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PubMed1996

Serum antibodies reactive with eye muscle antigens and the TSH receptor in a euthyroid subject who developed ophthalmopathy and Graves' hyperthyroidism.

Serum antibodies reactive with eye muscle autoantigens, in particular a 64-kDa protein that is also expressed in the thyroid, and the TSH receptor, are associated with the ophthalmopathy that occurs in about 50% of patients with Graves' hyperthyroidism. We have had the opportunity to study a euthyroid, apparently normal, 35-year-old woman with a family history of thyroid autoimmunity and "colitis" but no clinical or biochemical evidence for thyroid disease or ophthalmopathy, who developed Graves' hyperthyroidism and ophthalmopathy together 18 months later. Serum taken when the patient was first seen was positive for antibodies reactive with (i) 9 different eye muscle proteins ranging in size from 15 to 130 kDa, notably those of 64, 55, and 50 kDa, by immunoblotting with eye muscle membranes, (ii) eye muscle and Müller's muscle cell membrane antigens in antibody-dependent cell-mediated cytotoxicity (ADCC), (iii) an eye muscle cytoplasmic antigen in indirect immunofluorescence, and (iv) the TSH receptor as measured in a radioreceptor binding inhibition assay. When she developed Graves' disease, serum concentration of antibodies to the 55-kDa protein had decreased from +2 to +/-, those reactive with other eye muscle antigens had not changed significantly, and TSH receptor antibodies had increased 3-fold. This case report suggests that antibodies reactive with eye muscle antigens and the TSH receptor are markers of the ophthalmopathy and able to predict its development in predisposed subjects. The significance of these findings needs to be confirmed in a prospective study of first-degree relatives of patients with thyroid-associated ophthalmopathy and patients with Graves' hyperthyroidism without eye signs.

Adult↗
PubMed1982

Demonstration of a circulating autoantibody against a soluble eye-muscle antigen in Graves' ophthalmopathy.

Mouse monoclonal antibodies against antigens in human eye muscle, orbital connective tissue, and lacrimal tissue and guineapig harderian gland have been produced by means of the hybridisation technique. From 14 fusions, over 30 antibodies have been produced, of which 24 have been maintained and characterised for the present studies. All were IgG1. Most were organ-specific, but eye-muscle antibodies tended to cross-react with skeletal muscle, one eye-muscle antibody cross-reacted with thyroidal microsomes, and both lacrimal monoclonal antibodies reacted strongly with mucus-secreting cells in human small intestine. Only one of the antibodies fixed complement. Orbital monoclonal antibodies were used as probes to identify orbital antigens. Most antigens were in the cytosol fraction, but a few were demonstrated in cytoplasmic membranes. Circulating autoantibodies against a human-eye-muscle soluble antigen were detected in 17 of 23 patients with Graves' ophthalmopathy but in only 1 of 14 patients with Hashimoto's thyroiditis, in 2 of 11 patients with subacute thyroiditis, in no patient with Graves' hyperthyroidism without eye disease, and in none with multinodular goitre.

Adolescent↗
PubMed1998

Morphometric study of the muscles spindles of the eye muscle in human fetuses between 24-29 weeks.

The studies were carried out on human fetuses with the crow-rump length between 230 to 270 mm (24-29 weeks). The length of recti muscles varies from 12-15 mm in 24th week to 25-28 mm in 29th week. Number of muscle spindles varies from 29-36 in 24th week to 54-59 in 29th week. The length of the muscle spindles is from 30-300 microns in 24th week to 40-450 microns in 29th week. The diameter of the muscle spindles varies from 11-36 microns in 24th week to 15-70 microns in 29th week.

Embryonic and Fetal Development↗
PubMed1998

Registered eye position: short- and long-term effects of botulinum toxin injected into eye muscle.

