LAUSR

Dear Editor, Pupil perimetry is becoming more common for its utility as an objective method to evaluate visual fields using pupillary response. The pupillary response has two main pathways: an afferent and an efferent limb. The afferent pathway leaves the optic tract before the lateral geniculate body and terminates in the midbrain. Wilhelm et al. reported that there are pupillary response abnormalities in patients with homonymous visual field defects caused by postgeniculate lesions [1]. These findings challenge the neural pathway of the pupillary response. One of the possibilities is that retrograde trans-synaptic degeneration (RTSD) were observed within a few years after the onset of occipital damage using optical coherence tomography (OCT) [2, 3]. To clarify these findings, we have recorded the pupil fields in a patient with an Bearly-onset^ postgeniculate lesion using a newly developed head-mounted perimeter. A 40-year-old man noticed a loss of visual fields on the right side and visited our emergency center. Magnetic resonance imaging of the brain performed after admission showed unilaterally hyperintensity in the occipital lobes (Fig. 1a). Two days after the onset of occipital damage, several routine examinations revealed a visual acuity of 6/6 and spherical equivalent refraction of − 2.50 D in both eyes. Spectral domain OCT (3D-OCT2000, Topcon Corporation, Tokyo, Japan) of both eyes demonstrated normal findings (Fig. 1b). Visual field measurements were taken with a Humphrey field analyzer (HFA) using the 24-2 SITA standard program (Carl Zeiss Meditec, Dublin, CA, USA). The head-mounted perimeter Bimo^ (CREWT Medical Systems, Tokyo, Japan) can simultaneously record pupillary response during target presentation. A stimulus target with 1-s duration, 450-nm and 550-nm wavelengths, Goldmann V size, and 0 dB (10,000 asb = 3183 cd/m) light under a 31.4asb (10 cd/m) background was presented. Pupil fields during target presentation were recorded in correspondence to the HFA test points. More details were provided by Asakawa et al [4]. The tenets of the Declaration of Helsinki for research involving human subjects were followed, and informed consent was obtained. The protocol was approved by the Institutional Ethics Committee of Kitasato University (No. B17-031). This patient with a postgeniculate lesion generally showed good correspondence between the results (congruent quadrantanopia) for visual fields (Fig. 1c) and pupil fields (Fig. 1d), when percentage pupil constriction of < 7% was regarded as a pupil field defect. To our knowledge, this is the first reported pupil hemihypokinesia in a patient only 2 days after the onset of a postgeniculate lesion. In this case, the pupil field defect cannot be explained by RTSD. The afferent pathway of pupillary response terminates in the midbrain. What, then, is the mechanism of pupillary abnormalities? Recently, the melanopsin-containing retinal ganglion cells (mRGCs), novel photoreceptors, have projections to the olivary pretectal nucleus, and the EdingerWestphal (EW) nucleus in the midbrain, and play a role in pupillary response [5, 6]. However, mRGCs are most sensitive to blue light of 470 nm and require longer stimulation. It is unlikely to stimulate mRGCs effectively with short stimuli of 1 s [7, 8]. Maeda et al. concluded that the pupillary pathway used by mRGC is mainly subcortical, whereas there is another non-mRGC pathway runs via the occipital cortex [9]. A possible explanation for the pupil field defect in postgeniculate lesion might be a loss of sympathetic central inhibition of the EW nucleus [10]. These results corroborate our findings. A limitation of the present study is that the cutoff value for abnormal sensitivity remains unclear. In future studies, we * Ken Asakawa [email protected]