Stroke. 1999;30:1707-1710
(Stroke. 1999;30:1707-1710.)
© 1999 American Heart Association, Inc.
Decreases in Blood Pressure and Sympathetic Nerve Activity by Microvascular Decompression of the Rostral Ventrolateral Medulla in Essential Hypertension
Satoshi Morimoto, MD, PhD;
Susumu Sasaki, MD, PhD;
Kazuo Takeda, MD, PhD;
Seiichi Furuya, MD, PhD;
Shoji Naruse, MD, PhD;
Keigo Matsumoto, MD, PhD;
Toshihiro Higuchi, MD, PhD;
Mitsuru Saito, PhD
Masao Nakagawa, MD, PhD
From the Second Department of Medicine (S.M., S.S., K.T., M.N.),
Department of Radiology (S.F., S.N.), and Department of Neurosurgery (K.M.,
T.H.), Kyoto Prefectural University of Medicine, Kyoto, Japan, and Laboratory
of Applied Physiology, Toyota Technological Institute (M.S.), Nagoya, Japan.
Correspondence and reprint requests to Dr Satoshi Morimoto, Second Department of Medicine, Kyoto Prefectural University of Medicine, Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto, 602-8566, Japan. E-mail morimot{at}koto.kpu-m.ac.jp
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Abstract
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BackgroundNeurovascular
compression of the rostral ventrolateral
medulla, a major center
regulating sympathetic nerve activity,
may be causally related to
essential hypertension. Microvascular
decompression of the rostral
ventrolateral medulla decreases
elevated blood pressure.
Case DescriptionA 47-year-old male essential hypertension
patient with hemifacial nerve spasms exhibited neurovascular
compression of the rostral ventrolateral medulla and facial nerve.
Microvascular decompression of the rostral ventrolateral medulla
successfully reduced blood pressure and plasma and urine
norepinephrine levels, low-frequency to high-frequency
ratio obtained by power spectral analysis, and muscle
sympathetic nerve activity.
ConclusionsThis case suggests not only that reduction in blood
pressure by microvascular decompression of the rostral ventrolateral
medulla may be mediated by a decrease in sympathetic nerve activity but
also that neurovascular compression of this area may be a cause of
blood pressure elevation via increased sympathetic nerve activity.
Key Words: decompression hypertension sympathetic nervous system
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Introduction
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The rostral ventrolateral medulla (RVLM) contains neurons
that
are the major tonic source of supraspinal
sympathoexcitatory
outflow,
1 2 and
thus this area is considered to be an important
center for the
regulation of sympathetic and cardiovascular
activities.
Since the first report by Jannetta et al,
3
several clinical
studies have indicated a possible association between
neurovascular
compression of the RVLM and essential
hypertension.
4 5 6 7 8 Using MRI, we found that the incidence
of neurovascular compression
of the RVLM in an essential hypertension
group was significantly
higher than that in a secondary hypertension
group and in a
normotension group, although the stage of hypertension
did not
differ significantly between the 2 hypertension
groups.
9 10 Some investigators have reported that
microvascular decompression
(MVD) of the RVLM improves or normalizes
raised blood pressure
(BP).
8 11 12 13 We have found that
pulsatile compression of
the RVLM activates local
neurons
14 and elevates BP in rats.
10 These
observations together suggest that neurovascular compression
of the
RVLM may elevate BP.
In addition, we reported10 that pulsatile compression of
the RVLM elevates BP by increasing sympathetic outflow and that this
response is normalized after cessation of the compression in rats.
Thus, considering that chemical or electrical stimulation of the RVLM
increases sympathetic nerve activity (SNA), which in turn elevates
BP,1 2 we assume that in humans neurovascular compression
of the RVLM elevates BP via sympathetic activation, while MVD of the
RVLM decreases raised BP via sympathetic suppression. However, no human
data support our assumption, because SNA has not been measured in
patients with neurovascular compression of the RVLM or those who have
undergone MVD of the RVLM. Herein we describe the first investigation
of SNA in a hypertensive patient before and after MVD of the RVLM.
