| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
1 From the Institut de Recherche en Ophtalmologie, Sion, Switzerland; and 2 Istituto di Oftalmologia, Università Cattolica S. Cuore, Rome, Italy.
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
METHODS. In five normal volunteers, Fonh measured at the neuroretinal rim was monitored continuously by laser Doppler flowmetry. Stimuli were generated by green and red light emitting diodes and delivered to the fundus in Maxwellian view (field of 25o). Both green (G) and red (R) illuminances were square-wave modulated, 180o out of phase, with a maximum value of 10.4 for G and 2.64 lux for R. Flicker frequency was varied from 2 Hz to 40 Hz. RFonh was defined as the change in Fonh during stimulation relative to the prestimulus Fonh.
RESULTS. Defining the color ratio r as R/(R + G), the RFonh, measured for a 15-Hz flicker, was largest at pure luminance (r = 0 and 1), declined at mixed luminance and chromatic modulations, and reached a secondary maximum at r = 0.45, the value of psychophysical equiluminance. RFonh versus flicker frequency displayed the characteristics of a low-pass function for the equiluminance flicker stimulus and of a band-pass function, with a maximum at intermediate frequencies, for the luminance flicker stimulus.
CONCLUSIONS. RFonh in humans can be evoked by heterochromatic flicker, modulated either in luminance or chromatic equiluminant conditions. RFonh may be specific for luminance and chromatic modulations, similar to neural responses dominated by the magno- and parvocellular activity, respectively. These findings offer a new approach to study the neurovascular coupling at the optic nerve head in both physiological and diseased conditions involving predominantly or selectively the magno- and parvocellular pathways.
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
The primate visual pathway is characterized by two main cellular systems. The parvocellular system consists of tonic, wavelength-opponent retinal ganglion cells projecting to the parvocellular layers of the lateral geniculate nucleus. The majority of neurons belonging to this system receive antagonistic input from medium-wavelength–sensitive and long-wavelength–sensitive cones.7 The magnocellular system is made up of phasic, nonopponent ganglion cells that project to the magnocellular layers of the lateral geniculate nucleus. Magnocellular retinal ganglion cells receive combined input from medium- and long-wavelength–sensitive cones at both center and surround. Uniform field stimuli, whose luminance is varied periodically over time (i.e., the luminance flicker modulation) at relatively high temporal frequencies, are known to be optimal, though not specific, for evoking the response of the magnocellular neurons.7 On the other hand, low-temporal frequency, counter-phase modulation of red and green fields, whose luminance has been matched by heterochromatic flicker photometry (i.e., the equiluminant chromatic flicker modulation), represents a strong stimulus for the parvocellular neurons, eliciting predominantly their activity.7 8 At both retinal and postretinal levels, sensitivity of the human visual system to luminance modulation is maximal at intermediate temporal frequencies (10 Hz to 20 Hz) and falls off at both low and high frequencies, whereas sensitivity to equiluminant chromatic modulation is maximal at low temporal frequencies (<5 Hz) and falls-off at frequencies greater than 5 Hz to 10 Hz.7 9 10 11
It is presently unknown whether an RFonh can be evoked by chromatic, whole-field flicker modulation. The occurrence of such a response would imply that vascular changes in the ONH are associated, under specific experimental conditions, with the neural activity dominated by the parvocellular system. The aim of the present study was, therefore, to evaluate whether: an RFonh can be evoked in normal humans by red–green equiluminance flicker modulation and, if so, whether the temporal frequency dependence of RFonh evoked by this stimulus differs from that elicited by luminance flicker of either pure R or G luminance modulation.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
LDF Measurements
ONH blood flow was measured using the Topcon TRC-based
near-infrared laser Doppler system (Topcon, Inc., Tokyo, Japan)
described previously.1
12
Briefly, a probing laser beam
(wavelength, 810 nm; power at the cornea, 90 µW; diameter at the
fundus, 
150 µm) was directed at the ONH tissue at temporal sites
on the neuroretinal rim. The laser light scattered by the ONH was
collected by an optical fiber at the image plane of the fundus camera
and guided to a photograph-detector. The aperture of the
light-collecting optical fiber (diameter at the fundus approximately
180 µm) was centered on the site illuminated by the probing laser
beam.
