Ординатура / Офтальмология / Английские материалы / Electrophysiology of Vision_Lam_2005
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Chapter 4 |
NON-PHOTIC EOG RESPONSES
Changes in EOG are not always induced by light. A reduction in EOG amplitude occurs with intravenous infusion of hyperosmolar agents such as mannitol, and this is called the hyper- osmolarity-induced response (18). Carbonic anhydrase inhibitors such as acetazolamide inhibit the conversion of carbon dioxide to bicarbonate and reduce EOG amplitude by interfering with RPE function (19). Infusion of bicarbonate ions also reduces EOG amplitude most likely because of an increase in bicarbonate concentration on the basal RPE membrane which produces depolarization of the apical RPE membrane (20). In contrast, ingestion of ethyl alcohol increases the dark-adapted EOG amplitude in the absence of light (21). Similar to the effect of light, the alcohol-induced response is due to an increased in the Cl conductance in the basal and lateral surfaces of the RPE.
These non-photic EOG responses have been proposed as possible objective provocative tests of RPE function, and several reports have demonstrated abnormal non-photic EOG responses in various retinal conditions such as retinitis pigmentosa, Stargardt macular dystrophy, fundus albipunctatus, and Best macular dystrophy (22–24). Further investigations are needed to determine whether the nonphotic EOG responses are clinically useful.
FAST OSCILLATIONS OF THE EOG
The fast oscillation of the EOG occurs over 60–75 sec after the onset of light adaptation (3,25,26). The fast oscillation is produced by hyperpolarization of the basal RPE membrane in response to the decrease in extracellular Kþ of the photoreceptor outer segments. The clinical utility of EOG fast oscillations is unclear and specialized recording techniques are required. Brief alternating light and dark periods of 60– 80 sec each are recommended for recording the fast oscillation and a period of preadaptation is not essential. Continuous recording of the saccades is done over at least six completed
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light–dark cycles. The fast oscillations decrease with light and increase with darkness and are delayed by approximately 50% of the stimulus cycle.
REFERENCES
1.Dubois-Reymond EH. Chapter 3. Von dem ruhen Nervenstrome. Untersuchungen Uber Thierische Electricita¨t. Vol. 2. Berlin: G Reimer, 1849:251–288.
2.Marg E. Development of electro-oculography. Arch Ophthalmol 1951; 45:169–185.
3.Marmor MF, Zrenner E. Standard for clinical electro-oculo- gram. Arch Ophthalmol 1993; 111:601–604.
4.Steinberg RH, Linsenmeier RA, Griff ER. Three light-evoked responses of the retinal pigment epithelium. Vision Res 1983; 23:1315–1323.
5.Linsemeter RA, Steinberg RH. Origin and sensitivity of the light peak of the intact cat eye. J Physiol 1982; 331:653–673.
6.Miller SS, Edelman DJ. Active ion transport pathways in the bovine retinal pigment epitehlium. J Physiol 1990; 424:283– 300.
7.Miller SS, Steinberg RH. Active transport of ions across the frog retinal pigment epithelium. Exp Eye Res 1977; 25:235–248.
8.Steinberg RH, Griff ER, Linsenmeier RA. The cellular origin of the light peak. Doc Ophthalmol Proc Ser 1983; 39:1–11.
9.Ro¨ver J, Bach M. C-wave versus electrooculogram in diseases of the retinal pigment epithelium. Doc Ophthalmol 1987; 65:385–391.
10.Skoog K-O. The directly recorded standing potential of the human eye. Acta Ophthalmol (Copenh) 1975; 53:120–132.
11.Arden GB, Kelsey JH. Changes produced by light in the standing potential of the human eye. J Physiol (Lond) 1962; 161:189–204.
12.Franc¸ois J, Szmigielski M, Verriest G, DeRouck A. The influence of changes in illumination on the standing potential of the human eye. Ophthalmologica 1965; 150:83–91.
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13.Homer LD, Kolder HE. The oscillation of the human corneoretinal potential at different light intensities. Pflu¨ gers Arch Gesamte Physiol 1967; 296:133–142.
14.Kru¨ ger C, Baier M. Increment threshold function of the lightinduced slow oscillation of the EOG. Doc Ophthalmol Proc Ser 1983; 37:75–80.
15.Brigell M, Bach M, Barber C, Kawasaki K, Koojiman A. Guidelines for calibration of stimulus and recording parameters used in clinical electrophysiology of vision. Calibration standard committee of the international society for clinical electrophysiology of vision (ISCEV). Doc Ophthalmol 1998; 95:1–14.