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Case Report
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A 47-year-old man with a 4-year history of essential hypertension
was
admitted to our hospital in July 1998 for left hemifacial spasms.
His
family history was unremarkable. The patient was 169.5 cm in
height
and weighed 76.5 kg. BP was 152/110 mm Hg, and heart
rate was 64
beats/min under treatment with 5 mg amlodipine,
10 mg quinapril, and 2
mg doxazosin. Neurological physical examination
revealed nothing
abnormal except the left hemifacial spasms.
Initial laboratory evaluations showed normal renal function: serum urea
nitrogen was 13 mg/dL and creatinine was 0.80 mg/dL.
Creatinine clearance was 67.9 mL/min.
Electrocardiograms and echocardiograms were normal. MRI
of the medulla oblongata showed neurovascular compression of the RVLM
by the left vertebral artery (Figure 1A
).
The left facial nerve was seen just proximal to the left vertebral
artery, and thus neurovascular compression of the facial nerve was also
suspected. We decided to apply MVD to the facial nerve and RVLM.

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Figure 1. Serial axial MRI scans. A, before; B, after
MVD. In panels A, the left vertebral artery obviously compresses the
RVLM. In B, the vertebral artery is relatively separate from the RVLM.
Slices are arranged from the rostral to caudal side. V indicates
vertebral artery; FN, facial nerve; VN, vagal nerve; R, rostral
ventrolateral medulla; and Ant, anterior side.
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At surgery, a left lateral suboccipital craniectomy was performed with
the patient in the lateral position. The cerebellum was retracted
gently to expose the left facial nerve. Because we found compression at
the root-entry zone of the facial nerve by the vertebral artery, the
artery was moved away from the nerve, and a shredded Teflon felt (CR
Bard Inc) was inserted into the space between the nerve and the artery.
Consequently, the hemifacial spasms were improved just after the MVD.
The RVLM was also released from compression by the vertebral artery,
which was later confirmed by MRI (Figure 1B
).
This case provided an opportunity to study the effects of MVD of the
RVLM. The patient was followed up for 5 months after the MVD. BP,
hormone levels, power spectral analysis, and muscle SNA were
determined before and after the MVD. All examinations were approved by
the ethics committee of Kyoto Prefectural University of Medicine, and
informed consent was obtained for them from the patient.
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Study of MVD Effects
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Methods
BP Measurement
BP was measured with the patient in the sitting position after
resting
for at least 5 minutes with use of a standard mercury
sphygmomanometer.
Hormone Analysis
Plasma levels of norepinephrine,
epinephrine, renin activity, and aldosterone and
urine levels of norepinephrine and epinephrine were
estimated before and 1 month after MVD while the patient was admitted
and on a fixed-sodium diet of 120 mmol/d. The patient had not
received antihypertensive agents for 1 week prior to hormone studies,
and fasting peripheral blood was drawn via indwelling
catheter at 7:30 AM with the patient in the supine position
after 30 minutes of rest.
Power Spectral Analysis
Power spectral analysis of the R-R intervals was
performed before and 1 month after MVD from continuous 24-hour ECG
(SM-28, Fukuda Denshi Inc, Ltd.) recordings. The low-frequency
domain was obtained by integration of the power spectrum in the range
of 0.04 to 0.15 Hz. The high-frequency domain was calculated in the
range of 0.15 to 0.40 Hz. The average low-frequency to high-frequency
ratio was calculated as an index of sympathovagal
balance.15
Microneurographic Analysis
Muscle SNA was recorded from the tibial nerve before and 1
month after MVD, as described elsewhere.15 In
brief, a tungsten microelectrode was inserted
percutaneously with the patient in the supine position.
After identifying the muscle SNA, the microneurogram was amplified and
monitored. During the microneurographic recordings, BP was
monitored continuously from the middle finger by a servocontrolled
pressure measurement device (Finapres). Average burst rate (bursts/min)
and burst incidence (bursts/100 heart beats) were calculated from
20-minute recordings with the patient at rest in the supine
position.