An infrared video camera placed in the retinal image plane of the fundus camera allowed the operator to monitor the location of the beam and of the light-collecting aperture at the disc and, when necessary, reposition both at the desired site. The camera was positioned in front of the eye so that an edge of the pupil of the tested eye could also be observed on the video monitor. In this manner, the observer could monitor the position of the camera relative to the subject’s eye pupil and perform the necessary corrections to keep it steady. Guided by color photographs of the disc, care was taken to avoid recording from large vessels. The output signal of the detector was analyzed using a software implemented on a NeXT computer.13 It was monitored continuously in real time throughout the experiment. Fonh, in the volume sampled by the light collecting fiber, was obtained from the relationship Fonh = k x Velonh x Volonh, where k is an instrumental constant, Velonh is the first moment frequency of the Doppler shift spectrum, which is proportional to the mean velocity of the red blood cells, and Volonh is the relative number of red blood cells.2
Flicker Stimuli
Stimuli were generated by two independently controlled
ultrabright green and red light emitting diodes (Sloan, Precision
Optoelectronics, Model SL905GCU-15 and SL905OCU-16), with dominant
wavelengths at 524 and 630 nm, respectively. They were delivered to the
eye through the fundus illumination’s optical system of the Topcon
camera and uniformly illuminated in Maxwellian view, a 25°-diameter
area of the posterior pole. The currents of the diodes were square-wave
modulated, 180° out of phase, between zero and a maximum illuminance
of 10.4 lux for green and 2.64 lux for red. Temporal frequency of this
modulation ranged from 2 to 40 Hz. The color ratio defined
as14
r = R/(R +
G), where R and G represent the
illuminance of the red and green stimuli, was varied from 0 to 1.
r = 0 corresponds to a G–Black and
r = 1 to a R–Black modulation. Intermediate
values of r defined a R–G chromatic modulation.
CIE coordinates were x = 0.7, y = 0.3
for R and x = 0.17, y = 0.7
for G. The excitation of each cone type (i.e., the medium-
and long-wavelength–sensitive cones, the short-wavelength cone
excitation being negligible) was estimated by multiplying each LED
spectral component with the psychophysically based cone
fundamentals15
and integrating over the wavelength range.
Data showed that under the prior experimental conditions, long- and
medium-wavelength–sensitive cones do not modulate at r = 0.34 and r = 0.72, respectively, the r
values correspond to silent substitution.16
For
r = 0.46, the responses of long- and
medium-wavelength–sensitive cones were equal and opposite. At this
r value, cone modulation, expressed as Michelson luminance
modulation depth (see definition later), was 0.35 for the long- and
0.43 for the medium-wavelength–sensitive cones.
Experimental Protocols
In each subject, trial recordings of the LDF parameters were
performed for various locations of the probing laser beam in the
temporal region of the optic disc to obtain the largest response
possible. These consisted of 30 seconds of constant maximum
G or R illuminance, followed by 30 seconds of
flicker at 15 Hz. At the location of the disc where this response was
20% or more, the protocols pertinent to the various studies described
in this article were started. For each subject, attempts were made to
aim the laser beam at the same site of the optic disc in the various
experimental sessions. Some of the experiments described next were
performed in separate sessions on the same day. Most of them, however,
took place on different days.
Changes in blood flow were measured in response to three different modes of stimulation: pure green flicker stimulus of different modulation depths at 10 Hz; flicker stimulus with different color ratios at 15 Hz; and flicker stimuli of pure luminance and equiluminance, changing the temporal frequencies.
Pure Green Flicker Stimulus of Different Modulation Depths at 10 Hz
This measurement was performed to identify possible saturation
effects in RFonh at high luminance
modulation, which could represent a source of potential artifacts,
distorting the relationship between RFonh and
the parameters of chromatic flicker under investigation.