Botulinum toxin is sometimes injected into human eye muscles as an alternative to surgery in the correction of strabismus. Within minutes of botulinum injections into ungulate eye muscles, proprioceptive discharge from muscle spindles decreases dramatically. It is only over 7-48 h, however, that surgically treated strabismus patients usually show an altered proprioceptive signal about eye position, presumably from the palisade endings attached to the global multiply innervated fibers. How quickly will botulinum toxin alter proprioceptive registration of eye position in humans? First, to examine the short-term effects, we measured open-loop pointing responses (which requires knowledge of eye position) in six strabismus patients preinjection and then over a 45 min postinjection period, and in six normal controls over the same time period. Second, to examine the long-term effects, 13 strabismus patients were tested preinjection and then daily over the next 3 weeks, and three normal controls over the same time period. We compared their open-loop pointing responses with the injected eye fixating the target to the photographically determined position of the occluded other eye (a measure of where the patient would point if eye position were determined by efference, not proprioception). There were three groups of patients: esotropes with no previous injection, exotropes with no previous injection, and exotropes with previous injection. First, all patients showed significant correction of their tropias. Second, over the short-term, there was no difference in pointing responses found between the patients and the controls (t(18) = -1.427, P = 0.1706). Third, over the long-term, however, the difference between the pointing responses and eye position information was compared among the four groups across four posttests and a significant difference found (F3,12 = 58.988, P < 0.00001). Only in patients with no previous injections was there altered proprioceptive feedback about eye position. Also, injections into the medial rectus induced a significantly greater proprioceptive response than those injected into the lateral rectus. In humans, botulinum toxin alters proprioception from eye muscles only over the long-term. We suggest that the toxin temporarily affects proprioceptive feedback from palisade endings.

Adult↗
PubMed1998

Reevaluation of the prevalences of serum autoantibodies reactive with "64-kd eye muscle proteins" in patients with thyroid-associated ophthalmopathy.

Serum autoantibodies reactive with eye muscle proteins of "64 kilodaltons (kd)" are frequently found in patients with Graves' hyperthyroidism and thyroid-associated ophthalmopathy (TAO). Earlier, we cloned a 64-kd protein that was identified as calsequestrin, a calcium-binding protein localized in the sarcoplasmic reticulum of striated muscle and extensively studied another cloned 64-kd protein, called 1D, which is expressed in thyroid and eye muscle, and some other tissues. Using a monoclonal antibody against calsequestrin, a polyclonal antibody against 1D and a TAO patient serum reactive with the "64-kd protein," as probes, we performed Western blots of porcine eye muscle membrane. We identified three different proteins in the 63 to 67 kd molecular weight range that were targeted by antibodies in sera from patients with TAO. It was not possible to differentiate antibodies reactive with calsequestrin and 1D because these two proteins have very similar molecular weights--63 to 64 kd--and band appearance in Western blotting. A 67-kd protein was most frequently recognized by TAO patients' sera. Serum antibodies reactive with the 67-kd protein were detected in 73% of patients with active TAO of 1 year duration or less, in 37% of patients with TAO of more than 3 years' duration, in 35% with Graves' hyperthyroidism without evident ophthalmopathy, in 30% of patients with Hashimoto's thyroiditis, and in 16% of normal subjects. Serum antibodies reactive with calsequestrin/1D were detected in 47% of patients with active TAO of less than 1 year, in 22% of patients with TAO longer than 3 years, 17% with Graves' hyperthyroidism without evident ophthalmopathy, in 10% of patients with Hashimoto's thyroiditis, and in 21% of normal subjects. The prevalence of anti-67-kd protein antibodies in TAO patients corresponded to those reactive with the so called "64-kd protein" that we have reported previously. In conclusion, we were able to improve the accuracy of the Western blots by comparing the molecular weight of positive bands using specific antibodies reactive with eye muscle antigens as probes. The previously recognized, and extensively studied, "64-kd protein" is now shown to have a molecular weight of 67 kd. The role of the various eye muscle antibodies in the diagnosis and management of the ophthalmopathy associated with Graves' hyperthyroidism needs to be addressed in prospective studies using purified or recombinant full-length proteins.

Adolescent↗
PubMed1999

Serum antibodies against the flavoprotein subunit of succinate dehydrogenase are sensitive markers of eye muscle autoimmunity in patients with Graves' hyperthyroidism.

