Case Reports
Novel Representation of Astasia Associated With Posterior
Cingulate Infarction
Hiroshi Kataoka, MD; Kazuma Sugie, MD, PhD; Nobuo Kohara, MD, PhD; Satoshi Ueno, MD, PhD
Background and Purpose—The representation elicited in the cingulate motor area has been demonstrated in animals, but
remains unclear in humans. In particular, the representation and pathogenic mechanisms of the posterior cingulate cortex are
poorly understood, especially in humans. We describe a case of posterior cingulate infarction associated with contralateral
astasia.
Case Description—A 67-year-old right-handed man with a 10-year history of hypertension suddenly presented with
right-sided pulsion on attempting to stand or sit. On the following day, he could not maintain a sitting position. The
patient immediately fell to the floor because of instability, characterized by marked right-sided pulsion despite no
muscle weakness, sensorial deficits, or cerebellar ataxia. Magnetic resolution imaging of the brain showed abnormal
intensity in the posterior parts of the cingulate, with no other clinically significant lesions.
Conclusions—Because the cingulate motor area is connected to the vestibulocerebellar system through the thalamic nuclei,
disruption of this connection by posterior cingulate infarction may result in astasia. (Stroke. 2006;37:e3-e5.)
Keywords: astasia 䡲 behavioral neurology 䡲 cingulate gyrus 䡲 infarction 䡲 stroke

S

everal cortical motor areas have been identified on the
medial wall of the hemispheres of the brain. These include
a group of premotor regions located in the cingulate sulcus,
collectively termed the cingulate motor area (CMA). Cytoarchitectural studies have established that the CMA has 2 separate
motor representation areas: the rostral CMA (area 24c) and the
caudal CMA, encompassing both the dorsal CMA (CMAd, area
6c) and the ventral CMA (CMAv, area 23c). Each area has direct
projections to the spinal cord and connections with the premotor
cortex and primary motor cortex.1 Physiological studies indicate
that anatomical connections of the CMA with the motor system
are functionally linked to limb-movement generation. The representation elicited in the CMA has been demonstrated in
animals but remains unclear in humans. Damaged to the anterior
cingulate cortex in humans is associated with reduction in
spontaneous, compulsive, and emotional motor responses. Transient akinesia and mutism have been observed in large bilateral
anterior cingulate cortex lesions with slight encroachment on
adjacent cortical regions, such as the supplementary motor area.2
However, the representation and pathogenic mechanisms of the
posterior cingulate cortex are poorly understood, especially in
humans. We describe a case of posterior cingulate infarction
associated with contralateral astasia and discuss underlying
neurological mechanisms.

Case Reports
A 67-year-old right-handed man with a 10-year history of
hypertension suddenly noticed repetitive scrubbed move-

ments of the fingers of the right hand, lasting for ⬎15
minutes. He subsequently presented with right-sided pulsion
on attempting to stand. On the following day, right-sided
pulsion occurred while sitting, as well as while standing.
Finally, he could not maintain a sitting position and was
admitted to the hospital. He never lost consciousness or had
any sensory complaints. On admission, the blood pressure
was 162/104 mm Hg, and the pulse rate was 106 beats/minute
and regular. He was alert and fully oriented, with no impairment of higher functions, including auditory comprehension,
orientation, cognition, and mentation. He could sit up only by
pulling himself up with both hands while holding onto the
side rails of his bed; however, on attempting to sit by
releasing his hands, the patient immediately fell to the floor
because of instability, characterized by marked right-sided
pulsion. The muscle strength of the trunk and extremities was
not decreased. There was no ataxia on either side. The deep
tendon reflexes were normal, with no pathological reflexes.
The muscle tone of the extremities was normal. Cranial
nerves, superficial sensation, joint position senses, and vibratory senses were not impaired. Paper-and-pencil tests of
extrapersonal neglect (line bisection and figure copy) were
normal. The results of routine laboratory blood examinations
were normal. Anti-DNA, antinuclear, antiphospholipid, and
anticardiolipin antibodies and the results of lupus anticoagulant testing were negative. On day 2, fluid-attenuated inversion recovery image and diffusion-weighted and T2-weighted

Received June 7, 2005; final revision received August 29, 2005; accepted September 26, 2005.
From the Department of Neurology (H.K., K.S., S.U.), Nara Medical University, Kashihara, Nara, and the Department of Neurology (N.K.), Kobe City
General Hospital, Kobe, Japan.
Correspondence to Hiroshi Kataoka, Department of Neurology, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-8522, Japan. E-mail
hk55@naramed-u.ac.jp
© 2005 American Heart Association, Inc.
Stroke is available at http://www.strokeaha.org

DOI: 10.1161/01.STR.0000195046.89926.98

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Stroke

January 2006

Diffusion-weighted (A) and FLAIR magnetic resolution images (B) of the brain,
showing high intensity in posterior parts
of the cingulate. (C) FLAIR image showing high intensity in only the cingulate
gyrus with no other clinically significant
lesions.

