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Corticosteroid therapy and tourette syndrome.

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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.
~
From the Neurological Unit, Beth Israel Hospital, 330 Brookline
Ave, Boston, MA 02215.
Notes and Letters
495
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