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Enlargement of the Blind Spot Caused by Papilledema
Vol. 106, No. 3
to the depressor muscles of that eye, which also causes increased innervation to the de pressor muscles of the less affected eye (Hering's law). This results in an inhibition of the superior rectus muscle in the less affected eye (Sherrington's law), which negates the in creased stimulation to the superior rectus muscle because of the forced head tilt. This is similar to the explanation outlined by Dr. Souza-Dias and I agree with him, but with one exception. He suggests that contracture of the superior rectus muscle of the more af fected eye is part of this explanation. I believe that the mechanism I have outlined is not contingent upon contracture of the superior rectus muscle in the more affected eye. Secondly, Dr. Souza-Dias believes that his and my explanations of the bilateral masking of superior oblique palsy are not mutually ex clusive. Although I agree, I do not think that mechanical contracture of the superior rectus muscle of the more affected eye is an essential ingredient. I have examined a patient with what was later proven to be a traumatic bilat eral masked superior oblique palsy within 24 hours after head injury. At that time the palsy of the less affected eye was totally masked. Certainly, there was no time for con tracture to occur. Of the nine patients I de scribed, only two of them had clinically de tectable contracture of the superior rectus muscles in the more affected eye, as tested with intraoperative forced duction testing. Although I do not believe the presence of contracture of the superior rectus muscle of the more affected eye is an essential ingredi ent, the explanation offered by Dr. SouzaDias works nicely with the one that I hypoth esized. BURTON J. KUSHNER, M.D. Madison, Wisconsin
Enlargement of the Blind Spot Caused by Papilledema EDITOR: We would like to add some information to the article "Enlargement of the blind spot
Correspondence
373
caused by papilledema," by J. J. Corbett, D. M. Jacobson, R. C. Mauer, and H. S. Thompson (Am. J. Ophthalmol. 105:261, March 1988). The reduction in size of the blind spot in cases of papilledema by using progressively stronger plus lenses during perimetry is not unknown to us in Holland. The same principle may be used to reduce the field defects in many other elevations of the retina, specifically in cases of choroidal tu mors such as melanomas or choroidal metastases. One of us (J.J.v.E.) has developed a similar technique to map visual fields in patients with severe myopia. Many of these patients have a nasal fundus ectasia, which causes a relative temporal scotoma to appear on perimetry. Such a scotoma should be demonstrable theoretically on perimetry by adding minus lenses in front of the eye being examined. Such a superimposition of minus lenses is often ineffective, however, as it is simply overcompensated by the patient's accommo dation. Therefore we have been using a series of minus lenses from a trial set with 5-mm holes drilled through the centers. These lens es are superimposed over the patient's normal correction and the visual fields are plotted through progressively more minus holed lens es. The hole allows the patient to maintain central fixation while the peripheral retina is subjected to the higher minus power of the holed lens. With this technique one can determine whether degenerative changes have already taken place in a nasal staphyloma. That is, it is often possible to obtain a normal visual field in a young patient with progressive myo pia whereas in a patient in whom degenera tive changes have already taken place, the relative field defect over the area of the staph yloma is not completely reduceable. This technique also enables one to differentiate be tween field loss resulting from myopia as op posed to field loss resulting from a possible chiasmal tumor. J. J. VAN ENDT, M.D. H. A. WESSELS, M.D. Roosendaal, The Netherlands
to the depressor muscles of that eye, which also causes increased innervation to the de pressor muscles of the less affected eye (Hering's law). This results in an inhibition of the superior rectus muscle in the less affected eye (Sherrington's law), which negates the in creased stimulation to the superior rectus muscle because of the forced head tilt. This is similar to the explanation outlined by Dr. Souza-Dias and I agree with him, but with one exception. He suggests that contracture of the superior rectus muscle of the more af fected eye is part of this explanation. I believe that the mechanism I have outlined is not contingent upon contracture of the superior rectus muscle in the more affected eye. Secondly, Dr. Souza-Dias believes that his and my explanations of the bilateral masking of superior oblique palsy are not mutually ex clusive. Although I agree, I do not think that mechanical contracture of the superior rectus muscle of the more affected eye is an essential ingredient. I have examined a patient with what was later proven to be a traumatic bilat eral masked superior oblique palsy within 24 hours after head injury. At that time the palsy of the less affected eye was totally masked. Certainly, there was no time for con tracture to occur. Of the nine patients I de scribed, only two of them had clinically de tectable contracture of the superior rectus muscles in the more affected eye, as tested with intraoperative forced duction testing. Although I do not believe the presence of contracture of the superior rectus muscle of the more affected eye is an essential ingredi ent, the explanation offered by Dr. SouzaDias works nicely with the one that I hypoth esized. BURTON J. KUSHNER, M.D. Madison, Wisconsin
Enlargement of the Blind Spot Caused by Papilledema EDITOR: We would like to add some information to the article "Enlargement of the blind spot
Correspondence
373
caused by papilledema," by J. J. Corbett, D. M. Jacobson, R. C. Mauer, and H. S. Thompson (Am. J. Ophthalmol. 105:261, March 1988). The reduction in size of the blind spot in cases of papilledema by using progressively stronger plus lenses during perimetry is not unknown to us in Holland. The same principle may be used to reduce the field defects in many other elevations of the retina, specifically in cases of choroidal tu mors such as melanomas or choroidal metastases. One of us (J.J.v.E.) has developed a similar technique to map visual fields in patients with severe myopia. Many of these patients have a nasal fundus ectasia, which causes a relative temporal scotoma to appear on perimetry. Such a scotoma should be demonstrable theoretically on perimetry by adding minus lenses in front of the eye being examined. Such a superimposition of minus lenses is often ineffective, however, as it is simply overcompensated by the patient's accommo dation. Therefore we have been using a series of minus lenses from a trial set with 5-mm holes drilled through the centers. These lens es are superimposed over the patient's normal correction and the visual fields are plotted through progressively more minus holed lens es. The hole allows the patient to maintain central fixation while the peripheral retina is subjected to the higher minus power of the holed lens. With this technique one can determine whether degenerative changes have already taken place in a nasal staphyloma. That is, it is often possible to obtain a normal visual field in a young patient with progressive myo pia whereas in a patient in whom degenera tive changes have already taken place, the relative field defect over the area of the staph yloma is not completely reduceable. This technique also enables one to differentiate be tween field loss resulting from myopia as op posed to field loss resulting from a possible chiasmal tumor. J. J. VAN ENDT, M.D. H. A. WESSELS, M.D. Roosendaal, The Netherlands