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Br J Ophthalmol. 2007 April; 91(4): 406–407.
PMCID: PMC1994761

All in the timing

Short abstract

mfVEP as a measure of perimetry

In this issue of the BJO, the paper by Semela et al1 (see page 445) reports on the characteristics of the multifocal visual evoked potential (mfVEP) in six cases of compressive optic neuropathy (CON) secondary to optic nerve meningiomas. The mfVEP can be thought of as an objective measure of perimetry. With the display used by Semela's group, the 60 sectors tested comprise about the same area of visual field as the Humphrey 24–2 standard automated perimetry (SAP) test. Unlike SAP, the mfVEP does not require the subject to consciously register and respond to stimuli but rather is generated by the electrical potentials evoked by the individual pattern‐reversal stimuli at the primary visual cortex.2 The amplitudes of mfVEPs have been shown to correlate well with SAP in several optic neuropathies including ischaemic optic neuropathy (ION) and glaucoma.2,3,4,5,6,7,8 It is not surprising that the mfVEP amplitudes in optic nerve meningiomas follow suit. This is in agreement with work by Danesh‐Meyer et al9 using the AccuMap system of mfVEP, demonstrating good amplitude correlation with SAP in CON due to pituitary lesions.

However, unlike the mfVEPs seen in ION and glaucoma, Semela et al demonstrate that CON mfVEPs have significant latency delays.10,11 This is consistent with conventional VEP studies showing prolonged latencies in compressive neuropathies including those caused by chiasmal gliomas, orbital tumours and thyroid orbitopathy.12,13,14,15,16,17 Prolongations in latency have been attributed to disruptions of the saltatory conduction along the myelinated portion of ganglion cell axons and are the hallmark of demyelinating entities such as optic neuritis.7,18 Both mechanical and vascular mechanisms for CON have been proposed, and an experimental model of compressive peripheral neuropathy induced by a pneumatic tourniquet demonstrating anatomical disruption of the nodes of Ranvier and subsequent demyelination supports Semela et al's findings.17,19

Semela et al found that the latency delays occurred topographically at the interface between normal and abnormal regions of the visual field and could be seen in areas of visual field that test normal on SAP, as is shown in their cases 1 and 4. Delays may not be seen inside the scotoma owing to the fact that the mfVEP amplitudes are typically so diminished in areas of significant field loss that information on timing in these sectors is lost. However, the delays seen outside the areas of field loss are perhaps more interesting. Do these delays represent early signs of compressive optic nerve dysfunction? Although potentially interesting, this is clinically irrelevant in cases of optic nerve meningiomas as most of the cases are diagnosed only after presenting with visual loss. However, if true, it could prove a useful method for diagnosing early compressive neuropathy in thyroid orbitopathy and pituitary adenomas.

Unlike ION and glaucoma, which typically are not associated with any recovery of visual field, CONs frequently will improve when the compression is relieved. What happens to the latency changes after surgery or radiation? Are the latency changes somehow linked to the ability of nerves for recovery? Studies documenting visual outcomes after either surgical or radiation decompression of CONs show that 40–47% improved, 33–40% remain stable and about 20% worsen.20,21 Does the presence or absence of latency delays correlate with prognosis? It would be interesting to see how the mfVEPs and SAPs of Semela et al's six cases change after intervention.

Semela et al suggest monitoring changes in amplitude for evidence of progression or recovery of CON. This is good for modest visual field defects. We know, though, that mfVEP amplitudes can be completely wiped out when Humphrey visual field thresholds drop below –6 dB.22 Theoretically, a recovery from –20 to –10 dB in a localised area could go unnoticed since the mfVEP might not have a detectable amplitude in either case. However, since the latency changes frequently occur at the perimeter of the field deficit, and if we posit that in the presence of normal amplitudes they may represent the earliest detectable damage, changes in latency could signal the subtlest progression or recovery of disease.

As with all theory and conjecture, validation or rejection by experimentation is required. Semela et al's findings invite several interesting questions on the significance and relevance of latency shifts in compressive neuropathies. It is easy to hypothesise about them, but only further experimentation will provide real answers.

Footnotes

Competing interests: None declared.

References

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