RFonh was measured in 2 subjects for a pure G stimulus (r = 0, 10 Hz) as a function of modulation depth defined according to the Michelson formula, as (G1 - G2)/(G1 + G2). G1 and G2 represent the green illuminance during the first and second phase of the modulation, respectively. The mean illuminance (G1 + G2)/2 was kept constant and equal to 3 lux for all modulation depths. Two experimental protocols were followed:
Protocol 1.
After a 30-second baseline recording of Fonh with constant
illuminance (modulation depth = 0), stimuli with stepwise
ascending values of the modulation depth from 0.2 units up to 1 were
presented each for a duration of 40 seconds The same sequence was then
followed in reverse.
Protocol 2.
After delivery of each stimulus, Fonh was allowed to return
to baseline, which occurred in less than one minute, before the next
modulation depth was tested. The subjects were also tested twice, in
separate days, to determine the reproducibility of
RFonh as a function of modulation depth. In one
of them, reproducibility of RFonh was evaluated
from a number of successive measurements with a pure G
stimulus (r = 0, modulation depth = 0.6,
frequency = 10 Hz) and a pure R stimulus (1, 1, 25
Hz).
Flicker Stimulus with Different Color Ratios at 15 Hz
In 5 subjects, RFonh was
measured in response to R–G stimuli with different values
of r, from 0 to 1 (10 to 12 steps). The stimuli were
modulated at 15 Hz. Reproducibility of
RFonh versus r was obtained
from two subjects (stimulation at 15 Hz) each run on two separate
days.
Flicker Stimuli of Pure Luminance and Equiluminance, Changing
the Temporal Frequencies
For stimuli of pure luminance (i.e., r = 0
or r = 1) and stimuli with r corresponding
to the point of subjective equiluminance,
RFonh, was measured in three subjects
for several frequencies between 2 Hz and 40 Hz. The point of subjective
equiluminance was estimated psychophysically for every subject by
adjusting r to produce a minimum perceivable flicker of the
R–G modulation when alternating at 15 Hz. Mean r
at equiluminance was found to be 0.45 ± 0.02.
RFonh was also measured in response to pure luminance (modulation depth = 1) and equiluminance flicker stimuli alternating at 2 and 15 Hz. Four out of the five subjects were tested at both 2 and 15 Hz with the luminance flicker stimulus, while all the five subjects were evaluated with the equiluminance stimulus.
In one subject, RFonh induced by luminance flicker obtained with pure G stimuli of different modulation depths (1, 0.6, and 0.4), but with the same mean illuminance, were also recorded as a function of frequency.
Data Analysis
RFonh was defined as
AvFonh,st/AvFonh,bl,
where AvFonh,st represents the average over the
last 20 seconds of Fonh measured as the tested
eye was exposed to a specific flicker stimulus of 1 minute duration (if
not stated otherwise). AvFonh,bl
represents the average of Fonh over the last 20
seconds measured as the eye was exposed to a homogenous, unmodulated
field of approximately the same mean luminance as that of the flicker
stimulus (baseline condition). RFonh was plotted
as a function of r, modulation depth, and frequency of the
stimulus. Comparisons across conditions were performed by repeated
measures ANOVA (with post hoc adjusted t-tests) or paired
t-tests, assuming normal data distribution.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
|
RFonh versus Modulation Depth for Pure Green
Luminance Flicker at 10 Hz
Figure 2
shows RFonh versus modulation depth for a pure
G luminance flicker (r = 0) at 10 Hz, when
the modulation depth was varied in an ascending and descending manner
in one subject (protocol 1). Also plotted is the average of both
RFonh data. A linear model is adequate to fit
the RFonh versus modulation depth data
(P < 0.01), with correlation coefficients equal to
0.98, 091, and 0.98 for the ascending, descending and average data,
respectively. RFonh measured in one subject from
the temporal part of the disc, according to protocol 2 and a pure
G luminance flicker at 10 Hz and pure R luminance
flicker at 25 Hz are shown in Figure 3A and B
. The linear model adequately fits the
RFonh versus modulation depth data
(P < 0.01), with correlation coefficients of 0.92 for
Figure 3A
and 0.99for Figure 3B
, respectively. Linearity between
RFonh and modulation depth is improved by using
this second protocol, as indicated by the higher values of the
correlation coefficients in Figure 3
compared to those associated with
the data shown in Figure 2
.
