Sleep, 14(2):163-165
© 1991 Association of Professional Sleep Societies
Short Note
Periodic Movements of the Legs during Sleep
Associated with Rises in Systemic Blood Pressure
*N. J. Ali, *R. J. O. Davies, tJ. A. Fleetham, and *J. R. Stradling
*Osler Chest Unit, Churchill Hospital, Headington, Oxford OX3 7U, V. K.; and tDepartment of Medicine,
University Hospital (UBC), Vancouver, B.c., Canada V6T 2B5
Summary: We report the relationship between periodic leg movements during sleep and recurrent rises in systemic
blood pressure in a patient with narcolepsy. The mean increase in systolic blood pressure following leg movements
was 23%, which is ofthe same order as the rises seen in patients with obstructive sleep apnea. Following treatment
with temazepam, the swings in blood pressure were unchanged despite considerably less electroencephalographic
evidence of cortical arousal. Key Words: Periodic movement of the legs-Hypertension.
Among the more dramatic acute physiological consequences of obstructive sleep apnea (OSA) are the
large rises in systemic blood pressure (SBP) that follow
each apnea (1). The factors responsible for this have
not been clearly defined, but it is suggested that arterial
oxygen desaturation and arousal from sleep both contribute to this phenomenon (2,3). We report a patient
with narcolepsy and periodic leg movements (PLM),
but no sleep apnea or hypoxemia, who displayed large
rises in SBP following each leg movement similar to
those seen in patients with OSA.
time of 6.25 hr. The leg movements (in the right leg
only) were typical of PLM episodes and all were associated with return of alpha rhythm on EEG of at
least 2 sec. There was no evidence of snoring or sleep
apnea. Routine investigations were normal and human
leukocyte antigen typing showed him to be DR2 and
DQWl +ve, adding weight to the diagnosis of narcolepsy.
He underwent repeat polysomnography [electroencephalography (EEG), electrooculography (EOG), electromyography (EMG)-submental, and anterior tibial,
nasal airflow, and oximetry], and continuous monitoring of the arterial blood pressure waveform by an
CASE REPORT
infrared photoplethysmograph attached to the middle
The patient, a 46-yr-old male rally driver, presented finger ofthe right hand (Ohmeda 2300 Finapres Blood
with a IO-yr history of increasing hypersomnolence Pressure Monitor, Ohmeda Monitoring Systems, Enand kicking movements during sleep. On questioning glewood, CO) (4). The output was recorded onto a chart
he gave a history of mild cataplexy over the same recorder and a computer, which were accurately synperiod. There was no history of snoring. He smoked chronized for later analysis. The patient was monitored
15-20 cigarettes per day and drank alcohol only oc- throughout the study by closed circuit television to
casionally. There was no significant past medical his- ensure that there were no hand movements that could
tory and no family history of hypersomnolence, nar- affect blood pressure measurement.
colepsy, or PLM. He was normal on examination in
SBP was continually recorded for 10 min while awake
the outpatient department with a BP of 118176. Initial and supine and for a longer period asleep during pepolysomnography showed short rapid eye movement riodic leg movements, both before and 1 hr after taking
(REM) latency (24 min), PLM (511hr), and a total sleep 10 mg oftemazepam.
Figure 1 shows the rises in SBP following each leg
movement. There is associated return of a rhythmn
Accepted for publication January 1991.
Address correspondence and reprint requests to Dr. N. J. Ali, Osler and EMG tone consistent with cortical arousal. This
Chest Unit, Churchill Hospital, Headington, Oxford OX3 7U, U.K. was the case for all PLM episodes before the admin163
164
~
N. J. ALI ET AL.
I.
EEG
'\
EOG
\
.EMG-submental~~~~---t--~~~~~---~~---+~--~~------t------1I-~::~
I
I
. EMG-anterior tibial
1
'I' .
. Nasal Flow _----1--__I---+----t----+---i-----'---l--"-ti---l-rT
I;
I
~At:llrAtinn'~--~~--r_---~~~~~~-,.~~~~
t----fi
seconds-s--~
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,"'\
:
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JTIG, 1. Relationship between leg movements, return of a rhythm, and rise in systemic blood pressure.
istration of temazepam. Figure 2 shows the record 1
hr after temazepam administration where similar rises
in SBP are seen, but with considerably less EEG t:vidence of cortical arousal. Figure 3 shows the same data
as Fig. 1 run at a slower paper speed of 1 mm/sec: to
illustrate the repeated rises in SBP and their relation
to the leg movements more clearly.
Mean blood pressures and pulse rate during wakefulness, PLM, and PLM + temazepam are shown in
Table 1, along with their coefficients of variation to
simply quantify their variability. SBP and pulse rate
were significantly higher during wakefulness than during PLM or PLM + temazepam. The average maximum rise in systolic blood pressure following each leg
movement was 21.8 mmHg (SD 5.39) before temazepam was administered and 22.7 mmHg (SD 4.85)
'I
Nasal
afterwards. This represents a 23% and 24% rise in systolic BP, respectively, which is very similar to the 25%
rise reported by Shepard in patients with OSA (1), and
to our own observations, which will be reported elsewhere.
