10 days.

Gradual improvement of vision.

Frequently returning to normal level within 2-3

months.


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OPTIC NEURITIS-FUNDUS EXAM.:

Normal (60%), especially when the inflammation isretrobulbar.

Papillitis >> inflammation of the anterior optic nerve

causes disc swelling, and sometimes hemorrhages, cells inthe vitreous, and deep retinal exudates.

After the neuritis resolves, the disc is often pale (optic

pallor), most commonly in the temporal aspect.

Atrophy is seen over time, especially after lesions that

cause poor visual acuity and slowed evoked potentials.


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