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FUNDOSCOPY 101 for Neurosurgeons
The following illustrated tutorial covers some key concepts related to fundoscopy relevant to neurosurgeons. The author is grateful to Doctors HDM, WN, AN and IH for their input.
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Figure 1 (above). Basic visual pathway and associated lesional visual fields. Top left image: Output from the retina's ganglion cell layer constitutes the optic nerve (1). The nerve passes posteromedially to the optic chiasm (2). Fiber bundles here partially decussate as shown by the yellow and pink colouring in the top right image. Axons from nasal retinal fibers (inner/medial retina) cross the midline, while temporal (outer/lateral) retinal fibers stay ipsilateral. The post-chiasmatic fibers constitute the optic tract (3). Each optic tract therefore contains contralateral and ipsilateral fibers in almost equal proportions. The optic tract ends mainly in the lateral geniculate body (LGB) of the posterior thalamus. Note that some offshoots from the main optic tract pass as smaller tracts to (i) the pretectal area of the midbrain (*) and (ii) the superior colliculus (#) of the midbrain's quadrigeminal plate: such fiber tracts participate in pupillary light reflexes (parasympathetic Edinger-Westphal nucleus) and visually-guided eye movements, respectively. From each LGB, emerges the geniculo-calcarine tract (GCT; 5) aka the "optic radiation", which carries fibers from the thalamus to the cerebral cortex's primary visual processing area (posteromedial occipital lobe located around the calcarine fissure). The ventral-most fanning of the GCT is known as "Meyer's loop" (4). This loop passes close to the temporal horn and atrium of the lateral ventricle. The fibers in Meyer's loop represent the lower-inner retina output, and therefore damage to Meyer's loop produces an upper-outer ("pie in the sky") visual field defect. Effects of lesions of the left visual pathway at the various numbered locations are shown above in the lower right of the image. In the lesion numbered 5 involving the optic radiation or occipital cortex, there may or may not be "macular sparing". In cases of sparing, the central spot of the visual field is preserved, enabling some degree of reading ability to remain. The macular area of each visual cortex (located at the tip of the occipital pole) receives dual blood supply from the posterior and middle cerebral arteries.
Figure 2 (above). MRI diffusion tensor (tractography) imaging or "DTI" showing the optic radiation (O.R.)
Figure 3 (above). Normal fundus of the right eye ("Dexter"; OD) and left eye ("Sinister"; OS). [BTW, there's nothing sinister about being left-handed...author]. The image above shows the fundus displayed as a physician would see it looking into each eye via a hand-held ophthalmoscope or table-top slit lamp. Note that the apparently yellow optic disc (where the optic nerve starts) lies medial to the macula (OMM...). The macula mediates central, high-resolution vision especially via its small pit in the centre called the fovea, which contains the highest concentration of colour-processing cone cells (CC...). Visual acuity tests function of fovea and the papulo-macular bundle running between the macula and the optic disc. Output from the macula is eventually received by cells in the tip of each occipital pole. Note at the optic disc is where veins and arteries of the retina will converge/diverge from. The margin of the optic disc should be sharp, and the normal proportions are shown above. The blue arrows represent the direction of the optic nerve from the optic foramen, travelling anterolaterally in the optic canal with the attendant ophthalmic artery.
 
Figure 4 (above). Normal visual fields of the left and right eyes, respectively. The left eye's map is traditionally shown first and on the left, and the right eye's map follows or is on the right. The above "maps" are from formal perimetry in a normal subject who demonstrated no "fixation losses" during testing. Perfect fields. Each dark spot LATERALLY in the left and right eye fields shown above corresponds to the optic nerve's "physiological blind spot" (absence of photoreceptor cells at the optic disc) medially in each corresponding retina. Some "classic" examples of abnormal fields are given in the lower left hand corner of Figure 1. Remember, the projection of a fundus (Figure 3) is how a physician sees it looking through the pupil, while the representation of a visual field (Figure 4) is how the patient sees it out of each eye. Check the labeling to be sure. When testing a visual field one open eye at a time via confrontation, use a round-red-tip pin -- a wiggling finger is a poor proxy.
Figure 5 (above). Abnormal visual fields of the left and right eyes, respectively. The field defect shown above is a left homonymous hemianopia indicating involvement of the right optic radiation and/or right visual cortex (see Figure 1 for correlates). Reminder: When interpreting visual field charts, always check the name, date, and eye labeling. Also check the "fixation losses" number (red arrow, above) just to make sure that the result was not confounded by a "wandering eye" during testing.
 
