J Neurol (1994) 241 : 537-542
© Springer-Verlag 1994

J. Ghika
J. Bogousslavsky
J. Henderson
R Maeder
E Regli

Received: 6 July 1993
Accepted: 25 January 1994

J. Ghika ([~) - J. Bogousslavsky
J. Henderson • F. Regli
Service de Neurologie, CHUV,
CH-1011 Lausanne, Switzerland
P. Maeder
Service de Radiologie, CHUV,
CH-1011 Lausanne, Switzerland

The "jerky dystonic unsteady hand":
a delayed motor syndrome
in posterior thalamic infarctions

Abstract We report the cases of
three patients with a thalamic infarct
in the territory of the posterior
choroidal artery involving the posterior thalamic nuclei. These patients
developed delayed complex hyperkinetic motor syndromes, associating
ataxia, tremor, dystonia, myoclonus
and chorea, which we call "the jerky
dystonic unsteady hand". One patient
had a severe myoclonic and ataxicdystonic choreoathetosis; another
showed a so-called rubral tremor
(myoclonic ataxia with resting, action, and wing-beating tremor) with
dystonia; and the third one had a
dystonic and ataxic hand with intermittent mild action myoclonus. All
of them had sensory dysfunction;
two had also presented with a painful
Dejdrine-Roussy syndrome. All had

Introduction
Sensory and ataxic thalamic syndromes are well-recognized entities [1-12]. Motor hyperldnetic thalamic syndromes have been mentioned by Dej6rine and Roussy [1]
and Foix and Hillemand [2], but very few cases have been
reported and analysed [10-14]. We had the opportunity to
study three different delayed myoclonic complex hyperkinetic syndromes in CT or MRI-proven thalamic infarcts in
the territory of the posterior choroidal artery [ 15-19] from
the posterior cerebral artery territory with involvement of
the pulvinar nucleus. None of the 54 patients with thalamic infarcts in another territory that we examined (inferolateral, paramedian or polar territories) showed these abnormal movements, but they were all observed in the acute
phase [4]. Infarcts in this deep territory of the posterior

CT or MRI-proven infarcts in the
territory of the posterior cerebral
artery involving the posterior
choroidal territory with an abnormal
signal in the posterior area of the
thalamus (pulvinar nucleus) but sparing the other thalamic, subthalamic
and midbrain structures. These delayed myoclonic complex hyperkinetic syndromes have not been reported before, and we did not observe them in other topographic
forms of thalamic infarcts. They may
thus represent a new entity of movement disorders due to lesions in the
posterior thalamic nuclei, with specificity for posterior choroidal artery
infarcts.
K e y w o r d s Myoclonus - Chorea
Dystonia • Rubral tremor • Thalamus

cerebral artery are known to present with sensorimotor
syndromes and sectorial or quadrantic visual field defects,
coma, cognitive or behavioural syndromes [15-19]. A delayed tremor was recently reported in such an infarct [12],
but delayed complex myoclonic hyperkinetic syndromes
have not yet been reported to our knowledge. The posterior choroidal artery supplies the geniculate bodies, the
colliculi, the fornix, the pineal body, a part of the midbrain and the pulvinar nucleus of the thalamus, but not the
lateral or posterior nuclei [14, 18, 19] (Fig. 1).

Case Reports
Patient 1 was a 90-year-old hypertensive woman with atrial fib-

rillation associated with mitral valve disease. She was known to
have an essential familial action and postural tremor which became
symptomatic when she was in her sixties. In 1972, she had a verte-

