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Cellular infiltration of Cloquet’s canal
  1. TIBOR MILIBÁK
  1. 1st Department of Ophthalmology, Semmelweis University Medical School
  2. Budapest, VIII, Tömö u 25-29, H-1083, Hungary

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    Editor,—Biomicroscopic evaluation of the Cloquet’s canal is difficult in a normal eye. Although Goldmann, based on his extensive biomicroscopic studies,1 described as early as 1954 the detailed biomicroscopic anatomy of it, normally only parts of the Cloquet’s canal are available for direct biomicroscopic observation.

    In this report I present a case in which not only the entire course of the Cloquet’s canal became visible by a marked cellular infiltration of the vitreous, but the cell infiltration itself dramatically improved the visibility of fine structures of the surrounding vitreous.

    CASE REPORT

    A 9-year-old white boy discovered visual deterioration of the left eye by the incidental covering of his right eye. The patient’s previous medical history was uneventful: chickenpox and epidemic parotiditis occurred in early childhood.

    Uncorrected visual acuity was 20/20 right eye and 20/200 left eye, which improved to 20/40 with a −3.0 D correction. Intraocular pressures were 12 and 13 mm Hg, respectively. Biomicroscopic examination of the right eye was unremarkable. The left eye was quiet, slit lamp examination revealed partial cataract, a vitreous flare, and cell infiltration in the anterior vitreous. Biomicroscopy of the vitreous with a contact lens revealed diffuse flare and cell infiltration. Cloquet’s canal was made distinct by a marked cellular infiltration (Fig 1). The course of the central canal curved down in the vicinity of the retina and ascended towards the lens. Cell infiltration around the canal emphasised the radial structure of the child’s vitreous, surrounding the course of the Cloquet’s canal (Fig2). There were no abnormalities in the fundus or on the pars plana. Fluorescein angiography could not be performed because of the cataract, the vitreous haze, and the patient’s inability to cooperate.

    Figure 1

    Slit lamp biomicroscopic appearance of heavily infiltrated Cloquet’s canal seen through the QuadrAspheric contact lens. Central part of the vitreous space. The normal course of the central canal is altered by the cellular infiltration. Saccular dilatations are present at the anterior end of the tractus. The whole course of the Cloquet’s canal is surrounded by a layer of infiltrated cloudy vitreous where signs of the radial orientation can be seen.

    Figure 2

    Computer graphic of Figure 1 taken with embossed filter. Computer imaging enhances visibility of the subtle radial structures of the vitreous, surrounding the course of the Cloquet’s canal.

    Results of general physical examination and chest x ray were unremarkable. Laboratory evaluation showed an erythrocyte sedimentation rate of 5 mm in the first hour, a negative rheumatoid factor, a normal complete blood, normal titres againstToxoplasma, Toxocara, Brucella,Listeria, Lyme, and HIV. A clinical diagnosis of chronic posterior uveitis was made, but specific therapy was not considered.

    After follow up of 1 year, visual acuity and the partial cataract in the left eye remained unchanged, the structure of the vitreous had become disorganised, the vitreous haze and the infiltration of Cloquet’s canal disappeared, and only a limited number of cells in the retrolental space could be observed. Fundus examination showed no abnormality.

    COMMENT

    During development and early childhood Cloquet’s canal extends almost in a direct anteroposterior course from the optic disc towards the posterior capsule of the lens. With aging, Cloquet’s canal changes: in the adult it emerges from the optic nerve head, and in the posterior part of the vitreous cavity it curves down, while in the anterior vitreous it emerges again towards the lens.2 The canal becomes obliterated in its middle part in the adult eye. In some cases saccular dilatation of the canal may occur.1 Under pathological conditions the course or the visibility of the Cloquet’s canal can change considerably. Uveitis may cause greater delineation of the canal in the area of the retrolental space (ascending phenomena),23 whereas chorioretinitis of the posterior pole may cause the canal to turn downwards in front of the optic disc. Cells may even infiltrate the Cloquet’s canal in front of the retina. It has also been suggested that intravitreal traction on the optic pit by the anomalous Cloquet’s canal may have a role in the development of macular detachment in pits of the optic nerve.4 The present case clearly highlights these changes to the biomicroscopic anatomy of the vitreous caused by dense cellular infiltration of the vitreous. This case clearly demonstrates: the entire intravitreal course of the Cloquet’s canal an obliteration of its anterior parts the presence of saccular dilatation of the canal in the anterior third of the vitreous cavity the effect of the cellular infiltration on the intravitreal course of the infiltrated Cloquet’s canal and the subtle radial structures of the vitreous, surrounding the course of the Cloquet’s canal.

    References

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