Ординатура / Офтальмология / Английские материалы / Electrodiagnosis of Retinal Disease_Miyake_2005
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4.7 Age-Related Macular Degeneration 225
4.7.1How Does Subretinal Hemorrhage Damage the Retina?
A thick subretinal hemorrhage situated under the fovea occasionally has a natural course that leads to severely decreased visual function even in those without choroidal neovascularization. Animal experiments have shown that the photoreceptors can be damaged by the toxic effects of the iron released by red blood cells as well as by mechanical blockage by the hemorrhage, which hinders metabolic exchange between the photoreceptors and the RPE cells [1].
Subretinal macular hemorrhages can be successfully removed by vitrectomy using tissue plasminogen activator [2], leading to an improvement in the postoperative visual acuity of patients whose vision was good before the hemorrhage [3] (Fig. 4.31).
Changes in the focal macular ERGs elicited by a 10° spot in five patients who had a submacular hemorrhage removed by vitrectomy using tissue plasminogen activator are shown in Fig. 4.32. The submacular hemorrhage was caused by rupture of a macroaneurysm in three of the eyes, AMD in one of the eyes, and an unknown reason in the fifth eye. The duration of the subretinal hemorrhage ranged from 3 to 14 days. All of the patients had extremely poor visual acuity (from hand motion to 0.05) before
surgery, and the visual acuity improved to 0.1–0.7 after surgery.
Three points can be made based on these results. First, focal macular ERGs were undetectable in all of these patients before surgery regardless of the duration of the submacular hemorrhage. This is definitely different from the results from patients with idiopathic central serous chorioretinopathy, where serous fluid, not blood, accumulates between the photoreceptors and the RPE. Patients with central serous chorioretinopathy usually have much better visual acuity with good-amplitude focal macular ERGs (see Section 4.1). This difference indicates that blood can alter the function of the photoreceptors much more so than can serous fluid.
Second, the decline of photoreceptor function is partially reversible when blood is removed from the subretinal space even after 14 days, as shown by the recovery of the focal macular ERG in case 5. However, it is more likely that the earlier the blood is removed the better is the recovery. The third point is that there is little if any toxic effect of recombinant tissue plasminogen activator injected at clinically useful doses.
226 4 Acquired Macular Diseases
Fig. 4.31. Top: Preoperative fundus photograph with a 10° spot superimposed on the fovea. The image was obtained while recording the macular ERG in a patient with submacular hemorrhage. Bottom: Postoperative photograph. The retinal blood is almost completely removed. (From Terasaki et al. [3], with permission)
Fig. 4.32. Focal macular ERGs recorded from five patients with subretinal macular hemorrhage. The stimulus spot was 10° in diameter. The fellow eye of case 5 shows no response because of macular degeneration of unknown cause. After surgical drainage of the subretinal hemorrhage using human plasminogen activator, there is partial recovery of the ERG in all patients. (From Terasaki et al. [3], with permission)
4.7 Age-Related Macular Degeneration 227
4.7.2Removal of Choroidal Neovascular Lesions
Surgical removal of choroidal neovascular (CNV) lesions is undertaken to preserve or regain central neurosensory retinal function as an alternative treatment to conventional laser photocoagulation in eyes with AMD (Fig. 4.33). The focal macular ERGs elicited by a 15° spot before and after removing CNV lesions in three patients are shown [4] in Fig. 4.34. The amplitudes of the a-waves, b-waves, and OPs were markedly reduced or unrecordable with prolonged implicit times before surgery. These findings indicated severe impairment of macular cone function, which agrees with a histological report that there is marked photoreceptor loss in eyes with AMD. Most patients had
a significant recovery at 3 months after surgery, with the b-wave amplitude selectively increased without an increase in the a-wave amplitude. These findings suggest further recovery of inner retinal function, particularly the on bipolar cells.
The postoperative increase in b-wave amplitude in eyes with preoperative recordable b- waves significantly correlated with the decrease in the mean parafoveal thickness measured by OCT [4] (Fig. 4.35). This suggests that inner retinal function is impaired by retinal edema, and the decreased thickness of the macula contributes to the recovery of the inner layer function of the macula.
