VISUAL PATHWAY

DEFECTS
PRESENTED BY:
1. SSEMAMBO JOSHUA
2. KYENKYA ANGEL
3. ALINITWE JOSELINE
The visual pathway.
• Visual pathway or optic pathway is the nervous pathway that
transmits impulses from retina to the visual center in cerebral
cortex for interpretation.
• It consists of; the optic nerve, optic chiasma, optic tracts, lateral
geniculate bodies, optic radiation and occipital cortex.
• Light passes through the outer layers of the retina to reach the
photoreceptors, which convert light into electrochemical signals.
• These signals are then processed by bipolar cells and transmitted
to the retinal ganglion cells, whose axons converge to form the
optic nerve.
• Each optic nerve exits the posterior pole of its respective eye,
carrying all visual information from that eye.
• The two optic nerves meet at the optic chiasm. At this point;
• Fibers from the nasal (medial) half of each retina (carrying
information from the temporal/peripheral visual field) cross over to
the opposite side.
• Fibers from the temporal (lateral) half of each retina (carrying
information from the nasal/central visual field) remain on the same
side.
• After the chiasm, the fibers form the optic tracts. Each optic tract
contains fibers from both eyes but carries information only for the
contralateral visual field.
• Majority of the optic tracts terminate in the LGN that organizes
visual information before transmitting it to the cerebral cortex.
• Axons from the LGN form the optic radiations that pass through the
internal capsule to reach the primary visual cortex.
VISUAL FIELDS
DEFINITION:
• The visual field is the entire area of space, or field of
vision, that is visible to the eyes when the gaze is fixed on
a single central point.
• It includes everything that can be seen above, below, and
to either side of the point of focus.
MAPPING OF VISUAL FIELDS
• CONFRONTATION METHOD
• PERIMETRY[AUTOMATED]
cont’d
• The image of an object in the visual field is inverted and
reversed right to left on retina. – Temperal field of the left eye
is seen by nasal retina of the left eye.
• Nasal field of the left eye is seen by temperal retina of the left
eye
• Superior field of the left eye is seen by inferior retina of the
left eye
• Inferior field of the left eye is seen by the superior retina of
the left eye.
• Similary the image is inverted and reversed for the right eye.
 Confrontation visual fields tests
• Mannual test where the examiner uses their hands or a small object
to test the patients peripheral vision. It involves the patient covering
one eye and focussing on a central point while the examiner moves
his/her hand or an object into the patients peripheral vision.
• Minimal equipment is needed ,takes about 2mins for a basic
screening.
• Its often used as a preliminary screening tool to detect gross visual
defects mostly in settings when automated equipment is not
available.
• It can identify significant defects but it is less sensitive and specific
compared to automated methods
 AUTOMATED VISUAL FIELDS
• A computerized test where the patient looks into a bowl-
shaped instrument called perimeter.
• Small lights Are flashed and the patient presses a button when
they see the light.
• Requires specialized equipment like aperimeter machine and
takes about 10 mins per eye.
• Provides a detailed visual field assesment,dentifying small
defects.
• Mostly used to mornitor diseases like glaucoma.
Visual field defects(Scotomas): These are areas of partial/complete loss of vision
within the visual field.
• They can be classified according to the pattern of loss or the location of the lesion.
According to the loss pattern as follows;
• Quadrantanopia: defective vision or blindness in approx. ¼ of visual field.
• Hemianopia: defective vision or blindness in one half of the vision field.
• Homonymous defect: visual defect is restricted to either the right or the left visual
fields.
• Heteronymous defects: defects involving parts of both the right and left visual
fields.
• Congruous defects: defects are equivalent in each monocular visual field.
• Incongruous defects: defects are not equivalent on each monocular field.
• Altitudinal defects: defects are in the upper an lower aspects of the visual fields.
• Based on the location of the lesion;
• Optic nerve lesion(before chiasm):results in monocular blindness.
(total loss of vision in the ipsilateral eye.)
• Optic chiasm lesion: commonly from pitutary tumor or
craniopharyngioma compression. There is damage to crossing
nasal fibres which affects tenporal fields resulting in bitemporal
hemaniopia.(loss of the temporal half of the visual field in both
eyes)
• Optic tract lesion(between chiasm & LGN): There is damage to
ipsilateral and contralateral nasal fibres resulting in Contralateral
Homonymous Hemianopsia the opposite visual field of both eyes.
• LGN or Optic Radiations Lesion:Result in quadratanopsias.
• Primary Visual Cortex (Occipital Lobe) Lesion: Damage to the
primary visual cortex (V1) at the back of the occipital lobe typically
causes a highly congruous homonymous hemianopsia.
