Short-wavelength automated perimetry in patients with migraine

Abstract

Some patients with severe migraine have earlier defects on SWAP suggesting a common vascular insult of glaucoma and migraine, and all migraine cases with high MIDAS scores should be further evaluated for early glaucomatous visual field defects using SWAP.

Optic disc and visual test findings in patients with migraine

“…13 It was of interest to the investigators whether SWAP is more sensitive in detecting early visual field defects in migraine patients. 14,15 McKendrick et al studied 25 migraine subjects and 20 age-matched nonmigraine subjects and found that MD and PSD with SWAP were worse than SAP in half of the migraine subjects. 14 However, the Farnsworth-Munsell 100-hue test also utilizes the S-cone system, as SWAP was reported to be abnormal in migraine patients; therefore, it was suggested that migraine alone could interfere with SWAP, and could cause visual field defects in patients with migraine without ganglion loss.…”

Assessment of spatial–contrast function and short-wavelength sensitivity deficits in patients with migraine

“…The significance of these deficits to long-term ocular health in these individuals is currently unknown, but as we already mentioned before data resembling, a relationship between normal tension glaucoma and migraine either as a cause or a factor involved in disease progression is still evolving. [25][26][27][28][30][31][32] Beyond these, Harle and Evans 33 suggest an alternative explanation that migraine headache might cause a magnocellular-specific dysfunction unrelated to glaucoma and they claim that they are currently comparing visual fields, ocular tensions, and optic nerve head analysis in migraine and control subjects to investigate this hypothesis. 33 The findings of this study correlate with several other previous studies, which assessed precortical pathways by vision-related tests in the migraineurs population, which were found to be abnormal.…”

Clinical impact of migraine for the management of glaucoma patients

“…Fig. 1) (Comoglu et al, 2003;De Natale et al, 1993;Drummond and Anderson, 1992;Lewis et al, 1989;McKendrick and Badcock, 2004a, 2004b, 2004cMcKendrick et al, 2002McKendrick et al, , 2000Nguyen et al, 2014;Nizankowska et al, 1997;Yenice et al, 2006;Yucel et al, 2005), implying a pre-chiasmal and possibly retinal ganglion cell origin. Monocular defects identified in people with migraine can involve mild generalised depression in visual field sensitivity, as reflected by a reduction in the perimetric global indices, Average and Mean Defect (Dersu et al, 2013;Lewis et al, 1989;McKendrick and Badcock, 2004a;Yenice et al, 2006).…”

“…Certain perimetric techniques are customised to bias the assessment of specific precortical visual pathways, such as the fast-flickering luminancepedestal targets of temporal modulation perimetry (TMP), or flicker perimetry, that preferentially test the magnocellular pathway (Vingrys et al, 1994), or the blue-on-yellow stimuli of shortwavelength automated perimetry (SWAP), which preferentially tests the koniocellular pathway (Sample and Weinreb, 1990). Both TMP Badcock, 2004a, 2004b;McKendrick et al, 2000;Nguyen et al, 2014) and SWAP (McKendrick et al, 2002;Nguyen et al, 2014;Yenice et al, 2006;Yucel et al, 2005) have identified visual field defects in up to 50% of migraine cohorts. Note that these findings should not be interpreted as evidence for migraine producing a selective loss of one type of processing pathway, as dysfunction in both the magnocellular and parvocellular pathways has been demonstrated in people with migraine using perceptual stimuli designed to assess these channels separately (McKendrick and Badcock, 2003;McKendrick and Sampson, 2009).…”