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(BQ) Part 2 book “General ophthalmology” has contents: Neuro-Ophthalmology, ocular disorders associated with systemic diseases, immunologic diseases of the eye, special subjects of pediatric interest, ophthalmic genetics, ophthalmic trauma, ophthalmic therapeutics, vision rehabilitation,… and other contents.
14 Neuro-Ophthalmology Paul Riordan-Eva, FRCOphth The retinas and anterior visual pathways (optic nerves, optic chiasm, and optic tracts) (Figures 14–1 and 14–2) are an integral part of the brain, providing a substantial proportion of its total sensory input The pattern of visual field loss indicates the site of damage in the visual pathway (Figures 14–3 to 14–5) Eye movement disorders may be due to disease of cranial nerves III, IV, or VI, or a more central lesion Cranial nerves V and VII are also intimately associated with ocular function 626 Figure 14–3 Visual field defects due to various lesions of the optic pathways 627 Figure 14–4 Occipital lobe abscess Top: Automated perimetry and tangent screen examination showing homonymous, congruous, paracentral scotoma in right upper visual fields Bottom: Parasagittal magnetic resonance imaging showing lesion involving left inferior calcarine cortex (Reproduced, with permission, from Horton JC, Hoyt WF: The representation of the visual field in human striate cortex A revision of the classic Holmes map Arch Ophthalmol 1991;109:816 Copyright © 1991 American Medical Association All rights reserved.) 628 Figure 14–5 Bilateral occipital infarcts with bilateral macular sparing Top: Tangent screen and superimposed Goldmann visual fields of both eyes showing bilateral homonymous hemianopia with macular sparing, greater in the right hemi-field Bottom: Axial magnetic resonance imaging showing sparing of occipital poles (Reproduced, with permission, from Horton JC, Hoyt WF: The representation of the visual field in human striate cortex A revision of the classic Holmes map Arch Ophthalmol 1991;109:816 Copyright © 1991 American Medical Association All rights reserved.) 629 Figure 14–1 Magnetic resonance imaging of normal brain in sagittal section (upper left), coronal section (upper right), and axial section (lower left) The white arrows indicate the chiasm 630 Figure 14–2 The optic pathway The dotted lines represent nerve fibers that carry visual and pupillary afferent impulses from the left half of the visual field THE OPTIC NERVE A wide variety of diseases affect the optic nerve (Table 14–1) Clinical features indicative of optic nerve disease are reduction of visual acuity and field, afferent pupillary defect, poor color vision, and optic disk changes Table 14–1 Etiologic Classification of Diseases of the Optic Nerve 631 632 Optic disk swelling occurs predominantly in diseases directly affecting the anterior portion of the optic nerve but also occurs with raised intracranial pressure (papilledema) and compression of the intraorbital optic nerve It is also a feature of central retinal vein occlusion, ocular hypotony, and intraocular inflammation Peripapillary exudates occur with optic disk swelling due to inflammation (papillitis), ischemic optic neuropathy, raised intracranial pressure, or severe systemic hypertension The term neuroretinitis for retinal exudates, including a macular star, due to optic disk swelling of whatever cause is a misnomer in that there is no inflammation of the retina, the exudates being a response to the anterior optic nerve disease (Figure 14–6A) The term is more reasonably applied if there is inflammation of the retina and optic nerve (Figure 14–6B) Figure 14–6 A: Retinal exudates due to optic disk swelling B: Arcuate neuroretinitis due to acute retinal necrosis syndrome (B: Reproduced, with permission, from Margolis T et al: Acute retinal necrosis syndrome presenting with papillitis and arcuate neuroretinitis Ophthalmology 1988;95:937 Copyright © 1988 American Academy of Ophthalmology, Inc Published