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Another report of nonconvulsive status epilepticus after metrizamide myelography.

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inherited both essential tremor and Charcot-Marie-Tooth
neuropathy respond to the antitremor actions of propranolol
in the usual way despite their having no functional peripheral stretch reflex arcs.
Massachusetts General Hopsital
Boston, M A 02114
William C. Koller, MD, PhD
Dr Young raises several important issues regarding the treatment of essential tremor. His experience with amantadine,
which is similar to mine, indicates that the drug is of minimal
value in essential tremor therapy. The effectiveness of propranolol is established, but the clinical response is variable
and incomplete 121. Contraindications, particularly bronchospastic disease and adverse reactions, further limit propranolol’s usefulness. Until recently I thought, as did Dr
Young, that no worthwhile alternate drug was available. In
our continued search for such an agent, we have investigated
the dose-response relationship of primidone in 40 patients
with essential tremor. Postural hand tremor was measured by
an accelerometer and its amplitude determined by spectral
analysis. Propranolol decreased tremor by 37.2% in 25 patients. Primidone (50 mg at bedtime) further reduced tremor
by 60.1% and 250 mg at bedtime reduced tremor by 68.4%.
The effect was dramatic in some patients (e.g., from 7 to
70%). In 15 previously untreated patients, primidone (50
mg) decreased tremor by 52.1% and a 250-mg dose by
64.6%. The reduction was substantial in some patients (e.g.,
from 0 to 86%). Higher doses of primidone (500 to 1,000
mdday) caused similar or less tremor reduction than did
lower doses. Three patients had acute reactions (ataxia and
mental alterations) with a 50-mg dose and discontinued taking the drug. Higher doses commonly caused sedation and
were poorly tolerated. It is therefore not certain that
primidone is less toxic than propranolol as Dr Young suggests.
Low-dose primidone is effective treatment for reducing
essential tremor, whether used alone or in combination with
propranolol. Primidone appears to have efficacy in more patients and to cause greater tremor reduction than does propranolol. Time course studies suggest that the antitremor
effect is due to primidone itself rather than derived from
My recommendation for the treatment of essential tremor
is to start with primidone, 50 mg at bedtime. If tremor is not
controlled after a week, the dose should be increased to 250
mg. Propranolol (120 rndday in divided doses) should be
added if the clinical response remains inadequate and, if necessary, increased to a maximum dose of 320 mg a day.
Higher doses rarely cause additional benefit [3]. Propranolol
can be given in the long-acting form if once daily administration is desirable [4]. This drug regimen often results in
tremor control and increased functional capabilities.
Movement Disorders Center
Hines-Loyola Medical Center
2160 S 1st Ave
Maywood, I L 60153
1. Koller WC: Amantadine in essential tremor. Ann Neurol
16:621, 1984
2. Koller WC: The diagnosis and treatment of tremors. Neurol
Clinics 2(3):399-415, 1984
3. Koller WC: Propranolol therapy for essential head tremor. Neurology (Cleveland) 34:1077-1079, 1984
4. Koller WC: Long-acting propranolol in essential tremor. Neurology (Cleveland) (in press)
5. Manyam BV: Reply to letter. Ann Neurol 16:621-622, 1984
6. OBrien MD, Upton AR, Toseland PA: Benign familial tremor
treated with primidone. Br Med J 282:178-180, 1981
7. Young RR.Essential-familial tremor and enhanced physiological
tremors. In Johnson RT (ed): Current Therapy in Neurologic
Disease. Philadelphia, Decker, 1985, pp 270-275
8. Young RR,Growdon JH, Shahani B T Beta-adrenergic mechanisms in action tremor. N Engl J Med 298:950-953, 1975
Another Report of
Nonconvulsive Status
Epilepticus after
Metrkmide Myelography
John H. Wagner, Jr, M D
Drs Pritchard and O N e d [ l ) describe the occurrence of
nonconvulsive status epilepticus following metrizamide myelography. We had a similiar complication in a 54-year-old
man who was on maintenance phenytoin (300 mg daily) for
adult-onset idiopathic grand ma1 seizures.
The patient was admitted because of evidence of cervical
myeloradiculopathy. His phenytoin level on admission was
7.7 p.g/ml (therapeutic range, 10 to 20 pg’ml). The laboratory report had not been received by the time of myelography, so the dosage was kept at 300 mg daily, the patient
having been seizure-free for the preceding 6 months. A cervical and lumbar myelogram was carried out with 10 ml of
metrizamide (250 mgldl) by lumbar puncture, and no abnormality was found. Two hours after myelography, the patient
was noted to have facial twitches and to be withdrawn.
Phenytoin (200 mg) was given intravenously followed by
another 400 mg about 4 hours later. The patient continued
to be withdrawn and did not talk or respond appropriately to
Twenty-four hours after myelography, the patient would
look at the examiner and make largely unsuccessful attempts
to verbalize. H e could not follow commands appropriately.