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Results
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Effects of MVD on BP
BP decreased slightly and gradually after MVD of the RVLM (Figure
2

). Three months after MVD, the patient
complained of occasional
dizziness. Measurement in our outpatient
clinic demonstrated
that BP was lowered to 90/70 mm Hg, so we
decreased the antihypertensive
regimen. Five months after MVD, BP was
recorded at 108/74 mm
Hg under treatment with only 5 mg
quinapril. We are currently
attempting to discontinue the quinapril if
BP remains low.

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Figure 2. Clinical course of the patient. Hormone
analysis, power spectral analysis, and muscle SNA
analysis were performed at the times indicated by the white
arrows. sBP indicates systolic blood pressure; dBP,
diastolic blood pressure; Sept, September; Nov, November;
and Jan, January.
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Effects of MVD on Hormone Values
Plasma levels of norepinephrine, epinephrine,
renin activity, and aldosterone and urine levels of
norepinephrine and epinephrine were all
substantially reduced after MVD
(Table
).
Effects of MVD on Power Spectral Analysis
The low-frequency to high-frequency ratio showed a decrement after
MVD (Table
).
Effects of MVD on MSNA
Both average burst rate and burst incidence were clearly decreased
after MVD (Figure 3
and Table
).
 |
Discussion
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In the present case, BP values were lowered with concomitant
decreases
in plasma levels of norepinephrine,
epinephrine, renin activity,
and aldosterone and
urine levels of norepinephrine and epinephrine,
low-frequency
to high-frequency ratio by heart rate power spectral
analysis,
and muscle SNA after MVD of the RVLM. Plasma and
urine norepinephrine
values reflect SNA,
16 17
whereas epinephrine values are viewed
as indicators of adrenal
medullary activity.
18 Increased SNA
stimulates the
renin-angiotensin-aldosterone
system,
19 and
the low-frequency to high-frequency ratio by
power spectral
analysis is considered to be an index of
SNA,
20 which exhibits
a circadian rhythm similar to that
of plasma norepinephrine.
21 Muscle SNA
measured microneurographically reveals direct, precise,
and
reproducible sympathetic neuronal discharge from the
peripheral
nerves.
22 Considering that the RVLM
is a major center regulating
supraspinal sympathetic
outflow,
1 2 our data strongly indicate
that MVD improved
compression-induced increases in the sympathetic
nerve-renin-angiotensin-aldosterone
system to
thereby reduce BP in our patient.
Removal of a pheochromocytoma immediately reduces elevated levels of
catecholamines and BP.23 In contrast, in the
present case, MVD of the RVLM decreased BP gradually. The reason
for the discrepancy remains unknown. We suppose that existence of
target organ damage by hypertension might have inhibited reduction of
high BP even after MVD of the RVLM in our patient. However, this
remains only speculative and further studies are expected to resolve
this issue.
Also needing to be discussed in this case is whether decreases in BP
and SNA were due to MVD of the facial nerve but not of the RVLM.
Jannetta et al11 reported that in patients with
hypertension and neurological disorders such as trigeminal neuralgia
and hemifacial spasms, MVD of the cranial nerves did not reduce BP.
Geiger et al12 reported that in hypertensive patients, MVD
of only the RVLM itself decreased BP. Although SNA was not measured in
these studies, we suppose that in our case MVD of the RVLM but not of
the facial nerve may have decreased BP and SNA.
This case suggests not only that the reduction in BP by MVD of the RVLM
may be mediated by a decrease in SNA but also that neurovascular
compression of this area may be a cause of BP elevation via increased
SNA. To confirm this assumption, however, further studies in a larger
series of patients like ours are needed. In addition, a correlation
between hypertensive patients who do not show BP decrement despite MVD
of the RVLM and normotensive patients despite neurovascular compression
of the RVLM are to be investigated.
Received March 29, 1999;
revision received May 17, 1999;
accepted May 17, 1999.
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