Thyroid-associated ophthalmopathy is an autoimmune disorder of the extraocular muscles and orbital connective tissue, which is usually associated with Graves' hyperthyroidism. Well-studied markers of ophthalmopathy are eye muscle membrane antigens, reportedly of approximately 64-kDa molecular mass. One, originally identified only as the 64-kDa protein, has recently been shown to be the flavoprotein (Fp) subunit of mitochondrial succinate dehydrogenase, which has a correct molecular mass of 67 kDa. We have used purified beef heart Fp as antigen in an enzyme-linked immunosorbent assay for cross-reactive human autoantibodies. Sera have been screened from patients with thyroid-associated ophthalmopathy classified according to activity and presence or not of eye muscle disease, and from those with Graves' hyperthyroidism without eye involvement. Also examined were serum samples taken periodically from 20 patients with Graves' hyperthyroidism during 24 months of treatment of their hyperthyroidism with antithyroid drugs. Four of these patients had ophthalmopathy at the onset, 12 developed ophthalmopathy, and 4 did not develop any eye signs during treatment. Anti-Fp subunit antibodies were detected in 73% of patients with active ophthalmopathy and evidence of eye muscle involvement but only in 25% if there was only congestive ophthalmopathy. These values were 0% and 11% for patients with chronic ophthalmopathy, with or without eye muscle dysfunction, respectively. The antibodies were also detected in 14% of patients with Graves' hyperthyroidism without evident ophthalmopathy, 11% of patients with nonimmunologic thyroid disorders, 12% of type I diabetics, and 12% of age- and sex-matched normal subjects. Significantly, appearance of anti-Fp antibodies predicted the development of ophthalmopathy in 5 of the 6 patients with Graves' hyperthyroidism, who developed eye muscle dysfunction after treatment of the hyperthyroidism, and coincided with the onset of eye muscle signs in the other patient. Antibodies were not detected in any of 6 patients who developed congestive ophthalmopathy without evidence of eye muscle damage or in 4 patients who did not develop any eye signs. In conclusion, we have shown a close relationship between eye muscle disease and serum antibodies against the Fp subunit of succinate dehydrogenase in patients with Graves' hyperthyroidism.

Adult↗
PubMed1989

Re-evaluation of eye muscle autoantibody determination in Graves' ophthalmopathy: failure to detect a specific antigen by use of enzyme-linked immunosorbent assay, indirect immunofluorescence, and immunoblotting techniques.

Sera from 41 patients with Graves' ophthalmopathy were investigated for presence of autoantibodies directed against eye muscle preparations using different methods: 1. ELISA with pork eye muscle membrane preparations; 2. Immunoblotting with glycoprotein preparations from human eye muscle; 3. Indirect immunofluorescence with human eye muscle sections. The ELISA was not suitable for detection of specific immunoglobulin binding with sera from patients suffering from endocrine ophthalmopathy. Immunoblotting exhibited only nonspecific binding to some muscle proteins; it could be prevented by pre-adsorption procedures and was not different from the pattern observed with skeletal muscle as antigen. The indirect immunofluorescence technique revealed no binding of Graves' sera to human muscle sections, whereas sera containing antibodies against skeletal muscle bound to eye muscle as well. Thus far, an antigenic structure of eye muscle specific for Graves' ophthalmopathy is not detectable with the methodology used here. The possibility that retroorbital connective tissue may be the main target of the autoimmune process must be considered.

Animals↗
PubMed1987

Antibodies to porcine eye muscle in patients with Graves' ophthalmopathy: identification of serum immunoglobulins directed against unique determinants by immunoblotting and enzyme-linked immunosorbent assay.

The immunological mechanisms involved in Graves' ophthalmopathy are not known. To explore the pathophysiology of this disorder, we used an enzyme-linked immunosorbent assay to detect antibodies that bound to the 100,000 X g sediment fraction of porcine eye muscle. Serum from patients with Graves' ophthalmopathy had enhanced immunoglobulin binding to porcine eye muscle compared to serum from control subjects (P less than 0.0001); however, several individual normal serum samples also had elevated binding activity. Incubation of serum from some Graves' patients with skeletal muscle or liver tissue resulted in reduction in immunoglobulin binding to porcine eye muscle. Thyroglobulin and TSH reduced binding only at high concentrations. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis revealed some obvious differences in protein bands between porcine eye muscle and skeletal muscle. Serum from many normal subjects and patients with autoimmune thyroid disease formed bands with skeletal muscle protein fractions on immunoblotting, and no specific bands were found using serum from Graves' ophthalmopathy patients. Immunoblots of Graves' patients' serum after reaction with either porcine skeletal or eye muscle showed no reactivity with thyroglobulin (200K and 320K) or thyroid microsomal antigen (105K). Instead, immunoblots of eye muscle and serum from Graves' patients, with or without eye disease, showed two bands at 64K and 73K, which were shared by serum from normal subjects. In addition, several unique eye muscle determinants were detected in serum from 6 of 13 Graves' disease patients analyzed. These unique bands usually had mol wt of less than 50K, and 5 of the 6 patients whose serum reacted with these determinants had significant ophthalmopathy. Our findings support the presence of potential antigenic differences between eye muscle and skeletal muscle accounting for the immunological specificity of eye muscle as a target in Graves' ophthalmopathy.

