Unusual presentation of more common disease/injury

Isolated astasia in acute infarction of the
supplementary-motor area
Yuko Wada, Yo Nishimura
Department of Neurology, Nishi-Kobe Medical Center, Kobe, Japan
Correspondence to Yuko Wada, wada@nmc-kobe.org

Summary
Astasia, which is the inability to stand in the absence of motor weakness or marked sensory loss, is an uncommon clinical feature of stroke in
the thalamic ventrolateral region. The authors describe a patient with a unilateral supplementary motor area (SMA) infarction presenting with
contralateral astasia. On neurological examination, he would lean to the left side and would fall unless supported. He showed no muscle weakness, sensory deficits or cerebellar ataxia. Magnetic resolution imaging of the brain showed acute infarction only involving the right SMA. On the
basis of the anatomy that the SMA is connected to the vestibulocerebellar system through the ventrolateral nucleus of the thalamus, the authors
concluded that contralateral astasia probably resulted from disruption of this connection following infarction of the SMA.

BACKGROUND

INVESTIGATIONS

Astasia, which is the inability to stand unsupported despite
normal strength, resembles the marked balance impairment
in patients with vestibulocerebellar disease.1 Astasia is an
uncommon manifestation of thalamic syndrome2, and its
duration is transient when it occurs.3 It can be caused by
lesions of the thalamic ventrolateral region.3 Recently, there
has been one report of astasia associated with a cingulate
lesion.4 However, to the best of our knowledge, there have
been no reports of astasia associated with a lesion in the
supplementary motor area (SMA).
We describe the case of a patient presenting with transient contralateral astasia as the characteristic feature of an
infarction of SMA and discuss the underlying neurological
mechanisms of this phenomenon.

Laboratory test results, including those of rheumatological
(anti-DNA, antinuclear, antiphospholipid and lupus
anticardiolipin antibodies) and coagulative (antithrombin III,
prothrombin time, S and C-protein and fibrinogen) tests,
were normal. Transesophageal echocardiogram (TEE) with
air contrast showed a patent of foramen ovale with a right-toleft shunting, accentuated with the Valsalva maneuver. Right
atrial pressure was not elevated, and no involvement of the
valves was observed. On the day of admission, diffusionweighted and T2-weighted MRI of the brain revealed a highintensity lesion in the right SMA (figure 1). There were no
other abnormalities in the cerebrum, brainstem or cerebellum. MR angiography and carotid ultrasonography findings
were normal, as was that of Holter monitoring.

CASE PRESENTATION

OUTCOME AND FOLLOW-UP

A previously healthy 61-year-old right-handed man presented with a suddenly inability to stand; whenever he attempted to stand or walk, he would lean to the left. He noted
no other symptoms. On the next day, he was admitted to our
hospital. On admission, his blood pressure was 138/96 mm
Hg, and his pulse rate was 96 beats/min and regular. He
showednormalconsciousnessandorientation.Therewasno
personality change or apparent intellectual deterioration. No
deficit of language, visual cognition or praxis was observed.5
Therewasneithermotornorverbalinertia.Therewasnomotor neglect. He was unable to stand unsupported because
there was an inclination to veer his body toward the left,
characterised by marked left-sided pulsion, and needed supportonhisleftsidetopreventhimfromfalling.Whenaskedto
stand up from a sitting position, he was able to stand up by
pullinghimselfupwithbothhands.However,hisabilitytosit
straight was preserved. Cranial nerves were intact. His
strength and the muscle tone of the extremities and trunk
were normal. All the tendon reflexes were normal, with no
pathological reflexes. Superficial sensation, and joint position, and vibration senses were normal. His finger-to-nose,
heel-knee and shin-tapping test were normal.

Although we did not detect deep venous thrombosis of the
patient, we suspected that he had a paradoxical embolism.
Because TEE of the patient showed foramen ovale with a
right-to-left shunting.
The patient was treated with an anticoagulant. The next
day his symptom began to improve, and 2 days after admission he was able to walk independently.