538

Fig. 1 Territory of the posterior choroidal artery (mR) (modified
from Bogousslavsky et al. [4])

brobasilar minor ischaemic incident which lasted 24 h with vertigo, left sensorimotor deficit but a persistent increase in amplitude
of her action tremor on the left side. A physician thought she had
Parkinson's disease and treated her successively with amantadine,
trihexyphenidyt and tetrabamate with no effect. In May 1977, she
had a new ischaemic event with vertigo, diffuse headache, and increased weakness on the left side with paraesthesia and dysaesthesia of the hand. On examination, there was a left upper homonymous quadrantic visual field defect, a sensory deficit predominating on the left arm for all superficial, deep and complex sensory
modalities with sensory extinction but no hemineglect on the left
hemibody, and dysaesthesia of the left upper extremity. A mild,
slightly spastic, motor hemisyndrome was present on her left side
with brisk reflexes and a distal paresis of 20%, but no abnormal
movements except for the essential tremor could be observed. By
August 1977, she began to experience an hyperpathic disorder of
the left arm (D~jer~ne-Roussy syndrome) together with constant,
involuntary, high-amplitude involuntary movements and total loss
of control of her left upper extremity. On physical examination,
there was no change in the sensorimotor deficit, but a high-amplitude, hyperkinetic, very jerky hemichoreoathetotic syndrome was
described. She was successively treated with amitriptyline, haloperidol and tetrabenazine without benefit.
In 1991, she was examined in our movement disorder unit. She
was wheelchair-bound, totally unable to control or use her left arm
for any of her daily activities. The left arm, forearm and hand were
constantly restless, with irregular complex distal high-amplitude
involuntary choreoathetotic jerky motions of the distal upper extremity, which she attempted to decrease by holding her left forearm with her right hand against her body. The motions were increased on stress and became myoclonic and explosive on action,
sometimes ballistic-like. The fingers were in a dystonic posture in
extension. She was unable to hold a glass of water, to drink without spilling all the water, and could not eat or write, button or even
comb her hair or dress with her left arm. Her left shoulder had a
wing-beating type of tremor at rest, and she had a high-amplitude
4 Hz "no-no" type of head titubation, a tremulous voice, and a generalized resting and action tremor of the four extremities. There
was a severe left hemiataxia, much more pronounced in the upper
extremity, with gross hypermetria, asynergia, and asynchronometria, pathological rebound, and a total inability to perform a rhythm
or to make a ballistic coordinated motion. Only a few low-amplitude jerky motions were present on her left leg. The sensorimotor
deficits were unchanged on the left hemibody. CT in 1992 showed
an infarction in the territory of the posterior cerebral artery involving the territory of the posterior choroidal artery (Figs. 1,2), and no
evidence of subthalamic nucleus involvement; MRI was not performed.
Patient 2 was a 61-year-old male patient with a history of abrupt

headache and coma of several days duration in 1969. After regain-

Fig.2 Patient 1 (CT scan). Small infarct in the right posterior thalamic nuclei corresponding to the territory of the posterior
choroidal artery; enlargement of the occipital horn in relation to an
old superfical posterior cerebral infarct
ing consciousness, he presented with a memory deficit and a right
sensorimotor syndrome with a M 4 + distal deficit in strength. An
angiogram was performed, but was discarded together with his
chart after the legally prescribed period of time, and was therefore
not available. Neither CT or MRI were available at this time. A
few months later, he developed a painful D6jerine-Roussy syndrome in the right hand and upper extremity up to the shoulder and
on the right sole and calf with a constant burning sensation. He had
major difficulty in using his right hand owing to unawareness of its
position, as well as disproportionate strength and awkwardness,
but had no trouble walking. He consulted in March 1992 because
of an unrelated L4 sciatic pain on the right side. On physical examination, there was a right upper homonymous quadrantic visual
field defect complete loss of sensation for all superficial, deep and
complex sensory modalities on the whole right hemibody, a dystonic hand with athetosis of the fingers, a right kinetic hemiataxia
with hypermetria, asynergia, adiadokokinesia, asynchronometria
and rebound, difficulty in rhythmic and ballistic activity of the
right upper extremity, which was much less pronounced in the
right lower extremity. On performing the finger-to-nose manoeuvre, there were some jerky motions, better seen when he drank a
glass of water. The patient not only spilled all of the water from the
plastic cup, but completely broke it. MRI in 1992 (Fig.3) performed with a Magnetom SP 63 1.5 T with T1- and T2-weighted
images showed a posterior cerebral artery infarct with involvement
of the posterior choroidal territory (Fig. 1), with no abnormal signal in other thalamic or subthalamic nuclei or in the midbrain.
Patient 3 was a 32-year-old man with a familial and personal his-

tory of migraine without aura, but with no other cerebrovascular
risk factors. In April 1988, he complained of an abrupt, unusual
headache, which was followed, half an hour later, by a right sen-

