1
We agree that OCT can be used to guide the interpre- tation of visual field results, and in that respect, given a structure–function correspondence, it may be possible to use imaging data to confirm early, subtle visual field abnormalities such as that seen in our Case 3 that do not rise to the level of statistical significance with standard visual field software. JOEL S. SCHUMAN, MD ZINARIA Y. WILLIAMS, MD LISA GAMELL, MD AJIT NEMI, MD ELLEN HERTZMARK, MA CYNTHIA MATTOX, MD JULIE SIMPSON GADI WOLLSTEIN, MD Boston, Massachusetts JAMES G. FUJIMOTO, PhD Cambridge, Massachusetts REFERENCES 1. Williams ZY, Schuman JS, Gamell L, et al. Optical coherence tomography (OCT) measurement of nerve fiber layer thick- ness and the likelihood of a visual field defect (VFD). Am J Ophthalmol 2002;134:538 –546. 2. Keltner JL, Johnson CA, Quigg JM, et al. Confirmation of visual field abnormalities in the Ocular Hypertension Treat- ment Study. Arch Ophthalmol 2000;118:1187–1194. Correlation Between Retinal Abnormalities and Intracranial Abnormalities in the Shaken Baby Syndrome EDITOR: THE ARTICLE BY MORAD AND ASSOCIATES (AM J OPHTHAL- MOL 134:354-359, 2002) has serious deficiencies. First, the use of standard deviation implies a normal distribution. If indeed the subjects of this study were normally distrib- uted as to age, 15% would not have been born yet and 3% would not even have been conceived. This misunderstand- ing of statistics may well have implications for the remain- der of the article, but insufficient presentation of the data are given to evaluate this. Second, the statement, “In fact, it is well accepted today that retinoschisis in SBS is created by the shearing forces these (vitreous) attachments exert on the retina,” has two citations. The first is a self-citation and thus of limited value. The other is a paper about perimacular retinal folds. 1 Gaynon and associates, 2 talking about these folds, stated, “Perhaps the neurosensory retina is displaced later- ally by vitreous traction” (shearing); and Massicotte and associates 3 referenced this. However, Tongue 4 in a Guest Editorial commenting on the Massicotte article cautioned, “Until it is unequivocally proven that retinal folds are secondary to dynamic vitreous traction and shaking and not some other factors, it is imperative we not equate retinal folds with child abuse.” Perimacular retinal folds have also been reported in Terson syndrome, 5 the authors noting, “The presence of these folds in adults, without shaking, brings into question the mechanism of the folds arising from vitreoretinal traction induced by shaking.” One of the three cases in the Massicotte article has a “hemorrhagic retinoschisis cavity.” Retinoschisis was sug- gested to be from forward and backward movement of the lens producing traction, not shearing, by Greenwald 6 ; but the discussion by Tongue of this article notes, “Their hypothesis concerning the mechanisms of retinal damage and hemorrhage is interesting but not upheld by the pathologic specimen available to me.” Since no proof of vitreous traction has been produced, acceptance of this mechanism appears premature. Finally, the conclusion that correlation between retinal abnormalities and intracranial abnormalities supports any specific theory of causation overstates the data. Indeed, it may not even be consistent with an independent direct effect of trauma on intracranial and ocular tissues. If both are produced independently by similar intensities of trauma, since many cases of intracranial abnormalities without retinal abnormalities exist, cases of ocular findings without intracranial pathology would be expected to occur at least occasionally. Since all reported cases of retinal abnormalities have intracranial findings, it is most likely the ocular findings are secondary. Indeed, retinal hemor- rhages are seen in high altitude retinopathy with no trauma and factors such as hypoxia/anoxia and changes in intracranial pressure are seen in both shaken baby syn- drome and high altitude retinopathy. HORACE GARDNER, MD Manitou Springs, Colorado REFERENCES 1. Morad Y, Kim Y, Armstrong D, Huyer D, Mian M, Levin A. Correlation between retinal abnormalities and intracranial abnormalities in the shaken baby syndrome. Am J Ophthal- mol 2002;1434:354 –359. 2. Gaynon MW, Koh K, Marmor MF, Frankel LR. Retinal folds in the shaken baby syndrome. Am J Ophthalmol 1988;106: 423–425. 3. Massicotte SJ, Folberg R, Torczynski E, Gilliland MG, Luck- enbach MW. Vitreoretinal traction and perimacular retinal folds in the eyes of deliberately traumatized children. Oph- thalmology 1991;98:1124 –1127. 4. Tongue AC. The ophthalmologist’s role in diagnosing child abuse. Ophthalmology 1991;98:1009 –1010. 5. Keithahn MA, Bennett SR, Cameron D, Mieler WF. Retinal folds in Terson syndrome. Ophthalmology 1993;100:1187– 1190. 6. Greenwald MJ, Weiss A, Oesterle CS, Friendly DS. Traumatic retinoschisis in battered babies. Ophthalmology 1986;93:618 – 624. CORRESPONDENCE VOL. 135,NO. 5 745

Correlation between retinal abnormalities and intracranial abnormalities in the shaken baby syndrome

Embed Size (px)

Citation preview

We agree that OCT can be used to guide the interpre-tation of visual field results, and in that respect, given astructure–function correspondence, it may be possible touse imaging data to confirm early, subtle visual fieldabnormalities such as that seen in our Case 3 that do notrise to the level of statistical significance with standardvisual field software.

