Sleep Medicine 9 (2008) 465–467
www.elsevier.com/locate/sleep

Letters to the Editor
Unilateral periodic leg movements during wakefulness and
sleep after a parietal hemorrhage
To the Editor:
Although periodic leg movements (PLM) [1] following lesions in the cerebral white matter, basal ganglia,
or brainstem are known, abnormalities confined to a
lobar location have not been reported.
A 58-year-old man experienced a left parietal hemorrhage in 1993, shortly after a liver transplant (cirrhosis). He came to our attention 13 years later, after an
accidental left fronto-basal contusion. He had tacrolimus-induced chronic renal failure and a mild, symmetrical axonal polyneuropathy; medication included
benzodiazepines, vitamins, and electrolytes. He complained of rhythmic movements of his right leg,
appearing at rest, which prevented him from falling
asleep, starting a few weeks after the stroke; he denied
any associated unpleasant sensation or need to move.
This had been interpreted as symptomatic simple-partial seizures and was treated unsuccessfully with antiepileptic agents. On examination, he had a moderate
right hemibody ataxic hemiparesis with sensory impairment (postural sensation, graphesthesia) and a spastic
component. At rest, his right toes and foot began to
dorsiflex slowly and periodically, with a slight knee
flexion. This was abolished by voluntary posturing;
the left limb was not involved. Magnetic resonance
imaging (MRI) showed the old parietal lesion but no
basal ganglia abnormality (Fig. 1a). An afternoon
polysomnographic recording confirmed brief periodic
movements occurring every 20 s exclusively on the
right, during quiet wakefulness (Fig. 1b); they persisted
in light sleep (Fig. 1c and d), inducing periodic microarousals (Fig. 1c), and disappeared during rapid eye
movement (REM) sleep. Plasma ferritine was within
the normal range. Routine electroencephalograms
(EEGs) performed under the same conditions were
normal. The movements practically disappeared with
0.250 mg pramipexole.
These movements fulfill diagnostic criteria for PLM
[1]. Seizures are unlikely: the former displayed a relatively low frequency and lacked any myoclonic component; furthermore, the EEG was normal, and there was

a response to dopaminergic, but not to antiseizure,
drugs. Medication and uremia may have worsened
the picture, but PLM appeared just after the hemorrhage, before either could exert a durable action. The
strictly asymmetrical location argues against a substantial role of alcoholic polyneuropathy or hepatic-induced basal ganglia dysfunction. Our observation is
limited by the short polysomnographic recording, since
the patient refused an overnight study. In fact, PLM
may switch sides; however, we believe that his history,
our observations, and previous medical records reporting PLM only on the right are highly suggestive of unilateral PLM.
These movements have several interesting features.
They appeared shortly after the left parietal hemorrhage, strongly suggesting a causal relationship. To
our knowledge, this represents the most rostral lesion
inducing PLM: spinal lesions are relatively common
[2], whereas pontine lesions [3], subcortical stroke [4],
and corticobasal degeneration [5] are exceptional.
PLM pathophysiology remains unclear [6]. A functional MRI study showed activation of the brainstem
reticular formation and the red nuclei during PLM [7];
a dysfunction of a dopamine-modulated spinal pathway from the hypothalamus has also been postulated
[6]. PLM following spinal lesions suggest the presence
of a disinhibited spinal pacemaker [2]. Regardless of
the exact location of the putative pacemaker, in analogy to corticobasal degeneration [5], our description
suggests that parietal lobe impairment might disrupt
cortical excitatory inputs to the basal ganglia, altering
the physiological balance. Our patient’s PLM are
strictly unilateral, a rare finding described in symptomatic cases following central nervous system
(CNS) lesions [2–5]. In the absence of restless legs,
the complaint of PLM leading to insomnia represents
an intriguing feature. As in patients with spinal cord
impairment [2], the condition lasted for many years
before the correct diagnosis, but, as opposed to
PLM following brainstem lesions [4], it was resolved
by dopamine agonists. Considering the misdiagnosis
of partial epilepsy for years, our observation suggests
that similar conditions might represent an underreported cause of insomnia in stroke patients.

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Letters to the Editor / Sleep Medicine 9 (2008) 465–467

References
[1] Walters AS. Toward a better definition of the restless legs
syndrome. The International Restless Legs Syndrome Study
Group. Mov Disord 1995;10:634–42.
[2] Nogués M, Cammarota A, Leiguarda R, Rivero A, Pardal A,
Encabo H. Periodic limb movements in syringomyelia and syringobulbia. Mov Disord 2000;15:113–9.
[3] Kim JS, Lee SB, Park SK, Han SR, Kim YI, Lee KS. Periodic limb
movement during sleep developed after pontine lesion. Mov Disord
2003;18:1403–5.
[4] Kang SY, Sohn YH, Lee IK, Kim JS. Unilateral periodic limb
movement in sleep after supratentorial cerebral infarction. Parkinsonism Relat Disord 2004;10:429–31.
[5] Iriarte J, Alegre M, Arbizu J, de Castro P. Unilateral limb
movements during sleep in corticobasal degeneration. Mov Disord
2001;16:1180–3.
[6] Clemens S, Rye D, Hochman S. Restless legs syndrome. Revisiting
the dopamine hypothesis from the spinal cord perspective. Neurology 2006;67:125–30.
[7] Bucher SF, Seelos KC, Oertel WH, Reiser M, Trenkwalder C.
Cerebral generators involved in the pathogenesis of the restless legs
syndrome. Ann Neurol 1997;41:639–45.

Andrea O. Rossetti a,b,*
Raphaël Heinzer a
Fabrice Espa a
Mehdi Tafti a,c
a
Centre d’Investigation et Recherche du Sommeil (CIRS),
Lausanne, Switzerland
b
Service de Neurologie, CHUV, Lausanne, Switzerland
c
Centre Intégratif de Génomique (CIG),
University of Lausanne, Switzerland
E-mail address: andrea.rossetti@chuv.ch (A.O. Rossetti).
Received 17 March 2007; received in revised form 28
June 2007; accepted 28 June 2007
Available online 24 October 2007
*
Corresponding author. Address: Service de Neurologie, CHUVBH07, CH-1011-Lausanne, Switzerland. Tel.: +41 21 314 1220; fax:
+41 21 314 1290.
1389-945/$ - see front matter Ó 2007 Elsevier B.V. All rights reserved.
doi:10.1016/j.sleep.2007.06.014

Half of patients with obstructive sleep apnea have a higher
NREM AHI than REM AHI
To the Editor:

Fig. 1. T2 weighted axial and T1 weighted sagittal (right lower corner)
MRI, showing the old left superior parietal lobar hemorrhage (a);
polysomnographic recordings during wakefulness (b) stage 1 (c), and
stage 2 sleep (d), disclosing PLM in the right leg (black arrow; one
page corresponds to 60 s), with the induced micro-arousals (gray
arrow).

Siddiqui et al. [1] refer to our study [2] quite extensively and for that we are honoured and grateful. They
stated, however, that we studied patients with sleep apnea who were being evaluated for potential surgery.
That is not actually correct. Our patients, like theirs,
were patients presenting to a sleep disorders clinic for
evaluation and investigation of suspected sleep