CLINICAUSCIENTIFIC NOTES

356

4. Poewe WH, Lees AJ, Stem GM. Dystonia in Parkinson’s disease:
clinical and pharmacological features. Ann Neurol 1988;23:73-78.
5. Mandir AS, Rowland LH, Dougherty PM, Lenz FA. Microelectrode recording and stimulation techniques during stereotactic procedures in the thalamus and pallidum. Adv Neurol 1997 (in press).
6. Laitinen LV, Bergenheim AT, Hariz MI. Leksell’s posteroventral
pallidotomy in the treatment of Parkinson’s disease. J Neurosurg
1992;76:53-61.
7. Lozano AM, Lang AE, Galvez JN, et al. Effect of GPi pallidotomy
on motor function in Parkinson’s disease. Lancet 1995;346:13831387.
8. Iacono RP, Shima F, Lonser RR, Kuniyoshi S, Maeda C, Yamada
S . The results, indications, and physiology of posteroventral pallidotomy for patients with Parkinson’s disease. Neurosurgery
199S;36:11 18-1 125.
9. Sutton JP, Couldwell W, Lew MF, et al. Ventroposterior medial
pallidotomy in patients with advanced Parkinson’s disease. Neurosurgery 1995;36:I 112-1 116.
10. Nutt JG. Levodopa-induced dyskinesia: review, observations, and
speculations. Neurology 1990;40:340-345.
11. Verhagen Metman L, Van den Munckhof P, Klaassen AAG, Blanchet P, Mouradian MM, Chase TN. Effects of supra-threshold
levodopa doses on dyskinesias in advanced Parkinson’s disease.
Neurokogy 1997;49:711-713.
12. Boyce S, Clarke CE, Luquin R, et al. Induction of chorea and
dystonia in parkiusonian primates. Mov Disord 1990;5:3-7.
13. Mitchell IJ, Luquin R, Boyce S, et al. Neural mechanisms of dystonia: evidence from a 2-deoxyglucose uptake study in a primate
model of dopamine agonist-induced dystonia. Mov Disord 1990;
5:49-54.
14. lacono RP, Kuniyoshi SM, Lonser RR, Maeda G, Inae AM,
Ashwall S. Simultaneous bilateral pallidoansotomy for idiopathic
dystonia musculorum deformans. f‘ediutr Neurol 1996;14:145148.

15. Vitek JL, Evatt M, Zhang J, et al. Pallidotomy is an effective
treatment for patients with medically intractable dystonia [Ahstract]. Mov Disord 1997;12:31.
16. Marsden CD, Parkes .ID, Quinn N. Fluctuations of disability in
Parkinson’s disease-4inical aspects. In: Marsden CD, Fahn S,
eds. Movement disorders. London: Butterworth, 1981:96-122.
17. Nutt JG. Dyskinesia induced by levodopa and dopamine agonists
in patients with Parkinson’s disease. In: Lang AE,Weiner WJ, eds.
Drug-induced movement disorders. New York: Futura Publishing
Co, Inc, 1992:281-314.

Cortical Action Tremor and Focal Motor
Seizures After Parietal Infarction

Stroke is the most frequent cause of epileptic seizures in the
elderly.’-7 When the ischemic area is located subcortically,
tremor occasionally
The occurrence of both tremor
and focal motor seizures as a sequel to stroke has not been
reported. We describe a patient suffering from focal motor
seizures of the contralateral hand and forearm after right pari-

’

A videotape accompanies this article.

Received April 16, 1996; revisions received November 6, 1996, and
June 19, 1997. Accepted July 14, 1997.
Address correspondence and reprint requests to D ~ A,
, SchulzeBonhage at Neurologische Klinik, Stadtische Kliniken, Kassel,
Germany.

Movement Disorder,y, Voi. 13, No. 2,1998

etal infarction who also developed a rhythmic action tremor
restricted to the same region. Whereas the seizures were controlled by therapy with carbamazepine, the action tremor persisted for another year before disappearing spontaneously. The
association of tremor and seizures is discussed with regard to a
common pathogenesis.

