Ординатура / Офтальмология / Английские материалы / Visual Fields Examination and Interpretation_Walsh_2011
.pdf296 Visual Fields
2 m from the screen, the examiner may move 10 to 12 feet from the patient and use his or her hand as the test object. This test object is grossly larger than the target required for that distance. If the patient sees the hand as the test object at a distance of less than 7°, this will demonstrate the functional nature of the field defect.
One of the easiest tests for functional visual loss is to compare the distant (20-foot) and the near (14-inch) acuity with the appropriate distant prescription and add as indicated. Distant and near acuities should be essentially the same, or near acuity should be only slightly better than distant acuity because of the magnification. There should not be a discrepancy of four or five lines. The next step is to measure the acuity at different distances from the chart. If a patient reads the 20/200 large S-L letters at 20 feet, he should read the original 20/100 O-P-L-D line at 10 feet, which, at the new distance, is equal to the previous 20/200 S-L line. The patient can further be tested at 5 feet or for any line of letters with which he starts. If he continues to read only the original 20/200 S-L at all distances, he may then be considered to have functional visual loss.
A variation on the standard refraction is another useful test. The patient is given cycloplegia, and his best refraction is put in the phoropter. A +2.50 lens is then inserted in front of the eye about which he is complaining. If the patient compares both eyes alternately on the distant chart, his vision in the suspected eye will be blurred and he will not be able to read the letters. As long as both eyes are open behind the phoropter, he does not mind reading the distant chart, because he feels he is reading it with the uninvolved eye. The near card is now moved to 16 inches in front of him, and he is asked to read it. Presuming that his uninvolved eye still is doing the reading, the patient reads the near card. Because, however, he is under cycloplegia and only the involved eye has the appropriate +2.50 lens in front of it, he will be reading only with the eye with which he said he could not read the distant 20/200 S-L—an obvious discrepancy.
More sophisticated tests can be done with prisms. In these tests, the patient who says he has a monocular defect reads with both eyes open, and supposedly he is reading with the good eye only. If an 8-diopter base-out prism is placed in front of the affected eye and the patient makes a correcting fusional movement, evidence of reasonable vision is indicated. A similar movement in the opposite direction will occur when the prism is withdrawn. If the vision is as poor as the patient claims, there will be no reason for a fusional movement. This test can be reversed by putting a vertical 6-D prism in front of the affected eye. Vertical prisms of this magnitude cannot be fused and will cause diplopia and interruption of reading. If the vision in the suspected eye is so poor that it is not used in reading, the vertical prism will cause no interruption in reading and no diplopia symptoms. The far test with reading is similar to the vertical prism test.
The duochrome test can also be used when functional loss is suspected. This test uses the red-green filter in the projector and red-green glasses either on the patient or in front of the phoropter. If the patient reads both the red and the green letters, it belies his claim that he sees abnormally with one of his eyes, because he is seeing the red letters through the eye with the red lens in front of it and the green letters through the eye with the green lens. The success of this test presupposes that the patient does not close each eye alternately to check with which eye he is seeing.
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A clever variation of the duochrome test uses polarizing lenses instead of redgreen glasses. The red-green slide is replaced with a polarizing slide, half of the letters polarized vertically to 90° and the other half horizontally to 180°. A similar orienting glass is placed in front of each eye. As in the duochrome test, the patient can discover which eye sees which half of the line of letters by closing each eye separately. By a twist of the projector knob, however, the examiner can easily interchange the half of the letters having a horizontal orientation and the half having a vertical orientation. At one slight movement, the right eye sees the right half of the line of letters and, in the span of a blink, the left eye sees the same half. If the change of orientation is kept in mind and is done fast enough, the patient may be tricked into reading with his “poor” eye.
