Clinical Neurology and Neurosurgery 111 (2009) 633–635

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Clinical Neurology and Neurosurgery
journal homepage: www.elsevier.com/locate/clineuro

Case report

Dominant posterior-variant alien hand syndrome after acute left
parietal infarction
Jonathan Kessler, Gasser Hathout ∗
West LA VA Hospital, Radiology, 11301 Wilshire Blvd., Los Angeles, CA 90073, United States

a r t i c l e

i n f o

Article history:
Received 14 October 2008
Received in revised form 7 May 2009
Accepted 11 May 2009
Available online 12 June 2009
Keywords:
Alien hand syndrome
Stroke
Posterior-variant AHS
Parietal lobe

a b s t r a c t
Alien hand syndrome (AHS) is a complex clinical disorder in which patients develop a sense of estrangement from, and loss of volitional control of, an affected limb and non-purposeful complex motor actions
of the same limb. Several forms of AHS exist, including frontal, callosal, and posterior types with a series of
different associated neuroanatomical lesions and clinical symptoms. Most commonly, the lesions associated with AHS occur in the frontal lobes and corpus callosum. Rarely, lesions in the parietal lobes may be
associated with AHS, and most often occur within the non-dominant hemisphere. We describe a 57-yearold patient who developed symptoms of posterior AHS after an acute infarction in the left (presumably
dominant) parietal lobe. A review of the different clinical features of AHS and the underlying mechanisms
is also presented.
Published by Elsevier B.V.

1. Introduction
Alien hand syndrome encompasses a variety of clinical symptoms and neurological lesions and involves a sense of disconnection
between a patient’s will and action. It was first described in the
early twentieth century in a 57-year-old woman who developed a
“feeling of estrangement” from her left upper limb and associated
motor abnormalities that were distinct from both ataxia and paresis [1]. Roughly 60 years later, three patients were reported with
similar symptoms, which the authors termed “le signe de la main
étrangère” or alien hand sign [2]. Since that time, this terminology
has come to describe numerous different clinical and pathologic
entities involving areas of the frontal lobes, corpus callosum, and
more recently the parietal lobes, occipital lobes, and thalamus [3].
When the parietal lobes are involved, the lesions are almost exclusively found in the non-dominant hemisphere. Here we present a
case of a patient who developed AHS as his presenting symptom
following an acute left (presumably dominant) parietal infarction.
2. Case report
The patient is a 57-year-old, right-handed man with a history
of hyperlipidemia, hypertension, obesity, tobacco use, and chronic
obstructive pulmonary disease who noted abnormal movements
of his right arm, while driving his car. The patient described feeling that he had lost control of his arm and felt like it had “fallen

∗ Corresponding author.
E-mail address: ghathout@ucla.edu (G. Hathout).
0303-8467/$ – see front matter. Published by Elsevier B.V.
doi:10.1016/j.clineuro.2009.05.006

off.” He also reported that his right arm grabbed the steering wheel
“without me knowing it.” His symptoms continued intermittently
over the next several hours and the patient subsequently presented to the emergency department. The patient denied motor
or sensory problems in any other limb, visual or hearing changes,
loss of consciousness, or hallucinations. On examination, he had a
temperature of 97.8 F, blood pressure of 149/88, heart rate of 68,
respiratory rate of 18 and an oxygen saturation of 99% on room
air. His general physical examination revealed no significant abnormalities. On neurological examination, he was alert and oriented to
person, place and time. He had spontaneous and fluent speech, normal comprehension and was able to follow commands. His cranial
nerves were intact. On motor examination, the patient demonstrated normal strength bilaterally. However, the patient’s right arm
demonstrated spontaneous waving movements while his eyes were
closed. He denied knowledge or control of these movements. On
sensory examination, he had decreased sensation to pin prick testing on his right hand and arm. He was also noted to have decreased
graphesthesia and stereognosis on his right upper extremity compared to his left. His gait was normal.
MRI examination demonstrated a subacute infarction in the
left anterior parietal lobe along the posterior lip of the postcentral gyrus. This is expected to involve the posterior aspect of the
primary sensory strip (likely Brodmann’s area 2), as well as the tertiary somatosensory cortex in the superior parietal lobule (likely
in the location of Brodmann’s area 5) (Fig. 1A and B). No other
major lesions or infarcts were seen, though note was also made
of a very few punctuate foci of diffusion hyperintensity in the left
motor/premotor region. The remainder of the brain appeared normal. The patient also underwent time-of-flight MR angiography of

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J. Kessler, G. Hathout / Clinical Neurology and Neurosurgery 111 (2009) 633–635

Fig. 1. (A) FLAIR demonstrating hyperintensity in the left anterior parietal lobe along the posterior lip of the postcentral gyrus. (B) Diffusion weighted images demonstrating
corresponding hyperintensity in the left anterior parietal lobe.