JOEL S. SCHUMAN, MD

ZINARIA Y. WILLIAMS, MD

LISA GAMELL, MD

AJIT NEMI, MD

ELLEN HERTZMARK, MA

CYNTHIA MATTOX, MD

JULIE SIMPSON

GADI WOLLSTEIN, MD

Boston, MassachusettsJAMES G. FUJIMOTO, PhD

Cambridge, Massachusetts

REFERENCES

1. Williams ZY, Schuman JS, Gamell L, et al. Optical coherencetomography (OCT) measurement of nerve fiber layer thick-ness and the likelihood of a visual field defect (VFD). Am JOphthalmol 2002;134:538–546.

2. Keltner JL, Johnson CA, Quigg JM, et al. Confirmation ofvisual field abnormalities in the Ocular Hypertension Treat-ment Study. Arch Ophthalmol 2000;118:1187–1194.

Correlation Between RetinalAbnormalities and IntracranialAbnormalities in the ShakenBaby Syndrome

EDITOR:

THE ARTICLE BY MORAD AND ASSOCIATES (AM J OPHTHAL-

MOL 134:354-359, 2002) has serious deficiencies. First,the use of standard deviation implies a normal distribution.If indeed the subjects of this study were normally distrib-uted as to age, 15% would not have been born yet and 3%would not even have been conceived. This misunderstand-ing of statistics may well have implications for the remain-der of the article, but insufficient presentation of the dataare given to evaluate this.

Second, the statement, “In fact, it is well accepted todaythat retinoschisis in SBS is created by the shearing forcesthese (vitreous) attachments exert on the retina,” has twocitations. The first is a self-citation and thus of limitedvalue. The other is a paper about perimacular retinalfolds.1 Gaynon and associates,2 talking about these folds,stated, “Perhaps the neurosensory retina is displaced later-ally by vitreous traction” (shearing); and Massicotte andassociates3 referenced this. However, Tongue4 in a GuestEditorial commenting on the Massicotte article cautioned,

“Until it is unequivocally proven that retinal folds aresecondary to dynamic vitreous traction and shaking andnot some other factors, it is imperative we not equateretinal folds with child abuse.” Perimacular retinal foldshave also been reported in Terson syndrome,5 the authorsnoting, “The presence of these folds in adults, withoutshaking, brings into question the mechanism of the foldsarising from vitreoretinal traction induced by shaking.”One of the three cases in the Massicotte article has a“hemorrhagic retinoschisis cavity.” Retinoschisis was sug-gested to be from forward and backward movement of thelens producing traction, not shearing, by Greenwald6; butthe discussion by Tongue of this article notes, “Theirhypothesis concerning the mechanisms of retinal damageand hemorrhage is interesting but not upheld by thepathologic specimen available to me.” Since no proof ofvitreous traction has been produced, acceptance of thismechanism appears premature.

Finally, the conclusion that correlation between retinalabnormalities and intracranial abnormalities supports anyspecific theory of causation overstates the data. Indeed, itmay not even be consistent with an independent directeffect of trauma on intracranial and ocular tissues. If bothare produced independently by similar intensities oftrauma, since many cases of intracranial abnormalitieswithout retinal abnormalities exist, cases of ocular findingswithout intracranial pathology would be expected to occurat least occasionally. Since all reported cases of retinalabnormalities have intracranial findings, it is most likelythe ocular findings are secondary. Indeed, retinal hemor-rhages are seen in high altitude retinopathy with notrauma and factors such as hypoxia/anoxia and changes inintracranial pressure are seen in both shaken baby syn-drome and high altitude retinopathy.

HORACE GARDNER, MD

Manitou Springs, Colorado

REFERENCES

1. Morad Y, Kim Y, Armstrong D, Huyer D, Mian M, Levin A.Correlation between retinal abnormalities and intracranialabnormalities in the shaken baby syndrome. Am J Ophthal-mol 2002;1434:354–359.

2. Gaynon MW, Koh K, Marmor MF, Frankel LR. Retinal foldsin the shaken baby syndrome. Am J Ophthalmol 1988;106:423–425.

3. Massicotte SJ, Folberg R, Torczynski E, Gilliland MG, Luck-enbach MW. Vitreoretinal traction and perimacular retinalfolds in the eyes of deliberately traumatized children. Oph-thalmology 1991;98:1124–1127.

4. Tongue AC. The ophthalmologist’s role in diagnosing childabuse. Ophthalmology 1991;98:1009–1010.

5. Keithahn MA, Bennett SR, Cameron D, Mieler WF. Retinalfolds in Terson syndrome. Ophthalmology 1993;100:1187–1190.

6. Greenwald MJ, Weiss A, Oesterle CS, Friendly DS. Traumaticretinoschisis in battered babies. Ophthalmology 1986;93:618–624.

CORRESPONDENCEVOL. 135, NO. 5 745