|
|
|
Flicker Stimuli of Pure Luminance and Equiluminance, Changing
the Temporal Frequencies
Figure 5
shows how the average RFonh of the data obtained
from three subjects, for luminance and chromatic equiluminance flicker,
varied as a function of frequency. For luminance flicker a band-pass
function having a broad maximum at 5 Hz to 10 Hz was found. A response,
though small, was still consistently recorded at 30 Hz. For the
equiluminance flicker, a low-pass type of function was observed, with a
maximum at 2 Hz, an attenuation above 10 Hz, and no significant
contribution beyond 15 Hz. Repeated testing in two subjects showed that
these characteristics were reproducible.
|
|
|
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
RFonh decreased significantly when the ratio between the R and G illuminance of the chromatic flicker stimulus was varied at 15 Hz from a condition of pure luminance flicker modulation to a condition where mixed luminance and chromatic modulations were present (Figs. 4A and 4B) . In most experiments, RFonh also showed a local peak corresponding to the equiluminant point measured psychophysically. This peak is quite clear in Figure 4B .
The RFonh to luminance flicker displayed a different dependency on frequency compared to the response to equiluminance flicker. With the former stimulus, RFonh was band-pass tuned and well detectable up to 30 Hz (Fig. 5) ; with the latter stimulus, RFonh had a low-pass behavior with a cutoff at 15 Hz. The results of Figure 6 suggest that this difference is not attributable to a difference in cone modulation amplitude between luminance and equiluminance flicker because reducing the modulation depth of a G–G stimulus left unaltered the band-pass tuning behavior of RFonh. In accordance with the band-pass versus low-pass behavior of RFonh, the average ratio between the RFonh obtained at 2 and 15 Hz for luminance flicker was significantly smaller and reversed, compared with that for equiluminance flicker (Table 1) .
The dependence of RFonh on r and
frequency (Figs. 4B
and 5)
is similar to that observed for the magno-
and parvo-cellular retinal ganglion cells activity7
and
for the pattern electroretinogram (PERG), a response correlated with
ganglion cell activity.9
10
17
18
By recording the
responses of magno- and parvocellular ganglion cells to luminance and
R–G equiluminance flicker modulation in monkeys, it was
found that, at high frequency, response sensitivity of magnocellular
ganglion cells was substantially weaker for the equiluminance than for
the luminance flicker.7
By contrast, at low frequency, the
response sensitivity of parvocellular ganglion cells to chromatic
equiluminance was stronger than the corresponding responses to
luminance flicker. Recordings of the steady state PERGs at relatively
high temporal frequencies (
6 Hz) as a function of r of
R–G patterns revealed that the response amplitude decreased
significantly when r was changed from luminance to mixed
luminance and chromatic contrast modulation.9
18
10
Furthermore, in both humans and monkeys the PERG amplitude showed a
local maximum at equiluminance.9
10
By decreasing stimulus
temporal frequency, this maximum was relatively more pronounced,
compared to the responses to patterns of pure luminance
contrast.9
These similarities suggest a correlation
between the observed RFonh behavior and the
physiological responses of retinal ganglion cells to respectively
high-frequency luminance flicker modulation and low-frequency
equiluminance flicker chromatic modulation. Although the neural
responses to luminance flicker may have a contribution of both magno-
and parvocellular systems,9
18
it may be suggested that
the responses to equiluminance flicker reflect, selectively or
prevalently, the activity of the parvo system.7
8
It
should be noted, however, that the neural parvo-response might change
depending on the type of stimulus. It is indeed known, from single
cells studies7
that the temporal response function of the
parvo-system is low-pass with chromatic, but band-pass with luminance
modulation.