539

Fig.3 Patient 2 (MRI, T2-weighted image 2500,90). Left posterior cerebral infarct with involvement of the posterior thalamic nuclei in the territory of the posterior choroidal artery

1 S,EC
Fig.5 EMG recording of patient 3, showing a rubral tremor with
alternating patterns in antagonist muscles at 3 Hz (lower part) and
more dystonic-athetotic pattern (upper part)

Fig.4 Patient 3 (MRI; Tl-weighted image 500,40). Left posterior
thalamic infarct in the territory of the posterior choroidal artery
(superficial posterior cerebral artery not shown here)

sorimotor deficit. On physical examination° he had a right hemianopia, which resolved in an upper quadrantanopia, a slow pursuit
left optokinetic nystagmus, and a complete right hemibody sensory
deficit for all epicritic, protopathic and complex sensory modalities. There was also a sensory hemiextinction without neglect, and
a predominantly distal normotonic hyperreflexic motor paresis
20-30%, which resolved in 24 h. CT showed a left posterior cerebral infarct with involvement of the pulvinar. A left carotid and
vertebral angiogram showed arteriovenous shunts in the territory
of the left PCA compatible with a recent stroke; the posterior
choroidal artery could not be seen. The CSF examination was unremarkable. The EEG showed bradyrhythmia on the left temporoparieto-occipital lobes, and the temporo-parietal waves of sensory
evoked potentials were absent on the left. By September 1988, the
patient started to have "jerks of the right arm on action". He frequently dropped things, could not write, use buttons, or use his
right arm for any precise motion. MRI in September 1988 (Fig. 4),
performed with a Diasonics 0.35 T T1- and T2-weighted images,
showed a decreased signal in the posterior thalamic nuclei (pulvinar) and the lingual gyrus compatible with a left posterior cerebral

540

infarct with involvement of the posterior choroidal artery territory
(Figs. 2, 3): The subthalamic nucleus and midbrain were intact on
MRI. The patient was successively treated with propranolol 120
mg, clonazepam 1.5 mg, primidone 750 rag, trihexyphenidyl 20
mg and flunarizine 40 mg without any benefit.
He consulted our movement disorder unit in January 1992. On
examination, the above-mentioned deficits were all present, but in
the right upper extremity, there was a resting tremor of the right
arm with wing-beating of the shoulder. The tremor increased on
action and posture with large irregular amplitude of frequency
around 3 Hz. On wrist extension, there was an athetoid, oscillating,
low-frequency, high-amplitude, tremor-like movement with suggestion of dystonia of the fingers. On the finger-to-nose manoeuvre, and on drinking a glass of water with the right hand, there
were myoclonic high-amplitude jerks. There was a right hemiataxia, almost exclusively localized on the upper extremity, with
hypermetria, asynergia, adiadokokinesia, asynchronometria, pathological rebound, difficulty in beating a rhythm or producing a ballistic motion with his right hand. Writing showed ataxic tremor
and myoclonus. His gait and standing were normal except that they
increased the left arm tremor and dystonia. The surface EMG
recording (Fig. 5) shows the classical 3 Hz alternating pattern of a
rubral tremor (lower part of the recording) but also more dystonicathetotic patterns on occasion (upper part of the recording).