Fig. 4.33. OCT images obtained from a 56-year-old man with AMD before and after choroidal neovascular (CNV) lesion removal
228 4 Acquired Macular Diseases
Fig. 4.34. Focal macular ERGs recorded from a normal control and three patients with AMD before and after CNV removal. The visual acuity is also shown. (From Terrasaki et al. [4])
Fig. 4.35. Percentage increase in the amplitude of the b-wave and the percentage decrease in the mean parafoveal thickness measured at four points on four sides of the fovea in vertical and horizontal scans. The results are significantly correlated (r = 0.688, P = 0.0076). (From Terasaki et al. [4], with permission)
4.7 Age-Related Macular Degeneration 229
4.7.3Macular Translocation Surgery
Although surgical removal of a subfoveal CNV can be performed in some patients with AMD, the main disadvantage of the procedure is reduced visual function that results from damage to the RPE underneath the macula. Foveal or macular translocation surgery is an operative procedure in which the fovea is moved from diseased RPE onto healthy RPE [5]. This surgery has the potential to improve or preserve central visual function in eyes after removing a subfoveal CNV.
One common technique of macular translocation surgery involves a 360° circumferential retinotomy followed by a subretinal infusion of fluid to create total retinal detachment from the RPE. The completely detached retina is then rotated to move the macula from the original position on the RPE to healthy RPE, resulting in a new retina and RPE complex. This complicated surgery has been well performed by Terasaki, my colleague, in many patients, and the results have been evaluated [6–8]. The fundus photographs and OCT images of a patient with AMD before and after macular translocation surgery are shown in Fig. 4.36.
From the point of view of retinal physiology, this technique poses several interesting and important issues that should be considered. First, what is the visual function of the entire retina after it is translocated to the new RPE? To answer this question, full-field ERGs
recorded from three representative patients with AMD before and after macular translocation with 360° retinotomy were compared [6] (Fig. 4.37). In summary of many patients, the amplitudes of the rod and cone components of the full-field ERGs were reduced by 25%–40%, with slight prolongation of the implicit times after the surgery. Interpreting these results has not been easy because, in addition to translocating the entire retina to the new RPE, we had to take into consideration surgical trauma to the retina caused by transient total retinal detachment, the 360° circumferential retinotomy, and the massive photocoagulation after reattaching the retina. However, the degree of reduction of the full-field ERGs after surgery was surprisingly small, suggesting that the sensory retina can function well at the new RPE site.
Second, how does the shifted macula function on the new RPE? The answer is obtained from the changes in visual acuity and the focal macular ERG before and after surgery [7]. In our large series of patients, visual acuity improved significantly after surgery; moreover, the amplitudes of the focal macular ERGs increased and the implicit times decreased significantly after surgery (Fig. 4.38). These results indicate that the newly located macula does maintain and organize the neural components well, resulting in improved visual acuity.
230 4 Acquired Macular Diseases
