Transcript Visual field defect

CHAPTER-11: VISUAL SYSTEM
Najwa Al-Bustani
Neurology AHD
February 9-2011
EYES & RETINA:


Light >> lens >> retina
(inverted and reversed
image).
Right part of visual
space >> project to left
hemiretina of each eye,
vice versa.
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.
EYES & RETINA:


Optic disc: region
where axons leaving
the retina gather to
form the Optic 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.
PHOTORECEPTORS:


Rods: more numerous than
cons-20:1, have poor spatial
& temporal resolution of
visual stimuli, do not
detect colors >> vision in
low level lighting
conditions.
Cons: less numerous,
much more highly
represented in the fovea >>
have high spatial &
temporal resolution >>
they detect colors.
OPTIC NERVE, CHIASM AND TRACT:
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 the
calcarine fissure:
 Upper bank >> fibers from upper O.R.
 Lower bank >> fibers from lower O.R.

VISUAL PROCESSING PATHWAYS:
Dorsal Pathway:
Project to parietooccipital ass.
Cortex.
Ventral Pathway:
Project to occipitotemporal ass.
Cortex.
VISUAL DISTURBANCE –
LOCALIZATION:

Nature of visual disturbance: time course,
positive/negative phenomenon.

Description of regions of visual field for each eye.

Visual acuity.
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.

POSITIVE PHENOMENON:
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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.
POSITIVE PHENOMENON:


1.
2.
3.
4.
5.
6.
7.
8.
Formed visual hallucination: people, animals or
complex scenes >> arise from inferior temporooccipital visual association cortex.
Causes:
Toxic or metabolic disturbance.
Withdrawal from alcohol or sedatives.
Focal seizures.
Complex migraine.
Neurodegenerative diseases: CJD, LB disease.
Narcolepsy.
Midbrain ischemia >> peduncular hallucinosis.
Psychiatric disorders: less common than auditory.
CLINICAL CORRELATION:

Different field defect:
starting from optic
nerve >>> visual
cortex.
Describe the visual field defect ?
OPTIC NERVE-TYPE FIELD DEFECTS:


1.
2.
3.
Retinal fibers enter
optic discs in a
specific manner.
Nerve fiber
bundle (NFB)
defects are of the
following:
Papillomacular
bundle.
Sup. & Inf. Arcuate
bundle.
Nasal bundle.
PAPILLOMACULAR BUNDLE:
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1.
2.
3.
Macular fibers that enter the temporal aspect
of the disc.
Defect, result in the following:
Central scotoma: defect covering central
fixation.
Centrocecal scotoma: a central scotoma
conneted to the blind spot.
Paracentral scotoma: defect of some of the
fibers of the papillomacular bundle lying next
to, but not involving central fixation.
PAPILLOMACULAR BUNDLEDEFECTS:
ARCUATE NFB:
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
1.
2.
3.
4.
Fibers from the retina temporal to the disc
enter the superior and inferior poles of the
disc.
Defects, result in the following:
Arcuate scotoma: due to involvement of
arcuate NFB (extend from blind-spot).
Seidel scotoma: defect in the proximal
portion of the NFB >> comma-shaped
extension of the blind spot.
Nasal step: defect in distal portion of the
arcuate NFB (respect the horizontal meridian).
Isolated scotoma within arcuate area:
defect of the intermediate portion of the
arcuate NFB.
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.
CLINICAL PEARLS:
1.
Lesions at or behind the chiasm tend to cause
hemianopic field defects originating from the point
of fixation and respecting the vertical meridian.
2.
Optic nerve lesions cause field defects corresponding
to one of the 3 major NFB defects.

