(Hypertension. 1997;30:77-82.)
© 1997 American Heart Association, Inc.
Articles |
From the Second Department of Medicine (S. Morimoto, S.S., S. Miki, T.K., H.I., T.N., K.T., M.N.) and Department of Radiology (O.K., S.F., S.N., T.M.), Kyoto Prefectural University of Medicine, Kyoto, Japan.
| Abstract |
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Key Words: rostral ventrolateral medulla hypertension, essential magnetic resonance imaging magnetic resonance angiography
| Introduction |
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| Methods |
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Imaging Methods
MRI and MRA studies were performed with an SMT-150X imaging
device (1.5 T, Shimadzu) and a multipolarization head coil. In the MRI
studies, the slices were axial, parallel to the line connecting the
hard palatine and the great foramen, and coronal, parallel to the
fourth ventricle. Proton densityweighted fast spin echo (SE) images
(repetition time [TR]/effective echo time [TE], 5000/23
milliseconds) were obtained to avoid overestimation of the distance
between brain parenchyma and artery due to a partial volume effect
caused by a high signal of cerebrospinal fluid. A high-resolution
(0.4x 0.4 mm/pixel) 512x512 matrix was used to estimate the
precise distance between brain parenchyma and artery. Slice thickness
was 3 mm, and interslice gaps were covered in a second
measurement. MRA studies were performed to determine the courses of the
basilar artery, the bilateral vertebral arteries, and their branches
three dimensionally. The 3D-time of flight (TOF) method with
magnetization transfer contrast pulse was used (TR/TE/flip angle
[FA], 40 ms/8 ms/16°).
Two neuroradiologists, unaware of the subjects' medical histories, assessed all the MRI and MRA scans to determine whether there was neurovascular compression of the retro-olivary sulcus of the medulla oblongata at the level of the root-entry zone of the glossopharyngeal and vagus nerves, assumed to be the surface of the RVLM.14 The distances between the center of the retro-olivary sulcus (RVLM) and the nearest arteries and between the surface of the medulla oblongata and the nearest arteries in the axial view at the level of the root-entry zone of cranial nerves were measured. Strictly speaking, the cuts are not anatomically comparable among cases. Nonetheless, false readings due to anatomic cuts are not considered to be an important matter because the root-entry zone of the glossopharyngeal and vagus nerves lies in a small range. Borderlines of the low-intensity area (the inner lumen of the arteries) were substituted for the arterial walls because the arterial walls investigated in this study could not be determined in MRI images.
Statistical Analysis
A
2 test was applied to determine
significant differences between groups in the neurovascular
compression. Fisher's multiple range test was applied to determine the
significance of differences in the distances between the center of the
retro-olivary sulcus (RVLM) and the nearest arteries and between the
surface of the medulla oblongata and the nearest arteries among the
three groups.
| Results |
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Neurovascular compression of the RVLM was observed in 15 of 20
patients (75%) with essential hypertension, excluding 1 patient whose
images were inadequate for assessment. In contrast, neurovascular
compression was observed in only 1 of 10 patients (10%) with secondary
hypertension and in only 2 of 18 normotensive subjects (11%). The rate
of observed neurovascular compression in the essential hypertension
group was significantly higher than that in the secondary hypertension
group and normotensive group (P<.01 for both). The
compressing artery was the posterior inferior cerebellar
artery in 10 (67%), anterior inferior cerebellar artery in
2 (13%), and vertebral artery in 3 (20%) of 15 patients with
essential hypertension. The compressing artery in 1 patient with
secondary hypertension and in 2 normotensive subjects was the posterior
inferior cerebellar artery. Neurovascular compression was
seen on the left side in 7 and on the right side in 7 patients and on
both sides in 1 of 15 patients with essential hypertension.
Neurovascular compression in 1 patient with secondary hypertension and
in 2 normotensive subjects was seen on the right side (Table 2
). Although Fig 1a
might suggest neurovascular
compression of the glossopharyngeal nerve, cardiopulmonary
deafferentiation has not been reported to induce sustained blood
pressure elevation.19 Also, no such findings were observed
in the other subjects. Therefore, it is not likely that compression of
this nerve contributes to the occurrence of hypertension.
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Table 3
shows the results of quantitative evaluations of the
distances between the center of the retro-olivary sulcus (RVLM) and the
nearest arteries and between the surface of the medulla oblongata and
the nearest arteries. The distances between the center
of the retro-olivary sulcus (RVLM) and the nearest arteries were
1.1±3.0 mm in the essential hypertension group, 4.9±4.0 mm
in the secondary hypertension group, and 3.8±2.2 mm in the
normotensive group. The distances in the essential hypertension group
were significantly shorter than those in the secondary hypertension
group and normotensive group (P<.05 for both). In contrast,
the distances between the surface of the medulla oblongata and the
nearest arteries were 0.5±0.9 mm in the essential hypertension
group, 1.5±1.6 mm in the secondary hypertension group, and
1.6±2.1 mm in the normotensive group; there were no significant
differences among the three groups. These results suggest that
neurovascular compression of the RVLM, but not the other regions of the
medulla oblongata, is particularly related to essential
hypertension.