Fig. 4.36. Fundus photographs (top) and OCT images (bottom) obtained from a 77-year-old woman with AMD before and after macular translocation with 360° retinotomy. The macula was shifted to the inferior part of the retina, where the RPE underneath the macula was healthy. Her visual acuity improved from 0.06 to 0.60 following surgery. (From Terasaki et al. [8], with permission)
Fig. 4.37. Full-field ERGs recorded from three representative patients with AMD before and after macular translocation with 360° retinotomy. (From Terasaki et al. [6])
Fig. 4.38. Focal macular ERGs recorded from three representative patients with AMD before as well as early (6–12 months) and late (18–30 months) after macular translocation with 360° retinotomy. (From Terasaki et al. [7])
4.7 Age-Related Macular Degeneration 231
References
1.Glatt H, Machemer R (1982) Experimental subretinal hemorrhage in rabbits. Am J Ophthalmol 94: 762–773
2.Lewis H, Resnick SC, Flannery JG, Straatsma BR (1991) Tissue plasminogen activator treatment of experimental subretinal hemorrhage. Am J Ophthalmol 111:197–204
3.Terasaki H, Miyake Y, Kondo M, Tanikawa A (1997) Focal macular electroretinogram before and after drainage of macular subretinal hemorrhage. Am J Ophthalmol 123:207–211
4.Terasaki H, Miyake Y, Niwa T, Ito Y, Suzuki T, Kikuchi M, et al. (2002) Focal macular electroretinograms before and after removal of choroidal neovascular lesions. Invest Ophthalmol Vis Sci 43:1540–1545
5.Machemer R, Steinhorst UH (1993) Retinal separation, retinotomy, and macular relocation. II. A surgical approach for age-related macular degeneration? Graefes Arch Clin Exp Ophthalmol 231: 635–641
6.Terasaki H, Miyake Y, Suzuki T, Niwa T, Piao CH, Suzuki S, et al. (2002) Change in full-field ERGs after macular translocation surgery with 360° retinotomy. Invest Ophthalmol Vis Sci 43:452–457
7.Terasaki H, Ishikawa K, Niwa Y, Piao CH, Niwa T, Kondo M, et al. (2004) Changes in focal macular ERGs after macular translocation surgery with 360° retinotomy. Invest Ophthalmol Vis Sci 45:567–573
8.Terasaki H, Ishikawa K, Suzuki T, Nakamura M, Miyake K, Miyake Y (2003) Morphorogic and angiographic assessment of the macula after macular translocation surgery with 360° retinotomy. Ophthalmology 110:2403–2408
Subject Index
a-wave |
3 |
|
choroidal detachment |
183 |
endophthalmitis |
186 |
|
||||
Åaland Island eye disease 91 |
choroidal neovascular (CNV) |
enhanced S-cone syndrome |
68 |
||||||||
ABCR |
126, 161 |
|
lesions |
227 |
|
EOG 1, 41, 76, 165, 182, 183 |
|
||||
acute idiopathic blind spot |
choroideremia |
64 |
|
|
see also |
|
|
|
|||
|
enlargement syndrome |
see also |
|
|
|
base value |
|
|
|
||
|
187 |
|
carrier state |
|
|
|
dark trough |
|
|
||
acute zonal outer retinopathy |
complete form |
90, 136 |
L/D ratio |
|
|
|
|||||
|
(AZOOR) 187 |
cone 4 |
|
|
|
light peak |
|
|
|
||
adult-onset foveomacular |
cone (photopic) ERG |
11 |
ERGs from pediatric patients |
6 |
|||||||
|
vitelliform dystrophy 165 |
cone dysfunction |
114 |
|
|
|
|
||||
age-related macular degeneration |
cone dystrophy |
116, 123 |
familial optic atrophy with negative |
||||||||
|
223 |
|
see also |
|
|
|
|||||
amacrine cells |
3, 29 |
central cone dystrophy |
ERG |
150 |
|
|
|||||
APB |
8, 99 |
|
cone–rod dystrophy |
123 |
fingerprint pattern |
58 |
|
||||
arrestin |
119 |
|
cone–rod interaction |
11 |
first-order kernel |
35, 102 |
|
||||
|
|
|
|
congenital stationary night |
focal macular ERG |
20–32, 78, 88, |
|||||
|
|
|
|
blindness (CSNB) 90 |
102, 153, 176, 204, 209, 215, |
||||||
b/a ratio |
174, 180, 181, 186 |
see also |
|
|
|
221, 224, 229 |
|
||||
b-wave |
3 |
|
complete form |
|
|
foveal thickness 213 |
|
||||
base value 183, 184 |
incomplete form |
|
|
foveoschisis |
73 |
|
|
||||
