on his own subject; in this book the reader will not be disappointed. Moreover, the translation from the original French, with the inclusion of some new material, suffers from few of the defects so frequently seen, for it reads fluently and spontaneously as if it were the original text. The first chapter deals with the nature of light and its relation to other forms of radiant energy: a succinct and interesting review, followed by a full description of different types of illuminants including the various types of artificial lighting and natural lighting from the sun. This is followed by a description of the physiology of vision and the functioning of the eye shown by experiments carried out on the human eye by physical methods. This part comprises a full discussion of such problems as photometry, the illumination of the retina, luminance efficiency and the duality of the retina, colorimetry and the trivariance of the retina, colour vision and its anomalies, and the various thresholds, time effects, and the spatial interactions affecting vision. The second section of the book is more physiological and speculative. It is introduced by a description of the relevant anatomy of the eye, the photochemistry and electrophysiology of vision, the various theories of colour vision, and a physiological interpretation of the visual thresholds. The book is easy and good to read and gives a fair and critical exposition of its subject. It should be useful not only to the ophthalmologist but also to the physiologist and physicist.

https://bjo.bmj.com/content/bjophthalmol/53/1/66.1.full.pdf

Light, Colour and Vision

PURPOSE. To develop a quantitative measure of local damage to the ganglion cells/optic nerve based on an interocular comparison of multifocal visual evoked potentials (mVEP). METHODS. Multifocal VEPs were recorded from both eyes of six normal subjects and four patients; each eye was stimulated separately. Two of the patients had glaucoma, one had ischemic optic neuropathy, and one had unilateral optic neuritis. All four patients had considerably more damage in one eye than in the other, as indicated by their Humphrey visual fields. The multi-input procedure of Sutter was used to obtain 60 VEP responses to a scaled checkerboard pattern. The amplitude in each response was obtained using a root mean square measure of response magnitude. For each of the 60 pairs of responses, a ratio between the amplitude of the responses from the two eyes was obtained as a measure of the relative health of one eye compared with the other. The mean and SD of this ratio measure for the control group were used to specify confidence intervals for each of the 60 locations. All patients had Humphrey 24-2 visual fields performed. To allow a comparison of the mVEPs to the visual fields, a procedure was developed for displaying the results of both tests on a common set of coordinates. RESULTS. Except for a small interocular difference in timing attributable to nasotemporal retinal differences, the pairs of mVEP responses from the two eyes of the control subjects were essentially identical. Many of the pairs of responses from the patients were significantly different. In general, there was reasonably good agreement with the Humphrey 24-2 visual field data. Although some regions with visual field defects were not detected in the mVEP due to small responses from the better eye, other abnormalities were detected that were hard to discern in the visual fields. CONCLUSIONS. Local monocular damage to the ganglion cell/optic nerve can be quantitatively measured by an interocular comparison of the mVEP. (Invest Ophthalmol Vis Sci. 2000;41: 1580 ‐1587)

An interocular comparison of the multifocal VEP: a possible technique for detecting local damage to the optic nerve.

Physiological experiments and the exploitation of clinical conditions have provided compelling evidence that retinal ganglion cells and other inner retinal structures generate the pattern ERG (PERG). As an increasing number of clinical reports have been published some contradictory findings have been reported. These may be ascribed to variation in recording and measuring techniques. The PERG consists of two major portions, the early positive and the following negative component which can be investigated separately if the stimulus conditions allow isolated (or "transient") responses to be recorded. Care has to be taken in positioning the reference electrode, maintaining accurate refraction, and the influence of pupil size must be considered. Furthermore the PERG is contaminated by a luminance component which may be generated in the outer retina. The size of this increases with low spatial frequency (large check-sizes) and high mean luminance. The PERG permits the examination of an additional level of the retina and helps the understanding of pathophysiology of various eye diseases, and is of clinical importance in routine diagnosis and assessment. In glaucoma the PERG amplitude is often reduced before it is possible to detect a scotoma and it is therefore an important prognostic indicator in patients with ocular hypertension. In diabetic retinopathy, retinal ischaemia sufficient to lead to the pre-proliferative state can be demonstrated. The PERG also has a major clinical role in examining localised retinal pathology. If combined with VECP recording, it greatly extends the interpretations possible, since not only can damage to the optic nerve be detected by both tests, but the normal PERG in the presence of an abnormal PVECP implies that the losses are confined to the central pathway.