Several other tests can be used for patients who complain of bilateral visual loss. These tests have some use in unilateral loss as well. If a patient says he can see only light or hand motion, the optokinetic nystagmus and mirror tests are of particular value. The OKN tape is moved in front of the patient at a distance where he says he cannot see anything except, perhaps, light. If his eyes move appropriately as the tape is moved, he must see the tape. This test cannot be used with patients who will not cooperate with fixation. If the patient appears to fixate but no response is forthcoming, the direction of the movement of the tape should be changed from horizontal to vertical. This change may surprise or momentarily confuse the patient, putting him off his guard so that he will give the examiner the proper response.
In the mirror test, the examiner holds a mirror at the distance where the patient says he sees nothing. The patient is asked to fixate straight ahead and not to move his eyes, even if he cannot see anything on which to fixate. At this point, the examiner starts a conversation to distract the patient so that he does not realize the test is taking place. The examiner slowly moves the mirror horizontally or vertically. If the patient is fixating steadily on himself, his eyes will move slowly. If he does not see himself, he will have no reason to move his eyes as the mirror is moved.
The use of the visual evoked response is another method of testing for the integrity of the visual system, but it is not always available and is rarely needed. Furthermore, the test may not be helpful if a patient does not fixate adequately, such as occurs in young children. There is no one test that is better than another to make the diagnosis. To prove the problem is functional, multiple tests need to be done; the patient only needs to fail only one test.
REFERENCES
1.Fames TH: A study of tubular and spiral central fields in hysteria. Am J Ophthalmol. 1947;30:610–611.
2.Karp JJ: Functional disease in neuro-ophthalmology. Int Ophthalmol Clin. 1972;17: 157–167.
3.Miller B: A review of practical tests for ocular malingering and hysteria. Surv Ophthalmol. 1973;17:241–246.
4.Eggers H: Estimation of uncorrected visual acuity in malingerers. Arch Ophthalmol. 1945;33:23–27.
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Index
NOTE: An f following a page number indicates a figure, and a t following a page number indicates a table.
Abscess
in optic tract infection, 256 papilledema, 201
Absolute defect, in fields, 19, 144, 157 Acquired optic nerve diseases, 193
compressive optic neuropathy, 198–200 ischemic optic neuropathies, 196
arteritic ischemic optic neuropathy (AAION), 196–98
nonarteritic ischemic optic neuropathy (NAION), 196
metabolic optic neuropathies, 198 visual field effects of, 198
optic neuritis, 194–95 papilledema, 200–201
Acute zonal occult outer retinopathy (AZOOR), 217, 250
Advanced Glaucoma Intervention Study (AGIS), 132
Afferent field defect (APD), 44f, 60, 196, 253, 255 Alcohol
and stress, 184
teratogenic agent, for ONH, 178
Altitudinal defects, 16, 59, 72, 73, 179, 181, 196 Altitudinal field defects, 42t, 72–75
congruous, 73–75
noncongruous binocular and monocular, 72–73 Altitudinal hemianopia, 273
congruent, 73–74
localized monocular field defects, 42t, 44f, 59 nonconguent, 73f
Amblyopia, 37, 57, 77, 180 Ametropias, 177
Amsler grid, field testing techniques, 36, 226, 240 Aneurysms, 71, 73, 83, 109, 199, 236, 243, 247,
248, 249, 256
Anterior chiasmal syndrome, 240
Anterior choroidal artery, occlusion of, 45f, 61, 63, 259f
Anterior genu of von Wilbrand, 200
Anterior visual pathway, 45, 54, 72, 237 Anton syndrome, 281–82
Aphasia, color-naming, 37, 268, 286 Aplasia, 177
Arachnoiditis, optochiasmic, 71 Arc perimeter, 85
Arcuate defect, 27f, 101, 107f, 135f optic nerve and retina, 20