Lesions in the visual pathway
• Patients with neural pathway visual loss must be evaluated
for additional neurological symptoms like;
– Optic nerve disorders; ION, Optic Neuritis, Papilloedema,
Congenital Abnormalities, Tumors(Meningioma, Glioma)
– Chiasimal disorders
– Retrochiasma disoreders
 OPTIC NERVE DISORDERS.
• These usually cause monocular vision loss and can be
inflammatory or ischemic.
• Optic neuritis is the major cause of optic nerve disease in young
adults whereas ischemic optic neuropathy is the most common
etiology in older adults.
Signs of optic nerve dysfuction
• Reduced visual aquity, relative afferent pupillary defect,
dischromatopia, diminished light brightness sensitivity,
diminished contrast sensitivity and visual field defect
 OPTIC NEURITIS
• This is inflammation of the optic nerve associated with a lot of
variety of conditions most notably MS.
• Most cases of demyelinating optic neuritis occurs more in women
between the ages of 20 and 40 years.
• Optic neuritis is highest in populations at high latitudes and lower in
areas closer to the equator.
• It can be classified basing on opthalmoscopic appearance and
etiology.
• Basing on opthalmoscopic appearance,it can be: retrobulbar
neuritis (not involving the optic head), papillitis (involving the optic
head)
 Basing on etiology;
Demyelinating optic neuritis
• Involves loss of the myeline sheath of optic nerve fibre ,due to phagocytosis by
microglia and macrophages,disrupting impulse transduction. It's common in
conditions like MS, isolated optic neuritis, devic disease and schilders disease.
Parainfectious opyical neuritis
• Usually associated with viral infections like chicken pox, mumps, measles occurring 1
to 2 wks after the infection, presents with papillitis and neuroretinitis usually
bilateral.
Infectious optical neuritis
• Associated with bacterial infections of the sinus, syphyllis, lyme disease usually
unilateral.
Non infectious optical neuritis
• No pathogen is involved, associated with autoimmune disoreders like sarcoidosis.
Clinical manifestations
Acute features
– Vision loss
– Eye pain:dull pain on ocular movement
– Afferent pupillary defect in affected eye
– Visual field defects
– Papillitis with hyperemia and disc edema
– Photopsias
– Dischromatopsia
Chronic features
– Persistent visual loss
– A relative afferent pupillary defect
– Optic atrophy
– Pattern shift visual evoked response remains delayed.

On Examination:
• Reduced VA.
• Relative Affarent Pupillary Defect.
• Swollen hyperemic nerve head w/ obliterated optic
cup(Papillitis)
diagnosis
• Diagnosis is clinically based on history and examination.
Investigations
– MRI
– Lumbar puncture
• Management depends on the etiology of the optical neuritis.
Involves use of systemic anti-inflammatory drugs;
Corticosteroids. Intravenous/ Oral Methylprednisolone.
• Complications include Optic Nerve Atrophy.
 Ischemic optic neuropathy
• Damage to the optic nerve due to interruption in blood supply
leading to severe sudden and painless vision loss.
• Infact at the optical disc may result into an altitudinal defect
• The occlusion may be anterior [affecting the optical disc ] AION
or posterior[retrobulbo]PION
• Etiologically it can be post operative arteretic eg GCA[giant cell
arteritis] or non arteretic.
 Clinical presentation
• Monocular or binocular vision loss
• Dischromatopsia
• Afferent pupillary defect
diagnosis
Diagnostic creteria are as follows;
– Acute deficit in visual aquity
– Ipsilateral pupillary defect
– Normal optic disc apperence at onset
– Exclusion of other causes
– Abnormal visual evoked response
– Normal electroretinogram
– Development of optic disc pallor within 4 to 8 weeks.
Investigations;
– Esr and crp
– Neuroimaging via MRI
 Papilloedema
• Swelling of the optic nerve head secondary to increased
intracranial pressure.
• All patients of papilloedema should be screened for a
intracranial mass.
• Its nearly always bilateral but it can be asymmetrical and usually
evolves in three stages ;early, established and chronic
Congenital Abnormalities:
• Optic nerve dysgenesis: group of congenital anomalies
resulting from the abnormal or incomplete development of
the optic nerve during fetal growth.
• Optic nerve coloboma: congenital developmental anomaly of
the optic nerve head, resulting from incomplete closure of
the embryonic fissure during the development of the eye in
the first trimester of pregnancy.
• Morning glory syndrome: congenital malformation of the
optic nerve head and the posterior portion of the eye.
REFERENCES
• Basic Opthalmology 4th Edition pg 25-30
• KANSKIS