batten disease |
58 |
congenital syphilis |
196 |
(full-field) dome |
2 |
|
|||||
“bear-track” pigmentation |
53 |
|
congenital tritanopia |
141 |
full-field ERG |
2–20, 45, 76, 95, 153, |
||||||||||
Best’s disease |
165 |
|
|
|
|
contact lens electrode |
2 |
|
207, 224, 229 |
|
|
|||||
binary m-sequence |
36 |
|
|
|
CRX 8 |
126 |
|
|
|
|
see also |
|
|
|
|
|
blue cone ERG 142 |
|
|
|
|
crystalline retinopathy |
55 |
pediatic patients |
|
|
|||||||
blue cone monochromacy |
138 |
cystoid macular edema (CME) |
full-field stimulator |
2 |
|
|||||||||||
blue-sensitive opsin |
142 |
|
|
|
203, 205 |
|
|
|
fundus albipunctatus |
|
114 |
|||||
bone spicule pigmentation |
45 |
|
|
|
|
|
|
|
fundus flavimaculatus |
160 |
||||||
bull’s-eye maculopathy |
58, 114, |
|
|
|
|
|
|
|
|
|
|
|
||||
123, 132, 148 |
|
|
|
|
d-wave |
8, 9, 14 |
|
|
|
ganzfeld dome |
|
|
|
|||
Burian-Allen bipolar contact lens |
dark adaptation |
11, 93 |
|
6 |
|
|
||||||||||
23 |
|
|
|
|
|
dark choroid |
148, 160 |
|
golden tapetal-like fundus reflex |
|||||||
|
|
|
|
|
|
dark trough |
41 |
|
|
|
82 |
|
|
|
|
|
|
|
|
|
|
|
delay in dark adaptation |
114 |
grouped pigmentation of retina 53 |
||||||||
CACNA1F 91, 105 |
|
|
|
|
depolarizing bipolar cells |
8, 99 |
GTP 126 |
|
|
|
|
|||||
carrier state |
65 |
|
|
|
|
diabetic macular edema |
177 |
GUCA1A |
126 |
|
|
|
||||
– of X-linked ocular albinism |
|
diabetic maculopathy |
176 |
GUCY2D |
126 |
|
|
|
||||||||
194 |
|
|
|
|
|
diabetic retinopathy |
170 |
|
gyrate atrophy |
66 |
|
|
||||
central cone dystrophy |
128 |
|
diabetic vitreous hemorrhage |
|
|
|
|
|
||||||||
central retinal artery occlusion |
181 |
|
174 |
|
|
|
|
hexagonal elements |
|
|
||||||
central retinal vein occlusion |
180 |
diffuse unilateral subacute |
|
34 |
||||||||||||
central serous chorioretinopathy |
|
neuroretinitis |
191 |
horizontal cell |
13 |
|
|
|||||||||
200 |
|
|
|
|
|
dominantly inherited juvenile optic |
hyperpolarizing bipolar cells 8, 99 |
|||||||||
cGMP 126 |
|
|
|
|
|
|
atrophy |
141 |
|
|
hypotonic maculopathy |
183 |
||||
234 Subject Index
idiopathic epimacular membranes |
bull’s-eye maculopathy |
|
|
focal macular ERGs in – |
45 |
|||||||||||||||||||
|
209 |
|
|
|
|
|
|
familial optic atrophy |
|
|
see also |
|
|
|
|
|
|
|||||||
idiopathic macular hole |
215 |
|
nematodes |
191 |
|
|
|
|
|
full-field ERGs |
|
|
|
|
|
|||||||||
incomplete form |
136 |
|
|
neovascular glaucoma |
180 |
|
macular OPs |
|
|
|
|
|
||||||||||||
infrared television fundus camera |
Nettleship-Falls ocular albinism |
multifocal ERG |
|
|
|
|
|
|||||||||||||||||
|
21 |
|
|
|
|
|
|
|
87 |
|
|
|
|
|
|
|
rod (scotopic) ERG |
4 |
|
|
||||
inner retinal breaks |
73 |
|
|
neuronal ceroid-lipofuscinosis 58 |
rod bipolar cells |
8 |
|
|
|
|
||||||||||||||
intensity-response series |
3, 146 |
nonischemic types |
180 |
|
|
rod monochromacy |
|
136 |
|
|||||||||||||||
internal limiting membrane (ILM) |
nyctalopin |
105 |
|
|
|
|
|
rod-cone dysfunction syndrome |
||||||||||||||||
|
218, 219 |
|
|
|
|
nystagmus |
136 |
|
|
|
|
|
|
144 |
|
|
|
|
|
|
||||
interplexiform cells |
29 |
|
|
NYX |
91, 105 |
|
|
|
|
|
|
rod–cone dystrophy |
|
44 |
|
|
||||||||
interstitial keratitis |
196 |
|
|
|
|
|
|
|
|
|
|
|
rod–cone interaction |
13, 16 |
||||||||||
ISCEV |
4 |
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
rubella retinitis |
194 |
|
|
|
|||
ISCEV standards |
2, 6 |
|
|
occult macular dystrophy |
128, 153 |
|
|
|
|
|
|
|
|
|||||||||||
|
|
|
|
|
|
|
|
OCT |
42, 87, 158, 165, 178, 199, 202, |
|
|
|
|
|
|
|
|
|||||||
|
|
|
|
|
|
|
|
|
215, 221, 227, 229 |
|
|
salt and pepper retinopathy |
61 |