Pulse rate increased with each PLM episode by an
average of 8.1 beats per minute (bpm) (SD 2.6) before
temazepam and by 7.7 bpm (SD 2.7) after. Pulse rate
reached its maximum value before SBP did and was
begining to decline as blood pressure was still increasing.
DISCUSSION
We believe this is the first report linking PLM during
sleep with large swings in SBP, similar to those seen
Flow~----~~----1-------+-----_+~----~------4_------+-------+_~--
I
__
~ygen ~~[urc~lcln--r_----~----~_r~-~_r~--_r~_;--~-+--~_,~~~~~~~~
t.
I
Blood Pressure
II
i--J-~~
1---5
seconds-s----4'
FIG. 2. Relationship between rises in blood pressure and leg movements 1 hr after 10 mg temazepam.
Sleep, Vol. 14, No.2, 1991
LEG MOVEMENTS AND BLOOD PRESSURE DURING SLEEP
165
.I .JL. L,
I. EEG
r"P"'I,'
EOG~~~~~~~~~~~~~~~~~~~~~~~~~~~
I
-+--.,..............._,....._.;-......_ ......."""""......-+-oI-4II__-
. EMG-submental_....
I
..........- -.....__- .......
II'L ,it.~I~L.~i~·_MlM~r·.NW'"
• • • • • • • • • • • • •1.---..-:1 minute--"iI• • • • • • • •H
FIG. 3.
• •~
Relationship between rises in blood pressure and leg movements; at I mm/sec paper speed to illustrate their repetitive nature.
in OSA. A number of important issues are raised by
this case. It supports previous reports that arousal from
sleep alone is sufficient to cause a considerable rise in
SBP, probably through activation of the sympathetic
nervous system (3) and that associated hypoxemia is
not necessary. Interestingly, even after partial suppression of cortical arousal by temazepam (Fig. 2), SBP
rose nevertheless after each leg movement. It may be
therefore that PLM can cause arousal at brain stem
level, sufficient to activate the sympathetic nervous
system and raise SBP, but without necessarily any
change in cortical EEG activity. It is conceivable though
unlikely that the movements of one leg only caused
sufficient increase in venous return to raise BP by 22
mmHg.
We fixed hand position at the level of the sternum
(i.e. 5-10 cm above the level of the tricuspid valve)
with a bandage in order to avoid artifact on BP values
caused by changes in hydrostatic pressure associated
with hand movements, which are the major sources of
error associated with the Finapres (5).
TABLE 1. Mean systolic (SBP) and diastolic blood pressure
(DBP) (mmHg) and pulse rate (and coefficient of variation,
CV) during wakefulness, PLM, and PLM after 10 mg of
temazepam
Wakefulness
PLM
PLM + temazepam
SBP (CV)
DBP (CV)
Pulse rate
(CV)
96.3 (5.6)
93.7 (10.3)
92.2 (10.4)
64.3 (4.2)
63.7 (6.3)
59.1(7.7)
71.4 (5.6)
66.0 (6.5)
67.3 (7.9)
Increased arteriolar vasoconstriction at the periphery could increase systolic blood pressure measured in
the finger by the phenomenon of reflectance of the
pressure wave at the resistance vessels causing amplification and a rise in SBP (6). However diastolic pressure is virtually unaffected by this phenomenon (6).
We found a similar percentage increase in diastolic
pressure (see Figs. 1-3). This suggests that the BP rises
that we have observed are real and not due to this
artifact of pulse wave amplification.
Thus BP swings similar to those seen in OSA occur
in situations where recurrent arousal is due to other
mechanisms than apnea. The long-term consequences
of these BP swings are unknown.
REFERENCES
I. Shepard JW Jr. Gas exchange and haemodynamics during sleep.
Med Clin North Am 1985;69:1243-64.
2. Shepard JW Jr. Cardiorespiratory changes in obstructive sleep
apnea. In: Kryger MH, Roth T, Dement WC, eds. Principles and
practice of sleep medicine. Philadelphia: W. B. Saunders Company, 1989.
3. Snyder F, Hobson JA, Morrison DF et al. Changes in respiration,
heart rate and blood pressure in human sleep. J Appl Physiol
1964; 19:41 7-22.
4. Boehmer RD. Continuous, non-invasive monitor of blood pressure: Penaz methodology applied to the finger. J Clin Monit 1987;3:
282-7.
5. Smith NT, Wesseling KH, de Wit B. Evaluation of two devices
producing noninvasive, pulsatile calibrated blood pressure from
a finger. J Clin Monit 1985;1:17-29.
6. Wesseling KH, Settels JJ, Yav der Hoeven et al. Effects of peripheral vasoconstriction on the measurement of blood pressure
in a finger. Cardiovasc Res 1985;19:39-145.
Sleep, Vol. 14, No.2, 1991