Arcuate field defects, localized monocular field defects, 52–54
optic nerve head, 53–54 retina, 53
retrobulbar optic nerve, 54
Arcuate scotomas, 16, 52, 58, 100f, 128f, 141, 179, 196
Arcuate temporal retinal fibers, 128 Arteriovenous malformations, 250 Arteritic ischemic optic neuropathy (AAION), 193, 196–98
signs of, 196
visual field effects of, 197 Artery occlusions, 209, 259 Artifacts
in automated perimetry, 149 in corrective lens, 120
and learning effect, 118
corrective lens/frame artifacts, 120 eyelid and nose effects, 119
media opacities, 119
miosis and mydriasis, 118–19 refractive errors, 119–20
Atrial myxoma, visual loss after, 284f Automated perimetry
custom tests, 105–11
FASTPAC algorithm, 95, 108–9 grid size, 108
Nasal Step program, 110
Peripheral 60 and 60-4 program, 110 Programs 30-1 and 24-1, 109 stimulus size option, 111
299
300 Index
Automated perimetry (continued) evaluation
of series of tests, 144–61 of single test, 132–44
field testing, principles of, 86–94 frequency-of-seeing curves and
fluctuations, 92–94 kinetic perimetry, 88–90 static perimetry, 90
follow-up printout, 111–14
change analysis printout, 111–14 glaucoma progression analysis
printout, 114
guided progression analysis, 114 overview printout, 111
full threshold test, glaucoma-related advantages of, 129–30 disadvantages of, 130
future of, 161–73
altered stimuli, 161–69 altered strategies, 169–71 interpretive aids, 171–73
in glaucoma
automated perimetry options, 129–32 evaluation of series of tests, 144–61 evaluation of single test, 132–44 glaucomatous visual field defects, 127–29
historical overview of, 85–86 learning effect and artifacts, 118–20
corrective lens/frame artifacts, 120 eyelid and nose effects, 119
media opacities, 119
miosis and mydriasis, 118–19 refractive errors, 119–20
limitations of, 263–64
single test printout in, 99–105 Glaucoma Hemifield test, 102–5 global indices, 105
grayscale results, 101 numeric results, 101 pattern deviation, 101 reliability indices, 99–101 test selection, 99
total deviation, 101
test selection and algorithms, 94–99 fixation monitoring, 96–99 foveal threshold, 95
initial values, 95–96
Swedish Interactive Threshold Algorithm (SITA), 94–95
threshold testing, 99
visual field technician, role of, 121 visual function specific perimetric
technologies, 114–18
frequency doubling perimetry, 117 high-pass resolution perimetry (HPRP), 117 short-wavelength automated perimetry
(SWAP), 117 tendency-oriented perimetry, 118
Automated perimetry, field testing principles of frequency-of-seeing curves and fluctuations,
92–94
kinetic perimetry, 88–90 static perimetry, 90
suprathreshold techniques, 90–92 threshold techniques, 92
Automated perimetry, follow-up printout, 111–14 change analysis printout, 111–14
glaucoma progression analysis printout, 114 guided progression analysis, 114
overview printout, 111
Automated perimetry, future of, 161–73 altered stimuli, 161–69
color perimetry, 168–69 flicker perimetry, 165–67
frequency doubling perimetry/frequency doubling technology (FDP/FDT), 165
motion automated perimetry (MAP), 168 pattern-discrimination perimetry, 168 ring perimetry, 167
short-wavelength automated perimetry (SWAP), 161–65, 166–67f, 168–70f
altered strategies, 169–71 interpretive aids, 171–73
Automated perimetry, series of tests evaluation, 144–61
artifacts, 149–54
baseline establishment, 146–49
central abnormalities, follow-up of, 159–60
disc hemorrhage, early defect confirmed by, 148f glaucoma, confirmation of, 145–46f
glaucoma progression analysis, 157–59 inferior arcuate region, depression in, 147 long-term fluctuation, 155–56 progression
criteria for, 155–57 progression, nature of, 149
trend analysis, 159
Automated perimetry, single test evaluation, 132–44
abnormality, criteria for, 140–43, 143t advanced field loss, follow-up of, 144
apparent dense peripheral constriction, 137–38f field loss, staging of, 143–44