Animals↗
PubMed2003

Loss-of-function of an N-acetylglucosaminyltransferase, POMGnT1, in muscle-eye-brain disease.

Muscle-eye-brain disease (MEB), an autosomal recessive disorder, is characterized by congenital muscular dystrophy, brain malformation, and ocular abnormalities. Previously, we found that MEB is caused by mutations in the gene encoding the protein O-linked mannose beta1,2-N-acetylglucosaminyltransferase 1 (POMGnT1), which is responsible for the formation of the GlcNAcbeta1-2Man linkage of O-mannosyl glycan. Although 13 mutations have been identified in patients with MEB, only the protein with the most frequently observed splicing site mutation has been studied. This protein was found to have no activity. Here, we expressed the remaining mutant POMGnT1s and found that none of them had any activity. These results clearly demonstrate that MEB is inherited as a loss-of-function of POMGnT1.

Abnormalities, Multiple↗
PubMed2003

Worldwide distribution and broader clinical spectrum of muscle-eye-brain disease.

Muscle-eye-brain disease (MEB), an autosomal recessive disorder prevalent in Finland, is characterized by congenital muscular dystrophy, brain malformation and ocular abnormalities. Since the MEB phenotype overlaps substantially with those of Fukuyama-type congenital muscular dystrophy (FCMD) and Walker-Warburg syndrome (WWS), these three diseases are thought to result from a similar pathomechanism. Recently, we showed that MEB is caused by mutations in the protein O-linked mannose beta1,2-N-acetylglucosaminyltransferase 1 (POMGnT1) gene. We describe here the identification of seven novel disease-causing mutations in six of not only non-Finnish Caucasian but also Japanese and Korean patients with suspected MEB, severe FCMD or WWS. Including six previously reported mutations, the 13 disease-causing mutations we have found thus far are dispersed throughout the entire POMGnT1 gene. We also observed a slight correlation between the location of the mutation and clinical severity in the brain: patients with mutations near the 5' terminus of the POMGnT1 coding region show relatively severe brain symptoms such as hydrocephalus, while patients with mutations near the 3' terminus have milder phenotypes. Our results indicate that MEB may exist in population groups outside of Finland, with a worldwide distribution beyond our expectations, and that the clinical spectrum of MEB is broader than recognized previously. These findings emphasize the importance of considering MEB and searching for POMGnT1 mutations in WWS or other congenital muscular dystrophy patients worldwide.

Adult↗
PubMed1981

[Surgical treatment of eye muscle palsies (author's transl)].

The surgical treatment of an eye muscle palsy is indicated at the end stage of all possible conservative therapeutic measures. If after an interval of 8 to 12 months an eye muscle palsy manifests no change of pattern, the indication for surgical treatment is given, provided the pathologic process causing the palsy is no longer active. Of great importance for the evaluation of surgery are the forced duction test, measurement of saccadic velocity and electromyography. The aim of the surgical intervention is to eliminate diplopia and restore parallelism of the visual axes if possible with every line of vision, but above all with the largest possible visual field in the primary position and in downwards gaze. Any eye muscle palsy produces an overaction of the homolateral antagonist, an overfunction of the contralateral synergist and a secondary inhibition of the contralateral antagonist. Theoretically four surgical possibilities would result from these conditions. However, in practice the choice is reduced to weakening (recession, faden-operation) of the homolateral antagonist or the contralateral synergist or possibly both and to strengthening (resection, tucking) of the primary paretic muscle. Not infrequently, the surgical intervention has to be performed in different steps on different muscles of both eyes. In cases of total palsies muscles transposition or transplantation procedures (Hummelsheim-O'Connor, Jensen etc.) must be considered. A promising new method of restoring innervation to a paralyzed muscle is muscular neurotization (implantation of the inferior oblique muscle into the paralyzed denervated external rectus muscle in cases of abducens nerve paralysis).