16.Arden G, Fojas MR. Electrophysiologic abnormalities in pigmentary degenerations of the retina. Arch Ophthalmol 1962; 68:369–389.
17.Alexandridis E, Ariely E, Gronau G. Einfluss der Bulbuslage und der Bulbausala¨nge auf das EOG. Graefes Arch Ophthalmol 1975; 194:237–241.
18.Madachi-Yamamoto S, Yonemura D, Kawasaki K. Hyperosmolarity response of ocular standing potential as a clinical test for retinal pigment epithelial activity. Normative data. Doc Ophthalmol 1984; 57:153–162.
19.Madachi-Yamamoto S, Yonemura D, Kawasaki K. Diamox response of ocular standing potential as a clinical test for retinal pigment epithelial activity. Acta Soc Ophthalmol Jpn 1984; 88:1267–1272.
20.Segawa Y, Shirao Y, Kawasaki K. Retinal pigment epithelial origin of bicarbonate response. Jpn J Ophthalmol 1997; 41:231–234.
21.Arden GB, Wolf JE. The human electro-oculogram interaction of light and alcohol. Invest Ophthalmol Vis Sci 2000; 41:2722– 2729.
22.Arden GB, Wolf JE. The electro-oculographic responses to alcohol and light in a series of patients with retinitis pigmentosa. Invest Ophthalmol Vis Sci 2000; 41:2730–2734.
23.Gupta LY, Marmor MF. Sequential recording of photic and non photic electro-oculogram responses in patients with extensive extramacular drusen. Doc Ophthalmol 1994; 88:49–55.
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24.Yonemura D, Kawasaki K, Madachi-Yamamoto S. Hyperosmolarity response of ocular standing potential as a clinical test for retinal pigment epithelial activity. Chorioretinal dystrophies. Doc Ophthalmol 1984; 57:163–173.
25.Kolder H, Brechner GA. Fast oscillations of the corneoretinal potential in man. Arch Ophthalmol 1966; 75:232–237.
26.Weleber RG. Fast and slow oscillations of the electro-oculo- gram in Best’s macular dystrophy and retinitis pigmentosa. Arch Ophthalmol 1989; 107:530–537.
5
Visual Evoked Potential
In visual evoked potential (VEP), the electroencephalographic (EEG) signals of the brain elicited by visual stimuli are recorded with cutaneous electrodes placed on the scalp in the occipital region. Unlike the EOG and different types of ERG which measure activities of the retina or the retinal ganglion cells, VEP is the only electrophysiologic test that assesses visual cortical activity. Standard for VEP recording has been established by the International Society for Clinical Electrophysiology of Vision (ISCEV) and is available on the ISCEV Internet website. The standard is reviewed every 3 years and published periodically. A summary of the standard is provided in Table 5.1.
CLINICAL UTILITY OF VEP
The VEP provides a clinical measure of the function of the visual pathway. In the clinic, VEP is commonly performed to detect visual pathway deficits in patients with no apparent objective signs of ocular dysfunction, in other words, unexplained visual loss. For instance, the utility of VEP in
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Table 5.1 Summary of International Standard for Visual Evoked Potential (VEP)
Clinical protocol |
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Pupils |
Undilated |
Fixation |
Fixation target in center of stimulus |
Refraction |
Best-correction for testing distance for pattern reversal VEP |
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and pattern onset=offset VEP |
Normal values |
Each laboratory to determine age gender, and interocular difference norms |
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from direct tabulation of normal responses with median and 95% confidence |
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limits as minimum outer limits of normal |
Recording |
At least two replications of each stimulus to confirm responses |
Analysis time |
250 msec; 500 msec if both onset and offset responses are analyzed |
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for pattern onset=offset VEP |
Electrode placement |
International 10=20 system |
Stimulus parameters of the |
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three standard responses |
Abrupt alternating black and white checkerboard; white element > 80 cd m 2, |
Pattern reversal VEP |
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contrast between white and black elements > 75%, mean |
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luminance > 40 cd m 2, background 40 cd m 2; reversal rates |
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between 1 and 3 reversals per second (0.5–1.5 Hz); overall screen luminance |
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should not vary during testing (usually requires equal number of light and |
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dark elements); at least two pattern element sizes, 1 and 15 min checks |
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should be tested; visual field stimulated should subtend 15 visual angle |
Pattern onset=offset VEP |
Pattern similar to pattern reversal VEP with interspersed abrupt diffuse blank |
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luminance between pattern stimulus; no change in mean luminance as pattern |
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appears or disappears; 100 msec to 200 msec of pattern presentation separated |
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by at least 400 msec diffuse background |
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Flash VEP |
Standard flash (1.5–3.0 cd s m 2) as defined in ERG standards; background |
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light 15–30 cd m 2, subtend 20 visual angle |
Designation of waveform |
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components |
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Flash VEP |
N1, P1, N2, P2, N3, P3, N4 |
Pattern reversal VEP |
N75, P100, N135 |
Pattern onset=offset VEP |
C1, C2, C3 |
Pre-chiasmal, chiasmal, and |
Prechiasmal assessment |
postchiasmal assessment |
Pattern VEP with monocular stimulation recommended; pattern |