NFB defects originate from the blind spot, not from
the fixation point, & do not respect the vertical
meridian, but do respect the nasal horizontal
meridian.
KEY Q.: IN A PATIENT WITH
QUADRANTIC FIELD DEFECT: DOES
THE FIELD DEFECT GO TO FIXATION
OR TO THE BLIND SPOT ?
Describe the visual field defect ?
Junctional scotoma: lesion at junction of
optic nerve and chiasm
Describe the visual field defect ?
Bitemporal Homonymous Hemianopia
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, temporal
fibers remain uncrossed.
Chiasmal lesion >> bitemporal
hemianopia.
RULES OF THE ROAD FOR THE 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 of
fibers from the nerves through
the chiasm into the tract.
RULES OF THE ROAD FOR THE 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.
Describe the visual field defect ?
OPTIC TRACT DEFECTS:
1.
All retrochiasmatic lesions result in a contralateral
homonymous hemianopia.
2.
Congruity describes incomplete homonymous
hemianopic defects that are identical in all
attributes: location, shape, size, depth, slope of
margins.
3.
Remember: the more posterior ‘toward the occipital
cortex’ the lesion in the postchiasmal visual
pathways, the more likely the defects will be
congruous.
Describe the visual field defect ?
Left sector sparing homonymous hemianopia
>> lesion at LGN.
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.
LGN FIELD DEFECTS:
1.
Incongruous homonymous hemianopia.
2.
Unique sector & sector-sparing defects
due to dual blood supply of LGN from
anterior & posterior choroidal arteries.
Describe the visual field defect ?
Right superior quadrantanopia >>
temoporal lobe lesion
Describe the visual field defect ?
Left inferior quadrantanopia >> parietal
lobe lesion
Describe the visual field defect ?
CENTRAL HOMONYMOUS
HEMIANOPIA:
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In visual cortex, the macular representation, is
located on the tips of the occipital lobes.
A lesion affecting the tip of the occipital lobe
tends to produce a central homonymous
hemianopia.
Describe the visual field defect ?
Left homonymous hemianopia with
macular sparing
MACULAR SPARING:
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Watershed area with respect to
blood supply.
The ‘macular’ visual cortex is
supplied by terminal branches
of posterior & middle cerebral
arteries.
Visual cortex subserving the
midperipheral & peripheral
field is supplied only by the
PCA. The area is supplied by a
more proximal ‘not terminal’
vessel.
Describe the visual field defect ?
BILATERAL HOMONYMOUS
WITH MACULAR SPARING:
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1.
2.
3.
4.
5.
Differential Diagnosis:
Non-organic visual field loss.
Glaucoma.
Optic disc drusen.
Post-papilledema optic atrophy.
Retinitis pigmentosa.
HEMIANOPIA
Optic disc drusen: globules of
mucoproteins and
mucopolysaccharides that
progressively calcify in the optic
disc.
Retinitis Pigmentosa
Describe the visual field defect ?
Left incongruous homonymous hemianopia
Describe the visual field defect ?
Right congruous homonymous hemianopia
CONGRUITY:
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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 hemianopia cannot be
categorized as ‘’congruous’’ because it is complete.
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).
Describe the visual field defect ?
Enlarged Blind Spot
FUNDS EXAM. OF PREVIOUS
PATIENT:
Papilledema
PAPILLEDEMA-OPHTHALMIC
EXAM.:

V.A: retained because visual loss from papilledema
develops first in the visual field remote from the point
of fixation, unless optic nerve damage is severe.

VF: enlargement of the blind spots.
Visual field loss often occurs in the peripheral nasal
visual field first, eventually encroaching on the center
of the visual field in severe cases.

Pupils: generally normal (there is no afferent
pupillary defect).

EOM: normal/CN XI palsy.

PAPILLEDEMA- FUNDUS:
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Early Manifestation:
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Disc hyperemia.
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Obscuration of the optic disc margins: affecting the
inferior and superior poles of the nerve first, followed
by the nasal portion of the nerve and lastly by the
temporal nerve.
Splinter hemorrhage ‘hemorrhage within NFL’.
Absent venous pulsation (if pulsation present >> CSF
P. less than 20 cm), 20% of normal patients have
absent venous pulsation >>> helpful only if present.
PAPILLEDEMA-FUNDUS:
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
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Late Manifestation:
Nerve fiber layer swelling eventually obscures
the normal disc margins and the disc becomes
grossly elevated.
Venous congestion develops, and peripapillary
hemorrhages become more obvious, along with
exudates and cotton-wool spots.
The peripapillary sensory retina may develop
concentric or, occasionally, radial folds known as
Paton 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).
25 YR F, C/O LT. EYE BLURRING OF
VISION/COLORS, ? PAIN ON MOVING THE
EYE X 3 DAYS ?
HER FUNDUS EXAM. & VF ?
OPTIC NEURITIS:

Primary inflammation of optic nerve.

2 clinical forms of optic neuritis:
Papillitis: intraocular form in which disc
swelling is present.
2. Retrobulbar neuritis: optic disc appears
normal and inflammatory lesion along course of
optic nerve is behind globe.
1.
OPTIC NEURITIS:
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Pain: periocular, retrobulbar, tenderness of the
globe, 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.
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.

OPTIC NEURITIS-FUNDUS EXAM.:
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Normal (60%), especially when the inflammation is
retrobulbar.
Papillitis >> inflammation of the anterior optic nerve
causes disc swelling, and sometimes hemorrhages, cells in
the 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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