Humans↗
PubMed1994

Immunoglobulin class and subclass distribution of eye muscle and fibroblast antibodies in patients with thyroid-associated ophthalmopathy.

OBJECTIVE: The investigation of the antibody response in thyroid-associated ophthalmopathy (TAO) using different antigens and assays has given inconsistent results. We have analysed antibodies against eye muscle and control antigens in a large group of TAO patients to assess whether specific eye muscle antibodies exist in TAO. We have also evaluated the presence of IgA and IgM class antibodies and examined IgG subclass distribution. DESIGN: Sera were obtained from all patients (TAO, Graves' disease without ophthalmopathy and Hashimoto's thyroiditis) within one year of diagnosis. Sera were also collected from healthy controls, with no family history of autoimmune thyroid disease. PATIENTS: Thirty-eight patients had Graves' disease with Grade III or greater TAO; 15 patients had Graves' disease without ophthalmopathy and nine had Hashimoto's thyroiditis without any eye signs. The control group consisted of 14 subjects. MEASUREMENTS: Antibodies against porcine eye and skeletal muscle, human eye (membrane and soluble antigen) and skeletal muscle, human thyroid microsomal and thyroglobulin antigens and dermal and orbital fibroblast antigens were assessed using ELISA. Antibody isotypes and IgG subclasses were studied for porcine and human eye muscle antibodies. Eye muscle (porcine and human) and orbital fibroblast antibodies were further analysed by immunoblotting. RESULTS: There were no significant differences in the ability of either IgG or IgA in sera from the different groups to bind porcine and human eye muscle antigens. There was a significant correlation (P < 0.0001) between the binding to porcine eye muscle and skeletal muscle antigens (for both IgG and IgA). There was no difference between sera from TAO patients and control subjects in their binding to eye muscle fibroblasts for both IgG and IgA antibodies. However, IgA antibody activity against dermal fibroblasts differed significantly between TAO patients and controls (P < 0.05). By immunoblotting, the frequency of IgA antibodies recognizing 21 kDa (40% of patients) and 62 kDa (52%) bands in porcine eye muscle blots and 20, 24 and 38 kDa bands in blots of human eye muscle (soluble) antigen differed significantly between patients with TAO and controls (P < 0.05 in all cases). IgG antibodies recognizing 80 and 92 kDa bands in blots of the subcellular membrane antigen prepared from orbital fibroblasts were found more frequently in patients with TAO compared with controls (P < 0.05 in both cases). CONCLUSIONS: We found no evidence that eye muscle membrane or fibroblast antibodies are present in a significant proportion of TAO patients, using ELISAs based on antigens prepared from several sources. We have also failed to demonstrate the presence of previously described specific, TAO-associated antibodies, including those directed against a 64 kDa protein in eye muscle and a 23 kDa protein in fibroblasts. IgA class antibodies reactive with orbital components appeared to be more strongly associated with TAO than those of the IgG class, though even this relationship is weak. These results suggest that antibodies are of secondary importance in the pathogenesis of TAO, which is most likely a T cell-mediated disorder.

Animals↗
PubMed2000

Cloning and characterization of the novel thyroid and eye muscle shared protein G2s: autoantibodies against G2s are closely associated with ophthalmopathy in patients with Graves' hyperthyroidism.

