Biomedical subjects
Publications and source records attributed to D F Kamin.
The Wies procedure may be complicated by an overcorrection, which is in effect a cicatricial ectropion. Four cases of such a complication are presented. The mechanism of an overcorrection is related to the level of the incision in the lid and to the suture placement. Correction of this complication primarily involves lysing cicatricial bands maintaining the overcorrection. Placement of sutures maintains the lid in a normal position.
We used two surgical procedures to treat upper eyelid retraction in ten patients: either a posterior myectomy or the anterior levator muscle recession technique. Our choice was usually based on the amount of retraction. We used the posterior myectomy technique to treat up to 2 mm of retraction or localized retractions (five cases), particularly after blepharoptosis surgery. We used the anterior recession method to treat more than 2mm of retraction (five cases), particularly when associated with dysthyroid ocular disease. Complex eyelid contour abnormalities were treated with a combined recession-resection approach to the aponeurosis of the levator palpebrae superioris muscle (one case).
The Wies procedure may be complicated by an overcorrection, which is in effect a cicatricial ectropion. Four cases of such a complication are presented. The mechanism of an overcorrection is related to the level of the incision in the lid and to the suture placement. Correction of this complication primarily involves lysing cicatricial bands maintaining the overcorrection. Placement of sutures maintains the lid in a normal position.
Three male patients had paravenous pigmented retinochoroidal atrophy. Extensive retinal function tests showed characteristic retinal pigment epithelial abnormalities on fluorescein angiography, loss of peripheral visual field, diminution of the electroretinographic b-wave, and elevated rod threshold on dark adaptometry. The disease appears to be more progressive than previously indicated, and in late stages, may cause legal blindness through involvement of the posterior pole. No treatment is known.
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This is the first reported case of Wilson's disease where a global defect of saccadic eye movements has been documented by electro-oculography. The defect of rapid eye movements is discussed in relation to current anatomical, pathological, and experimental work relating to the descending frontobulbar saccadic eye movement system. It is suggested that the caudate nucleus pathology in Wilson's disease might be responsible for the defect of saccadic movement by interrupting a descending polysynaptic pathway.
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