The mechanisms underlying the flicker induced RFonh are still matter of investigation. In the cat, the extracellular K+onh concentration at the ONH increased in parallel with RFonh. Lack of evidence of a direct vasodilatory effect of K+onh on the ONH microvasculature raised doubt regarding the role of K+onh in the flicker-induced RFonh.4 The role of nitric oxide (NO) in ONH vaso-activity has been recently demonstrated.19 20 In the cat, flicker-evoked changes in NOonh concentration paralleled RFonh.19 In addition, inhibition of NO synthase markedly attenuated both the changes in NOonh concentration and RFonh. These data strongly implicate NO as a putative mediator of the coupling between blood flow and neuronal activity, although the role of other factors (pH, pCO2, circulating hormones) cannot be excluded. It is presently unknown whether the same or different mediators may underlie the specific vascular responses at the level of the ONH induced by luminance and chromatic equiluminance flicker stimuli observed in this study. Pharmacological approaches in experimental animal models could help clarify this issue.
The study described here was performed in volunteers who could maintain excellent target fixation and minimal head motion, since no bite bar was used. Subjects were instructed to fixate during the whole flicker period. This condition could be relaxed by having subjects fixate the target only during the last 20 seconds or so of the 1-minute flicker period, while the tested eye remains exposed to the flickered field during the whole period. From a clinical standpoint, the measurement of RFonh in response to luminance and chromatic equiluminance flicker stimulation, even if only applicable to patients selected for their adequate target fixation, could provide a new, powerful tool to investigate ONH and retinal diseases. First, it may bring new insights into the pathophysiology of blood flow, examined through its relationship with neural activity losses. For example, it is still unknown whether ischemic damage to the ONH in glaucoma is a primary determinant or whether it develops secondarily to compression-induced neural damage. In the former situation, it could be conceivable that an abnormal vascular response to flicker precedes any detectable neural loss, due to impaired vasoactivity. Investigation of the neurovascular coupling could also be of interest in early diabetes, where both ischemic and neural damage occur in the inner retina.21 Second, the present approach allows separate evaluation of neural visual activities, coupled with corresponding hemodynamic changes, carrying luminance and chromatic information. For instance, a considerable body of anatomic evidence indicates that, in early glaucoma, large retinal ganglion cells, subserving primarily the magnocellular pathway, are selectively or predominantly damaged.22 23 24 Although this selective vulnerability may not necessarily correlate with visual dysfunction,25 it may be of interest to investigate whether the measurement of RFonh reveal specific losses elicited by luminance versus chromatic stimulation. Electrophysiological and psychophysical results26 have shown that, in multiple sclerosis patients with or without optic neuritis, the function of the parvocellular pathway may show specific losses. The relationship of these losses to the neurovascular activity changes are still unknown.
In conclusion, the present findings indicate that changes in human ONH hemodynamics can be evoked by both luminance and equiluminance R-G flicker modulation, and that the temporal frequency response characteristics of these changes differ for the two types of stimulation, similar to the neural responses of retinal ganglion cells. These data suggest that equiluminance-evoked RFonh is associated with neural parvocellular activity, yet luminance flicker-induced RFonh may be correlated with the activity of both magno- and parvocellular neurons. The specificity of RFonh elicited by chromatic flicker modulation may offer new opportunities to study visually evoked vascular activity of the ONH in both physiological and diseased conditions involving predominantly or selectively the magno- and parvosubsystems.
|
Acknowledgements |
|---|
|
Footnotes |
|---|
Submitted for publication August 21, 2000; revised November 6, 2000; accepted November 22, 2000.
Commercial relationships policy: N.
