carotid sympathetic plexus, which lies on the surface of the internal carotid artery near the origin of the ophthalmic artery 141. Our patient was fortunate in having an unusually large right posterior communicating artery, making it possible to clamp the right common carotid artery safely despite the absence of communication between the right anterior cerebral and right internal carotid arteries. The resolution of her symptoms and signs following clamping strongly suggests that the aneurysm was their sole cause. Surgery was performed by Dr Erwin Hanson. Photographs are courtesy of E. E. Kingsky.

Referetires Derakhshan I: Superior branch palsy of the oculomotor nerve with spontaneous recovery. Ann Neurol4:478-479, 1978 2. Meadows SP: lntracavernous aneurysms of the internal carotid artery. Arch Ophthalmol 62:566-574, 1959 3. Trobe JD, Glaser JS. Post JD. Meningiomas and aneurysms of the cavernous sinus: neuro-ophthalmologic features. Arch Ophthalmol 963457-467, 1978 4. Walsh FB, Hoyt W F Clinical Neuro-ophthalmology. Third edition. Baltimore, Williams & Wilkins. 1969, pp 478-480 1.

Corticosteroid Theram and Tourette Syndmme Norman Geschwind, M D

I was interested in the article entitled “Improvement in Gilles d e la Tourette syndrome after corticosteroid therapy” by Drs Kondo and Kabasawa (Ann Neurol 4 : 3 8 7 , 1978). T h e authors state that postinfectious cases of this syndrome have rarely been described, and they suggest that corticosteroids may be useful in patients in whom the syndrome appears following an acute infection. Let me point o u t that the patient is described as having hypotonic muscles and small, recurrent. bizarre, brisk movements. His antistreptolysin 0 titer was elevated; the C-reactive protein and rheumatoid arthritis tests were positive; the sedimentation rate was elevated. The patient was treated with steroids and improved without recurrence. 1 would simply ask why this is not a case of rheumatic fever with associated Sydenham chorea. The clinical course in response t o steroids would be consistent with this diagnosis. Furthermore, the presence of sudclen cries and the utterance of obscenities, i.e., coprolalia, should not be surprising. D r Fred Quadfasel pointed out to me many years ago that these symptoms can occur in cases of Sydenham chorea. I have myself seen them in patients with that syndrome whose laboratory tests were as striking as those of this patient. If it is correct that the patient had rheumatic fever, then we should be very hesitant to accept this as a case of Tourette syndrome, which does not have this association, nor these laboratory findings, and which runs a quite different course.

Reply Kiyotaro Kondo, MD W e appreciate Dr Geschwind’s questions and attempt here to answer. Tics and choreic movements share some common features, but the former are more markedly characterized by repetitiveness and a stereotypic appearance that does not interfere with volitional movements. They can be voluntarily suppressed at least temporarily, but such an effort ultimately increases the movements. These movement patterns Characterized our patient. As stated by Dr Geschwind, hypotonia, sudden cries, and obscenities are encountered in a few cases of Sydenham chorea as well, and no objective clues exist that will unequivocally yield the correct diagnosis. Tourette syndrome has protean clinical manifestations and is often difficult to distinguish from other hyperkinetic conditions. As correctly pointed out by Dr Geschwind, Sydenham chorea may be particularly difficult to rule out. One of the reasons Dr Geschwind is hesitant to accept o u r patient as having Tourette syndrome was the transient course. It is true that the syndrome usually runs a chronic and recurrent course, whereas most cases of Sydenham chorea are transient. Shapiro et a1 [2] included a life-long course as one of their criteria for diagnosis of Tourette syndrome. Such a criterion, however, makes it impossible to diagnose Tourette syndrome except after a long time; it would be difficult to diagnose a young patient who shows a typical clinical picture but improves. Mindful of rhis difficulty, we waited five years before reporting our case, observing its course. Tourette syndrome is not an etiological entity but a syndrome in which various extrinsic factors may act on an inherited predisposition. Therefore, we find no reason to exclude clinically typical cases with abnormal laboratory findings as observed in our patient. In diseases conditioned by gene-environment interactions o r by triggering factors operating on a latent inheriteJ susceptibility, mild, abortive, or atypical cases are not unusual, depending on the relative importance of the factors involved. The symptoms can be transient in such diseases when the triggering factor acts transiently. We have discovered, to our regret, that we failed to acknowledge a report of beneficial effects of corticosteroids in Tourette syndrome. Dr S. Novick of the Tourette’s Syndrome Association, Bayside, N Y 11361, notes that Popielarska et al observed superior therapeutic results in 7 patients treated with prednisone ( 4 cases) and neuroleptic agents ( 3 cases) [l].

R eferenres 1. Popielarska A. Kuligowska M. Mazur M: On Gilles de la Tourerte syndrome and therapeutic trials in the light of o u r observations [in Polish]. Pediatr Pol 47110557-1 103, 1972 2. Shapiro IS, Bruun RD, Sweet RD: Gillrs de la Tourette Syndrome. New York. Raven, 1977, pp 254-255

From the Department of Neurology, Brain Research Institute. Niigata University, Niigara, Japan.

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From the Neurological Unit, Beth Israel Hospital, 330 Brookline Ave, Boston, MA 02215. Notes and Letters

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Corticosteroid therapy and Tourette syndrome.

carotid sympathetic plexus, which lies on the surface of the internal carotid artery near the origin of the ophthalmic artery 141. Our patient was for...
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