Small twitches of the orbicularis oculi muscle were noted.
An electroencephalogram (EEG) revealed continuous generalized high-voltage 2- to 3-Hz waves with interposed spikes
and polyspikes. A phenytoin level that morning was 23.1 pg’
ml. Diazepam (8 mg) was given slowly intravenously and the
patient rapidly became responsive and began to talk and
respond rationally. The EEG pattern changed to a diffusely
slow pattern without the spike activity.
Patients with preexisting convulsive disorders are at increased risk of seizures following the use of metrizamide.
Annals of Neurology
Vol 18 No 3 September 1985 369
This patient’s case highlights the importance of this problem
and has led us to use iophendylate instead of metritamide in
similar situations.
It is of interest that the nonconvulsive status continued
despite a phenytoin blood level above the therapeutic range,
but was promptly terminated by intravenous diazepam.
Department of Neurology
Kaiser P e m n e n t e
1526 North Edgemont St
Los Angeles. CA 90027
1. Pritchard PB 111, ONeal DB: Nonconvulsive status epilepticus
following metrizamide myelography. Ann Neurol 16252-254,
Taraive Dyskrnesia
in a Patient with Akathisia
R. Sandyk, MD, MSC
Both akathisia and tardive dyskinesia have been reported in
patients on neuroleptic medication, and have been attributed
to altered receptor sensitivity in the mesocortical and nigrostriatal dopamine system, respectively [51. In addition, noradrenergic mechanisms have recently been implicated in the
pathogenesis of neuroleptic-induced tardive dyskinesia [2].
The following report provides further support for a possible
role of noradrenaline in tardive dyskinesia.
A 5 3-year-old man experienced akathisia following administration of haloperidol (30 mg daily) for acute aggressive
behavior. H e had not received antipsychotic medication in
the past and there was no past history of extrapyramidal
disease. Neurological examination was unrevealing and there
was no clinical evidence of parkinsonism. Haloperidol was
discontinued but the akathisia persisted. Based on recent
reports advocating beta-adrenergic blockers in the management of akathisia [4], the patient was placed on propranolol
(40 mg twice daily). This resulted in almost complete disappearance of the *akathisiawithin 48 hours after initiation of
therapy. One week later, the patient developed severe
orobuccal dyskinesia with sucking and chewing movements
along with constant tongue protusion. Mild parkinsonian
signs were present, such as facial amimia, reduced blinking,
and difficulties in initiation of gait. There was no tremor or
limb rigidity. Propranolol was discontinued and the symptoms of tardive dyskinesia and parkinsonism disappeared
several days later, followed by recurrence of the akathisia.
One month later, the patient was again given propranolol(40
mg twice daily) with prompt disappearance of the akathisia.
Tardive dyskinesia and mild parkinsonism reappeared four
days later, however. He was then placed on lorazepam (3 mg
daily) which proved beneficial.
Tardive dyskinesia induced by a beta-adrenergic blocking
agent is most unusual as these agents have been reported to
be beneficial in patients with tardive dyskinesia [3f. It has
been suggested that noradrenaline enhances the sensitivity of
neuronal systems on which dopamine acts [I). Blockade of
central noradrenergic receptors could have caused increased
dopamine receptor sensitivity in both the mesocortical and
nigrostriatal systems, thus leading to the development of tardive dyskinesia. Alternatively, it is possible that propranolol
caused blockade of dopamine or other receptor sites allowing the emergence of the tardive dyskinesia, perhaps as ;i
“withdrawal emergent” syndrome seen during acute narcotic
withdrawal precipitated by naloxone.
Department of Experimental and Clinical Pharmacology
University of the Witwatersrand, School of Medicine
2192 Johannesburg
South Africa
1. Hornykiewicz 0:Brain catecholamines in schizophrenia-a good
case for noradrenaline. Nature 29’3484-486, 1982
2. Jeste DV, Doongaji DR, Linnoila M: Elevated cerebrospinal fluid
nor-adrenaline in tardive dyskinesia. Br J Psychiatry 114: 177180, 1984
3. Jeste DV, Wyatt RJ: Therapeutic strategies against tardive dys-kinesia: two decades of experience. Arch Gen Psychiatry
39~103-116, 1982
4. Lipinski JF, Zubenko GS, Cohen BM, Barreira PJ: Propranolol in
the treatment of neuroleptic-induced akathisia. Lancet 1:685,
5. Marsden CD, Jenner P: The pathophysiology of extrapyramidal
side effects of neuroleptic drugs. Psycho1 Med 10:55-72, 1980
370 Annals of Neurology Vol 18 N o 3 September 1985
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statue, report, metrizamide, epileptic, myelography, another, nonconvulsive
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