by Elsevier Inc.) 633 Optic atrophy (Figure 14–7) is a nonspecific response to optic nerve damage from any cause and also occurs in primary retinal disease, such as central retinal artery occlusion or retinitis pigmentosa In general, in optic nerve disease, there is a correlation between degree of optic disk pallor and loss of acuity, visual field, color vision, and pupillary responses, but the relationship varies according to the underlying etiology An important exception to this rule is compressive optic neuropathy, in which optic disk pallor is generally a late manifestation such that the optic disk may be normal even when there is severe reduction of visual acuity and field Hereditary optic neuropathies usually produce bilateral temporal disk pallor with preferential loss of papillomacular axons Figure 14–7 Examples of optic atrophy A: Primary optic atrophy due to nutritional amblyopia B: Secondary optic atrophy with retinochoroidal collaterals (arrows) due to optic nerve sheath meningioma C: Optic atrophy with optic disk drusen D: Pallor (atrophy) of right optic disk due to nerve compression by sphenoid meningioma The left disk is normal 634 Excavation of the optic nerve head (optic disk cupping) is generally but not necessarily a sign of glaucomatous optic neuropathy (see Chapter 11) OPTIC NEURITIS (INFLAMMATORY OPTIC NEUROPATHY) The most common cause of optic neuritis is demyelinative disease, including the typical acute demyelinative optic neuropathy that is associated with multiple sclerosis Retrobulbar means that the optic disk is normal during the acute stage, whereas papillitis means that the optic disk is swollen Loss of vision is the cardinal symptom of optic neuritis and is particularly useful in differentiating papillitis (Figure 14–8) from papilledema (Figure 14–9), with which it may be confused on ophthalmoscopic examination Figure 14–8 Mild disk swelling (A) in demyelinative papillitis, with disk leakage on fluorescein angiography (B) Because of major differences in management and outcome, optic neuritis is classified as typical or atypical Figure 14–9 Mild papilledema The disk margins are blurred superiorly and 635 Ultraviolet irradiation, 395 Ultraviolet radiation–induced superficial keratoconjunctivitis, 387 Uncorrected refractive errors, as cause of vision loss, 392, 393 Uncorrected visual acuity, 29 Uncover test, 256–257, 257f Unoprostone, 242 Unoprostone isopropyl, 421 Upbeat nystagmus, 319 Urea, 423–424 USEIR see US Eye Injury Register US Eye Injury Register (USEIR), 394 Uveal meshwork, 12 Uveal tract anatomy, 9–10, 10f–11f, 147, 148f glaucoma secondary to changes in, 248–249 Uveal tumors, 160 benign choristomas, 161 choroid osteoma, 163, 163f circumscribed choroidal hemangioma, 162, 162f diffuse choroidal hemangioma, 163, 163f hamartomas, 161 melanocytic uveal nevus, 161–162, 161f–162f, 164, 164f neoplasms, 161 intermediate atypical lymphoid hyperplasia, 164–165 nevoma, 164, 164f malignant 1188 evident features of, 165 glaucoma secondary to, 248–249 non-ophthalmic primary cancer metastatic to uvea, 167–168, 167f primary uveal lymphoma, 168, 168f primary uveal melanoma, 165–167, 165f–166f Uveitis, 361 anterior causes of, 152t classification, 148f Fuchs’ heterochromic iridocyclitis, 147–148, 152–153 joint disease associated with, 151–152, 152f lens-induced uveitis, 153 in childhood, 372 clinical findings, 147–150, 148f–149f, 148t complications, 150 corticosteroids and, 150–151, 151t, 152, 153, 156, 157, 158, 159 course and prognosis, 151 defined, 147 in developing countries cysticercosis, 160, 160f leptospirosis, 159 onchocerciasis, 159–160 differential diagnosis, 150 emergency management of, 65–67, 71 glaucoma secondary to, 248–249 granulomatous, 147–148, 148t hypopyon, 148 intermediate, 148–149, 148f, 153 1189 nongranulomatous, 147, 148t panuveitis causes, 157t classification, 148f classification of, 148f sarcoidosis, 158 sympathetic ophthalmia, 158–159, 159f syphilis and, 158, 158f