learning effect, recognition of, 141–42f patient reliability, 132–40
false-negative responses, 136 false-positive responses, 133–36 fixation losses, 133
full threshold algorithm, STF on, 136 stimuli number, 136–40
test duration, 133 test selection, 144
true dense peripheral constriction, 139–40f Automated perimetry options, 129–32
full threshold test advantages of, 129–30 disadvantages of, 130
Swedish Interactive Threshold Algorithm (SITA), 130–32
Automated threshold perimetry for chiasmal lesion, 240
Automated visual fields, 255f
Bacterial infection, 194, 256
Bacterial infection, in optic neuritis, 194 Bausch & Lomb colored test objects, 25, 31 Bjerrum region, 52
Best disease, 213, 215
“Big pumpkin test,” cecocentral scotoma, 37 Bilateral central depression, in DOA, 187 Bilateral central field defects, 42t, 77–78 Bilateral checkerboard scotomas, 42t, 79–80
Bilateral homonymous hemianopias, 42t, 80, 279, 280, 283
Bilateral peripheral field defects, 42t, 78–79 Binocular field defects
altitudinal field defects, 72–75 congruous, 73–75
noncongruous binocular and monocular, 72–73
bilateral central field defects, 77–78 bilateral checkerboard scotomas, 79–80 bilateral homonymous hemianopias, 80 bilateral peripheral field defects, 78–79 binasal field defects, 70–72
complete, 70–71 incomplete, 71
bitemporal hemianopias, 67–70 with central depression,
scotomatous, 69–70 complete, 67–69
homonymous hemianopias, 60–67 horizontal sectoranopia, 62–63 incomplete incongruous, 65–66 macular sparing, incomplete, 64 macular splitting, complete, 60–62 paramidline-sparing vertical
hemianopia, 63
two scotomas, incomplete, 64
unilateral defect of temporal crescent, 67 unilateral sparing of temporal crescent, 66
quadrantanopias, 75–77
inferior homonymous, complete, 76–77 superior homonymous, incomplete, 75–76
Bipolar cells, 12, 45, 46t, 52
Birdshot chorioretinopathy (BSCR), 217–26 Bitemporal hemianopias, 7, 16, 20f, 42t, 44f, 82f,
181, 234, 236, 249, 250 binocular field defects, 67–70
with central depression, scotomatous, 69–70 complete, 67–69
by confrontation testing, 240–41 and Cushing’s syndrome, 248 lesions affecting chiasm body, 243 and pituitary adenomas, 247
Bitemporal hemianopia plus, 83
Index 301
Blindness, 281
chiasmatic postfixation, 240–41, 248 complete, 16, 201, 239
cortical blindness, 283, 295 retinal lesions, 16
transient cerebral blindness, 283 using suprathreshold techniques, 90
Blind spot, 21, 26f, 27f, 28f, 52, 73, 88, 97f, 98, 99, 217, 242
false-positive responses, 133 Fuchs colobomata, 181 interpretation of, 4
and optical nerve, 194
Blind spot enlargement, 181, 182f, 250 reasons for, 7
Blue-on-yellow perimetry, 117. See also Shortwavelength automated perimetry (SWAP)
Bowl perimeter, 86 Brunescent cataract, 32
Calcarine artery occlusions, 64
Calcarine cortex, 14f, 45, 49f, 61f, 62, 78, 267, 268, 283
incomplete incongruous, 66 macular sparing, incomplete, 64
in occipital lobe field defects, 272, 273 visual field defects, 264–67
Calcarine cortex, anterior, 67 Calcarine cortex, basal superior or
inferior, 74–75 Calcarine cortex, posterior, 66
Calcarine fissure, 13, 15, 44, 46, 47, 48, 66, 273 Calcarine sulcus, 50f, 67, 75, 78, 79 Cancer-associated retinopathy (CAR), 228 Cataract, 32, 59, 60, 103, 105, 111, 119, 141–42,
152f, 157, 161, 279 blind spot interpretation, 4 and SITA Standard, 114
Cecocentral defect, 26f optic nerve and retina, 20
Cecocentral scotoma, 16, 38f , 243 in DOA, 186–87
field testing, difficulty in, 37
Central field examination, guidelines for, 27–31 Central fields exploration, perimetry, 6–7
vascular lesions, identification of, 6 in glaucoma patients, 6–7
Central scotoma or depression, 54–56 optic nerve head, 56
retina, 54–56
retrobulbar optic nerve, 56 Central scotoma, 16
in DOA, 186 and ONH, 179
in optic neuritis, 194
Central serous chorioretinopathy (CSCR), 207 Central visual field defect, 181, 182f.
