Biomedical subjects
Publications and source records attributed to W N Gillum.
A previously undescribed syndrome of bilateral blepharoptosis, ectopia lentis, and high myopia apparently was dominantly inherited and originated from a spontaneous genetic mutation. The syndrome seems to be caused by a decrease in the tensile strength of the levator aponeurosis, the zonules, and the sclera.
Essential blepharospasm is an idiopathic, progressively debilitating disease leading to blindness. Years of forceful spasms result in brow ptosis, dermatochalasis, and, frequently, levator aponeurosis and lateral canthal tendon defects. Following standard neurectomy procedures, the facies droop, brow ptosis and dermatochalasis worsen, and ptosis and canthal tendon laxity suddenly become more evident. We describe a procedure involving meticulous extirpation of all accessible orbicularis oculi, procerus, corrugator superciliaris, and facial nerves in postorbicular fascia. This extirpation of eyelid protractors is combined with browplasty with fixation to frontalis and reinforcement of the levator aponeurosis to strengthen the retractors. Our technique opens the eye just as effectively as standard facial neurectomy procedures, simultaneously corrects associated anatomical deformities, and avoids facial paralysis. Gratifying results were obtained in 15 patients followed up for six to 38 months.
A 19-year-old white male developed blindness in the left eye following a motor vehicle accident. Orbital echography and computerized axial tomography established the diagnosis of subperiosteal hematoma of the orbit. Emergency medical therapy and lateral canthotomy resulted in slight visual improvement but rebleeding occurred 12 hours after injury with visual loss. An emergency surgical decompression of the orbit was performed. Vision returned to 6/7.5 following decompression. This is the first report illustrating that orbital decompression can reverse complete visual loss from a subperiosteal hematoma of the orbit.
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The diagnosis and management of patients having had superior rectus suspension procedures for the correction of blepharoptosis can be quite difficult. Patients who have had these procedures frequently present with a syndrome which included 1) history of an unknown type of ptosis surgery performed at least ten years ago, 2) good eyelid excursion, 3) minimal lid lag associated with marked lagophthalmos, 4) hypotropia, and 5) corneal scarring. One must evert the upper eyelid to demonstrate the pathognomonic adhesion between tarsus and the superior rectus muscle. The correct management of this condition is virtually impossible until the diagnosis is made. To correct the corneal and motility problems that result from superior rectus suspension procedures, the adhesion between the superior rectus muscle and the upper eyelid must be released. It is very easy to overlook this syndrome if one is unaware of its presentation. We present five patients who illustrate the superior rectus suspension syndrome.