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| Discussion |
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Jannetta et al9 noticed 2 patients with glossopharyngeal neuralgia who had hypertensive strokes after microvascular decompression of the root of the glossopharyngeal nerve in 1973. On the basis of these 2 cases, the relationship between the role of the RVLM and high blood pressure was investigated. Neurovascular compression of the RVLM was found in 51 of 53 hypertensive patients and in none of 50 normotensive patients who underwent microvascular decompression for unrelated cranial nerve dysfunction. High blood pressure returned to normal in 32 and improved in 4 of 42 patients who were treated with left microvascular decompression of the RVLM. On the other hand, blood pressure remained unchanged in the 7 hypertensive patients who were treated with right microvascular decompression of the RVLM.9 Jannetta et al10 also reported the development of hypertension by pulsatile compression on the left RVLM and normalization of the blood pressure by the cessation of the pulsatile compression in an experimental baboon model. Angiographic and pathological studies further indicated that the neurovascular compression of the left RVLM was involved in essential hypertension.12 13 14 Although two investigations of neurovascular compression using MRI have been reported,15 16 quantitative analysis of the relationship between the RVLM and the neighboring arteries had not been evaluated. In the present study, quantitative analysis of the relationship between the RVLM and the nearest arteries and between the surface of the medulla oblongata and the nearest arteries could be estimated because we used proton densityweighted images with a high-resolution 512x512 matrix.
We considered obtaining MRI images by 3D reconstruction of the ventral portion of the medulla oblongata to know the specific nature of the compression. However, it is impossible to obtain images that are fine enough to give us any information about the specific nature of the compression with a low-resolution matrix. On the other hand, to obtain MRI images by 3D reconstruction using a high-resolution 512x512 matrix, which might give us more information about the compression, we needed highly developed new software, and in theory, it might have taken much time (more than 2 hours) to perform the MRI studies. For these reasons, we did not obtain MRI images by 3D reconstruction in the present study.
The distances between the center of the retro-olivary sulcus (RVLM) and the nearest arteries in the essential hypertension group were significantly shorter than those in the secondary hypertension group and the normotensive group (P<.05 for both). On the other hand, there were no significant differences between the essential hypertension group and secondary hypertension group, or the essential hypertension group and the normotensive group, in the distances between the surface of the medulla oblongata and the nearest arteries. Because the margin of the RVLM cannot be determined in MRI studies, the existing reports using MRI could not indicate the specific relationship between the RVLM and essential hypertension. In contrast, we found that the neurovascular compression of the RVLM, but not the other regions of the medulla oblongata, may be related to essential hypertension by using MRI with a high-resolution 512x512 matrix.
Neurovascular compression of the RVLM in essential hypertension has been reported to be seen more frequently on the left side.9 11 12 13 14 15 16 However, the number of observed neurovascular compressions of the RVLM was symmetrical in the present study. Jannetta et al9 reported that blood pressure remained unchanged in seven hypertensive patients who had been treated with right microvascular decompression of the RVLM as described above. These authors hypothesized that the left side of the medulla oblongata is more sensitive to compression because the major part of the afferent inputs from the myocardial receptors of the left ventricle and atrium to the nucleus tractus solitarii is conducted by the left vagus nerve.9 20 However, cardiopulmonary deafferentiation has not been reported to induce sustained blood pressure elevation19 as described above, or the RVLM has not been reported to be functionally asymmetrical in experimental studies. Therefore, the significance of the laterality of neurovascular compression at the RVLM requires further study.
In a pathological study, Naraghi et al14 described the involved vessels and three types of neurovascular compression: type I (monovascular), caused by a single vessel loop of a branch originating from the vertebral or basilar artery, eg, the posterior inferior cerebellar artery; type II (vertebral), caused by an ectatic vertebral artery; and type III (combined), a combination of types I and II. They reported that type I was the most common type, and our result is consistent with theirs. The specific branch of the vertebral artery was difficult to determine using only MRI. MRA was thus very useful for the de- termination of the specific branch because the branches of the vertebral artery could be visualized three-dimensionally.
Prolonged hypertension causes elongated and tortuous arteries. In the present study, however, only 1 of 10 patients in the secondary hypertension group had neurovascular compression of the RVLM, whereas in the essential hypertension group, 15 of 20 patients had neurovascular compression. The duration of hypertension, left ventricular mass, and hypertension stage (as classified by the extent of organ damage according to the WHO/ISH meeting) were not significantly different between the two hypertension groups. The distances in the secondary hypertension group are rather longer than those of the normotensive group, although they are not significantly different. Thus, it is not likely that neurovascular compression of the RVLM or a shorter distance between the RVLM and the nearest artery is the natural outcome of a chronic blood pressure elevation. This finding further supports our hypothesis that neurovascular compression of the RVLM might be a cause rather than a result of high blood pressure, at least in a subgroup of patients with essential hypertension.
In summary, with the use of proton densityweighted images with a high-resolution 512x512 matrix, we found that the distances between the surface of the RVLM, but not that of the other regions of the medulla oblongata, and the neighboring arteries are significantly shorter in essential hypertension. Accordingly, we conclude that neurovascular compression of the RVLM might be at least partly associated with essential hypertension.
| Footnotes |
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Presented in part at the 50th Annual Fall Conference and Scientific Sessions of the Council for High Blood Pressure Research, Chicago, Ill, September 17-20, 1996.
Received April 8, 1996; first decision July 22, 1996; accepted December 9, 1996.
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