Case Report
A 68-year-old man with preexisting atrial fibrillation, arterial
hypertension, and diabetes mellitus developed weakness of the
left arm that he considered too mild to see a physician. Some
weeks later, recurrent spontaneous focal motor seizures restricted to his left forearm occurred with consecutive Todd’s
paresis. The frequency of seizures without medication was one
every third or fourth day. At times, the jerking was vigorous
enough to make the patient lose his balance and fall. Neither
Jacksonian march nor secondary generalization of seizures occurred. In addition to these spontaneous motor seizures, opposition of his left thumb and index finger triggered rhythmic
tremor-likejerking of his left forearm muscles (see the videotape).
This action tremor was confined to the period of continuous voluntary muscle contraction and was not observed during Todd’s
paresis. The presence or absence of focal motor seizures did not
have considerable impact on tremor severity and frequency.
Clinical examination showed moderate weakness of the left
face and arm, with exaggerated tendon reflexes of the left arm.
Surface electromyographic recordings from left abductor pollick brevis and first dorsal interosseus as well as from forearm
flexor and extensor muscles showed rhythmic cocontractions of
agonist and antagonist muscles at a frequency of 4-5 s when
the thumb and index finger were voluntarily opposed; individual tremor bursts lasted 80-100 ms (Fig. 1). Even repeated
interictal electroencephalographic (EEG) recordings did not
show epileptic discharges during or in the absence of action
tremor; intermittent regional slowing was sometimes found
over the right parietal cortex. The amplitudes of cortical
sensory-evoked potentials were normal (4 pV with left median
nerve stimulation, 3.5 pV with right median nerve stimulation,
and 0.5 pV with either tibia1 nerve stimulation), with prolonged
latencies resulting from polyneuropathy. Also, motor-evoked
potentials in abductor pollicis brevis muscles were of normal
amplitude (2.0 mV) and latencies (23.0 ms, right; and 23.7 ms,
left). Transcranial magnetic stimulation did not induce repetitive tremor-like discharges or focal motor seizures. Cranial
computed tomography and magnetic resonance imaging
showed a hypodensity-hyperintensity in the white matter underlying the right parietal cortex (Fig. 2).
During the following year, the patient’s left facial and arm
paresis gradually improved, leaving a left forearm pronator
drift and slowness of rapid repetitive movements. With doses of
up to 600 mg phenytoin per day, therapeutically effective serum levels could not be established, and focal motor seizures
persisted. Thus, the patient was treated with carbamazepine,
which completely abolished spontaneous seizures for 1 year.
He was gradually tapered Off ‘arbamazepine, and his motor
seizures have not recurred for >I 8 months. Action tremor of the
left hand and forearm initially persisted, however, under medication with carbamazepine for 1 more year before gradually
disappearing without any additional medication.

357

CLINICAUSCIENTIFIC NOTES
A

end

voluntary muscle contraction

start

I .

left forearm extensors

I
500ms
B

without voluntary muscle contraction

during voluntary muscle contraction

I

200pv

I

500ms
FIG. 1. (A) Surface electromyographic recordings from left forearm flexor and extensor muscles during voluntary opposition of the left thumb and
index finger. During action, agonist and antagonist muscles discharge synchronously at 4-5 Hz. (B) Bipolar electroencephalographic (EEG)
recordings over the right central region with and without contralateral tremor activity from the same recording session. There is no evidence of
tremor-related EEG changes.

Discussion
Focal motor seizures after cerebral infarction are considered
to be the result of focal hyperexcitability in the cortical border
zonc of the infarct. There is experimental evidence that inhibition to paired electrical pulses in this region is diminished
probably as a result of reduced GABAergic input to pyramidal
cells.12 The mechanism of tremor generation after cortical infarction is less well understood.
There are reports of patients suffering from tremor of probable cortical originI3,'" without morphologically identifiable
lesions. These patients were reported to have rhythmic electromyographic discharges at frequencies of 9-1 8 s particularly
during action. Lance-Adams syndrome, myoclonus epilepsy,
and opsoclonus-myoclonus syndrome were the respective underlying causes. Surface EEG recordings were normal in most
cases. Back-averaging of EEG activity revealed a cortical premovement potential, and there were giant somatosensoryevoked potentials (SSEPs), from which the concept of rhythmic
cortical myoclonus underlying the clinical phenomenon of tremor
in these patients emerged (see also Hallettl'). Treatment with
clonazepam had some effect. In our patient, tremor frequency was
slower, and neither EEC spikes nor giant SSEPs were present.
The 5 s writing tremor after cortical infarction in the case