MRI of the brain showed high intensity in the posterior parts
of the cingulate (Figure). There were no other abnormalities
in the cerebrum, brain stem, or cerebellum. An electroencephalogram, transcranial Doppler ultrasonogram, and echocardiogram were all normal. The 24-Holter ECG showed no
abnormal arrhythmia. The transesophageal echocardiography
showed spontaneous echo contrast within the left atrium. The
patient was given anticoagulant therapy and regained stability. One week later, he became able to sit, but he was unable
to maintain a standing position because of right-sided pulsion.
Three weeks later, he was able to walk, although his gait was
slightly unstable. His steps were characterized by an irregular
amplitude and direction, sometimes directed laterally and
then suddenly stopping while attempting to take a right step,
leading to pulsion. The gait disturbance differed from cerebellar ataxia, because the gait was not broad based or
lurching. He could arise from a squat and maintain a closed
stance. The results of the other neurological examinations
were unremarkable, including a negative Romberg’s sign,
finger-to-nose test, heel-knee test, and shin-tapping test. The
patient regained more stability and became able to sit and to
walk alone. After 1 month, he was discharged, with no
residual signs or symptoms.

Discussion
Our patient had posterior cingulate infarctions associated
with marked truncal instability, characterized by contralateral
pulsion in the absence of other clinically significant lesions in
the premotor cortex, primary motor cortex, thalamus, brain
stem, cerebellum, and corpus callosum. Stimulation of the
cingulate is known to elicit bilateral and contralateral complex movements of the extremities accompanied by tonic
postures, deviation of the head and eyes, vocalization, and
automatic changes. Stimulation studies in humans have demonstrated stiffening of the wrist, supination of the forearm and
hand, and mild flexion in the fingers.3 However, the representation as contralateral pulsion has not been confirmed in
either humans or animals. We consider this manifestation an
astasia, because our patients could not maintain a stationary
sitting or standing position and had no other conditions that
could have accounted for pulsion, such as pyramidal or
sensorial deficits, including abnormal proprioceptive sensation, cerebellar ataxia, kinaesthesia, psychosis, or parkinsonism. To our knowledge, this is the first time to report an

association in humans between astasia and cingulate
infarctions.
Astasia can be caused by lesions of the thalamic ventrolateral region, resulting in “thalamic astasia,” or of the pons or
callosal region.4 – 6 Festigial fibers of the vestibulocerebellar
pathway project to the medial ventrolateral nucleus of the
thalamus, and disruption of this pathway may cause thalamic
astasia.7 Moreover, the nucleus ventroposterior lateralis and
the nucleus ventrolateralis of the thalamus as determined by
vestibular stimulation in animals are termed “vestibular
thalamic nuclei.”8 The CMAd and CMAv also receive a
major thalamic input from the ventrolateral nucleus of the
thalamus.9 The CMAd and CMAv may be connected to the
vestibulocerebellar system through the thalamic nuclei. Disruption of this connection by posterior cingulate infarction,
including the caudal CMA, may have been responsible for the
astasia in our patient.
However, the CMAd receives the major component of its
thalamic input from the nucleus ventralis lateralis pars oralis,
which receives inputs primarily from the caudate putamen, as
well as the supplementary motor area.10 Supplementary motor
area seizures are associated with severe gait disturbances
characterized by markedly impaired postural reflexes.11
Moreover, the CMAv receives a substantial component of its
input from the mediodorsal and intralaminar nuclei and
ventralis lateralis pars caudalis, which receive input primarily
from deep cerebellar nuclei.12 Ictal single-photon emission–
computed tomography in patients with nocturnal frontal
epilepsy has demonstrated increased blood flow in the cingulate gyrus and cerebellar cortex, suggesting a direct connection between these regions.13 Disruption of these connections
may also have partially contributed to the patient’s astasia.
In conclusion, astasia is a novel representation elicited in
the posterior CMA in humans by the disruption of the
connection between CMA and the vestibulocerebellar system
via thalamic nuclei.

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Novel Representation of Astasia Associated With Posterior Cingulate Infarction
Hiroshi Kataoka, Kazuma Sugie, Nobuo Kohara and Satoshi Ueno
Stroke. 2006;37:e3-e5; originally published online December 1, 2005;
doi: 10.1161/01.STR.0000195046.89926.98
Stroke is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright © 2005 American Heart Association, Inc. All rights reserved.
Print ISSN: 0039-2499. Online ISSN: 1524-4628

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