Serum autoantibodies against eye muscle antigens are closely linked with thyroid-associated ophthalmopathy (TAO), although their significance is unclear. The two antigens that are most often recognized are eye muscle membrane proteins with molecular masses of 55 and 64 kDa, as determined from immunoblotting with crude human or porcine eye muscle membranes. We cloned a fragment of the 55-kDa protein by screening an eye muscle expression library with affinity-purified anti-55 kDa protein antibody prepared from a TAO patient's serum. A complementary DNA (cDNA) encoding a novel protein, which we have called G2s, was sequenced on both strands, and its size was 411 bp. The open reading frame of G2s corresponded to a 121-amino acid peptide with a size of 1.4 kb. Using the rapid amplification of 5'-cDNA ends technique we were able to clone an additional 0.3 kb of the protein. G2s did not share significant homologies with any other entered protein in computer databases and had one putative transmembrane domain. Using the 1.4 kb cDNA as probe in Northern blotting of a panel of messenger ribonucleic acids prepared from human tissues, the parent protein was shown to correspond to a large molecule of about 5.8 kb with a calculated molecular mass of approximately 220 kDa, consistent with earlier immunoblot studies performed in the absence of reducing agents. G2s was strongly expressed in eye muscle, thyroid, and other skeletal muscle and to a lesser extent in pancreas, liver, lung, and heart muscle, but not in kidney or orbital fibroblasts. We tested sera from patients with Graves' hyperthyroidism with and without ophthalmopathy and from control patients and subjects for antibodies against a G2s fusion protein by immunoblotting and enzyme-linked immunosorbent assay. In immunoblotting, antibodies reactive with G2s were identified in 70% of patients with TAO of less than 3 yr duration, 53% with TAO of more than 3 yr duration, 36% with Graves' hyperthyroidism without evident ophthalmopathy, 17% with Hashimoto's thyroiditis, 3% with type 1 diabetes, 23% with nonimmunological thyroid disorders, and 16% of normal subjects. The prevalences, compared to normal values, were significant for the two groups of patients with TAO, but not for the other groups. Tests were positive in 54% of patients with active TAO, 33% with chronic ophthalmopathy, 36% with Graves' hyperthyroidism, 54% with Hashimoto's thyroiditis, 23% with type 1 diabetes, and in 11% of normal subjects using enzyme-linked immunosorbent assay. The antibodies predicted the development of the ocular myopathy subtype of TAO in six of seven patients and the congestive ophthalmopathy subtype in seven of eight patients, respectively, with Graves' hyperthyroidism studied prospectively during and after antithyroid drug therapy. Antibodies reactive with G2s may be early markers of ophthalmopathy in patients with Graves' hyperthyroidism. Because G2s is expressed in both thyroid and eye muscle, immunoreactivity against a shared epitope in the two tissues may explain the well known link between thyroid autoimmunity and ophthalmopathy.

Adult↗
PubMed2005

Isometric force measured in human horizontal eye muscles attached to or detached from the globe.

BACKGROUND: Human eye muscle tension has been measured directly only in detached condition. The purpose of this study is to compare force development in single, horizontal human eye muscle during saccadic eye movements, first when the muscle was still attached and later when it was detached from the globe. METHODS: Eleven horizontal muscles of eight patients were examined during surgery under topical anesthesia for concomitant strabismus. None of the muscles examined had been operated before. Isometric muscle tension was recorded with a strain gauge system, to which the muscle tendon was attached by a silk suture. The subjects made saccadic eye movements with the non-recorded eye by fixating light-emitting diodes in the center and at 10, 20, and 30 degrees horizontally to each side. Continuous and stepwise saccades were produced. In the tension signals, peak tension (Fp), steady tension (Fs), and the ratio Fp/Fs were measured. Statistical analysis was done with multivariate analysis of variance. RESULTS: The values of Fp, Fs, and Fp/Fs at different amplitudes of the saccadic eye movements were compared in the attached and the detached muscle. There were no consistent statistical differences between the values obtained in the two conditions. CONCLUSIONS: The muscle force development, measured at the tendon, was the same in muscles attached to the globe and in muscles free from the globe. Thus isometric muscle tension can be adequately recorded in muscles still attached to the globe, which increases the possibilities for studying contractile properties of various eye muscles during ophthalmic surgery procedures performed under topical anesthesia.

Adult↗
PubMed1990

Adaptation to tilt is not produced by eye-muscle potentiation.

The role of eye-muscle potentiation in adaptation to prismatic tilt was evaluated by assessing the presence of cyclotorsion induced by prolonged wearing of tilting prisms. Fundus photographs, containing the retinal image of the test line adjusted to the subjective vertical, were obtained before and after prism viewing that induced a 6 degrees aftereffect. The angular separation of the retinal images of the test line between pre- and post-prism photographs matched, in all cases, the difference in orientation between pre- and post-prism adjustment of the test line to the vertical. The data, therefore, clearly show that the eye is in exactly the same orbital position before and after substantial tilt aftereffects are induced. These results argue against the eye-muscle potentiation explanation of tilt aftereffects, that is, the explanation which says that tilt aftereffects are the result of prism induced changes in cyclotorsion.

Adaptation, Ocular↗