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Show Journal of Clinical Neuro- ophthnlmology 12(]): 73- 74, 1992. Letters to the Editor To the Editor: We read with interest the article by Hriso and colleague ( 1) who presented a patient with monocular elevation paresis and incomplete ptosis due to midbrain infarction involving the fascicular segment of the oculomotor nerve. Based on previously reported cases of complete and partial oculomotor nerve palsies ( 2- 5), we proposed ( 6) that the transverse oculomotor fascicular arrangement in the ventral midbrain tegmentum from lateral to medial was as follows: inferior oblique fascicles; superior rectus fascicles; medial rectus and levator palpebrae ( lid) fascicles; inferior rectus fascicles; and most medially, the pupillary fibers. The cases that were available at the time of that report were insufficient to determine whether the lid fascicles were intermediate between the medial rectus and inferior rectus fascicles or possibly positioned between the superior rectus and medial rectus fascicles ( 6), The case by Hriso and colleague documented the presence of inferior oblique, superior rectus, and levator palpebrae paresis, with simultaneous sparing of medial rectus function. Their case and two other similar cases ( 7) would favor the latter conclusion that the levator palpebrae fascicles are in an intermediate location between the superior rectus and medial rectus fascicles. The availability of such clinical cases has helped to advance our understanding of the transverse neuroanatomic organization of the fascicular fibers ~ f the oculomotor nerve ( 6). Future clinicopathologIc correlation is awaited. Acknowledgment: This research was aided in par~ by an unrestricted grant from Research to Prevent Bhndness. Leuworth N. Johnson, M. D. Othoniel Castro, M. D. Neuro- Ophthalmology Division Mason Institute of Ophthalmology University of Missouri- Columbia Columbia, Missouri REFERENCES 1. Hriso E, Masdeu JC, Miller A. Monocular elevation? weakness and ptosis: an oculomotor faSCIcular syndrome. JCIzn Neuro- ophthalmoI1991; 11: 111- 3. 73 c1j 1992 Raven Press, Ltd., New York 2. Nadeau SE, Trobe JD. Pupil- spring in oculomotor palsy: a brief review. Ann NeuroI1983; 13: 143- 8. 3. Shuaib A, Murphy W. Mesencephalic hemorrhage and third nerve palsy. J Comput Tomogr 1987; 11: 38~. 4. Keane JR. Isolated brain- stem third nerve palsy. Arch Neurol 1988; 45: 813-- 4. 5. Shuaib A, Israelian G, Lee MA. Mesencephalic hemorrhage and unilateral pupillary deficit. J CIin Neuro- Ophthalmol 1989; 9: 47- 9. 6. Castro 0, Johnson LN, Mamourian AC. Isolated inferior oblique paresis from brain- stem infarction: Perspective on oculomotor fascicular organization in the ventral mldbram tegmentum. Arch Neurol 1990; 47: 23>.- 7. . .. 7. Ksiazek SM, Repka MX, Maguire A, el al. DIVISIOnal oculomotor nerve paresis caused by intrinsic brainstem diSease. Amz Neurol 1989; 26: 714-- 8. To the Editor: We read with interest the article by Smith et al. ( 1) concerning a case of Leber's hereditary optic neuropathy with bilateral distended optic nerve sheaths. Optic nerve sheath decompression performed 8 months after onset of visual loss did not improve visual acuity. The authors were unaware of any previous cases of Leber's with distended optic nerve sheaths and questioned whether earlier intervention in such a case would be efficacious. We report a similar case in which optic nerve sheath decompression was performed 1 month after the onset of visual loss. Report of a case. A 19- year- old man with previously normal vision had sudden onset of reduced vision in his right eye in late November, 1990, followed by a similar episode in the left eye one month later. He had a family history of Leber's hereditary optic neuropathy in a maternal cousin and uncle. He was treated with oral prednisone for 2 weeks with no improvement. A computerized tomography ( CT) scan on January 4, 1991, was read as normal. Examination at University of Alabama at Birmingham on January 9, 1991 revealed visual acuity of 5/ 200 right eye and 20/ 400 