Corresponding author: Charles E. Riva, Institut de Recherche en Ophtalmologie, 64 Av. Grand Champsec, 1950 Sion, Switzerland. charles.riva{at}iro.vsnet.ch
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
This article has been cited by other articles:
|
|
 |
|
  G. Hanazono, K. Tsunoda, Y. Kazato, K. Tsubota, and M. Tanifuji Evaluating Neural Activity of Retinal Ganglion Cells by Flash-Evoked Intrinsic Signal Imaging in Macaque Retina Invest. Ophthalmol. Vis. Sci., October 1, 2008; 49(10): 4655 - 4663. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. Feigl, I. B. Stewart, B. Brown, and A. J. Zele Local Neuroretinal Function during Acute Hypoxia in Healthy Older People Invest. Ophthalmol. Vis. Sci., February 1, 2008; 49(2): 807 - 813. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Hanazono, K. Tsunoda, K. Shinoda, K. Tsubota, Y. Miyake, and M. Tanifuji Intrinsic Signal Imaging in Macaque Retina Reveals Different Types of Flash-Induced Light Reflectance Changes of Different Origins Invest. Ophthalmol. Vis. Sci., June 1, 2007; 48(6): 2903 - 2912. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. V. Lovasik, H. Kergoat, and M. A. Wajszilber Blue flicker modifies the subfoveal choroidal blood flow in the human eye Am J Physiol Heart Circ Physiol, August 1, 2005; 289(2): H683 - H691. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Garhofer, H. Resch, G. Weigert, S. Lung, C. Simader, and L. Schmetterer Short-Term Increase of Intraocular Pressure Does Not Alter the Response of Retinal and Optic Nerve Head Blood Flow to Flicker Stimulation Invest. Ophthalmol. Vis. Sci., May 1, 2005; 46(5): 1721 - 1725. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
V. Porciatti, N. Sorokac, and W. Buchser Habituation of Retinal Ganglion Cell Activity in Response to Steady State Pattern Visual Stimuli in Normal Subjects Invest. Ophthalmol. Vis. Sci., April 1, 2005; 46(4): 1296 - 1302. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. E. Riva, T. Salgarello, E. Logean, A. Colotto, E. M. Galan, and B. Falsini Flicker-Evoked Response Measured at the Optic Disc Rim Is Reduced in Ocular Hypertension and Early Glaucoma Invest. Ophthalmol. Vis. Sci., October 1, 2004; 45(10): 3662 - 3668. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Tsunoda, Y. Oguchi, G. Hanazono, and M. Tanifuji Mapping Cone- and Rod-Induced Retinal Responsiveness in Macaque Retina by Optical Imaging Invest. Ophthalmol. Vis. Sci., October 1, 2004; 45(10): 3820 - 3826. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. A. Phipps, T. M. Dang, A. J. Vingrys, and R. H. Guymer Flicker Perimetry Losses in Age-Related Macular Degeneration Invest. Ophthalmol. Vis. Sci., September 1, 2004; 45(9): 3355 - 3360. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G Garhofer, C Zawinka, H Resch, P Kothy, L Schmetterer, and G T Dorner Reduced response of retinal vessel diameters to flicker stimulation in patients with diabetes Br. J. Ophthalmol., July 1, 2004; 88(7): 887 - 891. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. Nagel, W. Vilser, and I. Lanzl Age, Blood Pressure, and Vessel Diameter as Factors Influencing the Arterial Retinal Flicker Response Invest. Ophthalmol. Vis. Sci., May 1, 2004; 45(5): 1486 - 1492. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E Nagel and W Vilser Flicker observation light induces diameter response in retinal arterioles: a clinical methodological study Br. J. Ophthalmol., January 1, 2004; 88(1): 54 - 56. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Garhofer, C. Zawinka, K.-H. Huemer, L. Schmetterer, and G. T. Dorner Flicker Light-Induced Vasodilatation in the Human Retina: Effect of Lactate and Changes in Mean Arterial Pressure Invest. Ophthalmol. Vis. Sci., December 1, 2003; 44(12): 5309 - 5314. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Polak, L. Schmetterer, and C. E. Riva Influence of Flicker Frequency on Flicker-Induced Changes of Retinal Vessel Diameter Invest. Ophthalmol. Vis. Sci., August 1, 2002; 43(8): 2721 - 2726. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. Falsini, C. E. Riva, and E. Logean Flicker-Evoked Changes in Human Optic Nerve Blood Flow: Relationship with Retinal Neural Activity Invest. Ophthalmol. Vis. Sci., July 1, 2002; 43(7): 2309 - 2316. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