tuberculous uveitis, 157–158 posterior AIDS and, 157, 157f causes, 153t diagnosis and clinical features, 154–155 histoplasmosis, 156 laterality of, 154 ocular toxocariasis, 156–157, 156t ocular toxoplasmosis, 155–156, 155f overview of, 148f, 149, 153–154 sequelae, 150 treatment, 150–151, 151t tuberculous, 157–158 V Vaccination, optic neuritis, 351 Valacyclovir (Valtrex), 102, 349, 430 Valganciclovir, 350, 430 Vancomycin, 277 Varicella (chickenpox), 348–349, 349f Varicella-zoster virus (VZV), 348–349, 349f 1190 blepharoconjunctivitis, 102, 102f keratitis, 132–133, 133f Varix, 84 Vascular abnormalities, orbital arteriovenous malformation, 278 carotid-cavernous fistula, 278–279 Vascular disease, ocular disorders associated with, 328–339 see also specific disorders acute ocular ischemia, 328, 330f–333f, 331–333, 333t anatomy and physiology, 328 central retinal vein occlusion and, 68, 71 chronic ocular ischemia, 333–335, 334f–336f clinical manifestations, 328–337 hemorrhages, 328, 329f, 329t hypertensive retinochoroidopathy, 337, 338t, 339f idiopathic (benign) intracranial hypertension, 338–339 infective endocarditis, 339, 339f retinal branch vein occlusion and, 68–69 retinal vein occlusion, 336–337, 337f, 337t, 338f Vascular endothelial growth factor inhibitors (VEGF), 430 Vascular insufficiency occlusion of internal carotid artery and, 320–321 of vertebrobasilar arterial system, 321 Vasoconstrictors, 425–426 Venous drainage system, 4f, 5, 6f VER see Visual evoked response Vergences (disjunctive movements), 253, 258–259, 258f–259f Vernal keratoconjunctivitis (VKC), 104–105, 105f, 361 1191 Versions, 32, 253, 257, 258f Vertebrobasilar arterial system vascular insufficiency of, 321 Vertex distance, change of, 407 Vestibular nystagmus, 318–319 central, 319 downbeat, 319 peripheral, 318–319 upbeat, 319 Vestibulo-ocular response (VOR), 317 Video magnifiers, 462f–463f Viral conjunctivitis see also Acute viral follicular conjunctivitis causes, 93t chronic, 101–102, 101f–102f of newborn, 372 signs, 94t Viral diseases, ocular disorders associated with, 348–351, 349f–351f acute retinal necrosis, 350, 350f bulbar poliomyelitis, 350 cytomegalovirus, 350 Epstein-Barr virus, 350 herpes simplex virus, 348 measles, 350 mumps, 350 progressive outer retinal necrosis, 350 rubella, 350 vaccination, 350 varicella-zoster virus (chickenpox and herpes zoster), 348–349, 349f, 350f 1192 Viral keratitis, 130–134, 131f–134f Acanthamoeba, 134, 134f adenovirus, 133 HSV, 130–132, 131f varicella-zoster virus, 132–133, 133f Visceral larva migrans, 156t Viscocanalostomy, 243–244 Vision, reduction of, 390 Vision abnormalities Amsler grid, 44–45, 46f brightness acuity testing, 45 color vision testing, 45–46, 47f–49f contrast-sensitivity testing and, 46–47, 50f diagnosis of, 41–50, 43f–50f functional visual loss, 49–50 in ocular history, 27–28 perimetry, 41–44, 43f–45f visual aberrations, 28 visual loss, 27–28 Vision examination basic, 29–31, 29f–30f children, 368, 368t infants, 368, 368t neonatal, 367 pinhole test, 29–30 refraction, 30, 30f visual acuity testing, 29, 29f–30f visual field testing, 31 1193 Vision loss acute painful, without red eye, 69–70 acute painless, 68–69 aspects of, 469, 469f binocular vs monocular, 68 causes of, 390–393, 392t cataract, 392–393 glaucoma, 393 onchocerciasis, 393 other, 393, 393t trachoma, 393 uncorrected refractive error, 393 definitions, 390–392 driving privileges, 390–392 functional, tests for, 49–50 prevalence, 392 prevention of, 394–400 acquired ocular infection, 395–397, 396t amblyopia (lazy eye), 399–400 diabetic retinopathy, 399 due to drugs, 398–399 early detection of treatable ocular disease, 399–400 genetic disease with ocular involvement, 398 iatrogenic ocular and nonocular infection, 397 JIA, 400 nonoccupational injuries, 395 occupational injuries, 394–395, 395t ocular damage due to congenital infections, 397–398 1194 ocular damage due to systemic diseases, 398 ocular injuries, 394–395, 395t primary open-angle