See also Blind spot enlargement Central visual loss, in optic neuritis, 194
302 Index
Centrocecal scotoma or depression, 42t, 57–58 optic nerve, 57–58
retina, 57
Cerebral artery occlusions, 272, 273 Cerebral dyschromatopsia, 286, 288–89 Chamlin step technique
field testing, 31–34
temporal lobe field defects, 268 Checkerboard scotoma, bilateral, 42t, 79, 80 Chediak-Higashi syndrome, 215
Chiasmal compression, 245, 249 Chiasmal dysfunction, 234, 250 Chiasmal region lesions
aneurysms, 249 craniopharyngiomas, 249 dilatation of the third ventricle, 250 meningiomas, 248
parasellar meningiomas, 249 suprachiasmatic meningiomas, 249 suprasellar meningiomas, 248–49
pituitary tumors, 247–48 Chiasmal tumor, 20f, 21f
Chiasmal visual field defects, 241–46 Chiasmatic postfixation blindness, 240–41 Chorioretinal disorders, 207–32
congenital and genetic diseases, 211–17 retinitis pigmentosa (RP), 211
inflammatory/infectious diseases, 217–26 acute zonal occult outer retinopathy
(AZOOR), 217
birdshot chorioretinopathy (BSCR), 217 Chediak-Higashi syndrome, 215
cone dystrophy, 215 Hermansky-Pudlak syndrome, 215 multiple evanescent white dot syndrome
(MEWDS), 217
ocular histoplasmosis, 217 white dot syndromes, 217
macular diseases, 207–9 causes of, 207
pathologic myopia, 207–9
peripheral retinal abnormalities, 226–32 peripheral tumors, 228
toxicity, 226
vascular diseases, 209–11
intraretinal hemorrhages and exudates, 222–23f
microaneurysms and macular ischemia, 218f
progressive retinal dysfunction, 217 retinal emboli, 209
Choroidal neovascular membrane, 207, 209 Choroideremia, visual field defects by, 211
HVF 10-2 showing, 224–25f
Circle of Willis, in optical chiasm, 235, 238f, 249, 256
Clinical perimetry, 4, 86 Cloverleaf field, 96, 97f, 136, 137
Cocaine, teratogenic agent, for ONH, 178
Coenzyme Q10, mitochondrial energy production, 184
Cogan’s rule, 66
Collaborative Initial Glaucoma Treatment Study (CIGTS), 132
Collaborative Normal Tension Glaucoma Study, 127
Color agnosia, field defects, 288 Color blindness, 37
Color perimetry. See Blue-on-yellow perimetry; Short-wavelength automated
perimetry (SWAP) Color testing, 36–38, 285 Color vision recording, 5
Compressive optic neuropathy, 193, 198–200 visual field findings of, 199
Computer graphics, understanding retinotopic projection, 46
Computerized field examination of arcuate defect, 27f
of bitemporal hemianopia, 20f of cecocentral defect, 26f
of chiasmal tumor, 21f
incongruous field defect., representation of, 17–19f, 22f
of paracentral defects, 26f and tangent screen, 3
Computerized perimeter advantage of, 27
use of, 6, 10–11f
in central field exploration, 6
in neuro-ophthalmic patients, 9–10 Computerized representation
of homonymous hemianopia, 265f Computerized visual field assessment, 85 Cone dystrophy, 228–29f
visual field defect, 215–16 Confluent central field loss, 171f Confrontation testing
for chiasmal lesion, 240–41 Congenital and genetic diseases, 211–17 Congenital color defect, 32
Congenital optic disc anomalies, 177–82 anomalous disc elevations, 180–81 aplasia and dysplasia, 177–79
optic nerve colobomas and pits, 179–81 Congruity, visual field testing, 264–67, 267f
incongruous superior quadrantanopia, 266f temporal lobe visual field defects, 268
Congruous defects, 16
Congruous left inferior quadrantic scotoma, 275f
Congruous quadrantanopia, 273 with macular sparing, 274f
Congruous scotomas, 273
Conjugate-gaze deviations, and occipital lobe lesions, 285
