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Chorea in long-term use of pemoline.

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extrinsic spread from contiguous nerves. A similar mechanism of spread to the ophthalmic and central retinal arteries
via the nasociliary nerve may be implicated in our patient.
Antidromic spread of HZ angiitis was recently suggested
by MacKenzie e t al [4].Noting that the ophthalmic nerve
innervates the dura, venous sinuses, large cerebral veins,
and arteries at the base of the brain, they suggested spread
of varicella zoster virus along the intracranial branches of
the ophthalmic nerve. Such a mechanism might explain the
well-described arteritis of the carotid, middle cerebral, and
anterior cerebral arteries seen ipsilateral to HZ ophthalmicus. Similarly, the proximity of the ophthalmic nerveinnervated dura to the middle meningeal artery might explain its involvement in our patient. Oculosympathetic
paralysis is a rare complication of HZ infection and has
been ascribed to sympathetic interruption at the middle ear
[2] or internal carotid artery [5].In our case, it seems more
likely that the paralysis resulted from antidromic spread of
varicella zoster virus to the long ciliary nerve.
Department of Neuvology
Bowman Gray School of Medicine
Winston-Salem. NC 271 03
1. Hollenhorst RW: Symposium on Neuro-ophthalmology. St.
Louis, Mosby, 1976, chap 13, pp 168-190
2. Jarrett WH: Horner’s syndrome with geniculate zoster. Am J
Ophthalmol 63:326-329, 1967
3. Linneman CC Jr, Alvira MM: Pathogenesis of varicella-zoster
angiitis in the CNS. Arch Neurol 37:239-240, 1980
4. MacKenzie RA, Forbes GS, Karnes WE: Angiographic findings
in herpes zoster arteritis. Ann Neurol 10:458-464, 1981
5. Victor DI, Green WR: Temporal artery biopsy in herpes zoster
ophthalmicus with delayed arteriris. Am J Ophthalmol
82:628-630, 1976
social skills of the 10- to 11-months’ level. The patient had
a seizure disorder with a right temporal lobe epileptic focus
controlled by primidone, 50 mg twice daily. Examination of
cranial nerves and of the sensory and motor systems
showed no abnormalities.
In 1976, the patient became progressively hyperactive in
spite of therapy with chlorpromazine, 75 mg twice a day.
Results of general physical and neurological examination
and laboratory work were unchanged. Primidone was discontinued and the patient was given phenytoin, 50 mg
twice daily, and diazepam, 5 mg three times per day.
Thioridazine, 15 mg three times daily, was given from
March, 1977, to March, 1978, without improvement. From
March, 1978, to October, 1979, methylphenidate at a dosage of 10 mg daily was tried without success.
I n November, 1979, magnesium pemoline, 37.5 mg per
day, was started and increased to 7 5 mg daily after five
weeks, resulting in an improvement in behavior. In July,
1980, the patient was noted to have violent choreiform involuntary movements of all the extremities and dyskinetic
movements of the face and tongue. Other findings were
unchanged. Pemoline was discontinued, and the abnormal
movements slowly diminished and completely disappeared
over the next 48 hours. At present, the patient is taking
phenytoin alone and is slowly becoming hyperactive.
Experiments in guinea pigs suggest that pemoline increases central dopaminergic activity, but the exact mode
of action is unknown. High doses of amphetamine produce
psychosis as well as abnormal choreiform movements due
to indirect stimulation of dopaminergic receptors. Prolonged use of amphetamines produces hypersensitivity of
the dopaminergic neurons in the basal ganglia [2]. A similar
effect may explain the chorea observed in this child after
therapeutic doses of magnesium pemoline.
New York Medical College
Mental Retardation Institute
Westcbester County Medical Center
Valhalla, NY 10595
Chorea in Long-term
Use of Pemoline
Baldev Kaur Singh, MD, Avtar Singh, MD,
and Emanuel Chusid, MD
Magnesium pemoline has been used to treat hyperactivity
in children because of its central stimulant action, which is
comparable to the effect of dextroamphetamine [ 11.
Chorea has been reported in a child suffering from
pemoline overdose 131 but not previously following
therapy in the usual dosage.
A 9-year-old boy with normal prenatal and perinatal
history developed hyperactive behavior after the age of 1
year. He stood at 2 years and spoke and walked at age 3. In
1975, at the age of 6 years, he was initially treated because
of uncontrolled hyperactivity and psychomotor retardation. H e had received chlorpromatine and diazepam for his
behavior. General physical examination was normal. The
head circumference was average; height and weight were in
the second percentile. He was hyperactive, had a short attention span, performed up to the level of 22 months in
motor coordination, and possessed adaptive, verbal, and
218 Annals of Neurology
Vol 1 3 No 2
February 1983
1. Conners CK, Taylor E, Meo G, Kurrz MA, Fumier M: Magnesium pemoline and dextroamphetamine: a controlled study
in children with minimal brain dysfuncrion. Psychopharmacologia 26:32 1-336, 1972
2. Klawans HL, Margolin DL: Amphetamine induced dopaminergic hypersensitivity in guinea pigs. Arch Gen Psychiatry
32:725-732, 1975
3. Nausieda PA, Koller WC, Weiner WJ, Klawans HL: Pemolineinduced chorea. Neurology ( N Y ) 31:356-360, 1981
Electromyography in
Myotonic Dystrophy
Erich Streib, MD, and Sallie F. Sun, MD
Drs Pryse-Phillips, Johnson, and Larsen, the authors of a
study of a large kinship with myotonic dystrophy (MyD) recently published in the Annals, should be congratulated for
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terms, long, chorea, pemoline, use
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