glaucoma, 399 retinopathy of prematurity, 399 from retinal emboli, 320–321 transient, causes of, 333t as vision abnormality, 27–28 Vision rehabilitation aspects of vision LOSS, 469, 469f comprehensive, 469–471 comprehensive plans, 470, 471f examination, 470 history and goal setting, 469–470 levels of competence in, 470 stages of visual processing, 468–469 vision enhancement, 470–471 Vision substitution, 470 Visual aberrations, 28 Visual acuity in clinical evaluation of strabismus, 255 development of, 368t driving privileges and, 390–392 optics and, 412 testing, 29, 29f–30f Visual axis, 39 Visual confusion, 254 Visual distortion, 28 Visual evoked response (VER), 62–63, 63f 1195 Visual field examination, in glaucoma assessment, 240–242, 241f testing, 31 Visual field defects due to lesions of optic pathway, 284, 287f pattern of, 284 Visual neglect, 31 Visual processing, stages of, 468–469 Vitamin A deficiency, 345, 345f prevention of, 398 retinal atrophy in, 345f sterile keratitis and, 135–136 Vitamin B deficiency, 345 Vitamin B1 (thiamin) deficiency, 345 Vitamin B12 deficiency (pernicious anemia), 345 Vitamin C (ascorbic acid) deficiency (scurvy), 345 Vitamin deficiencies, ocular disorders associated with, 345, 345f vitamin A, 345 vitamin B, 345 vitamin C, 345 vitamin E, 345 Vitamin E deficiency, 345, 345f Vitrectomy, 189 Vitreomacular disease, 189 Vitreomacular traction syndrome (VMT), 189 Vitreoretinal disease diabetic retinopathy, 190, 190f–191f retinal breaks, 189–190, 190f 1196 rhegmatogenous retinal detachment, 189–190, 190f symptoms, 188–189, 189f vitreomacular disease, 189 vitreomacular traction syndrome, 189 Vitreoretinal interface, examination of, 186–188, 187f–188f Vitreoretinal surgery, 186 Vitreous anatomy, 13, 186, 187f cataract surgery complications and, 190–191, 191f congenital abnormalities of, 370 cortex, 186, 187f embryology, 25–26 examination of, 186–188, 187f–188f hemorrhage, 385 acute painless visual loss from, 68–69 as symptom, 188 mobility, 192 posterior detachment of, 188–189, 189f traction, 191f transparent, 186, 187f trauma, 192, 192f volume, reduced, 242–243 VKC see Vernal keratoconjunctivitis VKH see Vogt-Koyanagi-Harada disease VMT see Vitreomacular traction syndrome Vogt-Koyanagi-Harada (VKH) disease, 356, 357f, 363 von Hippel-Lindau disease, 323, 376 VOR see Vestibulo-ocular response 1197 Vortex dystrophy, 142 V patterns, in strabismus, 266 VZV see Varicella-zoster virus W Wall-eyed bilateral internuclear ophthalmoplegia (WEBINO) syndrome, 311 Warfarin, 114f Wavefront aberrometry, 51, 52f Wavelength , of light, 403 WEBINO see Wall-eyed bilateral internuclear ophthalmoplegia syndrome Wegener’s granulomatosis see Granulomatosis with polyangiitis Wernicke’s encephalopathy, 345 White dot syndromes, 218 White pupil (leukocoria), 373 White without pressure, 211 White with pressure, 211 WHO see World Health Organization Wolfram’s syndrome, 301 Working distance, 417 World Health Organization (WHO), 390, 392, 394 Worth four-dot test, 259 Wyburn-Mason syndrome, 324 X Xalacom, 423 Xeroderma pigmentosum, 377 Xerophthalmia, vision loss due to, 393t Xerostomia, 354 X-linked juvenile retinoschisis, 218–219, 219f X-linked recessive inheritance, 377 1198 X-linked retinoschisis, 377 Y Yoke muscles, 254, 254t Y sutures, of lens, 10, 12f Z Zonular fibers, 178 Zonule, 10 Zygomatic bone, 1199 1200 1201 1202 ... Clinical features • Subacute loss of vision developing over 2 7 days • Reduced visual acuity (one-third better than 20 /40, one-third worse than 20 /20 0) • Visual field defect • Reduced color vision •... vision is normal apart from blind spot enlargement Chronic, particularly atrophic or vintage, papilledema is associated with gradual constriction of the peripheral visual field, particularly inferonasal... withdrawal of the toxic agent is the primary treatment Figure 14 21 Nutritional amblyopia showing centrocecal scotoma VA = 20 /20 0 Tobacco-Alcohol Amblyopia Nutritional amblyopia is probably a