BMJ Case Reports 2010; doi:10.1136/bcr.01.2010.2618

DISCUSSION
Our patient presented with a transient inability to stand
unsupported and marked truncal instability, characterised
by contralateral pulsion due to an acute SMA infarction. He
noted no other neurological symptoms or signs, such as
motor weakness, sensory deficit, incoordination or parkinsonism. Thus, we consider this manifestation as an astasia.
Astasia, which is the inability to stand unsupported despite
normal strength, resembles the marked balance impairment
observed in patients with vestibulocerebellar disease.1 Masdeu and Gorelick2 first described the cases of patients with
thalamic astasia, and their patients fell toward the side contralateral to the side of lesions. They also described that thalamic astasia may mimic cerebellar disease. In other reports
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Figure 1 Diffusion-weighted (A) and T2-weighted (B) MR images show a high-intensity lesion in the medial frontal lobe (supplementary
motor area). (C) T2-weighted MR image demonstrates a high-intensity lesion in only the supplementary motor area.

Learning points

â–²

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inability to stand unassited lasted for an average of 3 days in
six patients with infarction, and two of these patients presented with the inability to stand for only 1 day. They considered that the bilateral representation of fastigial
vestibulocerebellar projection to the medial ventrolateral
nucleus of the thalamus may be one of the factors for the
transient nature of thalamic astasia. This finding may
explain in part the transience of astasia in our patient.
In summary, the present finding raises the possibility that
unilateral small SMA lesions can cause transient astasia following the disruption of the connection between SMA and
the ventrolateral part of the thalamus.

â–²

of astasia associated with other lesions, the direction of
astasia was also contralateral to the site of lesions, such as
the midbrain or posterior cingulate region.4 6
Our patient has only one lesion located in the unilateral
SMA, in the absence of other lesions in the primary motor
cortex, thalamus, brainstem or cerebellum. It has been
shown that SMA lesions cause various abnormalities of
motor function, such as the planning or initiation, including
speech function.7 8 Chung et al7 reported the case of a
patient who developed severe gait disturbance characterised by markedly impaired postural reflexes after apparent
SMA seizure. However, their patient did not show contralateral pulsion. The exact mechanism of contralateral
pulsion associated with SMA lesion has not been confirmed
in either humans or animals. To the best of our knowledge,
no cases of unilateral SMA lesions that cause contralateral
pulsion as the sole symptom have been reported.
Astasia as the main clinical manifestation of supratentorial involvement has been associated with the thalamic ventrolateral region,1 3 or midbrain tegmental lesions.6
According to Solomon et al2 fastigial fibers of the vestibulocerebellar pathway project to the medial ventrolateral
nucleus of the thalamus, and disruption of this pathway
may be responsible for thalamic astasia. SMA also receives
a thalamic input from the ventrolateral part of the thalamus,
which receives inputs from cerebellar nuclei in animals.9
Disruption of this connection by SMA infarction may have
been responsible for astasia in our patient.
Contralateral astasia associated with medial frontal
lesions has rarely been described, and recently, only one
case has been reported.4 Kataoka et al4 described a patient
with posterior cingulate infarction who showed contralateral pulsion similar to that of our patient. They considered
their patient’s manifestation as astasia. Because the cingulated motor area receives a major thalamic input from the
ventrolateral thalamus, disruption of this connection by a
posterior cingulate infarction may be responsible for astasia
in their patient. Moreover, SMA is also connected to the
ventrolateral part of the thalamus, which receives inputs
from the basal ganglia9 as well as the cingulated motor area.
Disruption of this connection by SMA infarction also have
contributed to the patient’s astasia.
Astasia in our patient was transient, with resolution
within 2 days. This finding was in accordance with those of
previous reports.1 3 In Masdeu and Gorelick’s report3 the

Astasia is an uncommon clinical feature of stroke, such
as thalamic infarction.
The role of SMA has been demonstrated in animals,
but remains unclear in humans. Clinicians should be
aware of the possibility of a SMA stroke in patients
with contralateral astasia.

Competing interests None.
Patient consent Obtained.

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BMJ Case Reports 2010; doi:10.1136/bcr.01.2010.2618

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