Figure 6 (above).Papilledema fundoscopy, early/mild (above left) and late/severe (above right). Papilledema arises from raised intracranial pressure, with build up of back-pressure along the venous drainage pathways of the eye/optic nerve sheath. In papilloedema, parameters such as visual acuity and (red saturation) colour vision are preserved early on, while the earliest parameter compromised in papilledema is the VISUAL FIELD, whose abnormality in this condition starts as enlargement of the blind spot (central scotoma). Fundoscopy in patients with papilloedema may show blurring of the optic disc margin early on (left), or the margin's near-obliteration later (above right). Note, despite the possible presence of hemorrhages, exudates and blurred margins of acute papilloedema, visual acuity is preserved till late. A relative afferent pupillary defect (RAPD) develops late, corresponding to the progressive (late) loss of visual acuity.
- Optical coherence tomography (OCT; see below) of an eye affected by papilloedema shows evidence of thickening of the retina as fluid builds up. This occurs to the point of so much fluid/pressure building up that the retina starts to infarct, following which the retina will thin out, and become more pale. The end stage of papilloedema is therefore the same as severe optic atrophy (see below)...i.e., a pale, atrophic disc with RAPD and blindness in the affected eye(s).
Figure 7 (above).Optic neuritis fundus. In optic neuritis - inflammation of the optic nerve (e.g., associated with multiple sclerosis, Devic's neuromyelitis optica), the patient's visual acuity, red/colour perception, and visual field are ALL LOST EARLY. A RAPD is present early. The visual field loss is a central scotoma that enlarges from early on. Interestingly, despite the severe affect on the above parameters, the retina/fundus may actually look quite normal (especially in retrobulbar neuritis). However, the end-stage of optic neuritis is (like the of end-stage papilloedema) optic atrophy with a pale and enlarged disc region. In optic neuritis, the additional symptom that may be present from early on is pain on eye movement.
 
Figure 8 (above). Optic atrophy fundoscopy (left image) and visual fields (right image). Optic atrophy is the end- stage of papilledema, optic neuritis and glaucoma. At this point, visual acuity is lost, colour/red perception is lost, visual fields are lost, a RAPD is present and there are symptoms and signs of blindness in the affected eye(s). The optic disc is pale and enlarged.
Figure 9 (above). Optical coherence tomography (OCT). OCT is akin to ultrasound of retina or macula except that the technique uses light wave physics to determine focal thickness of the fundus region being examined. Thickness can be depicted graphically via the curvilinear graphs shown at the left of the image above, or via the retinal cross-sections shown at the right of the image above. In graphs, look to see if the black line wanders in the normal green range or into the abnormal (thinned) red range. A line wandering above the green zone (implying focally thickened retina) should correspond with early papilloedema, while a line wandering in the red zone should correspond with optic atrophy (which may be the end-stages of either optic neuritis, glaucoma or papilloedema). The normal retinal thickness is 100-120 microns. Note: If a good quality OCT test is done, visual field and/or visual acuity defects should be reversible if the OCT is normal or near-normal. In a pituitary macroadenoma, the physical pressure on the chiasm may be severe, and OCT will expectedly show thinning of the retina.
Figure 10 (above). Fundus in hypertensive retinopathy. Grade 1. Arteriolar constriction – “silver wiring” and tortuosity. Grade 2 = Gr 1 + tight constrictions or “AV nicking”. Grade 3 = Gr 2 + cotton wool spots (multifocal puffy damage/neuronal loss) and flame haemorrhages. Grade 4 = Gr 3 + swollen blurred disc/papilloedema. There is an association between increased Grade and mortality.
Figure 11 (above). Fundus in Terson’s syndrome. This syndrome is commonly seen in aneurysmal subarachnoid haemorrhage patients, with an incidence of 10-15% in that group of patients. It typically presents with a vitreous hemorrhage associated with raised intracranial pressure. Papilloedema and decreased level of consciousness are therefore part of the syndrome.
MISCELLANEOUS NOTES:
- Colour vision loss is an early sign of compressive neuropathy. The Ishihara test can detect red-desaturation/red perception loss early, that's why a red colour pin is also used for visual field assessment. The first of a total of fifteen plates in the Ishihara test has the number 12 and is a "control plate". Therefore, forget about further colour testing if a patient can't see the number 12 in the control plate (implies, e.g., the patient has a severe cataract or is retinally blind). Note how many plates are read by patient, one eye at a time, and how fast.
- Relative afferent pupillary defect (RAPD): direct and swinging light tests. The abnormal side's pupil does not constrict to direct light, but does constrict to indirect light (i.e., light shone in the other eye). When the light source is rapidly swung from the normal to the abnormal eye, the affected RAPD pupil paradoxically dilates.
- Foster Kennedy syndrome: Papilloedema is contralateral to the mass, and atrophy is ipsilateral to the mass. In end-stage papilloedema, there is optic atrophy, so in a long standing tumour such as an olfactory groove meningioma, there may be classic FKS (with differential findings in each eye),..or atrophy in both eyes.
- The optic cup is a lighter divot appearing within the optic disc's margins that enlarges as intraocular pressure (IOP) increases (i.e., in glaucoma). In glaucoma, the optic cup:disc ratio is greater than 0.6
- In macroadenomas, the most common field defect is "BTH plus" (i.e., bitemporal heminanopia plus one eye loses a nasal field in part or whole too) owing to frequent eccentricity of the tumour.
- Optic compression has different stages:
- Conduction block (reversible)
- Axoplasmic stasis (reversible)
- Demyelination (surgery may be helpful in facilitating remyelination with most of the recovery seen in 4-6 wks)
- Atrophy (IRREVERSIBLE)
- In pituitary apoplexy, a neurosurgical emergency, the fundoscopic findings may be that of acute or acute-on-chronic pailloedema. There is acute field loss and headache. The field loss usually is an asymmetric scotoma rather than classic bitemporal hemianopia as the macroadenoma's necrosis-related haemorrhage here is usually eccentric to one side.
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