Contraction, as field defect, 294 Corneal scar, 119
Corrected pattern standard deviation (CPSD), 105
glaucomatous visual field defects, 129 Cortical blindness, 283, 295 Craniopharyngioma, 64, 68–69, 199, 243, 244f,
247, 248, 249 optic tract lesions, 256
Cushing’s syndrome of the chiasm, 248 Custom tests, automated perimetry, 105–11
FASTPAC algorithm, 95, 108–9 grid size, 108
Nasal Step program, 110
Peripheral 60 and 60-4 program, 110 Programs 30-1 and 24-1, 109 stimulus size option, 111
Cycloplegia, 296
Cystoid macular edema, 211, 217, 226 HVF 24-2 showing, 220f
Dazzle test and papillary responses, 5
de Morsier syndrome. See Septo-optic dysplasia Defects in fields, interpretation of, 16–21
anatomic locations, types of defects, 16 computerized perimetry, use of, 9 margin, definition of, 20
in optic nerve and retina, 20–21 tangent screen representation in, 17–19f
Déjérine-Roussy syndrome, 260
Differential light sensitivity, static perimetry, 87 Diffuse depression, in optic neuritis, 194 Dilatation of the third ventricle, 250
Dominant optic atrophy (DOA), 185–88 visual finding of, 186
Double-ring sign, 178, 178f Drusen, macular pathology, 207
Duochrome test, for functional loss, 296–97 Dyscalculia, 23, 270
Dyschromatopsia, 37–38, 182, 288–89 in color testing, 37
in dominant optic atrophy (DOA), 186 in LHON, 183
Early Manifest Glaucoma Trial (EMGT), 157 Early-crossing fibers, 239
Edinger-Westfall nucleus, 256 Electro-oculography (EOG), macular diseases,
207, 215
Electroretinographic (ERG) testing, macular diseases, 207, 215
and cancer-associated retinopathy (CAR), 228 melanoma-associated retinopathy (MAR), 232
Embolic disease, 49 multiple emboli, 273, 279 retinal emboli, 209
Energy depletion, 183
Enlarged blind spot, in papilledema, 200 Enlarged physiologic blind spot, 56–57
optic nerve, 57 peripapillary retina, 56–57
Index 303
Equatorial annular scotoma or depression, 58–59
equatorial retina, 58 preretinal media, 58
Esophoria, 241
Exophoria, 241 Extrinsic lesion, 247t
Eyelids, and nose effects, 119
False-negative responses
automated perimetry in glaucoma, 136 False-positive responses
automated perimetry in glaucoma, 133–36 False-positive errors, 133–36
superimposed on glaucomatous defects, full threshold test, 135f
FASTPAC algorithm, 95, 108–9 Field testing, techniques of, 21–38
Amsler grid, 36
central field technique, 24–31 central field examination, 27–31
No. 966 Eagle Prismacolor pencil, 29–31 paracentral defects, 26f
spherical test object, 25
tangent screen representation, 25f Chamlin step technique, 31–34
homonymous fields, 34 color testing, 36–38
big pumpkin test, cecocentral scotoma, 37 confrontation technique, 21–24
tangent screen examination, 22f temporal and nasal fields, comparison
of, 23–24
finger counting method, 23 for peripheral field defect, 31
peripheral field technique, 34–35 Riddoch phenomenon, 35 temporal and nasal fields,
comparison of, 35f Finger counting, 23
Finger movement technique, 23 Fixation losses, 136
Flat test object, 25
Folate, mitochondrial energy production, 184
Frequency-of-seeing curves and fluctuations, field testing principles, 92–94
Fuchs colobomata, 181
Full threshold testing strategy, 129–30 Functional MRI (fMRI), understanding
retinotopic projection, 46, 48 Functional visual loss
field loss types, 294–95 patient types, 293
tests for, 295–97
Fundus flavimaculatus, 213. See Stargardt disease Fundus photography, band atrophy, 256