the circle of Willis and neck vessels that demonstrated no significant intracranial stenoses. Neck MRA showed moderate stenosis of
the left internal carotid artery.
His symptoms continued to improve during his hospitalization,
but were still present upon discharge 5 days later. The patient was
seen again in neurology clinic eight days after his discharge, when
he noted moderate improvement in his symptoms with residual
discomfort using his right hand.
3. Discussion
Alien hand syndrome (AHS) is one of the most fascinating disconnection syndromes in neurology. It is a complex disorder that
may result from a variety of central nervous system lesions that
may present with several different signs and symptoms. The common factor between all cases of AHS is the patient’s experience of
dissociation between his intention and the subsequent motor activity [4,5]. Typical symptoms include a sense of foreignness of a limb,
failure to recognize ownership of a limb, and autonomous motor
activity perceived as involuntary [6].
Several different mechanisms of neurologic injury may cause
AHS including infarction, surgical resection, seizure, and corticobasal degeneration [5,7,8,4]. Early research in AHS divided the
disorder into two clinical and pathologic categories [9]. The first
type presented in patients with damage to the dominant hemisphere in the supplementary motor area, anterior cingulate gyrus,
or medial prefrontal cortex. These patients tended to develop motor
signs of AHS that included grasping or groping activities with their
right hand. The second type of AHS presented in patients with damage to the anterior corpus callosum, and presented primarily with
complex movements of the affected limb that counteracted the
movements of the unaffected limb, often referred to as intermanual
conflict. For example, in one case a thirsty patient filled a glass of
water with one hand, only to pour it out with the other [10].
However, it later became clear that there existed a group of
patients who demonstrated symptoms of AHS, but lacked an identifiable lesion in the anterior structures typically thought to produce
the syndrome. Often, these patients also presented with more
prominent feelings of estrangement from the affected limb and less
complex motor activity, such as limb levitation, than in the other
types of AHS [3,11–14]. This variant became known as posterior AHS
[10,12,15].
Though the specific pathways remain unknown, several authors
have proposed theories of the neuronal mechanisms underlying
the posterior forms of AHS. The inferior parietal lobule has been
described as a multimodal association area that receives input

from multiple neuronal pathways and coordinates motor output
[5,15,16]. Thus, disruption to this system may lead to the interruption of normal motor output, such as that seen in AHS. Alternatively,
some have hypothesized that posterior AHS may represent a variation of neglect syndromes [12]. In typical neglect syndromes
patients suffer damage to the parietal lobe and subsequently ignore
the contralateral hemispace. In comparison, posterior AHS patients
may suffer damage to a portion of the parietal lobe and subsequently disregard the activities of their own contralateral limb,
while maintaining normal interactions with the contralateral external world.
Most reports of the posterior-variant AHS have involved the right
parietal lobe and the left hand [11,14,17]. There have been very few
reports of isolated lesions in the left (presumably dominant) parietal lobe causing posterior AHS of the right upper extremity [16]. In
one case, a patient developed seizures and subsequent right limb
AHS after surgical removal of an arteriovenous malformation from
the left parietal lobe [5]. Other published reports have described
posterior AHS symptoms in patients with non-ischemia related
atrophy in the left parietal lobe [11,18].
In our review of the literature, we were able to identify only
one more case of a patient with AHS whose imaging demonstrated
an infarct in the left parietal lobe [19]. This patient was a 63year-old woman, who presented with acute right hemiparesis and
dysarthria. Several months later, after substantial improvement in
her hemiparesis, she began demonstrating symptoms of posterior
AHS, including a feeling of estrangement from her limb and involuntary limb levitation.
Our patient differs in two important ways from the other
reported cases of dominant parietal lobe AHS. Firstly, to our knowledge, no other cases of left parietal AHS have been reported in the
setting of acute infarction. Second, though commonly described in
the frontal and callosal forms of AHS, complex motor movements
are quite rare in the posterior form. Though some authors have
described simple groping movements in patients with posteriorvariant AHS, more frequently the motor component of posterior
AHS involves non-purposeful movements or limb levitation [3]. In
contrast, our patient manifested complex movements, including
seemingly purposeful manipulation of the steering wheel of his car.
It is unclear what mechanisms underlie the symptoms of AHS in
our patient. Though his anatomic lesions are posterior, our patient’s
clinical symptoms are more similar to those described in the anterior forms of AHS. This combination of findings raises the possibility
that AHS disorders may represent a spectrum ranging from purely
frontal to purely posterior forms. More specifically, our patient’s
case provides interesting correlations because the infarct is rela-

J. Kessler, G. Hathout / Clinical Neurology and Neurosurgery 111 (2009) 633–635

tively discreet along the cortical ribbon of the posterior lip of the
postcentral gyrus, rather than a massive lesion which would preclude specific neuroanatomic correlation. In our patient, one of the
main structures involved is expected to be the posterior portion
of the sensory strip (e.g., Brodmann’s area 2), which subtends the
kinesthetic sense (as opposed to Brodmann’s areas 3a and 3b in the
anterior portion of the sensory strip, which subtend sensations of
pain and temperature) [20]. Another main structure involved would
appear to be Brodmann’s area 5, just posterior to Brodmann’s area
2, corresponding to a portion of the tertiary somatosensory cortex,
which subtends stereognosis [21]. Thus, the lesions in our patient
seem to involve a sense of where the limb is and what it is touching, logically correlating to an alien limb syndrome presentation, as
opposed to a simple hypesthesia.
Further imaging research is needed into the neural pathways
that are disrupted in patients like the one presented here to
more clearly elucidate the neuroanatomic correlates. However, our
patient illustrates that alien hand symptomatology may occur in
the right upper extremity from a left parietal acute infarct, and
may present acutely with complex motor movements once thought
typical only of anterior-variant alien hand syndromes.
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