The HRA2 instrument affords detailed high-resolution images of FA and ICGA. Notably, recurrence of myopic CNV developed in areas surrounded by new small crack fragments and LCs are considered to be important in the development of myopic CNV.
Indocyanine green angiography (ICGA) can provide valuable information on choroidal vessels because of its longer wavelength fluorescence with limited diffusion within the choriocapillaries compared with fluorescein angiography (FA).14, 15, 16 Many characteristic findings of myopic CNV are observed using ICGA such as lacquer cracks (LCs), peripapillary choroidal atrophy, any dark rim, and late-phase hyperfluorescence. In particular, LCs are considered important in the development of the condition,13, 17, 18 but the associated mechanism remains unclear so far.
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In patients with linear-type LCs, the location of myopic CNV was either within the area of the LC (11 eyes, 50.0%) or at the tip of the LC (11 eyes, 50.0%). However, CNV always occurred in the LC, the location nearest to the fovea and, especially, in a region surrounded by very tiny crack fragments. Therefore, the spatial relationship between LC and fovea was important to detect the site of myopic CNV (Figure 2). In patients with stellate-type LCs, myopic CNV was located near the center of the LC (14 eyes, 93.3%) or at the tip of the LC (1 eye, 6.7%). The center of the LC usually did not coincide with the fovea, and CNV tended to occur in the inner corner of the radiating arm nearest to the fovea. Figure 3 shows instances of myopic CNV associated with stellate-type LCs.
Patients with myopic CNV associated with linear-type LCs. FA shows fluorescein dye leakage (white circle) from myopic CNV (a and c). Late phase ICGA indicates small fragments of LCs (white circle; b and d). The area surrounded by these small crack fragments is the location of myopic CNV. The white circle indicates an identical region on both FA and ICGA.
Myopic CNV did not develop from the precise position of the LC per se. An LC consisted of a collection of small dot-shaped crack fragments and CNV was located in the area surrounded by these fragments, as shown in Figures 2 and 3. Small LC fragments were clearly noted in 25 eyes and the location of CNV corresponded with the region surrounded by such tiny dot-shaped crack fragments in 23 eyes.
LC progression was associated with the production of increasing amounts of small crack fragments. These fragments appeared slowly, in three different patterns, arising from the tip of an existing LC (elongation, 66.7%), the side of an existing LC (branching, 26.7%), or remote from an existing LC but later connecting with the LC (bridging, 46.7%; Figures 4 and 5). The progression pattern often appeared as a mixture of these three types. LCs of fellow eyes with no treatment showed 50% elongation, 33.3% branching, and 50% bridging pattern. Conversion of a linear-type LC to the stellate type occurred in one patient (Figure 4).
Patients showing LC progression. A linear-type LC is shown on late-phase ICGA (a). At 26 months later, a new small crack, showing a bridging pattern, developed remote from the previous LC (white arrow; b). At 6 months later, another new crack (black arrow) bridged over to the first LC, progressing toward the crack that developed at 26 months (white arrow; c). A linear LC is horizontally located, from the disc to the fovea (d). This LC became extended from a tip with an elongation pattern (white arrow; e). A new crack appeared, remote from the pre-existing LC in a bridging pattern (black arrow; f).
Patients showing LC progression. A stellate-type LC is evident near the disc, extending to the fovea, and small crack fragment in a bridging pattern lies separate from the main LC (white arrow; a). At 21 months later, newly developed LCs (black arrows) bridged the pre-existing LCs (white arrow; d). No definite LC was noted at first (b). At 13 months later, multiple new crack fragments appeared (white arrows; e). Irregular, multiple LCs lie near the disc (c). At 18 months later, new crack fragments in an elongation pattern are evident (white arrows; f).
Patients showing LC progression and recurring myopic CNV. FA shows fluorescein dye leakage (white circle) from myopic CNV (a) and late phase ICGA demonstrates an LC surrounding CNV (d). PDT was performed twice and myopic CNV recurred at 9 months later. Fluorescein dye leakages are apparent, from prior and newly developed CNV (b). ICGA reveals an area surrounded by new small crack fragments in a branching pattern (black arrow) that corresponds to CNV (white circle; e). New crack fragments, showing an elongation pattern, appeared at 6 months later (white arrows; c). These cracks progressed slowly in a branching pattern at 19 months later (white arrows; f).
Among 37 eyes with myopic CNV associated with LCs, CNV had developed along the LCs in 36. In both LC types, each LC consisted of a collection of small dot-shaped crack fragments. In linear-type LC, the location of CNV was in the LC region nearest to the fovea. More precisely, the area of origin was surrounded by small fragments of the LC in a region into which the LC did not extend. The occurred site of CNV in the center or at the tip of linear-type LC depended on the location of LC with respect to the fovea. When the LC lay over the fovea, CNV usually developed in the center. However, CNV occurred at the tip of the LC nearest to the fovea when the LC lay outside of the fovea. With stellate-type LCs, the location of CNV was in the inner corner of the radiating arm nearest to the fovea. Detailed imaging and analysis of LCs were possible in this study because of the high sensitivity of the confocal ICGA system.
Progression of LC was also observed on the development of myopic CNV. Five treated eyes showed LC progression and recurrence of CNV at newly developed LCs. Progression of LCs and development of new myopic CNV were detected simultaneously in non-CNV fellow eyes. Outbreak of CNV was associated with recently formed LCs. Axer-Siegel et al17 reported that extension of LCs accompanied newly developed myopic CNV and that vigorous healing of new LCs might have contributed to the development of CNV. In this study, LCs progressed with an increase in the number of small crack fragments and myopic CNV was usually located in an area surrounded by these fragments. A possible explanation is that the area surrounded by new small crack fragments, as well as the LC per se, is engaged in a vigorous healing process resulting in initiation of myopic CNV.
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Chronic anal fissure is a cut or crack in the anal canal or anal verge that may extend from the muco-cutaneous junction to the dentate line [1] . It can be observed as the buttocks are parted and it is often suspected when there is marked spasm of the anus. The typical symptom of chronic anal fissure is pain on or after defecation that is often severe and may last from minutes to several hours. Indeed, digital or proctoscopic examination is often impossible because of the pain experienced by the patient. Furthermore, bright blood is often observed on the toilet paper. Most fissures occur in the posterior midline of the anal canal; they are located in the anterior midline in only 10% of women and 1% of men [2-4] . Multiple or lateral fissures arise suspicion of other diseases, including inflammatory bowel diseases, tuberculosis, HIV infection and syphilis. The cause of chronic anal fissures and the reasons for their failure to heal remain unclear [5] . There is a history of constipation in 25% of patients, and diarrhea is considered a predisposing factor in approximately 6% of cases. The main characteristics of this painful condition, including the predilection of chronic anal fissure for the posterior midline and the lack of granulation tissue at the fissure site, are unexplained. Several theories have been advanced to disclose the underlying causes of anal fissure [3] . However, most of them are conflicting and none have given a satisfactory explanation for the characteristic features of chronic anal fissure. Recognized features common to most chronic anal fissures include a high resting anal pressure owing to hypertonicity of the internal anal sphincter (IAS), reduced vascular perfusion index at the site of the anal fissure, and the presence of 'ultraslow' pressure wave activity in the IAS [5-7] . Furthermore, anodermal blood flow could depend not only on the 'mechanical' force of sphincters, but also on biochemical processes that occur in the fissure region [8] . 2ff7e9595c
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