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Br J Ophthalmol. 2007; 91(12): 1709–1710.
PMCID: PMC2095554
Transient macular dysfunction determined by focal macular electroretinogram
Naoki Terauchi, Kaoru Fujinami, Kei Shinoda, Kazushige Tsunoda, Gen Hanazono, Yozo Miyake, and Koichi Inomata
Naoki Terauchi, Kaoru Fujinami, Kei Shinoda, Kazushige Tsunoda, Gen Hanazono, Yozo Miyake, Laboratory of Visual Physiology, National Institute of Sensory Organs, National Hospital Organization, Tokyo Medical Center, 2‐5‐1 Higashigaoka, Meguro‐ku, Tokyo 152‐8902, Japan
Koichi Inomata, Department of Ophthalmology, School of Medicine, Nihon University, 1‐8‐13 Surugadai, Kanda, Chiyoda‐ku, Tokyo 101‐8309, Japan
Correspondence to: Dr Kei Shinoda
Laboratory of Visual Physiology, National Institute of Sensory Organs, National Hospital Organization, Tokyo Medical Center, 2‐5‐1 Higashigaoka, Meguro‐ku, Tokyo 152‐8902, Japan; shinodakei@kankakuki.go.jp
Accepted February 3, 2007.
Keywords: transient ischemic attack, focal macular electroretinogram, retinal artery occlusion
Rapid diagnosis of patients with acute visual loss is critical1 but is difficult if the retina appears normal ophthalmoscopically. We report the case of a patient who presented with acute unilateral visual loss and a central scotoma.
A 75‐year‐old man complained of a sudden and painless decrease of vision in his left eye. He had undergone surgery for an unruptured intracranial aneurysm 20 years earlier and was taking 7 mg/day of systemic prednisolone for rheumatoid arthritis. He had also had diabetic mellitus without retinopathy for 5 years. He was being followed for a left hemianopsia and normal tension glaucoma for the previous 3 years.
On examination, a left relative afferent papillary defect (RAPD) was observed, and visual acuity (VA) was 20/30 OD and 20/2000 OS. All of the ocular findings were normal except for enlarged disc cupping OU (fig 11).). Fluorescein angiography showed a delay in the arm‐to‐retina circulation time of 20.0 s (fig 11).). Neither retinal emboli nor localised filling delay were observed. Goldmann perimetry showed a left quadrantic homonymous hemianopsia and a small central scotoma with peripheral constriction. The alterations in the left eye were new (fig 11).). Focal macular electroretinograms (FMERGs) were recorded 2 h after onset as described (see the supplemental figure available at http://bjo.bmj.com/supplemental).2,3
figure bj113373.f1
Figure 1 Fundus photograph and fluorescein fundus angiograms of the patient's left eye. Top left: Fundus photograph showing enlarged cupping of the left optic disc. Top right: Fluorescein angiogram with delayed arm‐to‐retina circulation (more ...)
The FMERGs were decreased in the left eye (fig 22)) indicating that the visual dysfunction was retinal in origin. Left VA improved to 20/250 spontaneously 3 h later. On the following day, VA had improved to 20/30, and the amplitudes of the FMERGs, full‐field ERGs and pattern visual evoked response (VEP) were normal (fig 22).). The visual field obtained 3 months later showed that the central scotoma was not present and an expansion of the peripheral visual fields. The fundus remained normal. Ultrasound echography revealed no stenosis of the carotid artery. Blood examination revealed rheumatoid factor and high HbA1c but was otherwise normal.
figure bj113373.f2
Figure 2 Focal macular electroretinogram (FMERG, top), full field electroretinogram and visual evoked response (VEP) from both eyes (bottom). Top: Upper three recordings show the photopic a‐ and b‐waves, and lowest recordings show (more ...)
We conclude that the acute visual loss and central scotoma with reduced FMERGs were consistent with transient macular ischaemia, and prophylactic anti‐coagulation treatment was considered.
Our patient had an acute monocular visual loss and a fundus that appeared normal except for the relatively delayed angiographic retinal filling time and enlarged disc cups. The RAPD, central scotoma and systemic complications made it difficult to determine the site of the alterations. The reduced FMERGs pointed to the retina as the site.
However, an abnormally long‐lasting visual decrease is not typical for amaurosis fugax,1 and ophthalmoscopy did not show retinal oedema typical of arteriolar occlusion. Conventional electrophysiological examinations such as full‐field ERGs and VEPs might be useful except when the ischaemic site is in the macular region.
The clinical course in our case was compatible with a transient retinal ischaemia with a possibility of a transient central retinal artery occlusion, although additional more generalised abnormalities cannot be completely excluded. The FMERG within the 5° area is similar to that of the ERG of a monkey treated with 2‐amino‐4‐phosphonobutyric acid (APB) and cis‐2,3‐piperidine dicarboxylic acid (PDA) to suppress both on and off synapses.4,5 This implies that the inner retinal layers have serious dysfunction. Because of the systemic complications, the risk of utilising prophylactic anticoagulant agents was discussed. However, the VA and central scotoma quickly recovered accompanied by an improvement in the FMERGs without any intervention.
These findings indicate that clinicians should consider focal macular dysfunction in cases of acute vision loss and normal retinal appearance; multifocal ERGs or FMERGs are useful in determining the site of the pathology.
Acknowledgements
This study was supported by the Suzuken Memorial Foundation.
The supplemental figure is available at http://bjo.bmj.com/supplemental.
Supplementary Material
[web only figure]
Footnotes
Competing interests: None of the authors have any financial or proprietary interest in any material or methods mentioned.
The supplemental figure is available at http://bjo.bmj.com/supplemental.
1. Rizzo J F., III Neuroophthalmologic disease of the retina. In: Daniel MA, ed. Principles and practice of ophthalmology, 2nd ed. Philadelphia: WB Saunders, 2000. 4083–4108.4108.
2. Miyake Y, Shiroyama N, Horiguchi M. et al Oscillatory potentials in electroretinograms of the human macular region. Invest Ophthalmol Vis Sci 1988. 291631–1635.1635. [PubMed]
3. Miyake Y. Focal macular ERGs. In: Miyake Y, ed. Electrodiagnosis of retinal diseases. Tokyo: Springer, 2005. 20–32.32.
4. Ueno S, Kondo M, Niwa Y. et al Luminance dependence of neural components that underlies the primate photopic electroretinogram. Invest Ophthalmol Vis Sci 2004. 451033–1040.1040. [PubMed]
5. Sieving P A, Murayama K, Naarendorp F. Push‐pull model of the primate photopic electroretinogram: a role for hyperpolarizing neurons in shaping the b‐wave. Vis Neurosci 1994. 11519–532.532. [PubMed]
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