reported by Kim and Lee" shares some clinical characteristics
with the tremor of our patient, but their patient's tremor was not
task specific. The simultaneous appearance of spontaneous focal motor seizures and action-induced tremor in the same part
of the body after cortical infarction suggests some common
mechanism in their generation. Focal motor seizures may be the
clinical manifestation of spontaneous repetitive firing of neurons
in the border zone of the infarction. The propensity of the same
region to discharge rhythmically may also become clinically apparent in the form of tremor-like contractions resulting from excitatory input during voluntary contraction of forearm muscles.
Carbamazepine administration suppressed the seizures,
whereas action-induced tremor persisted for some time. During
action, the tonically active pyramidal tract neurons may have
been depolarized sufficiently to relay the otherwise subthreshold inputs from the border zone of infarction (see also Ferbert
and Gerwig*); alternatively, tonic pyramidal cell output might
have activated the region generating rhythmic discharges either
axon collaterals or indirectly by way of recurrent sensory input.
Similar to our patient with focal motor seizures, spontaneous
resolution of epilepsia partialis continua is well recognized"
and may be the result of some local synaptic reorganization in
the border zone of infarction, resulting i n reduced excitability
or inhibition of the spread of discharges.

Movement Disorders, Vol. I3, No. 2, I998

358

CLIMICAWSCIENTIFIC NOTES

A

The simultaneous development of motor seizures and action
tremor in the same region in our patient suggests that hyperexcitability and synchronized rhythmic neuronal activity in the
border zone of infarction may be the common cause of both
focal epileptic seizures and cortical action tremor.

Legend to the Videotape
A few months after right parietal infarction, opposition of
left thumb and index finger would trigger rhythmic action
tremor restricted to the activated muscles. This tremor lasts as
long as voluntary contraction is maintained. Tremor is also
evident bringing the left index finger to the nose.
A. Schulze-Bonhage
A. Ferbert
Neurological Clinic
City Clinics
Kussel
Germany

References

0

FIG. 2. Coronal T1-weighted (A) and axial T2.Weighted (B) magnetic
resonance images showing the extension of right parietal infarction 3%
months after the onset of symptoms.

Movement Disorden, Vol 13, No. 2, 1998

1. Jackson JH. On the scientific and empirical investigation of epilepsies. In: Taylor J, ed. Selected writings of John Hughlings Jackson. London: Hodder and Stoughton, 1931:233.
2. Liihdorf K, Jensen LK, Plesner AM. Etiology of seizures in the
elderly. Epilepsiu 1986;47:458-463.
3. Cocito L, Favale E, Reni L. Epileptic seizures in cerebral arterial
occlusive disease. Stroke 1982;13: 189-195.
4. Gupta SR, Naheedy MH, Elias D, Rubino FA. Postinfarction seizures. Srroke 1988;19:1477-148 1.
5. Olsen TS, Hogenhaven H, Thage 0. Epilepsy after stroke. Neurology 1987;37:1209-1211.
6. Lesser RP, Liiders H, Dinner DS, Morris HH. Epileptic seizures
due to thrombotic and embolic cerebrovascular disease in older
patients. Epilepsiu 1985;26:622-630.
7. Lancman ME, Golimstok A, Norscini J, Granillo. Risk factors for
developing seizures after a stroke. Epilepsiu 1993;34: 14 1-143.
8. Ferbert A, Gerwig M. Tremor due to stroke. Mov Disord 1993;8:
179-182.
9. Kim JS. Delayed onset hand tremor caused by cerebral infarction.
Stroke 1992;199:292-294.
10. Kim JS, Lee MC. Writing tremor after discrete cortical infarction.
Stroke 1994,25:2280-2282.
11. Dethy S, Luxen A, Bidaut L, Goldman S. Hemibody tremor related
to stroke. Stroke 1993;242094-2096.
12. Domann R, Hagemann G, Kraemer M, Freund HJ, Witte OW.
Electrophysiological changes in the surrounding brain tissue of
photochemically induced cortical infarcts in the rat. Neurosci Lett
1993;155:69-72.
13. Ikeda A, Kakigi R, Funai N, Neshige R, Kuroda Y, Shibasaki H.
Cortical tremor: a variant of cortical reflex myoclonus. Neurdogy
1990;40: 1561-1565.
14. Toro C, Pascual-Leone A, Deuschl G, Tate E, Pranzatelli MR,
Hallett M. Cortical tremor: a common manifestation of cortical
myoclonus. Neurology 1993;43:2346-2353.
15. Hallett M. Myoclonus: relation to epilepsy. Epilepsia 1985%:
S67-S77.
16. Cockerell OC, Rothwell J, Thompson PD, Marsden CD, Shorvon
SD. Clinical and physiological features of epilepsia partialis continua. Bruin 1996;119:393407.