Discussion
Hyperkinetic syndromes are sometimes encountered in
the acute phase of a stroke. Acute hemichorea-hemiballism, asterixis, or hemidystonia, or "dyskinesias" have
been reported [1-14, 20-37], and have been described
more frequently with striatal or subthalamic rather than
thalamic lesions. Delayed hyperkinetic syndromes are less
frequently reported after strokes [12, 22-25]. Well described are delayed athetosis and dystonia [22-25], but
delayed tremor has only recently been reported [12].
Thalamic motor hyperkinetic syndromes are infrequent. D6jerine and Roussy in 1906 reported choreoathetotic motions and ataxia in the "thalamic syndrome",
which were described as "small movements localized to
the fingers and hand, sometimes disorganized like chorea,
sometimes slow and sinuous like athetosis" [1]. Foix and
Hillemand [2] wrote about the "superior syndrome of the
nucleus ruber or rubrothalamic syndrome" to describe a
coarse intentional tremor accompanying the cerebellar
ataxia, and reported choreoathetotic movements in thalamogenicular infarcts infarcts and the rubrothalamic syndrome. The choreoathetosis is described as spontaneous
or motion-dependent [2]. These authors, and later Garcin
[10], also reported a "thalamic dystonic hand". The socalled rubral tremor [28, 29, 34-37] is a controversial entity, characterized by large-amplitude resting and action
tremor associated with "wing-beating" tremor of the arm
at around 3 Hz, and a kinetic cerebellar ataxia. Lesions
along the dentato-rubro-thalamic cerebellar efferent pathway can cause this syndrome, which is reported in patients with multiple sclerosis, meso-diencephalic infarcts,
tumours, abscesses or vascular malformations, but also in
the postanoxic myoclonic syndrome [30, 32]. Stereotactic

surgery in the ventrolateral nucleus abolished this syndrome in a case of postanoxic intention myoclonus reported by Lhermitte [32]. Myoclonus [33], rhythmic hemiballista [21] or action-induced rhythmic dystonia [21, 26]
have been described in lesions in or near the ventrolateral
nucleus. Stereotaxic surgery in this region has shown improvement in various dyskinesias [38, 39].
We have reported the cases of three patients with a
thalamic infarct in the territory of the posterior choroidal
artery [15-19] who suffered from a rubral-like tremor
syndrome associated with a complex myoclonic hyperldnetic syndrome that could be further analysed on videotaping. One patient had a complex choreoathetotic myoclonic syndrome with total loss of control of the arm.
The movements were spontaneous, markedly increasing
on action with ataxo-ballistic-myoclonic features. Another
patient presented with a more classical "rubral tremor"
with ataxia, low-frequency, high-amplitude resting and
action "tremor" with wing-beating of the arm, but myoclonic on action and posture, with a slightly dystonic
posture of the fingers. The third patient had a dystonic
"thalamic hand" syndrome with ataxia and rare action
myoclonic jerky motions. All had presented with a mild
and almost totally regressive corticospinal syndrome with
normal or even increased uncontrollable strength; all had
a sensory thalamic syndrome, and two of them presented
with a delayed central painful syndrome of D6jerineRoussy [1]. All had a superior homonymous quadrantanopia, b,ut none had oculomotor abnormalities.
The most striking feature was that the syndrome was
delayed, appearing months or years after the stroke. The
reason for this delay, which is also found with the D6jerine-Roussy syndrome and posthemiplegic dystonia, is still
obscure and may be due to late effects of reorganizing
processes in the brain after deafferentation. All patients
had an ischaemic lesion in the territory of the posterior
cerebral artery with involvement of the posterior choroidal
artery territory, and a decreased signal in the posterior
thalamus, a region corresponding to the pulvinar nucleus,
but no lesion was visualized in the lateral thalamic nuclei,
even though the patients presented with a sensory thalamic syndrome (possibly due to involvement of the thalamic sensory radiations in the adjacent internal capsule),
and a "rubral syndrome", with probable involvement of
the cerebello-rubro-thalamic pathway. We did not encounter this syndrome in the acute phase of 54 patients
with a thalamic infarct in the other topographical vascular
territories of the thalamus [4].
The pulvinar nucleus is mainly connected to parietal
areas and is not a part of the cerebello-efferent pathways
to the ventrolateral nucleus of the thalamus, probably responsible for the "rubral syndrome" [27, 34-36]. Acuna et
al. [40, 41] clearly showed in monkeys that the unit cell
activity in the pulvinar nucleus was essentially correlated
with the intention of movement, the projection and hand
manipulation, with different thresholds according to the