Fungal infection, 256
Fusion testing, macular area evaluation, 5
304 Index
General contraction, 16 Generalized constriction
papilledema, 201, 202–3f Generalized defects, monocular field
defects, 59–60
generalized depression or peripheral contraction, 59–60
Generalized depression or peripheral contraction, 59–60
optic nerve, 60 preretinal media, 59–60 retina, 60
Geniculocalcarine fibers, visual pathway, 13 Geographic atrophy
mimicking paracentral glaucomatous field loss, patient with, 156–57f
Gerstmann syndrome, 270–71 Giant aneurysm, 250 Glaucoma hemifield test (GHT)
abnormally high sensitivity, display of, 134 Glaucoma, 295
progression analysis printout, 115f Glaucomatous cupping, 128 Glaucomatous field loss, single field
printout, 100f
deviation and the pattern standard deviation, 107f
Glaucomatous scotomas, detection of by manual perimetry, 128
Glaucomatous visual field loss, and automated perimetry, 127–29
advanced field loss, 150–51f age-related macular degeneration, 156 dense superior and inferior arcuate-type
defects, 158–59f
diagnosing acquired glaucomatous damage, 144t
early glaucomatous generalized depression, 130–31f
and elevated mean deviation, 129 evaluation of series of tests, 144–61
artifacts, 149–54
baseline establishment, 146–49
central abnormalities, follow-up of, 159–60 glaucoma progression analysis, 157–59 long-term fluctuation, 155–56
progression, criteria for, 155–57 progression, nature of, 149 trend analysis, 159
evaluation of single test, 132–44 abnormality, criteria for, 140–43, 143t advanced field loss, follow-up of, 144 field loss, staging of, 143–44, 149t patient reliability, 132–40
test selection, 144 full threshold test
advantages of, 129–30 disadvantages of, 130
generalized depression on, 130–31f
and glaucoma management, identification of, 127
high pass resolution perimetry in, 173f central scotomas, occurrence of, 129 multiple confounding variables, 152–55f ocular hypertension, 160f
Gliomas, 193, 198–99, 247t, 250 Goldmann perimeter, 4, 11, 86, 111
advantage of, 27
central field exploration, 6 for chiasmal lesion, 240
for peripheral field technique, 34–35 and tangent screen, 3
Goldmann visual field
with superior depression, peripheral retinal abnormalities, 231–32f
Guided Progression Analysis (GPA), 157, 162–65f PROGRESSOR trend analysis, 165f
Gun barrel field, 295 Gustatory hallucinations, 269
Gyrate atrophy, visual field defects by, 211
Hallucinations
occipital lobe field defects and, 285 temporal lobe field defects and, 268–69
gustatory hallucinations, 269 Halved vision, 233
Headache
in dilatation of third ventricle, 250 in papilledema, 200, 201
in pituitary tumor, 233
inarteritic ischemic optic neuropathy, 196 nonsecreting tumors, 247
pituitary apoplexy, 248 suprasellar meningiomas, 248–49
Heijl-Krakau blind spot monitoring technique, 96 Hemianesthesia, 61, 256, 260
Hemianopia, 179, 256 Hemianopic pupillary sign, 254 Hemianopsia, 16
and Chamlin step technique, 32 Hemifield slide phenomenon, 240–41 Hemiretinal suppression, 31 Heredodegenerative optic atrophies, 182–83
dominant optic atrophy (DOA), 185–88 Leber’s hereditary optic neuropathy
(LHON), 183–85
recessive optic atrophy (ROA), 189 Hermansky-Pudlak syndrome, oculocutaneous
albinism, 215
High-resolution optical coherence tomography (OCT), 226
Histiocytosis, 247t, 250
Homonymous defects, incongruous, 16 Homonymous hemianopia, 16. See also Halved
vision
