BACKGROUND: This prospective study was undertaken to investigate whether spectral sensitivity can be useful in determining the prognosis of fellow eyes of eyes with macular holes.
METHODS: Spectral sensitivity measurements using a one degree test spot presented at a rate of 1 Hz and 25 Hz on a bright (1000 td) white background were carried out on 10 patients aged between 67 and 74 years (mean age 70.3 +/- 2.6 years). Each patient had a full thickness macular hole in one eye and a normal contralateral fellow eye. The spectral sensitivity measurements were made with eccentric fixation in the eyes with macular holes and with central fixation in the normal fellow eye. A year later, the patient files were reviewed to look at the patient's ocular condition. Another 10 subjects between the ages of 50 and 80 years (mean age 69.5 +/- 4.2 years) were also seen. These control group subjects had visual acuities of 6/9 or better with minimal ocular media changes and no ocular or systemic pathology that could affect colour vision.
RESULTS: The 1 Hz and 25 Hz spectral sensitivities of all patients were reduced for both eyes. Despite the good eye without a macular hole having a VA of 6/6, the spectral sensitivity was similar to that of the eye with the macular hole and markedly reduced visual acuity.
CONCLUSION: The present investigation enabled us to examine the chromatic and achromatic mechanisms by testing spectral sensitivity at 1 Hz and 25 Hz, respectively. The data revealed that both chromatic and achromatic processing could be damaged in the eye with a macular hole. Surprisingly, the spectral sensitivities of both 1 Hz and 25 Hz are equally reduced in the good fellow eye with no macular hole. A one-year follow-up showed that two of the 10 patients (20 per cent) did eventually develop a macular hole in the normal fellow eye. This indicates that there is some subclinical foveal dysfunction in the normal fellow eye, the nature of which is unclear.
Study site: Manchester Royal Eye Hospital (MREH), United Kingdom
The majority of patients with dysthyroid eye disease have an acquired colour vision defect. However, no psychophysical investigation of selective damage to colour or flicker pathways has been carried out. In order to clarify the nature of the visual pathology, we have used a psychophysical technique (spectral sensitivity) to selectively stimulate the chromatic and achromatic mechanisms. Spectral spots of size 1 degree presented at a rate of 1 Hz on a bright 1000 td white background are detected by the chromatic mechanism but a rate of 25 Hz reveals the achromatic mechanism. Fifteen patients (28 eyes) between the ages of 50-70 years were tested. The study showed that all patients had reduced spectral sensitivity, either 1 Hz, 25 Hz or both. The patients with reduced 1 Hz or 25 Hz spectral sensitivity only had a shorter systemic and ocular duration of the condition, had no proptosis, normal intraocular pressures in primary gaze, slightly higher intraocular pressures on upgaze, normal visual field plots and FM 100-Hue error scores higher than the normal age-matched values. The patients with reduced both 1 Hz and 25 Hz spectral sensitivities had a longer systemic and ocular duration of the condition, had proptosis, normal intraocular pressures in primary position, higher intraocular pressures on upgaze and higher FM 100-Hue error scores than the age-matched normals and those in Groups 1 and 2. A total of 50% of patients in Group 3 had defective visual field plots. These data suggest that there is a damage of the large achromatic fibres and small chromatic fibres in dysthyroid eye disease. The mechanism of the damage could be one of ischaemic or mechanical or both.