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onset=offset VEP has greater inter-subject variability than pattern |
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reversal VEP but has little intra-subject variability. Pattern onset=offset |
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VEP is less prone to deliberate patient defocusing of stimulus and is most |
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effective for estimating visual acuity; flash VEP used for any assessments |
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for patients with poor fixation and=or dense media opacities |
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Chiasmal and postchiasmal assessment |
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Not part of standard; multiple electrodes at midline and laterally |
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recommended; pattern stimulation |
Reporting results |
Indicate whether the international standard were met; inclusion of the |
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following are recommended-eye tested, designated electrode position of |
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the recording channel, field size of stimulus, flash intensity, pattern |
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element size, and contrast of pattern stimuli; two replications of |
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waveforms obtained |
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(Continued) |
Potential Evoked Visual
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Table 5.1 Summary of International Standard for Visual Evoked Potential (VEP) (Continued)
Basic technology |
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Stimulus calibration |
Flash stimulus intensity measured by an integrated photometer |
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Photometer in non-integrating mode or spot photometer for white |
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stimulus areas, luminance 80 cd m 2; field luminance uniform, varying by |
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< 30% between center and periphery of tested field; contrast maximal (not |
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< 75%) between black and white squares or gratings |
Electrode |
Standard silver–silver chloride or gold disc electroencephalography (EEG) |
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electrodes ( 5 kO impedance); fixed to scalp and maintained as recommended |
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by manufacturer |
Recording parameters |
Analog high pass and low pass filters set at 1 Hz and 100 Hz, analogue |
Amplification and |
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averaging systems |
filter roll-off slopes 12 dB per octave for low frequencies and 24 dB per |
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octave for high frequencies |
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Amplification of input signal by 20,000–50,000, channel to channel |
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amplification difference < 1%; impedance of preamplifiers 10 MO |
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Analogue signal digitized 500 samples per second per channel, 8 bit |
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minimal resolution |
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Automatic artifact rejection to exclude signals exceeding 50–100 mV |
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Number of repetition or sweeps for each stimulus, 64 for each trial |
Repetition rate |
Low temporal frequency, < 2 stimuli per second |
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identifying occult visual pathway dysfunction in patients with multiple sclerosis has been demonstrated. An impaired VEP can be produced by a deficit large enough anywhere along the visual pathway including the retina, optic nerve, and brain. Therefore, an impaired VEP is anatomically non-speci- fic unless it is used in combination with a thorough ocular examination and other clinical modalities such as visual field, ERG, and neuroimaging. In short, VEP should not be performed in place of a comprehensive ophthalmic examination or neuroimaging. Impaired VEP responses may be produced in some normal persons by deliberate poor fixation, defocusing, or conscious suppression (1–3). Pattern onset=offset and flash VEP are less susceptible to this effect than pattern reversal VEP. The use of VEP in cortical blindness and nonorganic visual loss are discussed in Chapters 17 and 16, respectively. The VEP as a measure of visual function in infants and young preverbal children is detailed in Chapter 6.
Physiologic Origins of VEP
The physiologic basis of VEP is predominantly from the activity of the primary visual cortex located at the posterior tip of the occipital lobe (Fig. 5.1). The primary visual cortex, referred to as the striate cortex and anatomically designated as V1, is not a flat surface but folds inward to form the calcarine sulcus. The striate cortex receives visual projections from the lateral geniculate neurons by way of the optic radiations. These projections terminate in alternating eye-specific columns called ocular dominance columns of cortical layer IV of the striate cortex. The signals of the two eyes are combined beyond this cellular layer so that most cortical neurons are binocular with receptive fields that are in the same visual field location in each eye. As a consequence of the semidecussation of the retinal ganglion cell fibers at the optic chiasm, the right hemifield is represented in the left striate cortex and the left hemifield is represented in the right striate cortex. In addition, the upper visual field is represented below the calcarine sulcus, and the lower visual field is represented above the calcarine sulcus.