(Stroke. 1997;28:2169-2173.)
© 1997 American Heart Association, Inc.
Articles |
From the Department of Medicine and Geriatrics, Kochi Medical School (K.M., K.O., T.W., Y.O., M.F., Y.D.), Kochi, Tokyo Metropolitan Geriatric Hospital (T.O.), Tokyo, Japan.
Correspondence to Kozo Matsubayashi, MD, Department of Medicine and Geriatrics, Kochi Medical School, Okocho, Kohasu, 783, Nankoku City, Kochi, Japan.
| Abstract |
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Methods The study population consisted of 334
community-dwelling elderly adults, aged 75 years or older (mean age, 80
years). Postural changes in systolic blood pressure (SBP) were
assessed using an autosphygmomanometer (BP-203 I). By the difference
between the mean of two measurements of SBP at standing and at supine
position (dSBP=SBP at upright-SBP at supine position), we divided the
subjects into three groups: (1) 20 subjects with postural hypotension
(d-SBP
-20 mm Hg), (2) 29 subjects with postural hypertension
(dSBP
20 mm Hg), and (3) 285 subjects with postural
normotension (20<dSBP<20 mm Hg). We defined the former two
groups as the postural dysregulation group. Scores in four
neurobehavioral function tests (Mini-Mental State Exam, Hasegawa
Dementia Scale Revised, computer-assisted visuospatial cognitive
performance score, and the Up and Go Test) and activities of
daily living were compared among the three groups. Brain lesions on
MRI, including number of lacunes and periventricular
hyperintense lesions, were compared among 15 age- and sex-matched
control subjects with postural hypotension, 15 with postural
hypertension, and 30 with postural normotension.
Results Twenty subjects (6.0%) exhibited postural hypotension and 29 (8.7%) postural hypertension. Scores in neurobehavioral functions and activities of daily living were significantly lower in the postural dysregulation group (both postural hypotension and hypertension groups) than in the postural normotension group. The postural dysregulation group exhibited significantly more advanced periventricular hyperintensities than the normotension group.
Conclusions Asymptomatic community-dwelling elderly individuals with postural hypotension as well as those with postural hypertension had poorer scores on neurobehavioral function tests and more advanced leukoaraiosis demonstrated on MRI than those without exaggerated postural changes in SBP.
Key Words: blood pressure elderly leukoaraiosis
| Introduction |
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Since 1991, we have conducted a comprehensive geriatric assessment in the community-dwelling elderly in Kahoku, a rural Japanese town in which 32% of the population is 65 years or older (Kahoku Study).12 13 14 We assessed postural variability in BP and neurobehavioral functions in elderly subjects aged 75 or older in Kahoku in a cross-sectional study and found some elderly subjects who showed exaggerated postural changes in SBP associated with worsened scoring on neurobehavioral function tests. We have also reported incidental leukoaraiosis associated with cognitive and neurobehavioral impairments in apparently normal elderly individuals.15 In this report, we discuss the association between postural variability in SBP and neurobehavioral functions as well as silent brain lesions on MRI in community-dwelling elderly individuals in Japan.
| Subjects and Methods |
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Blood Pressure Measurements and Classification
Two BP and pulse readings were recorded first with subjects
in the sitting position. Subsequently, subjects were supine for at
least 5 minutes, and then two BP and pulse readings were recorded
in the next 5 minutes. BP and pulse rate were measured with a
autosphygmomanometer (BP-203 I), with an appropriately sized cuff
around the upper arm, resting next to the chest wall. We used the mean
of two measurements of BP and pulse rate taken in the supine position
as the baseline. The subject was then asked to stand upright without
support, and BP and pulse rate were again measured in the same arm,
relaxed at the side, at approximately the same level, relative to the
heart, as while supine. The measurements were recorded at 1 and 2
minutes after standing.5 7 17 After the measurements,
subjects were queried about any symptoms that developed while they were
standing. We similarly used the mean of two measurements of BP and
pulse rate taken in the standing position.
Using differences between the mean of two measurements of SBP while
subjects were standing and while supine (dSBP=SBP at upright-SBP at
supine position), we divided the subjects into three groups: (1) 20
subjects with postural hypotension (dSBP
-20
mm Hg),5 17 (2) 29 subjects with postural hypertension
(dSBP
20 mm Hg), and (3) 285 subjects with postural
normotension (20<dSBP<20 mm Hg). We defined the former two
groups as the postural dysregulation group.