/pdf/the-pattern-electroretinogram-2reg13ppw7.pdf

The pattern electroretinogram

Several lines of evidence suggest that the large optic nerve fibers, which form the magnocellular retinocortical pathway, are preferentially susceptible to early glaucomatous damage. It is evident from studies of the functional architecture of the visual system that the magnocellular pathway underlies the global perception of motion. Therefore, we have developed a psychophysical technique for assessing motion detection thresholds in patients with ocular hypertension (OHT) and primary open-angle glaucoma (POAG). For this purpose we employed a dynamic random dot display that contained varying degrees of a coherent motion signal embedded within a background of random motion noise. We used this technique to measure motion thresholds in POAG patients (n = 37), OHT patients (n = 14), and age-matched controls (n = 39). Motion thresholds were elevated by 70% for the POAG group and 44% for the OHT group relative to controls. In the same patients, no significant deficit in form discrimination was found as measured by Pelli-Robson charts. Our results demonstrate that significant motion perception deficits are evident in POAG and OHT. These findings support the suggestion that significant and selective damage to the magnocellular pathway occurs in OHT and POAG and indicate that motion threshold testing may reveal preclinical optic nerve disease in early POAG.

Motion perception is abnormal in primary open-angle glaucoma and ocular hypertension.

A hallmark of early diabetic retinopathy is the selective loss of the retinal mural cells (pericytes) from vessels. Using antibodies prepared against purified human placental aldose reductase, the presence of the enzyme aldose reductase can be demonstrated immunohistochemically in the cytoplasm of retinal mural cells of trypsin-digested human retinal vessels. This enzyme, which reduces various hexose sugars to their sugar alcohols, has been implicated in the pathogenesis of several diabetic complications.

Aldose reductase localization in human retinal mural cells.

In order to determine the optimum stimulus conditions for the detection of optic nerve damage due to glaucoma and ocular hypertension, checkerboard pattern reversal visual evoked potentials (VEPs) were recorded from 20 glaucoma patients, 20 ocular hypertensive patients, and 20 age-matched normals. Two check sizes (12' and 48'), two field sizes (14 degrees and 28 degrees), and two alternation rates (1.9 and 7.5 alt/sec) were used. All subjects had visual acuities of 20/40 or better in each eye and equal pupils of 2 to 5 mm diameter. The largest number of VEP abnormalities were found with large checks (48') reversing at a fast rate (7.5 alt/sec). After correcting for the effects of age, visual acuity, and pupil size, 16 of 30 eyes with glaucomatous visual field defects had abnormally long VEP latencies under this condition (beyond the 99% confidence limit of the normal subjects). Nine of 40 ocular hypertensive eyes also had abnormally long latencies. Increased pattern VEP latency was significantly correlated with both the severity and location of visual field defects and the degree of cupping and pallor of the optic disc. VEP latency was not significantly related to intraocular pressure.

The visual evoked potential in glaucoma and ocular hypertension: effects of check size, field size, and stimulation rate.

The latency of the first major positive component (P1) of the pattern reversal visually evoked potential (VEP) and constrast sensitivity, using the Arden grating plates, were measured in 3 groups of age matched subjects. One group consisted of 14 normal subjects (mean age 66 yrs.) with no ocular disease; a second group contained 21 patients (mean age 58 yrs.) with ocular hypertension; and a thrid group contained 20 patients (mean age 66 yrs.) with glaucoma. Analysis of the Arden grating scores revealed no significant differences between the 3 groups. These findings indicate that the Arden gratings have limited usefulness in the detection of glaucoma, at least in older patient populations. On the other hand, the VEP data showed that the mean P1 latency for the glaucomatous eyes was significantly longer than the P1 latency for the normals and ocular hypertensives. Further, there was no significant difference in mean P1 latency between the normals and ocular hypertensives.

Pattern Evoked Potential Latency and Contrast Sensitivity in Glaucoma and Ocular Hypertension

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The visual evoked potential in glaucoma and ocular hypertension: effects of check size, field size, and stimulation rate.

Pattern Evoked Potential Latency and Contrast Sensitivity in Glaucoma and Ocular Hypertension