Ординатура / Офтальмология / Английские материалы / Electrophysiology of Vision_Lam_2005

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Optic neuropathies:

Glaucoma

Optic neuritis=multiple sclerosis

Ischemic optic neuropathy

Papilledema

Compression of optic nerve or chiasm

Traumatic optic neuropathy

Optic nerve head drusen

Hereditary optic neuropathies Central nervous system disorders:

Cortical blindness

Spinocerebellar degeneration, olivopontocerebellar atrophy, and Friedreich ataxia

Alzheimer disease

Parkinson disease

Leukodystrophies

OPTIC NEUROPATHIES

Glaucoma

Glaucoma is a progressive optic neuropathy characterized by loss of retinal ganglion cells associated with increased cupping of the optic nerve head, progressive nerve-fiber-layer visual field defects, and usually, but not always, high intraocular pressure. There are many types of glaucoma with primary open-angle glaucoma being the most common. Glaucoma is one of the leading causes of blindness worldwide, and its prevalence increases with age. Patients with increased intraocular pressure without glaucomatous optic nerve and visual field damage are designated as having ‘‘ocular hypertension’’ and are at risk of developing glaucoma.

Medical and surgical treatments aimed at lowering intraocular pressure have shown to decrease glaucomatous progression and the likelihood of developing glaucoma in ocular hypertension. Early detection of glaucoma and glaucomatous progression is critical so that treatment can be initiated or modified to prevent permanent or future visual loss. Diagnostic tests that are of value in glaucoma must be sensitive

enough to detect early glaucoma progression and to identify those ocular hypertensive patients who are at higher risk of developing glaucoma. At the same time, a diagnostic test that is not specific enough will have a high false positive rate rendering the test less useful. Most patients with ocular hypertension do not develop glaucoma, and the rate of conversion to glaucoma is about 1.5% per year (1). Topical antiglaucomatous medication is effective in delaying or preventing the onset of glaucoma in patients with ocular hypertension by reducing this conversion rate to about 0.7% per year (1). Serial examinations with intraocular pressure measurement, visual field testing, and optic nerve head evaluation are recommended for glaucoma and ocular hypertension. However, loss of more than one-third of nerve fibers may occur before a visual field defect becomes detectable.

Despite numerous studies, electrophysiologic testing has yet to gain general acceptance in glaucoma. Long-term prospective studies are needed to determine whether electrophysiologic abnormalities are clinically meaningful in the diagnosis and treatment of glaucoma and ocular hypertension.

The pattern ERG is a measure of retinal ganglion cell function and has been proposed as a diagnostic test in glaucoma (Fig. 17.1). The N95 component of the pattern ERG is generated by retinal ganglion cell function while the P50 component is generated by both retinal ganglion cells and intraretinal cellular elements. For transient pattern ERG responses, earlier studies of P50 in glaucoma yielded variable results (2–4), but subsequent investigations noted more consistent impairment of the N95 in glaucoma and ocular hypertension (5–7). Studies examining correlation between pattern ERG abnormalities and other clinical parameters such as changes in visual field and optic nerve head appearance have yielded inconsistent results (8–12). For instance, one study found that pattern ERG and computerized optic nerve head analysis do not agree in their estimation of glaucomatous risk

(8) while a correlation between pattern ERG and nerve fiber layer thickness was reported in another study (13). This lack of consistent correlation is likely due in part to the varied

Figure 17.1 Simultaneous recordings of pattern-reversal VEP and pattern ERG. Note the delayed VEP P100 and pattern ERG P50 implicit times and the reduced VEP P100 and pattern P50– N95 amplitudes in the patient with primary open-angle glaucoma (POAG). The recordings were obtained with 15-min check sizes with the stimulus subtending 18 (From Ref. 13 with permission from the American Academy of Ophthalmology.)

effects of glaucoma on multiple physiologic mechanisms. In a cross-sectional study of 203 glaucoma patients, Martus et al. (14) compared optic disc morphometry, automated perimetry, temporal contrast sensitivity, blue-on-yellow VEP, and pattern ERG using confirmatory factor analysis in which the results are not dependent on the preselection of a specific gold standard (14). The investigators found that glaucomatous damage was quantified best by perimetry followed, in order, by neuroretinal rim of the optic disc, temporal contrast sensitivity, pattern ERG, and VEP. However, a combination of short-wavelength automated perimetry (SWAP) and pattern ERG improve the predictive power of progressive defects on standard automated perimetry and could detect glaucomatous optic neuropathy in eyes with normal standard perimetry (13,15,16).

The waveforms of steady-state pattern ERG are dominant by the N95 component, and abnormal steady-state pattern ERG in glaucoma and ocular hypertension have also been noted by several studies (17–20). A comparison of upper hemifield and lower hemifield transient or steady-state pattern ERG responses to detect glaucomatous damage has been demonstrated (21). Reports of correlations between steadystate pattern ERG changes and other clinical parameters are inconsistent (22,23).

In general, pattern ERG abnormalities are found in about 10–40% of patients with ocular hypertension (7,12,17,24,25). This prevalence rate is considerably higher than the approximate 1% per year conversion rate to glaucoma reported in clinical studies. A significant although weak correlation between pattern ERG amplitude and shape of the optic nerve head has been noted (26). Although ocular hypertensives with abnormal pattern ERG are likely to have a greater risk of developing glaucoma when compared to those with normal pattern ERG, the relatively high prevalence of abnormal pattern ERG in ocular hypertensives suggests a false positive rate that is likely too high to be potentially clinically useful in identifying those who would develop glaucoma.

Glaucomatous damage is detectable by multifocal VEP, but further studies are needed to determine whether these changes can be clinically meaningful and better than other clinically measures (Fig. 17.2) (27,28). The second-order response of the multifocal ERG may be reduced in glaucoma but this reduction is variable (29). In one study, multifocal pattern ERG did not reflect localized ganglion cell loss whereas multifocal pattern VEP to a similar stimulus showed the scotoma (30).

The photoreceptors are unaffected in glaucoma and conventional full-field ERG responses are normal (31). The photopic negative response (PhNR), a negative component that immediately follows the full-field ERG b-wave, is related to ganglion cell activity and is reduced in glaucoma (Fig. 17.3) (32). Optimal recording of the PhNR requires specialized techniques and its clinical usefulness requires further study. Mild waveform changes of the first-order multifocal ERG have also