|||||||||||
kearns-sayre syndrome |
61 |
|
off bipolar cells |
70, 90 |
|
|
salt-and-pepper change |
194 |
||||||||||||||||
KYN |
9, 99 |
|
|
|
|
|
off response |
|
8 |
|
|
|
|
|
Schubert-Bornschein type |
90 |
||||||||
|
|
|
|
|
|
|
|
Oguchi’s disease |
119 |
|
|
|
S-cone ERG |
10, 68, 77, 101 |
||||||||||
|
|
|
|
|
|
|
|
on bipolar cells |
70, 90 |
|
|
scotopic threshold response (STR) |
||||||||||||
L/D ratio |
41, 183 |
|
|
|
on response |
|
8 |
|
|
|
|
|
|
3, 97 |
|
|
|
|
|
|
||||
LED |
5, 9 |
|
|
|
|
|
|
OPA1 |
142 |
|
|
|
|
|
|
|
second-order kernel |
|
35, 102 |
|||||
light adaptation |
11 |
|
|
|
origin of ERG |
1 |
|
|
|
|
|
short-flash b-wave |
14 |
|
|
|||||||||
light peak |
41 |
|
|
|
|
ornithine aminotransferase |
66 |
sign-inverting synapses |
8 |
|
||||||||||||||
LM cone ERG |
10 |
|
|
|
oscillating potentials |
|
2, 170 |
|
sign-preserving synapses |
|
8 |
|||||||||||||
long-flash photopic ERG |
8, 9 |
|
|
|
|
|
|
|
|
|
|
silent choroid |
160 |
|
|
|
|
|||||||
luetic chorioretinitis |
196 |
|
|
|
|
|
|
|
|
|
|
Stargardt disease |
148, 160 |
|
||||||||||
|
|
|
|
|
|
|
|
panretinal photocoagulation |
171 |
stray light 20 |
|
|
|
|
|
|||||||||
|
|
|
|
|
|
|
|
paravenous retinochoroidal atrophy |
subjective blue sensitivity |
101 |
||||||||||||||
m-sequence |
34 |
|
|
|
|
|
51 |
|
|
|
|
|
|
|
subretinal hemorrhage |
225 |
||||||||
macular hole surgery |
217 |
|
PDA |
9, 99 |
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|||||
macular OPs |
27–32, 46 |
|
|
perimetry |
158 |
|
|
|
|
|
30-Hz flicker ERG |
|
96 |
|
|
|||||||||
macular pseudohole |
221 |
|
peripheral cone system |
128 |
|
|
|
|
||||||||||||||||
macular translocation 229 |
|
peripheral retinoschisis |
73 |
|
tritan |
138, 141 |
|
|
|
|
|
|||||||||||||
MEWDS |
187 |
|
|
|
|
peripherin/RDS |
126 |
|
|
|
two-color perimetry |
|
131, 133, 158 |
|||||||||||
mitochondrial DNA |
61 |
|
|
photophobia |
123, 136 |
|
|
|
|
|
|
|
|
|
|
|||||||||
mitochondrial myopathy |
61 |
|
photopic hill phenomenon |
14 |
unilateral cone dysfunction |
|
||||||||||||||||||
mixed cone–rod ERG |
4 |
|
|
photopic long-flash ERGs |
15 |
132 |
||||||||||||||||||
Mizuo phenomenon |
119 |
|
photoreceptor potential |
13 |
|
|
|
|
|
|
|
|
|
|||||||||||
monitoring ERGs |
7 |
|
|
|
plasminogen activator |
226 |
|
VER |
|
|
|
|
|
|
|
|||||||||
monitoring during surgery |
7 |
PNR |
68 |
|
|
|
|
|
|
|
23, 24 |
|
|
|
|
|
|
|||||||
Mueller cells |
3, 74, 219 |
|
|
proliferative diabetic retinopathy |
visual acuity |
75, 92 |
|
|
|
|||||||||||||||
multifocal ERG |
34–40, 46, 79, 102, |
|
174 |
|
|
|
|
|
|
|
vitelliform macular dystrophy |
|||||||||||||
|
153, 188, 215, 224 |
|
|
pseudohypopyon |
165 |
|
|
|
165 |
|
|
|
|
|
|
|||||||||
multiple evanescent white dot |
|
|
|
|
|
|
|
|
|
|
vitelliruptive |
165 |
|
|
|
|
||||||||
|
syndrome (MEWDS) |
187 |
|
|
|
|
|
|
|
|
|
vitreous fluorophotometry |
123 |
|||||||||||
multiple white flecks |
86 |
|
|
RDH |
86 |
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
||||
|
|
|
|
|
|
|
|
RDH5 |
116 |
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
refractive error |
75, 92 |
|
|
X-linked ocular albinism |
87, 194 |
|||||||||||
nasotemporal asymmetry |
28 |
|
retinal detachment |
183 |
|
|
X-linked retinoschisis |
72, 148 |
||||||||||||||||
negative ERG |
90, 147, 191 |
|
retinitis pigmentosa |
|
44, 45 |
|
XLRS1 |
148 |
|
|
|
|
|
|
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see also |
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atypical – |
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X-wave 16 |
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