Cognitive and Neurobehavioral Functional Assessment
We assessed cognitive and neurobehavioral function using four
tests: the MMSE,18 the HDSR, the VCPS (mentioned
elsewhere15 19 ), and the UG.20 In the
HDSR,21 a Japanese screening test for dementia that
assesses verbal memory, scores range from 0 to 30. The VCPS is an
eye-tracking and vigilance task. Briefly, a computer displays 10
circles, each of which corresponds to 1 of 10 keys on the keyboard. At
random intervals any 1 circle abruptly changes to a star for several
seconds. If a subject can correctly tap the corresponding key in time,
the duration of the star's appearance (appearance time) is
progressively shortened. If the tap is delayed or wrong, the next
appearance time of star becomes one step longer. A test session
consists of 40 trials. The accumulated shortening of each appearance
time of 100 arbitrary units was regarded as the VCPS. The mean±SD
score of the 68 normal Japanese elderly (mean age, 70 years) was
2261±194, while that of 25 dementia patients (mean age, 68 years) was
1090±860.22 This test measures attention, nonverbal
visuospatial orientation, and reaction time, with a high score
indicating better visuospatial performance. The UG is reliable
and valid scale assessing balance, gait speed, and postural
impairment.20 The subject is observed and timed while he
or she rises from an armchair, walks 3 meters, turns, walks back, and
sits down again. The mean±SD time of the 68 normal Japanese elderly
individuals (mean age, 70 years) was 12.5±2.8 seconds. We also
evaluated eight ADL (walking, ascending stairs, feeding, dressing,
toileting, bathing, grooming, and taking medicine) and rated them from
3 to 0 (score of 3=completely independent, 2=needs some help, 1=needs
much help, and 0=completely dependent).12 ADL was
self-reported 1 month before the examination and confirmed by a
physician when the subject was examined. The items were added to
provide scores ranging from 0 to 24, with low scores indicating
disability.
Brain MRI
MRI of the brain was conducted using a superconducting magnet
with a main field strength of 0.5 T (G-50, Hitachi) on 15 subjects with
PH, 15 with postural hypertension, and 30 with postural normotension.
The brain was imaged in the axial plane in 10-mm-thick slices.
T1-weighted images were obtained using a short spin-echo pause sequence
with a repetition time of 600 ms and an echo time of 20 ms. Proton
density and T2-weighted images were obtained using a long spin-echo
pulse sequence with a repetition time of 2000 ms and echo times of 60
and 120 ms, respectively. Lacunes were defined as low-signal-intensity
areas (3 mm
diameter
10 mm) on T1-weighted images that
were visible as hyperintense areas on T2-weighted images. Hyperintense
punctate lesions on T2-weighted images were not counted as lacunes if
they were not visible as low-intensity areas on T1-weighted images.
Proton density images were evaluated for the extent of patchy or
diffuse PVHs. The lesions were classified into four grades, as
previously described.15 23 24 Specifically, grade 1 was
defined as no white matter lesions, except for small triangular foci
surrounding the frontal horns. Grade 2 was defined as caps in both
anterior and posterior horns of the lateral ventricles or additional
discrete patchy subcortical white matter lesions adjacent to or above
the lateral ventricles. More extensive punctate
periventricular white matter lesions and their early
confluent stages were classified as grade 3. Marked areas of high
signal intensity that reached confluence completely surrounding the
lateral ventricles were defined as grade 4. The numbers of subjects
with grade 1 or 2 and grade 3 or 4 in the postural hypotensive,
hypertensive, and normotensive groups were compared. One author, a
neurologist who was blinded to the clinical status of the subjects
interpreted all MRI scans.
Statistical Analysis
Data are reported as mean±SD. ANOVA was used for 3-group
comparison, and Fisher's PLSD was used for between-group comparison.