occipital cortex field defects, 273 with macular sparing, 275 bilateral, 280–81
Homonymous hemianopias horizontal sectoranopia, incomplete
congruous, 62–63 incomplete incongruous, 65–66 macular sparing, incomplete, 64
macular splitting, complete, 60–62 paramidline-sparing vertical hemianopia, 63 two scotomas, incomplete, 64
unilateral defect of temporal crescent, incomplete, 67
unilateral sparing of temporal crescent, incomplete, 66
Homonymous hemianopic scotoma detection of, 263
multiple sclerosis and, 283 Horizontal sectoranopia, incomplete
congruous, 62–63 Hormone-secreting adenoma, 247 HRR plates, 37,
Humphrey 24-2 visual field, 243–44f, 245f Humphrey perimeter, 9
depicting variations, fields defects, 19 Humphrey Visual Field Analyzer, 85, 88, 93,
95, 293
fixation monitoring by, 96–99 graytone symbols, use of, 87f
visual threshold, measurement of, 88f Hydroxychloroquine toxicity, 226 Hyperphoria, 241
Hyperplasia, 177
Hypoplasia, 177, 178, 179, 215 Hysteric patients, 293
Iatrogenic lesion, 247t Idiopathic blind spot, 250
Idiopathic intracranial hypertension (IIH), 193
and papilledema, 201
Illuminance, measurement of light, 87 Incomplete incongruous, binocular field
defects, 65–66 anterior optic tract, 65 occipital lobe, 66 optic radiation, 65–66
Internal carotid artery (ICA) aneurysms, 243
Intracranial aneurysm, 199, 249 Intraretinal hemorrhages and exudates,
HVF 24-2, 222–23f Intravenous steroids
in arteritic ischemic optic neuropathy (AAION), 197
in optic neuritis, 194 Intrinsic lesion, 247t Ipsilateral optic tract, 239
Ischemic optic neuropathies, 193 Isopter
clinical perimetry, 4 perimetry chart, 85
Index 305
Junctional field defects, 80–83 bitemporal hemianopia plus, 83 complete monocular plus incomplete
contralateral ocular, 80–81 homonymous hemianopia plus, 81–83
Junctional scotoma, 241, 242f
Kinetic perimetry, 5
field testing principles, 88–90
visual field, localized shallow depressions of, 89f
Kinetic stimuli, measurement of light, 87 Kinetic testing, blind spot interpretation, 4 Kjer’s optic neuropathy. See Dominant optic
atrophy (DOA)
Knapp’s description, and blind spot, 7 Kollner’s law, in color testing, 36
Lateral choroidal artery, occlusion of, 260f Lateral geniculate body field defects, 258–61 Lateral geniculate nucleus (LGN), 239, 253 L-carnitine, mitochondrial energy
production, 184
Learning effect and artifacts, automated perimetry, 118–20
corrective lens/frame artifacts, 120 eyelid and nose effects, 119
media opacities, 119 miosis, 118–19 mydriasis, 118–19 refractive errors, 119–20
Leber’s hereditary optic neuropathy (LHON), 183–85
characteristics of, 183
dense central visual field defect, 185f Light, measurement of, 87
Linear magnification factor, 277–78 Localization, visual field testing, 264–67
of hemianopic field defect, 268
Localized defects, monocular field defects, 48–59 altitudinal hemianopia, 59
arcuate and paracentral field defects, 52–54 central scotoma or depression, 54–56 centrocecal scotoma or depression, 57–58 enlarged physiologic blind spot, 56–57 equatorial annular scotoma or
depression., 58–59
wedge-shaped temporal field defect, 48–52 Localized scotoma, 105, 106f, 111, 129,
130f, 133
Los Angeles Latino Eye Study, 127 Luminance, measurement of light, 87
Macroaneurysm, 209 Macular area, evaluation of, 5
Macular degeneration, dry age-related, 36f, 57, 156, 207, 208f, 209f
geographic atrophy in, 209
Macular diseases, visual field defects by, 207–9