541

direction o f the m o v e m e n t s [41]. This c o r r e s p o n d s to the
o b s e r v a t i o n in our patients. The p u l v i n a r nucleus, h o w ever, cannot be h e l d r e s p o n s i b l e for either the h e m i s e n sory deficit or the painful D d j e r i n e - R o u s s y s y n d r o m e present in our patients, nor for the c e r e b e l l a r type o f ataxia.
W e suspect the lesion to i n v o l v e the fascicular c e r e b e l l a r
and sensory p a t h w a y s within the t h a l a m u s b e f o r e their entry in r e s p e c t i v e l y the ventrolateral and v e n t r o - p o s t e r o lateral nuclei respectively. This m a y account for the d e l a y
in the a p p e a r a n c e o f both the sensory and m o t o r synd r o m e , in p r e s e n t i n g as a deafferentation s y n d r o m e , but
the i m p r o v e m e n t and partial r e c o v e r y o f the c o r t i c o s p i n a l
m o t o r function through plastic r e o r g a n i z a t i o n s or reinnervation c o u l d also b e n e c e s s a r y for these h y p e r k i n e t i c behaviours to occur, since it is w e l l e s t a b l i s h e d that lesions
o f the c o r t i c o s p i n a l tracts alleviate all h y p e r k i n e t i c m o v e ments disorders.
A c o m m o n characteristic for the three clinical pictures
p r e s e n t e d b y our patients is the j e r k y m y o c l o n i c or ballistic aspect o f the dystonic, choreoathetotic or t r e m u l o u s
syndromes, which we coined "jerky unsteady dystonic
hand", b e c a u s e w e thought this d e s c r i p t i o n best fits the
p o l y m o r p h o u s c o m p l e x i t y o f the motion. E a c h o f the
three patients d e s c r i b e d here presents a p r e d o m i n a n c e o f
either m y o c l o n u s , dystonia, t r e m o r or c h o r e o a t h e t o t i c

m o v e m e n t s but a l w a y s in a m i x e d c o m p l e x presentation.
T h e m o s t striking feature was a clear-cut w o r s e n i n g o f the
signs b y v o l u n t a r y activity or intention, w h i c h m a k e s this
presentation unique to lesions in this region o f the brain
and m a y be due to the i n v o l v e m e n t o f the p u l v i n a r nucleus and the strategic crossing o f p r o p r i o c e p t i v e , cerebellar, p y r a m i d a l and s u b t h a l a m i c p a t h w a y s . The potential
role o f the u n d e r l y i n g essential t r e m o r in the first patient
r e m a i n s unclear. In any case, pure p r o p r i o c e p t i v e deafferentation is u n l i k e l y to be r e p o n s i b l e for such a c o m p l e x
m o v e m e n t disorder, even though dystonic and ataxic presentations o f parietal and thalamic lesions are a l r e a d y well
known. T h e i n v o l v e m e n t o f the territory o f the posterior
c h o r o i d a l artery (Fig. 1) [26] seems to be a prerequisite for
this s y n d r o m e to a p p e a r after a p o s t e r i o r c e r e b r a l infarct,
b e c a u s e we did not find such a presentation in other thala m i c infarcts [26]; this c o u l d also be a n e w de~ayed lacunar s y n d r o m e .
In conclusion, w e suggest that a d e l a y e d c o m p l e x
h y p e r k i n e t i c s y n d r o m e (choreoathetosis, dystonia, m y o clonus and action tremor) together with u p p e r quandrantanopia, h e m i s e n s o r y dysfunction, and transient or m i l d
h e m i p a r e s i s is e v i d e n c e o f an infarct in the territory o f the
posterior c h o r o i d a l artery.

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