CHAPTER11 VISUAL SYSTEM Najwa AlBustani Neurology AHD February

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: 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: Formed visual hallucination: people, animals or complex scenes >> arise from inferior temporo-occipital 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. 1. 2. 3. 4. 5. 6. 7. 8.

CLINICAL CORRELATION: Different field defect: starting from optic nerve >>> visual cortex.

Describe the visual field defect ?

OPTIC NERVE-TYPE FIELD DEFECTS: 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. 1. 2. 3.

PAPILLOMACULAR BUNDLE: 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 BUNDLE-DEFECTS:

ARCUATE NFB: 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 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 ~ 4 mm in the contralateral optic nerve (Wilbrand’s knee) before turning back to join uncrossed inferotemporal 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: 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: 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 HEMIANOPIA WITH MACULAR SPARING: Differential Diagnosis: 1. Non-organic visual field loss. Glaucoma. Optic disc drusen. Post-papilledema optic atrophy. Retinitis pigmentosa. 2. 3. 4. 5.

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: 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: Early Manifestation: Disc hyperemia. 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: 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: 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: 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. : 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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