left eye, There was no afferent pupillary defect. Color vision was reduced bilaterally. Slit- lamp exam was normal. Ophthalmoscopy showed clear media with mild temporal pallor of the right disc and minimal peripapillary telangiectatic vessels on the left. Visual fields demonstrated bilateral central scotomas. Fluorescein angiography showed no leakage from the discs or peripapillary vessels. Blood sent for mitochondrial 74 LETTERS TO THE EDITOR DNA studies was positive for the Wallace 11778 point mutation. An electrocardiogram revealed a right bundle branch block. The CT scan was reviewed and the intraorbital segments of each optic nerve appeared enlarged ( Fig. 1). Quantitative ultrasonography showed both optic nerve sheaths to be distended. The difference in neural and dural diameters was 1.90 mm on the right and 1.80 mm on the left. The upper left of normal is 1.50 mm in this laboratory. The optic nerve proper was also slightly enlarged in each eye. An optic nerve sheath decompression through a medial approach was performed on the left eye on January 25, 1991. At surgery, the optic nerve sheath appeared mildly distended and as incisions were made there was prompt release of cerebrospinal fluid. Orbital ultrasonography done on February 7, 1991, showed no change in the size of the left optic nerve, but the difference in neural and dural diameters decreased to 1.50 mm. The perineural space decreased slightly on the right to 1.78 mm.; however, this difference of 0.12 mm. from the preoperative exam was too small to be considered a definite decrease. Unfortunately, the vision did not improve following the procedure. The patient was last seen March 6, 1991, with vision remaining 5/ 200 on the right and 20/ 400 on the left. Both optic discs showed temporal pallor, the right more than the left. There was no improvement in visual fields. Comment. Optic nerve sheath decompression was performed 1 month after visual loss in this FIG. 1. Preoperative axial CT scan reveals enlargement of both optic nerves. patient with Leber's hereditary optic neuropathy. Although ultrasonography demonstrated reduction of the perineural space to normal limits, there was no improvement in visual function. The cause of the sheath distension, and its effect, if any, on optic nerve function is uncertain. Further evaluation is needed to determine if early optic nerve sheath decompression is of any benefit in cases of Leber's hereditary optic neuropathy. REFERENCE 1. Smith JL, Tse DT, Byrne SF, et al. Optic nerve sheath distension in Leber's optic neuropathy and the significance of the " Wallace mutation." f Clin Neuro- ophtha[ mo[ 1990; 10: 231-- 8 Douglas R. Wilson, M. D. Lanning B. Kline, M. D. Department of Ophthalmology University of Alabama School of Medicine Birmingham, Alabama To The Editor: I suppose all of us believe that our technique for doing superficial temporal artery biopsies is the best. The technique described by Dr. Tomsak in the Journal of Clinical Neuro- ophthalmology 1991; 11( 3): 202- 204 was so opposed to what I have taught my students I felt it necessary to reexamine what I had been doing. I conclude that there are some problems with what he suggests. Early in my practice I encountered two patients who had had superficial temporal artery biopsies by general surgeons in the location described in his article. Both of these patients had painful masses under the scar, which we assumed were neuromas. I think that the problem is that the site suggested by Dr. Tomsak is a bit crowded. As he mentions, the superficial temporal vein lies next to the artery in front of the ear. Also, a branch of the auriculotemporal nerve usually lies directly on the artery in this region. I am sure that Dr. Tomsak is a careful surgeon who can dissect the vein and nerve free without any damage. It seems to me, however, to be a lot of work for the routine case and perhaps in less experienced hands, a somewhat more dangerous procedure than a biopsy done more peripherally. Don C. Bienfang, M. D. Brigham and Women's Hospital 75 Francis Street Boston, Massachusetts |