2 tests were used to compare proportions of selected
variables among the groups of individuals with postural
hypotension, hypertension, or normotension. Student's t
tests were used to compare scores of neurobehavioral function tests
between postural normotension and postural dysregulation group. A
probability value of .05 was considered statistically significant.
| Results |
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20 mm Hg, and 29 subjects (8.7%) exhibited postural
hypertension, defined as a postural elevation in SBP of
20
mm Hg. The other 285 subjects had postural normotension, defined as a
postural change in SBP from -20 to 20 mm Hg. Only 2 subjects
with postural hypotension, 1 with postural hypertension, and 2 with
postural normotension complained of mild dizziness developed while
standing. Table 1
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| Discussion |
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20 mm Hg, called "postural hypertension" in our study.
Although "orthostatic hypertension" was reported in
several case studies, the definition of orthostatic
hypertension remains to be established. Sapru et al10
defined orthostatic hypertension as marked hypertension at
upright position with normal pressures at supine position. Streeten et
al11 also defined orthostatic hypertension as
an increase in diastolic BP from below 90 to above 90
mm Hg after standing. In proportion to the definition of PH, we
defined postural hypertension as an elevation of SBP
20 mm Hg
at 1 to 2 minutes after standing. It may be noteworthy that there were
not only 20 subjects (6.0%) with PH but also 29 (8.7%) with postural
hypertension in our older elderly population. Of particular note in our study is that our detailed and quantitative neurobehavioral function tests revealed significantly poorer neurobehavioral functioning not only in subjects with PH but also in those with postural hypertension compared with those functions in subjects with postural normotension. Scores in function tests in the postural dysregulation (postural hypotension and hypertension) group were significantly worse than those in the postural normotension group. This finding was independent of the effect of age, mean education, antihypertensive or other medications, or diabetes mellitus in our elderly population.
The association between postural dysregulation and poorer neurobehavioral functioning may have two possible explanations. The first is that postural dysregulation in SBP may be an indicator of "functional aging" as opposed to chronological age. More advanced functional aging of cerebral cortex resulted in worsening neurobehavioral function, and brain stem dysfunction resulted in changes altered BP regulatory mechanisms that led to poor maintenance of BP at upright posture and in exaggerated BP fluctuation. The second explanation is that long-standing, excessively altered changes in BP in the elderly may impair cerebral perfusion and bring changes, such as lacunes or leukoaraiosis, that cause neurobehavioral decline. The combined association of postural dysregulation in SBP, neurobehavioral function, and silent lesions on MRI in our study seems to support the latter hypothesis. Although PH associated with cerebral ischemia is controversial,26 a few authors have reported primary orthostatic cerebral ischemia27 or cerebral ischemic attacks caused by postprandial hypotension.28 Recently, quantitative neurobehavioral function tests detected latent minor impairment of neurobehavioral functions in otherwise healthy older persons.14 29 Recent studies,29 30 31 including ours,15 have also revealed that leukoaraiosis in the apparently healthy elderly is associated with poorer scoring in neurobehavioral functions. In addition, there are several studies that report a significant association between leukoaraiosis and BP variation. Tohgi et al32 reported the importance of short-term variations in BP for the pathogenesis of Binswanger- and lacunar-type dementias in patients receiving antihypertensive medication. Ginanneschi et al33 also reported the association between BP fluctuation and the pathogenesis of leukoaraiosis, and Raiha et al34 reported the hemodynamic significance for the genesis of leukoaraiosis. Because reproducibility of PH is reported to be low even in symptomatic elderly individuals whose autonomic function is apparently normal,7 exaggerated postural change in SBP may be not always reproducible but sometimes latent. However, these potential BP dysregulatory mechanisms may be associated with latent neurobehavioral dysfunction as well as silent cerebrovascular disease. Further investigation is needed to determine whether these subjects with BP dysregulation and neurobehavioral dysfunction had unexplored risk factors, such as silent cerebrovascular occlusions.
In conclusion, asymptomatic subjects with postural hypotension as well as those with postural hypertension showed poorer scoring on neurobehavioral functions and more advanced leukoaraiosis than subjects without exaggerated postural changes in SBP in a sample of the community-dwelling elderly. A prospective study is needed to determine the prognostic significance of these findings.
| Selected Abbreviations and Acronyms |
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| Acknowledgments |
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Received April 18, 1997; revision received July 8, 1997; accepted July 8, 1997.
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